# AmericanPeptide.com — Full Peptide Catalog > 49 research peptides with PubChem-enriched chemistry, mechanisms, research areas, and FAQs. License: CC BY 4.0, attribution: AmericanPeptide.com. Curated index: https://www.americanpeptide.com/llms.txt · JSON API: https://www.americanpeptide.com/api/catalog · Docs: https://www.americanpeptide.com/developers # Semaglutide > Long-acting GLP-1 receptor agonist for glycemic control and weight management. - Also known as: Ozempic, Wegovy, Rybelsus - Class: Metabolic - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/semaglutide ## Overview Semaglutide is a 31-amino-acid GLP-1 receptor agonist engineered for once-weekly dosing via fatty-acid acylation and amino-acid substitutions that resist DPP-4 degradation. Approved by the FDA for type 2 diabetes (2017) and chronic weight management (2021). Semaglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist built on the backbone of human GLP-1. Two engineering changes define it: a C18 fatty-diacid chain attached through a linker that promotes reversible binding to albumin, and amino-acid substitutions that resist degradation by the enzyme DPP-4. Together these extend its half-life to roughly a week, enabling once-weekly administration. It reached the market first for type 2 diabetes (Ozempic, 2017; oral Rybelsus, 2019) and then for chronic weight management (Wegovy, 2021). Large cardiovascular-outcome and weight-management trials have made it one of the most studied metabolic peptides of the past decade, and its template — acylation plus DPP-4 resistance — now informs the broader incretin class. ## Mechanism GLP-1 receptor agonism → glucose-dependent insulin secretion, slowed gastric emptying, central appetite suppression. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C187H291N45O59 | | Molecular weight | 4113.6 Da | | CAS number | 910463-68-2 | | PubChem CID | [56843331](https://pubchem.ncbi.nlm.nih.gov/compound/56843331) | ## Research areas Studied in: Type 2 diabetes, Obesity, MASH, Cardiovascular risk reduction. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. ## Key research - Glycemic control — studied for glucose-dependent insulin secretion and glucagon suppression in type 2 diabetes. - Weight management — chronic-weight-management trials reported substantial mean body-weight reduction versus placebo. - Cardiovascular outcomes — investigated for reduction of major adverse cardiovascular events in at-risk populations. - MASH / hepatic fat — examined as an endpoint in metabolic liver-disease research. - Half-life engineering — fatty-acid acylation and DPP-4-resistant substitutions are the basis of its once-weekly profile. ## Storage, handling & synthesis **Storage.** Lyophilized: store frozen and protected from light; stable for extended periods. Reconstituted: refrigerate at 2–8 °C and use within weeks, not months. **Handling.** Reconstitute gently — swirl rather than shake, since agitation can shear the peptide. Protect from heat and minimize freeze–thaw cycles. **Synthesis.** Beyond its 31-residue chain, semaglutide carries a fatty-diacid side chain on a linker — extra synthetic steps that each add cost and another opportunity for impurities to form. Genuine material is purified to a defined spec and documented on a certificate of analysis, never judged by appearance. ## FAQs ### What is semaglutide? Semaglutide is a long-acting GLP-1 receptor agonist approved for type 2 diabetes and chronic weight management. It is marketed as Ozempic, Wegovy, and Rybelsus. ### How does semaglutide promote weight loss? In studies it slows gastric emptying and acts on appetite centers in the brain while enhancing glucose-dependent insulin release, which together reduce caloric intake. ### Why is it dosed once weekly? Fatty-acid acylation promotes reversible binding to albumin and amino-acid substitutions resist DPP-4 breakdown, extending its half-life to about a week. ### What is the difference between Ozempic, Wegovy, and Rybelsus? All three are semaglutide. Ozempic and oral Rybelsus are approved for type 2 diabetes; Wegovy is approved for chronic weight management. This page is a research reference, not medical advice. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/semaglutide Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Tirzepatide > Dual GIP / GLP-1 receptor agonist with industry-leading weight-loss endpoints. - Also known as: Mounjaro, Zepbound - Class: Metabolic - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/tirzepatide ## Overview Tirzepatide is a 39-amino-acid synthetic peptide acting as a dual agonist at GIP and GLP-1 receptors. Approved by the FDA for type 2 diabetes (2022) and chronic weight management (2023). Tirzepatide is a synthetic 39-amino-acid peptide that activates two incretin receptors at once — GIP (glucose-dependent insulinotropic polypeptide) and GLP-1. It carries a fatty-acid chain for albumin binding and once-weekly dosing, and is sometimes described as a "twincretin" for its dual mechanism. Developed by Eli Lilly, it was approved for type 2 diabetes (Mounjaro, 2022) and chronic weight management (Zepbound, 2023). In placebo-controlled and head-to-head trials it produced some of the largest weight reductions reported for a pharmacologic agent, which has driven intense research interest in multi-receptor incretin design. ## Mechanism Co-activation of GIP + GLP-1 receptors; complementary insulinotropic and satiety effects. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C225H348N48O68 | | Molecular weight | 4813.5 Da | | CAS number | 2023788-19-2 | | PubChem CID | [166567236](https://pubchem.ncbi.nlm.nih.gov/compound/166567236) | ## Research areas Studied in: Type 2 diabetes, Obesity, Obstructive sleep apnea. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. - [Sleep & Circadian Rhythm](https://www.americanpeptide.com/research-areas/sleep-circadian): Peptides studied for sleep architecture and circadian regulation. ## Key research - Glycemic control — dual GIP/GLP-1 activation studied for insulin secretion and HbA1c reduction. - Weight management — trials reported weight reductions exceeding those of single GLP-1 agonists. - Obstructive sleep apnea — investigated as an endpoint in people with obesity. - Cardiometabolic markers — examined for effects on lipids, blood pressure, and hepatic fat. - Dual-agonism rationale — GIP is studied as complementary to GLP-1 for insulinotropic and satiety effects. ## Storage, handling & synthesis **Storage.** Lyophilized: keep frozen and shielded from light. Reconstituted: store at 2–8 °C and use within weeks. **Handling.** Swirl to dissolve rather than shaking; keep away from heat and minimize repeated freeze–thaw. **Synthesis.** At 39 residues with a fatty-acid chain and a dual-receptor design, tirzepatide is a long, demanding synthesis — more coupling cycles mean more deletion and truncation impurities for purification to remove. Its length is exactly why a credible purity figure and an actual chromatogram matter here. ## FAQs ### What is tirzepatide? Tirzepatide is a dual GIP/GLP-1 receptor agonist approved for type 2 diabetes (Mounjaro) and chronic weight management (Zepbound). ### How is tirzepatide different from semaglutide? Semaglutide activates the GLP-1 receptor alone; tirzepatide activates both GIP and GLP-1 receptors, a dual mechanism studied for greater metabolic effect. ### What does "twincretin" mean? It is an informal term for a peptide that engages two incretin pathways — here GIP and GLP-1 — within a single molecule. ### Is tirzepatide FDA approved? Yes, for type 2 diabetes and chronic weight management under the brand names Mounjaro and Zepbound. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/tirzepatide Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Retatrutide > Investigational triple agonist (GIP / GLP-1 / glucagon) in late-stage trials. - Also known as: LY3437943 - Class: Metabolic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/retatrutide ## Overview Retatrutide is an Eli Lilly–developed triple agonist targeting GIP, GLP-1, and glucagon receptors. Phase 2 trials reported ~24% mean weight reduction at 48 weeks at the highest dose. Retatrutide (development code LY3437943) is an investigational single peptide that activates three receptors — GIP, GLP-1, and glucagon. Adding glucagon-receptor agonism to the incretin pair is studied as a way to increase energy expenditure and lipolysis on top of the insulinotropic and satiety effects of GIP and GLP-1. Developed by Eli Lilly, it remains investigational and has not been approved. Phase 2 results reported notably large mean weight reductions at the highest doses over roughly a year, placing it among the most closely watched "triple agonist" candidates in late-stage metabolic research. ## Mechanism GIP + GLP-1 (insulinotropic, satiety) plus glucagon (energy expenditure, lipolysis). ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C221H342N46O68 | | Molecular weight | 4731.5 Da | | PubChem CID | [171390338](https://pubchem.ncbi.nlm.nih.gov/compound/171390338) | ## Research areas Studied in: Obesity, Type 2 diabetes, MASH. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. ## Key research - Triple agonism — combines GIP/GLP-1 (insulin, satiety) with glucagon (energy expenditure, lipolysis). - Weight reduction — Phase 2 trials reported among the largest mean reductions seen for an investigational agent. - Type 2 diabetes — studied for glycemic endpoints alongside weight. - MASH / hepatic fat — examined as a metabolic-liver-disease endpoint. - Investigational status — not approved; under continued clinical evaluation. ## FAQs ### What is retatrutide? Retatrutide is an investigational triple agonist targeting the GIP, GLP-1, and glucagon receptors, studied in late-stage trials for obesity and type 2 diabetes. ### How does a triple agonist differ from dual or single agonists? It adds glucagon-receptor activation — studied for increased energy expenditure and fat breakdown — to the insulinotropic and satiety effects of GIP and GLP-1. ### Is retatrutide approved? No. It is investigational and has not received FDA approval; all data comes from clinical research. ### Who develops retatrutide? Eli Lilly. This page is a research and educational reference, not medical advice or an offer for sale. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/retatrutide Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Cagrilintide > Long-acting amylin analog studied alongside semaglutide as CagriSema. - Class: Metabolic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/cagrilintide ## Overview Cagrilintide is a 37-amino-acid acylated amylin analog with affinity at all five amylin receptor subtypes. Investigated by Novo Nordisk both as monotherapy and in combination with semaglutide (CagriSema). Cagrilintide is a long-acting, acylated analog of amylin — the pancreatic hormone co-secreted with insulin that signals satiety and slows gastric emptying. It binds across the amylin and calcitonin receptor subtypes and carries a fatty-acid chain that supports once-weekly dosing. Developed by Novo Nordisk, it is investigational and studied both on its own and in a fixed combination with semaglutide known as CagriSema, where the amylin and GLP-1 pathways are paired for additive weight effect. ## Mechanism Amylin and calcitonin receptor agonism → satiety, slowed gastric emptying. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C194H312N54O59S2 | | Molecular weight | 4409.2 Da | | CAS number | 1415456-99-3 | | PubChem CID | [171397054](https://pubchem.ncbi.nlm.nih.gov/compound/171397054) | ## Research areas Studied in: Obesity, Combination metabolic therapy. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. ## Key research - Satiety signaling — amylin-receptor agonism studied for appetite suppression and slowed gastric emptying. - Combination therapy — investigated with semaglutide (CagriSema) for additive weight reduction. - Obesity endpoints — Phase 2 trials reported meaningful mean weight loss alone and in combination. - Half-life engineering — acylation supports a once-weekly profile. - Investigational status — not FDA-approved. ## FAQs ### What is cagrilintide? Cagrilintide is an investigational long-acting amylin analog studied for weight management, both alone and combined with semaglutide (CagriSema). ### What is CagriSema? CagriSema is the investigational fixed combination of cagrilintide (amylin) and semaglutide (GLP-1), pairing two appetite pathways for additive effect. ### How does amylin differ from GLP-1? Both promote satiety, but amylin acts through amylin and calcitonin receptors while GLP-1 acts through the GLP-1 receptor; combining them is studied for complementary effects. ### Is cagrilintide approved? No — it is investigational. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/cagrilintide Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Insulin (human) > The archetypal protein biologic — a 51-amino-acid two-chain hormone, disulfide-linked, and the first recombinant DNA drug ever marketed. - Also known as: Recombinant human insulin, rhInsulin, regular insulin, Humulin, Novolin - Class: Metabolic - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/insulin ## Overview Insulin is the hormone that defined the biologic era. It is a small but genuinely complex protein: two peptide chains — an A chain of 21 residues and a B chain of 30 — held together by two interchain disulfide bonds, with a third disulfide looping within the A chain. At ~5.8 kDa it is the smallest hormone in this catalog’s biologic tier, yet it is assembled, folded, and processed exactly like the larger proteins, and it was the molecule that proved recombinant human therapeutics were possible. Insulin is synthesized in the body as a single chain — preproinsulin → proinsulin — that folds and forms its disulfide bonds before a connecting C-peptide is excised, leaving the mature two-chain hormone. That biosynthetic detail is why early recombinant manufacturing expressed the A and B chains (or proinsulin) in bacteria and then handled folding and disulfide pairing as a controlled step: the chemistry that the body does enzymatically has to be reproduced and verified in a reactor. Get the disulfides wrong and you get a misfolded, inactive — or immunogenic — product. Its history is foundational twice over. Insulin was discovered in 1921 in Toronto by Banting, Best, Macleod, and Collip, and the patent was famously sold to the university for one dollar on the principle that "insulin belongs to the world." Six decades later, in 1982, recombinant human insulin (Humulin) became the first recombinant-DNA drug ever approved — the proof of concept for the entire modern biologic industry, including most of the engineered peptides elsewhere in this catalog. And then the American drama. Despite the dollar patent and a century of manufacturing experience, US insulin list prices roughly tripled between 2002 and 2013, pushing some patients to ration a drug they cannot live without — a recurring, deadly access failure that sits uncomfortably against the molecule’s origin story. For a reference that takes provenance and honest pricing seriously, insulin is the clearest case study in the gap between what a medicine costs to make and what it is sold for. Insulin is also widely misunderstood at the edges: it is occasionally misused in bodybuilding for its anabolic effects, where dosing errors cause life-threatening hypoglycemia, and the modern GLP-1 era has shifted public perception of what "diabetes medicine" even means. It remains, first and foremost, essential replacement therapy for type 1 diabetes and an important tool in advanced type 2. ## Mechanism Binds the insulin receptor, a tyrosine kinase, triggering autophosphorylation and the PI3K/AKT cascade that drives GLUT4 translocation and glucose uptake into muscle and fat, suppresses hepatic glucose output, and promotes glycogen, lipid, and protein synthesis. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C257H383N65O77S6 | | Molecular weight | 5808 Da | | CAS number | 11061-68-0 | ## Sequence ``` A chain: GIVEQCCTSICSLYQLENYCN | B chain: FVNQHLCGSHLVEALYLVCGERGFFYTPKT ``` ## Research areas Studied in: Type 1 diabetes, Type 2 diabetes, Glucose metabolism, Anabolic signaling. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. ## Key research - Type 1 diabetes — life-sustaining replacement therapy; the body produces no insulin without it. - Type 2 diabetes — used when oral agents and incretins no longer maintain glycemic control. - Insulin-receptor signaling — the PI3K/AKT and MAPK pathways that make it a central anabolic and metabolic hormone. - Analog engineering — rapid-acting (lispro, aspart) and long-acting (glargine, detemir) analogs re-engineer the sequence/formulation to reshape the absorption curve. - First recombinant drug — Humulin (1982) established recombinant human protein manufacturing. - Hypoglycemia risk — narrow therapeutic margin; misuse outside medical supervision is dangerous. ## Storage, handling & synthesis **Storage.** Unopened insulin is refrigerated (2–8 °C); in-use vials/pens are typically kept at room temperature for a limited number of days per the product label. It must not be frozen — freezing denatures the protein and destroys activity — and should be protected from heat and direct light. **Handling.** As a folded protein it is sensitive to heat, freezing, and agitation, which can cause aggregation (visible as clumping or frosting) and loss of potency. Aggregated insulin should never be used. **Synthesis.** Recombinant human insulin is expressed in E. coli or yeast — historically as separate A and B chains or as proinsulin — then folded, disulfide-paired, and (for the proinsulin route) enzymatically processed to remove C-peptide. Release testing is protein-specific: identity by peptide mapping and mass spectrometry, correct disulfide connectivity, potency by bioassay, plus host-cell-protein and endotoxin limits. This is biologic manufacturing, not peptide synthesis. ## FAQs ### What is human insulin? A 51-amino-acid protein hormone made of two disulfide-linked chains that lowers blood glucose by driving its uptake into cells. Recombinant human insulin is produced in engineered bacteria or yeast and was the first recombinant-DNA drug approved (1982). ### Why is insulin considered a biologic and not just a peptide? It is a folded, multi-chain protein whose activity depends on correct disulfide pairing, and it is produced in living cells. Its manufacturing and quality control are protein-grade, not the solid-phase synthesis used for short research peptides. ### Why is insulin so expensive in the US if the patent was sold for a dollar? The original patent was sold for $1, but modern insulin products, manufacturing, and the US pricing system are separate from that history. List prices rose sharply in the 2000s–2010s, a widely documented access problem. ### Is this medical advice? No. This is a research and educational reference. Insulin has a narrow safety margin and is a prescription medicine; nothing here is dosing guidance. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/insulin Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Glucagon > Insulin’s counter-hormone — a 29-amino-acid peptide that raises blood glucose, the emergency rescue for severe lows, and the "G" in the new triple agonists. - Also known as: GlucaGen, Baqsimi, Gvoke - Class: Metabolic - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/glucagon ## Overview Glucagon is the metabolic mirror image of insulin. Released by the pancreatic alpha cells when blood sugar falls, this 29-amino-acid peptide tells the liver to break down glycogen and make new glucose, pushing blood sugar back up. It is the body’s primary defense against hypoglycemia, the basis of emergency rescue products, and — in a development that has put it back at the center of metabolic drug design — one of the three receptors the newest weight-loss agonists deliberately engage. Glucagon and insulin are a push-pull pair: insulin lowers blood glucose, glucagon raises it, and health depends on their balance. When blood sugar drops dangerously — most often in insulin-treated diabetes — glucagon is the rescue, which is why it is sold as emergency kits: the classic reconstituted injection (GlucaGen), a nasal powder (Baqsimi, 2019), and a ready-to-use autoinjector (Gvoke). It is also used in radiology and endoscopy to relax smooth muscle. As a molecule it is a 29-residue peptide derived from the same precursor (preproglucagon) that gives rise to GLP-1 and GLP-2 — a family relationship that matters more than it first appears. For decades glucagon was framed only as the hormone you suppress in diabetes. The reframing came from drug design: adding glucagon-receptor agonism to incretin drugs increases energy expenditure and fat mobilization, and the glucagon receptor is the "G" in the GIP/GLP-1/glucagon triple agonists (such as retatrutide) now posting the largest weight-loss numbers in trials. That is the forward-looking turn — the same hormone that, unopposed, worsens diabetic hyperglycemia becomes, when balanced against incretin signaling, a lever for greater fat loss and metabolic rate. It is a clean example of how a "bad" hormone in one context is a deliberate design ingredient in another. ## Mechanism Binds the glucagon receptor on hepatocytes, raising cAMP and driving glycogenolysis and gluconeogenesis to increase blood glucose. It opposes insulin in the moment-to-moment regulation of blood sugar. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C153H225N43O49S | | Molecular weight | 3485 Da | | CAS number | 16941-32-5 | ## Sequence ``` HSQGTFTSDYSKYLDSRRAQDFVQWLMNT ``` ## Research areas Studied in: Severe hypoglycemia, Glucose counter-regulation, Triple-agonist metabolic drugs. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. ## Key research - Severe hypoglycemia rescue — the approved use; raises blood glucose fast via hepatic glycogenolysis. - Insulin counter-regulation — the opposing arm of moment-to-moment glucose control. - Triple-agonist drugs — glucagon-receptor agonism is the "G" in GIP/GLP-1/glucagon agonists studied for large weight loss. - Procedural use — relaxes GI smooth muscle for imaging and endoscopy. - Preproglucagon family — shares a precursor with GLP-1 and GLP-2. ## Storage, handling & synthesis **Storage.** Older glucagon kits are stored as lyophilized powder + diluent and reconstituted immediately before use; ready-to-use and nasal products follow their own label storage. The peptide is unstable in solution and is not kept reconstituted. **Handling.** Reconstituted glucagon should be used promptly — it can aggregate/fibrillate in solution. Emergency products are designed for immediate single use. **Synthesis.** Glucagon is a 29-residue peptide produced by chemical synthesis or recombinant expression. It is prone to aggregation and fibrillation in aqueous solution, which is why traditional products are lyophilized and reconstituted at the point of use, and why newer formulations engineered for ready-to-use stability were a meaningful advance. ## FAQs ### What does glucagon do? Glucagon raises blood sugar — it is the counter-hormone to insulin. The pancreas releases it when glucose falls, signaling the liver to release stored glucose. As a drug it is the emergency rescue for severe hypoglycemia. ### Why is glucagon in weight-loss drugs? Glucagon-receptor agonism increases energy expenditure and fat mobilization. It is the "G" in the GIP/GLP-1/glucagon triple agonists (like retatrutide) that show the largest weight-loss effects in trials. ### How is it related to GLP-1? Both come from the same precursor protein, preproglucagon. Glucagon raises blood sugar; GLP-1 lowers it and curbs appetite — different products of one parent molecule. ### Is this medical advice? No — this is a research and educational reference, not dosing guidance. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/glucagon Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # BPC-157 > Synthetic gastric pentadecapeptide investigated for tendon, ligament, and GI repair. - Also known as: Body Protective Compound 157, PL 14736 - Class: Healing & Repair - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/bpc-157 ## Overview BPC-157 is a 15-amino-acid sequence derived from a protective protein found in human gastric juice. Preclinical work suggests pro-angiogenic and cytoprotective activity across tendon, ligament, muscle, and GI tissue. BPC-157 (Body Protective Compound-157) is a synthetic 15-amino-acid sequence derived from a protective protein identified in human gastric juice. It is studied as a cytoprotective and pro-angiogenic agent, with most of the interest centered on connective-tissue and gastrointestinal repair. Essentially all of the evidence is preclinical — cell cultures and rodent models — and BPC-157 is not approved by the FDA for any use. It is widely discussed in the tissue-repair literature but lacks the controlled human trials that characterize approved peptides, so model choice and endpoint definition are central caveats. ## Mechanism Activates the VEGFR2–Akt–eNOS pathway (with upstream Src / Caveolin-1 signaling), driving nitric-oxide–dependent angiogenesis; also modulates growth-factor signaling and the gut–brain axis. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C62H98N16O22 | | Molecular weight | 1419.5 Da | | PubChem CID | [9941957](https://pubchem.ncbi.nlm.nih.gov/compound/9941957) | ## Sequence ``` GEPPPGKPADDAGLV ``` ## Research areas Studied in: Tendinopathy, Wound healing, IBD models. Guides on this site: - [Wound Healing & Tissue Repair](https://www.americanpeptide.com/research-areas/wound-healing): Regenerative peptides studied for soft-tissue, tendon, and vascular repair. - [Immune & Inflammation](https://www.americanpeptide.com/research-areas/immune-inflammation): Thymic and host-defense peptides studied for immune modulation. ## Key research - Angiogenesis mechanism — repair effects are attributed largely to activation of the VEGFR2–Akt–eNOS pathway (with upstream Src / Caveolin-1 signaling), increasing nitric-oxide–dependent new-vessel formation in hypovascular tissue such as tendon. - Nitric-oxide modulation — the Sikiric research group first linked the gastric-protective effect to NO generation; subsequent L-NAME / L-arginine co-treatment studies support NO involvement across multiple tissue-injury models. - Tendon, ligament & GI repair — the most-replicated preclinical domains, spanning musculoskeletal injury and ulcer / inflammatory-bowel models. - Compared to TB-500 — both are studied as healing peptides but differ mechanistically: BPC-157 is perfusion-led (angiogenesis / NO) while TB-500 is migration-led (actin regulation), which is why the two are often examined together. - Evidence quality — extensive rodent data (much of it from a single research group) but no controlled human trials; not FDA-approved. ## Storage, handling & synthesis **Storage.** Lyophilized: store frozen and protected from light for long-term stability. Reconstituted: refrigerate at 2–8 °C and use within weeks. **Handling.** Reconstitute gently and avoid shaking; protect from heat, light, and repeated freeze–thaw. **Synthesis.** At 15 residues BPC-157 is a comparatively short synthesis, which makes it cheap to produce — and cheap to fake. The short, low-cost sequence is exactly why the market is flooded with under-characterized material; a batch-specific certificate of analysis is the only way to tell real from filler. ## FAQs ### What is BPC-157? BPC-157 is a synthetic 15-amino-acid peptide derived from a protein in gastric juice, studied in preclinical models for tissue repair and cytoprotection. ### What is BPC-157 studied for? Research contexts include tendon, ligament, and muscle repair, gastrointestinal protection, and angiogenesis — almost entirely in cell and animal models. ### Is BPC-157 FDA approved? No. BPC-157 is not approved for any medical use and the evidence base is preclinical. This page is a research and educational reference only. ### What is the proposed mechanism? Studies point to upregulation of the VEGFR2 receptor and modulation of nitric-oxide and growth-factor pathways, though the mechanism is not fully established. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/bpc-157 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # TB-500 > Synthetic fragment of thymosin β4 studied for cell migration and tissue repair. - Also known as: Thymosin Beta-4 fragment - Class: Healing & Repair - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/tb-500 ## Overview TB-500 corresponds to the active actin-binding region of thymosin β4. Preclinical studies report effects on endothelial cell migration, angiogenesis, and wound healing. TB-500 is a synthetic peptide corresponding to the actin-binding region of thymosin β4, a naturally occurring protein involved in cell migration and tissue repair. By sequestering G-actin, thymosin β4 influences cytoskeletal dynamics, and TB-500 is studied as a fragment that reproduces part of this activity. As with BPC-157, the evidence for TB-500 is largely preclinical and it is not FDA-approved; it is also a prohibited substance in regulated sport. Research interest centers on endothelial cell migration, angiogenesis, and wound healing, with cardiac and dermal repair among the contexts studied. ## Mechanism G-actin sequestration; modulation of cell migration and angiogenesis. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C38H68N10O14 | | Molecular weight | 889 Da | | PubChem CID | [62707662](https://pubchem.ncbi.nlm.nih.gov/compound/62707662) | ## Sequence ``` LKKTETQ ``` ## Research areas Studied in: Wound healing, Cardiac repair models, Hair growth. Guides on this site: - [Wound Healing & Tissue Repair](https://www.americanpeptide.com/research-areas/wound-healing): Regenerative peptides studied for soft-tissue, tendon, and vascular repair. - [Skin & Hair](https://www.americanpeptide.com/research-areas/skin-hair): Peptides studied for skin aging, pigmentation, and hair follicle biology. ## Key research - Actin regulation — corresponds to the actin-binding motif of thymosin β4; promotes G-actin sequestration and the polymerization / depolymerization cycle that mobilizes cells to injury sites. - Angiogenesis & re-epithelialization — thymosin β4 research reports accelerated wound closure in rodent full-thickness models, with increased collagen deposition and new-vessel growth. - Cardiac & dermal repair — investigated in myocardial-injury and dermal wound models, and explored in hair-follicle biology. - Compared to BPC-157 — complementary mechanism: TB-500 is migration-led (actin / cell mobilization) while BPC-157 is perfusion-led (angiogenesis / NO). - Evidence quality — much of the data derives from thymosin β4 rather than the TB-500 fragment specifically; preclinical, not FDA-approved, and prohibited by WADA. ## Storage, handling & synthesis **Storage.** Lyophilized: store frozen and protected from light for long-term stability. Reconstituted: refrigerate at 2–8 °C and use within weeks. **Handling.** Reconstitute gently and avoid shaking; protect from heat, light, and repeated freeze–thaw. ## FAQs ### What is TB-500? TB-500 is a synthetic peptide based on the actin-binding region of thymosin β4, studied in preclinical models for cell migration and tissue repair. ### How is TB-500 related to thymosin β4? TB-500 corresponds to the active actin-binding fragment of the larger thymosin β4 protein, reproducing part of its cytoskeletal activity. ### Is TB-500 approved or allowed in sport? No — it is not FDA-approved and is prohibited by the World Anti-Doping Agency. This page is a research and educational reference. ### What is TB-500 studied for? Research contexts include wound healing, angiogenesis, cardiac repair, and hair-follicle biology, primarily in animal and cell models. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/tb-500 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # GHK-Cu > Endogenous copper-binding tripeptide widely studied in skin and hair biology. - Also known as: Copper Peptide, Tripeptide-1 Copper, Copper Tripeptide-1 - Class: Cosmetic, Healing & Repair - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/ghk-cu ## Overview GHK-Cu is the copper complex of the tripeptide glycyl-L-histidyl-L-lysine, an endogenous fragment first isolated from human plasma. Reported to modulate ECM remodeling, fibroblast activity, and antioxidant defense. GHK-Cu is the copper(II) complex of glycyl-L-histidyl-L-lysine (GHK), a tripeptide first isolated from human plasma in 1973. The free GHK sequence binds copper with high affinity, and the resulting complex is generally regarded as the biologically active species. Plasma GHK is highest in early adulthood and declines with age, which has motivated long-standing interest in its role in tissue maintenance and repair. Because copper is a cofactor for enzymes involved in extracellular-matrix (ECM) remodeling and antioxidant defense, much of the research framing treats GHK-Cu as a signaling and copper-delivery molecule rather than a simple nutrient source. It is one of the most extensively studied "copper peptides" in the dermatologic and wound-healing literature and is widely used as a topical cosmetic ingredient under the INCI name Copper Tripeptide-1. ## Mechanism Copper delivery, ECM gene modulation, antioxidant pathway activation. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C14H22CuN6O4 | | Molecular weight | 401.9 Da | | CAS number | 49557-75-7 | | PubChem CID | [139035031](https://pubchem.ncbi.nlm.nih.gov/compound/139035031) | ## Sequence ``` GHK ``` ## Research areas Studied in: Skin aging, Hair follicle biology, Wound healing. Guides on this site: - [Wound Healing & Tissue Repair](https://www.americanpeptide.com/research-areas/wound-healing): Regenerative peptides studied for soft-tissue, tendon, and vascular repair. - [Skin & Hair](https://www.americanpeptide.com/research-areas/skin-hair): Peptides studied for skin aging, pigmentation, and hair follicle biology. ## Key research - Extracellular-matrix remodeling — studied for effects on collagen, elastin, glycosaminoglycan, and decorin synthesis in dermal fibroblast models. - Wound healing & angiogenesis — investigated for fibroblast activation and new-vessel formation in tissue-repair models. - Antioxidant & anti-inflammatory signaling — reported to modulate oxidative-stress and inflammatory pathways. - Hair-follicle biology — examined for effects on follicle size and the growth (anagen) phase. - Gene expression — a widely cited transcriptomic analysis (originating from Loren Pickart's work) reported GHK can shift the expression of a large set of human genes, often framed as a move toward a more youthful profile. - Compared to other copper / collagen peptides — GHK-Cu is the most-studied for skin remodeling; AHK-Cu is oriented toward the hair follicle, while Matrixyl (palmitoyl pentapeptide-4) stimulates collagen via matrikine signaling and contains no copper. ## Storage, handling & synthesis **Storage.** Lyophilized: store frozen and protected from light. Reconstituted: refrigerate at 2–8 °C and use within weeks; copper complexes are light- and oxidation-sensitive. **Handling.** Reconstitute gently; protect from light and air, since the copper(II) complex is prone to oxidation. The characteristic blue color indicates copper binding but is not a substitute for assay. ## FAQs ### What is GHK-Cu? GHK-Cu is the copper complex of the naturally occurring tripeptide glycyl-L-histidyl-L-lysine (GHK), first isolated from human plasma. The copper-bound form is considered the active species in most research. ### What is GHK-Cu studied for? Research focuses on skin remodeling (collagen and elastin), wound healing and angiogenesis, antioxidant and anti-inflammatory signaling, and hair-follicle biology. It is a reference compound in the "copper peptide" literature. ### Why does it contain copper? The GHK tripeptide binds copper(II) with high affinity, and copper is a cofactor for matrix-remodeling and antioxidant enzymes — so the complex is studied as both a signaling molecule and a copper-delivery vehicle. ### Is GHK-Cu the same as the copper peptides used in skincare? Yes — cosmetic "copper peptide" ingredients are typically GHK-Cu (INCI name Copper Tripeptide-1), applied topically. This page is a research and educational reference, not a product or usage recommendation. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/ghk-cu Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # AHK-Cu > Copper-binding tripeptide (Ala-His-Lys) studied for hair-follicle stimulation and dermal repair. - Also known as: Copper Tripeptide AHK, Ala-His-Lys Copper - Class: Cosmetic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/ahk-cu ## Overview AHK-Cu is the copper complex of the tripeptide alanyl-L-histidyl-L-lysine, structurally related to GHK-Cu but studied primarily in hair-follicle biology rather than facial-skin remodeling. AHK-Cu is the copper(II) complex of the tripeptide alanyl-L-histidyl-L-lysine (AHK). It shares the histidine–lysine copper-binding motif of the better-known GHK-Cu but differs at the first residue (alanine in place of glycine), and the research interest is oriented toward the hair follicle rather than facial skin. Like other copper peptides it is studied as both a copper-delivery vehicle and a signaling molecule. The evidence base is preclinical — cell and ex-vivo follicle models — and it is used as a cosmetic ingredient rather than an approved drug. ## Mechanism Copper delivery with VEGF upregulation and anti-apoptotic signaling in dermal papilla cells. ## Sequence ``` AHK ``` ## Research areas Studied in: Hair growth, Dermal repair. Guides on this site: - [Skin & Hair](https://www.americanpeptide.com/research-areas/skin-hair): Peptides studied for skin aging, pigmentation, and hair follicle biology. ## Key research - Dermal papilla cells — studied for stimulating proliferation and reducing apoptosis (raised Bcl-2/Bax ratio, lower cleaved caspase-3 / PARP) in DPCs (Pyo & Yoo et al., 2007). - Hair-follicle elongation — promotes elongation of human hair follicles ex vivo in preclinical work. - Angiogenesis — upregulates VEGF and stimulates dermal fibroblast proliferation while reducing TGF-β1 secretion. - Compared to GHK-Cu — the same copper-binding chemistry but oriented toward the follicle, where GHK-Cu is the reference compound for facial-skin remodeling. - Preclinical / cosmetic — not FDA-approved as a drug. ## Storage, handling & synthesis **Storage.** Lyophilized: store frozen and protected from light. Reconstituted: refrigerate at 2–8 °C and use within weeks; copper complexes are light- and oxidation-sensitive. **Handling.** Reconstitute gently; protect from light and air, since the copper(II) complex is prone to oxidation. ## FAQs ### What is AHK-Cu? AHK-Cu is the copper complex of the tripeptide alanyl-histidyl-lysine, a copper peptide studied primarily for hair-follicle stimulation and dermal repair. ### How does AHK-Cu differ from GHK-Cu? They share the same histidine–lysine copper-binding motif but differ at the first residue. GHK-Cu is the reference compound for facial-skin remodeling; AHK-Cu research is oriented toward the hair follicle. ### What is it studied for? Dermal-papilla-cell proliferation, hair-follicle elongation, and angiogenesis (VEGF) — mostly in cell and ex-vivo models. It is used as a cosmetic ingredient, not an approved drug. ### Is AHK-Cu FDA-approved? No. It is a research and cosmetic compound, not an approved drug. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/ahk-cu Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Matrixyl (Palmitoyl Pentapeptide-4) > Palmitoylated matrikine peptide that signals fibroblasts to synthesize collagen — contains no copper. - Also known as: Palmitoyl Pentapeptide-4, Pal-KTTKS, Matrixyl - Class: Cosmetic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/matrixyl ## Overview Matrixyl is palmitoyl pentapeptide-4 (Pal-KTTKS), a lipidated peptide whose KTTKS core is a fragment of type-I procollagen. Rather than delivering copper, it acts as a matrikine signal that stimulates extracellular-matrix synthesis. Matrixyl is the trade name for palmitoyl pentapeptide-4, a five-amino-acid sequence (KTTKS) joined to a palmitic-acid chain that improves skin penetration. The KTTKS sequence is a fragment naturally cleaved from the C-terminal propeptide of type-I procollagen during collagen assembly. The body uses that fragment as a feedback signal — a "matrikine" — telling fibroblasts to keep producing matrix. Matrixyl exploits this: it is studied not as a copper peptide but as a signaling molecule that drives collagen synthesis, and it is one of the better-evidenced cosmetic peptide ingredients. ## Mechanism Matrikine signaling — mimics a procollagen-I fragment to upregulate collagen and fibronectin synthesis. ## Chemistry | Property | Value | | --- | --- | | Molecular weight | 802 Da | | CAS number | 214047-00-4 | ## Sequence ``` KTTKS ``` ## Research areas Studied in: Skin aging, Collagen synthesis. Guides on this site: - [Skin & Hair](https://www.americanpeptide.com/research-areas/skin-hair): Peptides studied for skin aging, pigmentation, and hair follicle biology. ## Key research - Matrikine signaling — the KTTKS core mimics a procollagen-I breakdown fragment, signaling fibroblasts to upregulate collagen I, collagen IV, and fibronectin. - Clinical cosmetic data — a 12-week split-face randomized controlled trial (Robinson et al., 2005) reported improvements in wrinkle depth and skin roughness at low concentration. - Palmitoylation — the lipid chain improves penetration of the otherwise hydrophilic peptide through the stratum corneum. - Compared to copper peptides — unlike GHK-Cu or AHK-Cu, Matrixyl contains no copper and works purely by signaling, not metal delivery. - Cosmetic ingredient — topical use; not a drug. ## Storage, handling & synthesis **Storage.** Store the lyophilized peptide frozen and protected from light; in cosmetic formulation, follow the product’s stability guidance. **Handling.** Palmitoylation makes it amphiphilic — disperse carefully in formulation. Protect from heat and light. ## FAQs ### What is Matrixyl? Matrixyl is palmitoyl pentapeptide-4 (Pal-KTTKS), a lipidated peptide whose KTTKS core is a procollagen-I fragment that signals fibroblasts to produce collagen. It is a widely used cosmetic ingredient. ### Is Matrixyl a copper peptide? No. Unlike GHK-Cu and AHK-Cu, Matrixyl contains no copper. It works as a matrikine signal, not by delivering a metal. ### What is the evidence for Matrixyl? A 12-week split-face randomized controlled trial (Robinson et al., 2005) reported improvements in wrinkle depth and skin roughness, making it one of the better-evidenced cosmetic peptides. ### How does it work? Its KTTKS sequence mimics a collagen-breakdown fragment, signaling fibroblasts to upregulate collagen I, collagen IV, and fibronectin synthesis. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/matrixyl Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # EPO (Erythropoietin) > A glycoprotein hormone that drives red-blood-cell production — a recombinant biologic famous in medicine for treating anemia and infamous in sport for blood doping. - Also known as: Erythropoietin, Epoetin alfa, Epogen, Procrit, recombinant human erythropoietin, rhEPO - Class: Healing & Repair - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/epo ## Overview Erythropoietin is the hormone the kidneys release to tell the bone marrow to make more red blood cells. It is a 165-amino-acid glycoprotein, roughly 30–34 kDa once its sugar chains are counted, and like other glycoprotein hormones its carbohydrate is not optional — the glycosylation governs its stability and circulating half-life. Recombinant versions (epoetin alfa and its relatives) are produced in mammalian cells so that human-like glycosylation occurs, and beyond its core role in red-cell production it has a substantial research literature in tissue protection. EPO is a glycoprotein, and that places it firmly in the biologic tier of this catalog. Its 165-residue chain folds into a four-helix bundle (the same architectural family as growth hormone) and is decorated with three N-linked and one O-linked glycan. Those sugars are functionally decisive: more heavily glycosylated, engineered versions (such as darbepoetin) circulate far longer. This is why EPO is made in mammalian cell culture rather than bacteria — only a eukaryotic cell adds the human-style glycosylation the molecule needs. In medicine it is well established and genuinely important: recombinant EPO treats the anemia of chronic kidney disease, chemotherapy, and other marrow-suppressed states, sparing transfusions for millions. Its receptor turns up in the nervous system and elsewhere, which has driven a long research thread into EPO as a cytoprotective and neuroprotective agent after ischemic injury — promising in models, unproven as therapy. Then there is the doping. EPO became the defining drug of endurance-sport scandals: by raising red-cell mass it boosts oxygen delivery and stamina, and it sat at the center of professional cycling’s doping era. The misuse carries real danger — thickened blood raises the risk of clots, stroke, and heart attack — and the same caution emerged in medicine, where trials showed that over-correcting hemoglobin to normal or high targets increased cardiovascular events and mortality. EPO is a clean example of a molecule whose reputation splits sharply between its legitimate, life-improving medical use and its dangerous performance misuse. ## Mechanism Binds the erythropoietin receptor on red-cell progenitors in the bone marrow, activating JAK2/STAT5 signaling that promotes their survival, proliferation, and maturation into erythrocytes — raising the blood’s oxygen-carrying capacity. The same receptor is expressed in other tissues, the basis for its cytoprotective research. ## Chemistry | Property | Value | | --- | --- | | Molecular weight | 30400 Da | | CAS number | 113427-24-0 | | UniProt | [P01588](https://www.uniprot.org/uniprotkb/P01588) | ## Research areas Studied in: Anemia, Tissue protection, Neuroprotection, Erythropoiesis. Guides on this site: - [Cognition & Neuroprotection](https://www.americanpeptide.com/research-areas/cognition-neuroprotection): Nootropic and neurotrophic peptides studied for cognition and recovery. ## Key research - Anemia of chronic kidney disease — the core approved use, replacing the EPO failing kidneys no longer make. - Chemotherapy-induced anemia — used to reduce transfusion need in selected patients. - Hemoglobin-target caution — trials found that normalizing/over-correcting hemoglobin raised cardiovascular events and mortality, reshaping dosing. - Tissue/neuroprotection — EPO-receptor signaling outside marrow is studied for cytoprotection after ischemic injury (research, not approved). - Endurance doping — banned in sport; raising red-cell mass increases clot, stroke, and heart-attack risk. - Glycosylation engineering — added glycans (darbepoetin) extend half-life, underscoring that the sugar defines the drug. ## Storage, handling & synthesis **Storage.** Recombinant EPO is stored refrigerated (2–8 °C) and protected from light; it must not be frozen or shaken. Glycoprotein integrity is sensitive to heat and freeze–thaw. **Handling.** A glycosylated protein sensitive to heat, freezing, and agitation, which can aggregate it and reduce potency. Aggregated protein is also an immunogenicity concern — historically linked to rare pure red-cell aplasia from anti-EPO antibodies. **Synthesis.** EPO is produced recombinantly in mammalian (CHO) cell culture so that its essential N- and O-linked glycosylation is human-like; its ~30–34 kDa mass is approximate and varies with glycosylation, so it has no single molecular formula. Characterization is glycoprotein-grade — glycan/isoform profiling, identity by mass spectrometry and peptide mapping, and cell-based potency — far beyond an HPLC purity figure. ## FAQs ### What is EPO? Erythropoietin — a glycoprotein hormone, mainly from the kidneys, that signals the bone marrow to produce red blood cells. Recombinant EPO (epoetin alfa) treats anemia in kidney disease and chemotherapy. ### Why is EPO a biologic rather than a peptide? It is a folded, glycosylated 165-amino-acid protein whose sugar chains are essential to its activity and half-life. It is produced in mammalian cells so that human-like glycosylation occurs — something bacterial peptide synthesis cannot do. ### Why is EPO associated with doping? By increasing red-cell mass it raises oxygen delivery and endurance, which made it a notorious performance drug, especially in cycling. The misuse is dangerous — it thickens the blood and raises clot, stroke, and heart-attack risk. ### Is this medical advice? No — this is a research and educational reference. EPO is a prescription biologic with significant cardiovascular risks when misused. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/epo Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Teriparatide (PTH 1-34) > The active fragment of parathyroid hormone — a recombinant peptide that builds bone, exploiting a paradox: the same hormone resorbs bone when continuous, but builds it when pulsed. - Also known as: PTH(1-34), Forteo, Bonsity, recombinant parathyroid hormone - Class: Healing & Repair, Longevity - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/teriparatide ## Overview Teriparatide is the first 34 amino acids of parathyroid hormone (PTH), the body’s master regulator of calcium. It is one of the few osteoporosis drugs that is genuinely anabolic — it builds new bone rather than just slowing its loss — and it does so by exploiting a striking biological paradox. The same PTH signal that dissolves bone when it is chronically elevated stimulates bone formation when it is delivered as a brief, once-daily pulse. Teriparatide turns that timing trick into a therapy. Parathyroid hormone is the body’s calcium thermostat, and the N-terminal 1-34 fragment retains its full receptor activity — which is why teriparatide is that fragment rather than the whole 84-residue hormone. Its defining feature is the dose-pattern paradox: a continuously high PTH level (the disease state of hyperparathyroidism) leaches calcium from bone, but a short daily spike tips the balance toward the bone-building osteoblasts. Teriparatide (Forteo, approved 2002) was among the first treatments to add bone rather than merely preserve it, used in severe osteoporosis and high fracture risk. It also carries one of the more instructive drug-safety stories. Teriparatide launched with a black-box warning for osteosarcoma, a bone cancer seen when rats were given very high, lifelong doses — which translated into a strict two-year lifetime limit on use in people. Over nearly two decades of post-marketing data that signal did not materialize in humans, and in 2020 the FDA removed the boxed warning and the lifetime restriction. It is a useful case of a precautionary animal-derived warning being revised as real-world human evidence accumulated. For a reference catalog, teriparatide is a clean example of how *timing*, not just the molecule, determines a hormone’s effect — and of how a peptide fragment can outperform the full hormone for a specific therapeutic goal. ## Mechanism Agonist at the PTH1 receptor on osteoblasts. Intermittent (once-daily) exposure favors osteoblast activity and new bone formation; continuous elevation (as in hyperparathyroidism) instead drives osteoclastic resorption. The therapeutic effect depends entirely on the pulsatile dosing. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C181H291N55O51S2 | | Molecular weight | 4117.8 Da | | CAS number | 52232-67-4 | ## Sequence ``` SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNF ``` ## Research areas Studied in: Osteoporosis, Bone formation, Fracture healing, Calcium regulation. ## Key research - Anabolic osteoporosis therapy — builds new bone, distinct from antiresorptives that only slow loss. - The dose-pattern paradox — intermittent PTH builds bone; continuous PTH resorbs it. - Fracture-risk reduction — the approved use in severe osteoporosis and high fracture risk. - Boxed-warning reversal — the rat osteosarcoma warning and 2-year limit were removed by the FDA in 2020 after human data. - PTH1-receptor signaling — acts on osteoblasts; the 1-34 fragment retains full activity of the 84-residue hormone. ## Storage, handling & synthesis **Storage.** Teriparatide is supplied as a refrigerated (2–8 °C) solution pen; it must not be frozen and is protected from light, with an in-use window defined by the label. **Handling.** A peptide in aqueous solution — kept cold, not frozen or shaken. Pen devices deliver fixed daily doses to maintain the pulsatile exposure the mechanism depends on. **Synthesis.** Teriparatide is recombinant human PTH(1-34), expressed in E. coli and purified to a defined 34-residue peptide. Because it is the minimal active fragment rather than the full 84-residue hormone, it can be manufactured and characterized more like a long synthetic/recombinant peptide than a large folded protein — identity by mass spectrometry and peptide mapping, with potency confirmed functionally. ## FAQs ### What is teriparatide? Teriparatide is PTH(1-34), the active fragment of parathyroid hormone, used as a recombinant injectable (Forteo) for osteoporosis. Unlike most bone drugs, it is anabolic — it builds new bone. ### How can parathyroid hormone both build and break down bone? It is about timing. A brief once-daily pulse of PTH favors bone-building osteoblasts, while a continuously high level (as in hyperparathyroidism) drives bone resorption. Teriparatide uses the pulsatile pattern deliberately. ### Is teriparatide still limited to two years? The original 2-year lifetime limit and osteosarcoma boxed warning — based on high-dose rat studies — were removed by the FDA in 2020 after long-term human data did not show that risk. ### Is this medical advice? No — this is a research and educational reference, not dosing guidance. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/teriparatide Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Somatropin (rHGH) > Recombinant 191-amino-acid human growth hormone — a folded protein biologic identical in sequence to pituitary GH, not a synthetic research peptide. - Also known as: Recombinant human growth hormone, rhGH, 191aa HGH, Human growth hormone, Genotropin, Humatrope, Norditropin, Nutropin, Saizen, Omnitrope, Serostim - Class: Growth Hormone, Longevity - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/somatropin ## Overview Somatropin is recombinant human growth hormone (rHGH): a single 191-amino-acid polypeptide, ~22.1 kDa, with the exact sequence of the major form secreted by the human pituitary. Unlike the short synthetic peptides elsewhere in this catalog, it is a folded protein biologic — produced in engineered cells, stabilized by two internal disulfide bonds, and dependent on its three-dimensional structure for activity. It is FDA-approved for several growth-hormone-deficiency and short-stature indications, and is simultaneously one of the most misunderstood molecules in the anti-aging conversation. Somatropin is a biologic, and that distinction is the point of including it here. The research peptides in this catalog are mostly short chains built by solid-phase synthesis; somatropin is a full 191-residue protein with defined secondary and tertiary structure — a four-helix bundle held by two disulfide bridges (Cys53–Cys165 and Cys182–Cys189). Its sequence is identical to the dominant 22 kDa form of growth hormone the pituitary releases, which is why it is called "recombinant human" growth hormone rather than an analog. Activity lives in the fold: denature the protein and you do not get a weaker peptide, you get an inactive one. The molecule also carries its own history. Until 1985, growth hormone was extracted from cadaveric pituitaries — a supply that was abruptly halted when several recipients developed Creutzfeldt–Jakob disease from prion contamination. Recombinant production solved both the supply and the safety problem. The first recombinant product (somatrem) carried an extra N-terminal methionine, a 192-amino-acid artifact of bacterial expression; somatropin is the true 191-amino-acid, native-sequence version that followed and now defines the class across brands such as Genotropin, Humatrope, Norditropin, and Saizen. Mechanistically, growth hormone is a relay, not a direct effector. It binds and dimerizes the GH receptor, triggering JAK2/STAT5 signaling, and much of what people attribute to "GH" is actually the work of IGF-1 produced downstream in the liver. GH does have direct actions — it mobilizes fat and antagonizes insulin — but the growth and anabolic story runs largely through the GH/IGF-1 axis. This is also why the secretagogues elsewhere in this catalog (the GHRH analogs and GHRPs) exist: they coax the pituitary into releasing this same molecule, preserving the body’s pulsatile feedback rather than supplying a flat exogenous dose. Then there is the drama. In 1990 a small New England Journal of Medicine study by Daniel Rudman gave GH to twelve older men and reported reduced fat and increased lean mass over six months. That single paper — 12 subjects, no functional endpoints — became the founding myth of the GH anti-aging industry. The journal’s own editors later published an unusual note cautioning against using it to justify anti-aging treatment, and subsequent work documented the costs of supraphysiologic GH in healthy adults: fluid retention, carpal tunnel syndrome, joint pain, and insulin resistance. The headline rarely traveled with the footnotes. The deepest irony is the longevity science. Across model organisms, it is reduced GH/IGF-1 signaling — not elevated — that tracks with extended lifespan: GH-receptor-knockout mice are among the longest-lived strains known, and humans with Laron syndrome (GH-receptor insensitivity) show strikingly low rates of cancer and diabetes. So a hormone marketed for "longevity" sits on an axis whose downregulation is one of the most reproducible pro-longevity signals in biology. That tension — real, FDA-approved medicine for genuine deficiency; oversold and legally restricted as an anti-aging tonic; and pointing the opposite direction from the longevity data — is exactly why it belongs in an honest reference. ## Mechanism Binds a single GH receptor that then dimerizes, activating JAK2/STAT5 signaling. Most anabolic and growth effects are mediated indirectly through hepatic IGF-1 induction; GH also acts directly to drive lipolysis and oppose insulin. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C990H1528N262O300S7 | | Molecular weight | 22124 Da | | CAS number | 12629-01-5 | | UniProt | [P01241](https://www.uniprot.org/uniprotkb/P01241) | ## Sequence ``` FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF ``` ## Research areas Studied in: Growth hormone deficiency, Body composition, Anti-aging (off-label), Longevity, GH/IGF-1 axis. Guides on this site: - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - Growth hormone deficiency — the core approved use, in both pediatric and adult GHD, restoring GH/IGF-1 signaling to a physiologic range. - Approved short-stature and wasting indications — Turner syndrome, Prader-Willi syndrome, chronic renal insufficiency, SHOX deficiency, idiopathic short stature, AIDS wasting, and short bowel syndrome, depending on the specific product label. - Body composition — supraphysiologic GH reduces fat mass and increases lean/water mass, the effect that drives off-label anti-aging and athletic use; functional and long-term benefit in healthy adults is not established. - Documented adverse effects — fluid retention/edema, carpal tunnel syndrome, arthralgia, and insulin resistance are recurrent findings when GH is given above physiologic need. - Longevity paradox — reduced GH/IGF-1 signaling (GH-receptor knockout models, Laron syndrome) is associated with extended lifespan and lower cancer/diabetes risk, complicating the "anti-aging" rationale. - Legally restricted — U.S. federal law (21 U.S.C. § 333(e)) makes distribution of hGH for any use not specifically authorized by the FDA a crime; this is a near-unique statutory restriction among prescription drugs. ## Storage, handling & synthesis **Storage.** Lyophilized somatropin is stored refrigerated (2–8 °C); most products must stay cold and are reconstituted with a supplied diluent. Reconstituted solution is typically used within days to weeks under refrigeration and must not be frozen — freezing and agitation can denature and aggregate the protein. **Handling.** As a folded biologic it is sensitive to heat, freeze–thaw, vigorous shaking, and surface adsorption, any of which can unfold or aggregate it and destroy potency without changing appearance. Aggregated protein is also a potential immunogenicity concern, which is why protein therapeutics carry a tighter cold chain than small peptides. **Synthesis.** Somatropin is not made by solid-phase peptide synthesis. It is expressed recombinantly — historically in E. coli (often as inclusion bodies requiring refolding) and in mammalian cell lines — then purified by multi-step chromatography and verified for correct folding and disulfide pairing. Identity and potency rest on protein-specific methods (peptide mapping, mass spectrometry, bioassay/cell-based potency, host-cell-protein and endotoxin testing), not an HPLC purity percentage alone. This is the defining difference between a complex biologic hormone and the short synthetic peptides in the rest of this catalog. ## FAQs ### What is somatropin (191aa rHGH)? Somatropin is recombinant human growth hormone — a 191-amino-acid protein, ~22 kDa, with the same sequence as the growth hormone made by the human pituitary. It is a folded biologic, not a synthetic peptide, and is FDA-approved for several growth-hormone-deficiency and short-stature conditions. ### Why is it described as a biologic rather than a peptide? Its activity depends on three-dimensional structure — a four-helix fold stabilized by two disulfide bonds — and it is produced in living cells, not by solid-phase synthesis. That makes its manufacturing, characterization, and quality control much closer to a protein drug than to a short research peptide. ### Is it really used for anti-aging? Off-label, yes — that use traces largely to a small 1990 study whose authors and journal later warned against extrapolating it. Healthy-adult use carries documented side effects (edema, carpal tunnel, joint pain, insulin resistance), and U.S. law specifically restricts distributing hGH for uses the FDA has not authorized. ### Does growth hormone extend lifespan? The reverse is better supported in research: lower GH/IGF-1 signaling is associated with longer lifespan in animal models and with reduced cancer and diabetes in people with GH-receptor insensitivity (Laron syndrome). The popular "longevity" framing runs against much of the aging biology. ### Is this medical advice? No. This is a research and educational reference. Somatropin is a prescription biologic with specific approved indications and significant legal restrictions; nothing here is a recommendation to obtain or use it. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/somatropin Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # IGF-1 (Mecasermin) > The downstream effector of growth hormone — a 70-amino-acid recombinant protein, structurally a cousin of proinsulin, that carries out most of GH’s growth signal. - Also known as: Insulin-like growth factor 1, Mecasermin, Increlex, Somatomedin C, rhIGF-1 - Class: Growth Hormone, Longevity - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/igf-1 ## Overview IGF-1 is the molecule that does much of growth hormone’s work. It is a 70-amino-acid single-chain protein (~7.6 kDa) with three disulfide bonds, structurally homologous to proinsulin — which is why insulin and IGF-1 signaling overlap. Produced mainly in the liver under GH stimulation, it is the mediator most responsible for GH’s anabolic and growth-promoting effects. The recombinant therapeutic version, mecasermin, is FDA-approved for severe IGF-1 deficiency. It pairs naturally with somatropin in this catalog: GH is the signal, IGF-1 is the message that actually reaches the tissues. Where somatropin is the broadcast, IGF-1 is the signal received. Growth hormone acts on the liver and other tissues to induce IGF-1, and it is IGF-1 — acting through its own tyrosine-kinase receptor — that mediates most of the downstream growth and anabolic effects. Its structural kinship to proinsulin is not a coincidence: the IGF and insulin systems are evolutionary relatives, which is why IGF-1 has weak insulin-like (hypoglycemic) activity and why dosing is constrained by that overlap. The therapeutic form, mecasermin (Increlex), is recombinant human IGF-1 approved in 2005 for children with severe primary IGF-1 deficiency or growth-hormone insensitivity — the Laron syndrome population, in whom GH itself does not work because the receptor or its signaling is broken. In those patients, supplying IGF-1 directly bypasses the failed step. IGF-1 carries the same two layers of drama as growth hormone, sharpened. It is banned in sport and has been a recurring doping target; the most public episode was the 2013 "deer antler velvet spray" affair, in which an IGF-1-marketed product was tied to several athletes — a reminder that much of what is sold as IGF-1 outside medicine is unverified. And the longevity paradox is, if anything, cleaner here: low IGF-1 signaling is one of the most reproducible pro-longevity signals in biology, with IGF-1-pathway mutants living longer across species and Laron-syndrome individuals showing strikingly low cancer and diabetes incidence. A protein marketed for anti-aging sits on the very axis whose suppression extends life. ## Mechanism Binds the IGF-1 receptor (a tyrosine kinase) and, with lower affinity, the insulin receptor, activating PI3K/AKT and MAPK signaling to drive cell growth, proliferation, and survival. Circulating IGF-1 is largely bound to IGF-binding proteins, which modulate its availability. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C331H512N94O101S7 | | Molecular weight | 7649 Da | | CAS number | 68562-41-4 | | UniProt | [P05019](https://www.uniprot.org/uniprotkb/P05019) | ## Sequence ``` GPETLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA ``` ## Research areas Studied in: Severe primary IGF-1 deficiency, GH/IGF-1 axis, Growth disorders, Longevity. Guides on this site: - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - Severe primary IGF-1 deficiency — the approved use of mecasermin, supplying IGF-1 where GH signaling has failed. - GH/IGF-1 axis — IGF-1 is the principal mediator of growth hormone’s anabolic effects. - Insulin cross-talk — structural homology to proinsulin gives it weak hypoglycemic activity, a dosing constraint. - Longevity paradox — reduced IGF-1 signaling tracks with extended lifespan and lower cancer/diabetes risk (Laron syndrome). - Doping target — WADA-banned; "deer antler velvet" IGF-1 products are a notable case of unverified marketing. - IGF-binding proteins — circulating IGF-1 is mostly protein-bound, which regulates its activity and half-life. - Research analogs & splice variants — IGF-1 LR3 is a long-acting modified analog studied for systemic hypertrophy, while MGF (mechano growth factor) is a local IGF-1 splice variant studied for satellite-cell activation after muscle damage. ## Storage, handling & synthesis **Storage.** Mecasermin is stored refrigerated (2–8 °C) and protected from light; it must not be frozen, and reconstituted/in-use solution is used within the label’s limited window. **Handling.** A folded disulfide-bonded protein, sensitive to heat, freeze–thaw, and agitation. Because of its insulin-like activity, hypoglycemia is a specific handling/clinical concern. **Synthesis.** Recombinant IGF-1 is expressed (classically in E. coli), refolded to its native three-disulfide structure, and purified by chromatography. Release testing is protein-grade — peptide mapping, mass spectrometry, correct disulfide pairing, cell-based potency, host-cell-protein and endotoxin limits — not an HPLC purity figure alone. ## FAQs ### What is IGF-1? Insulin-like growth factor 1 — a 70-amino-acid protein, made mainly in the liver under growth-hormone stimulation, that carries out most of GH’s growth-promoting effects. The recombinant drug mecasermin (Increlex) is approved for severe IGF-1 deficiency. ### How is IGF-1 related to growth hormone? GH stimulates the liver to produce IGF-1, and IGF-1 then does much of the actual signaling to tissues. That is why IGF-1 can treat people whose GH does not work (Laron syndrome). ### Why is it called "insulin-like"? IGF-1 is structurally homologous to proinsulin and binds the insulin receptor weakly, giving it mild insulin-like (glucose-lowering) effects. ### Is this medical advice? No — this is a research and educational reference. Mecasermin is a prescription biologic; much of what is sold as IGF-1 outside medicine is unverified. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/igf-1 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # IGF-1 LR3 > A long-acting modified IGF-1 analog with reduced IGFBP binding and prolonged systemic activity. - Also known as: Long R3 IGF-1, LR3 IGF-1 - Class: Growth Hormone - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/igf-1-lr3 ## Overview IGF-1 LR3 (Long R3 IGF-1) is an 83-amino-acid analog of IGF-1 with an arginine substitution at position 3 and a 13-residue N-terminal extension. These changes reduce binding to IGF-binding proteins, extending its half-life and potency versus native IGF-1. IGF-1 LR3 ("Long R3 IGF-1") is a modified version of insulin-like growth factor 1, engineered for a much longer duration of action. Two changes define it: arginine replaces glutamic acid at position 3, and a 13-amino-acid extension is added to the N-terminus. Together these reduce the analog’s affinity for IGF-binding proteins — the carriers that normally sequester circulating IGF-1 — so more remains free and active, extending half-life and increasing potency roughly two- to three-fold over native IGF-1 (~9.1 kDa). It is a research compound, widely used in cell culture, and is not FDA-approved; it is also prohibited in sport. ## Mechanism IGF-1 receptor agonism with reduced IGFBP binding → prolonged systemic anabolic signaling. ## Chemistry | Property | Value | | --- | --- | | CAS number | 946870-92-4 | ## Research areas Studied in: Muscle hypertrophy, Cell proliferation, GH/IGF-1 axis. Guides on this site: - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - Reduced IGFBP binding — the R3 substitution lowers affinity for IGF-binding proteins, leaving more peptide free and active. - Prolonged potency — systemic, long-acting anabolic signaling roughly two- to three-fold more potent than native IGF-1. - Cell-culture standard — widely used as a serum-free supplement to promote cell proliferation in bioprocessing. - Compared to MGF — IGF-1 LR3 is systemic and long-acting (hypertrophy), while MGF is a local, transient splice variant (satellite-cell activation). - Preclinical / prohibited in sport — not FDA-approved; WADA-banned. ## Storage, handling & synthesis **Storage.** Lyophilized: store frozen and protected from light. Reconstituted: refrigerate at 2–8 °C and minimize freeze–thaw — a folded, disulfide-bonded protein. **Handling.** A disulfide-bonded protein sensitive to heat, agitation, and freeze–thaw. Reconstitute gently (swirl, do not shake). ## FAQs ### What is IGF-1 LR3? IGF-1 LR3 (Long R3 IGF-1) is a modified, long-acting analog of IGF-1 with an arginine-3 substitution and an N-terminal extension that reduce IGF-binding-protein binding and extend its activity. ### Why does the R3 modification matter? It lowers the analog’s affinity for IGF-binding proteins, so more remains free and active in circulation — extending half-life and increasing potency versus native IGF-1. ### How does it compare to MGF? IGF-1 LR3 is systemic and long-acting, studied for hypertrophy; MGF is a local, transient IGF-1 splice variant studied for satellite-cell activation. The two are typically sequenced, not combined. ### Is IGF-1 LR3 approved? No. It is a research compound (also common in cell culture), not FDA-approved, and is prohibited in sport. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/igf-1-lr3 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # MGF (Mechano Growth Factor) > A splice variant of IGF-1 expressed after muscle damage; studied for satellite-cell activation. - Also known as: Mechano Growth Factor, IGF-1Ec, IGF-1 Ec - Class: Growth Hormone - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/mgf ## Overview MGF is the IGF-1Ec splice variant — produced locally in muscle after mechanical overload or injury. Its distinct C-terminal E-peptide is studied for activating satellite cells, upstream of IGF-1’s hypertrophic role. Mechano growth factor (MGF) is a splice variant of IGF-1, also called IGF-1Ec. A 49-base-pair insert in exon 5 introduces a reading-frame shift, producing a distinct C-terminal peptide (the "E-domain") not found in the main circulating IGF-1 isoform. MGF is expressed rapidly and locally in muscle after mechanical overload or damage — the experimental basis was established by Geoffrey Goldspink and colleagues (UCL) beginning in the late 1990s. Its proposed role is to begin repair by activating satellite cells before differentiation, complementing the longer-acting hypertrophic signal of IGF-1 itself. It is a research compound, not FDA-approved. ## Mechanism Local IGF-1 splice variant; the E-peptide activates muscle satellite (stem) cells, complementing IGF-1-receptor signaling. ## Research areas Studied in: Muscle repair, Satellite-cell activation. ## Key research - Satellite-cell activation — the E-peptide is proposed to act upstream, promoting satellite-cell proliferation before differentiation. - Damage-induced expression — produced locally and rapidly after mechanical overload or muscle injury (McKoy, Ashley, Yang et al., 1999). - Splice-variant origin — an exon-5 insert gives IGF-1Ec a distinct C-terminal peptide versus the main IGF-1 isoform. - Compared to IGF-1 LR3 — MGF is local and transient, driving satellite-cell activation; IGF-1 LR3 is systemic and long-acting, driving hypertrophy. The two are sequenced rather than combined. - Preclinical / prohibited in sport — not FDA-approved; WADA-banned. ## Storage, handling & synthesis **Storage.** Lyophilized: store frozen and protected from light. Reconstituted: refrigerate at 2–8 °C and use within weeks; minimize freeze–thaw. **Handling.** Reconstitute gently and avoid shaking; protect from heat and light. PEGylated forms (PEG-MGF) are handled similarly but differ in half-life. ## FAQs ### What is MGF? MGF (mechano growth factor) is a splice variant of IGF-1 (IGF-1Ec) produced locally in muscle after damage. Its distinct E-peptide is studied for activating satellite cells. ### How is MGF different from IGF-1? MGF is a splice variant with a unique C-terminal peptide, expressed locally after mechanical stress. Where standard IGF-1 sustains hypertrophy systemically, MGF is studied for initiating repair by activating satellite cells. ### How does MGF compare to IGF-1 LR3? MGF is local and transient (satellite-cell activation); IGF-1 LR3 is systemic and long-acting (hypertrophy). They are generally studied in sequence rather than together. ### Is MGF approved? No. It is a research compound, not FDA-approved, and is prohibited in sport. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/mgf Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # CJC-1295 (no DAC) > Modified GHRH(1-29) analog with short plasma half-life. - Also known as: Modified GRF (1-29), Mod GRF 1-29 - Class: Growth Hormone - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/cjc-1295-no-dac ## Overview CJC-1295 without DAC is a 30-amino-acid analog of GHRH(1-29) with four substitutions that improve stability against DPP-4. Half-life ~30 minutes; commonly studied alongside GHRPs for pulsatile GH release. CJC-1295 without DAC — also called Modified GRF(1-29) — is a 30-amino-acid analog of the first 29 residues of growth-hormone-releasing hormone (GHRH). Four amino-acid substitutions improve stability against the enzyme DPP-4 while preserving GHRH-receptor activity. Without the Drug Affinity Complex (DAC), its plasma half-life is short — on the order of 30 minutes — so it produces a brief GH pulse. It is commonly studied alongside a GHRP such as ipamorelin, where the two receptor classes act synergistically. It is not FDA-approved. ## Mechanism GHRH receptor agonism on pituitary somatotrophs. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C165H269N47O46 | | Molecular weight | 3647.2 Da | | PubChem CID | [91971820](https://pubchem.ncbi.nlm.nih.gov/compound/91971820) | ## Sequence ``` YADAIFTQSYRKVLAQLSARKLLQDIMSR ``` ## Research areas Studied in: GH pulsatility, Body composition models. Guides on this site: - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - Pulsatile GH release — GHRH-receptor agonism studied for short, physiologic GH pulses. - DPP-4 resistance — substitutions extend stability versus native GHRH(1-29). - GHRP synergy — frequently paired with ghrelin-receptor agonists for amplified release. - Body composition — examined in models for lean-mass and fat endpoints. - Not FDA-approved — research compound. ## FAQs ### What is CJC-1295 (no DAC)? It is a stabilized GHRH(1-29) analog (Modified GRF 1-29) studied for short, pulsatile growth-hormone release. ### What does "no DAC" mean? DAC (Drug Affinity Complex) is an albumin-binding addition that greatly extends half-life. Without it, the peptide acts briefly, producing a short GH pulse. ### Why is it studied with GHRPs? GHRH analogs and ghrelin-receptor agonists (GHRPs) act on different receptors; combining them is studied for synergistic GH release. ### Is it approved? No — it is a research compound, not FDA-approved. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/cjc-1295-no-dac Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # CJC-1295 (with DAC) > Long-acting GHRH analog with a Drug Affinity Complex for albumin binding. - Also known as: CJC-1295 DAC - Class: Growth Hormone - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/cjc-1295-with-dac ## Overview Adds a maleimidopropionic acid (DAC) moiety to modified GRF(1-29), enabling covalent binding to serum albumin and extending half-life to roughly 6–8 days. CJC-1295 with DAC adds a Drug Affinity Complex — a maleimidopropionic acid group — to Modified GRF(1-29), allowing the peptide to bind covalently to serum albumin. This extends its half-life to roughly 6–8 days, replacing the brief pulse of the no-DAC form with prolonged elevation. The trade-off studied in the literature is physiologic: sustained GHRH-receptor exposure raises baseline GH and IGF-1 but blunts the natural pulsatility of the GH axis. It is a research compound and is not FDA-approved. ## Mechanism GHRH receptor agonism with albumin-mediated extended exposure. ## Research areas Studied in: Sustained GH release, IGF-1 elevation. Guides on this site: - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - Sustained exposure — albumin binding extends half-life to roughly 6–8 days (Teichman et al., 2006, J Clin Endocrinol Metab). - GH / IGF-1 elevation — in early human study a single dose produced dose-dependent ~2–10-fold mean GH elevations and sustained IGF-1 increases lasting about 9–11 days. - Pulsatility trade-off — continuous exposure raises baseline GH and IGF-1 but blunts the body’s natural pulsatile pattern. - Compared to sermorelin / no-DAC — the same GHRH(1-29) backbone, but the DAC converts a minutes-long pulse into multi-day elevation. - Not FDA-approved — research compound. ## FAQs ### What is CJC-1295 with DAC? A long-acting GHRH analog whose Drug Affinity Complex binds albumin, extending its half-life to roughly a week for sustained GH and IGF-1 elevation. ### How does it differ from the no-DAC version? The no-DAC form produces a brief GH pulse; the DAC form gives prolonged elevation by binding albumin, at the cost of natural pulsatility. ### What is a Drug Affinity Complex? A chemical group that lets the peptide covalently attach to serum albumin, dramatically slowing its clearance. ### Is it approved? No — it is a research compound. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/cjc-1295-with-dac Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Ipamorelin > Selective ghrelin receptor agonist (GHRP) with minimal cortisol / prolactin release. - Class: Growth Hormone - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/ipamorelin ## Overview Ipamorelin is a pentapeptide GHRP that selectively activates the GHS-R1a (ghrelin) receptor, releasing growth hormone with minimal impact on ACTH, cortisol, or prolactin. Ipamorelin is a pentapeptide growth-hormone-releasing peptide (GHRP) that selectively activates the ghrelin receptor (GHS-R1a) on pituitary somatotrophs. Its defining feature is selectivity: it releases GH with minimal effect on ACTH, cortisol, or prolactin compared with earlier GHRPs. Because of that clean profile, it is one of the most studied GHRPs in the research literature and is frequently paired with a GHRH analog such as CJC-1295. It is not FDA-approved. ## Mechanism Selective GHS-R1a agonism. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C38H49N9O5 | | Molecular weight | 711.9 Da | | CAS number | 170851-70-4 | | PubChem CID | [9831659](https://pubchem.ncbi.nlm.nih.gov/compound/9831659) | ## Sequence ``` Aib-His-D-2-Nal-D-Phe-Lys-NH2 ``` ## Research areas Studied in: GH secretion studies, Pituitary function. Guides on this site: - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - Selective GH release — characterized as the first GHRP to release GH without meaningfully raising ACTH, cortisol, or prolactin (Raun et al., 1998). - GHRH synergy — commonly studied alongside GHRH analogs (CJC-1295 / sermorelin) for amplified, pulse-preserving release. - Compared to hexarelin — trades raw potency for selectivity: hexarelin releases more GH per dose but recruits cortisol / prolactin and desensitizes the receptor faster. - Lower desensitization — its clean receptor profile is studied as more sustainable over repeated exposure. - Not FDA-approved — research compound. ## FAQs ### What is ipamorelin? Ipamorelin is a selective ghrelin-receptor agonist (a GHRP) studied for growth-hormone release with minimal effect on cortisol or prolactin. ### How is it different from other GHRPs? Its selectivity — releasing GH without significantly raising ACTH, cortisol, or prolactin — distinguishes it from earlier, less selective GHRPs. ### Why is it paired with CJC-1295? GHRPs and GHRH analogs act on separate receptors; combining them is studied for synergistic GH release. ### Is it approved? No — it is a research compound. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/ipamorelin Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Tesamorelin > GHRH analog FDA-approved for HIV-associated lipodystrophy. - Also known as: Egrifta - Class: Growth Hormone, Metabolic - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/tesamorelin ## Overview Tesamorelin is a stabilized 44-amino-acid GHRH analog approved by the FDA in 2010 for reduction of excess abdominal fat in HIV-infected patients with lipodystrophy. Tesamorelin is a stabilized 44-amino-acid analog of growth-hormone-releasing hormone (GHRH). By stimulating the pituitary to release endogenous GH, it preserves more of the body’s natural feedback than exogenous GH would. It is FDA-approved (Egrifta, 2010) specifically to reduce excess visceral abdominal fat in people with HIV-associated lipodystrophy. Beyond that indication it has been studied for visceral adiposity more broadly and, in research settings, for effects on cognition. ## Mechanism GHRH receptor agonism → endogenous GH release. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C221H366N72O67S | | Molecular weight | 5135.9 Da | | CAS number | 218949-48-5 | | PubChem CID | [16137828](https://pubchem.ncbi.nlm.nih.gov/compound/16137828) | ## Research areas Studied in: Visceral adiposity, HIV-associated lipodystrophy, Cognition. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. - [Cognition & Neuroprotection](https://www.americanpeptide.com/research-areas/cognition-neuroprotection): Nootropic and neurotrophic peptides studied for cognition and recovery. ## Key research - Visceral fat reduction — the approved use, lowering excess abdominal fat in HIV-associated lipodystrophy. - GH axis — GHRH-receptor agonism raising endogenous GH and IGF-1. - Cognition — examined in research for effects related to GH signaling. - Hepatic fat — studied as a metabolic endpoint. - FDA-approved (Egrifta) — for a specific HIV-related indication. ## FAQs ### What is tesamorelin? Tesamorelin is a GHRH analog FDA-approved (Egrifta) to reduce excess abdominal fat in people with HIV-associated lipodystrophy. ### How does it work? It stimulates the pituitary to release the body’s own growth hormone, rather than supplying GH directly. ### What is it approved for? Reduction of excess visceral abdominal fat in HIV-associated lipodystrophy. Other uses described here are research contexts, not approved indications. ### Is this medical advice? No — this page is a research and educational reference, not medical advice or a dosing protocol. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/tesamorelin Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Sermorelin > Truncated GHRH(1-29) — historically the first GHRH analog approved by the FDA. - Also known as: GRF 1-29, Geref - Class: Growth Hormone - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/sermorelin ## Overview Sermorelin is the first 29 amino acids of endogenous GHRH and was approved by the FDA in 1990 (subsequently discontinued commercially) for diagnostic and pediatric GH deficiency use. Sermorelin is the first 29 amino acids of endogenous GHRH — the shortest fragment that retains full GH-releasing activity. As a GHRH-receptor agonist it prompts the pituitary to release the body’s own growth hormone. It was FDA-approved in 1990 (Geref) for diagnostic evaluation of pituitary GH reserve and for pediatric GH deficiency, but was later discontinued commercially. It remains a widely referenced GHRH analog in research. ## Mechanism GHRH receptor agonism. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C149H246N44O42S | | Molecular weight | 3358 Da | | CAS number | 86168-78-7 | | PubChem CID | [16132413](https://pubchem.ncbi.nlm.nih.gov/compound/16132413) | ## Sequence ``` YADAIFTNSYRKVLGQLSARKLLQDIMSR ``` ## Research areas Studied in: GH axis evaluation, Pediatric GH deficiency (historical). Guides on this site: - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - GHRH-receptor agonism — binds GHRHR on pituitary somatotrophs, activating adenylyl cyclase / cAMP to drive endogenous GH synthesis and release. - Physiologic pulsatility — the short half-life is a design feature, producing a discrete GH pulse that preserves somatostatin negative feedback rather than sustained elevation. - GH-axis evaluation — historically used to test pituitary GH reserve; a former approved use in pediatric GH deficiency, since discontinued. - Compared to CJC-1295 — the same GHRH(1-29) backbone; CJC-1295 stabilizes and (with DAC) extends it for multi-day action, trading pulsatility for duration. - Discontinued commercially — referenced today as a research compound. ## FAQs ### What is sermorelin? Sermorelin is GHRH(1-29), the shortest active fragment of growth-hormone-releasing hormone, historically approved to assess and treat GH deficiency. ### Is sermorelin still FDA-approved? It was approved in 1990 (Geref) but later discontinued commercially. It is referenced today largely as a research compound. ### How does it differ from CJC-1295? CJC-1295 is a stabilized, longer-acting modification of the same GHRH(1-29) backbone; sermorelin is the unmodified fragment with a short half-life. ### Is this medical advice? No — this page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/sermorelin Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Hexarelin > Synthetic hexapeptide GHRP with potent GH-releasing activity. - Class: Growth Hormone - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/hexarelin ## Overview Hexarelin is a synthetic GHRP-6 analog and a potent GH secretagogue with documented cardioprotective effects in preclinical models, mediated in part via CD36. Hexarelin is a synthetic hexapeptide in the GHRP family — a close analog of GHRP-6 — and one of the more potent growth-hormone secretagogues studied. It activates the ghrelin receptor (GHS-R1a) on pituitary somatotrophs. A distinctive research thread is its action at the CD36 receptor, through which preclinical studies report cardioprotective effects independent of GH release. It is not FDA-approved. ## Mechanism GHS-R1a and CD36 agonism. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C47H58N12O6 | | Molecular weight | 887 Da | | CAS number | 140703-51-1 | | PubChem CID | [6918297](https://pubchem.ncbi.nlm.nih.gov/compound/6918297) | ## Sequence ``` His-D-2-MeTrp-Ala-Trp-D-Phe-Lys-NH2 ``` ## Research areas Studied in: GH release, Cardioprotection models. Guides on this site: - [Wound Healing & Tissue Repair](https://www.americanpeptide.com/research-areas/wound-healing): Regenerative peptides studied for soft-tissue, tendon, and vascular repair. - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - Potent GH release — among the strongest GHRP secretagogues; at equivalent doses releases more GH than GHRP-2, GHRP-6, or ipamorelin. - Cardioprotection — CD36-mediated effects studied in preclinical cardiac models, independent of GH release. - Compared to ipamorelin — more potent but less selective: hexarelin can elevate cortisol and prolactin where ipamorelin does not. - Receptor desensitization — its broader, stronger activation shows greater tolerance / desensitization with sustained exposure. - Not FDA-approved — research compound. ## FAQs ### What is hexarelin? Hexarelin is a potent synthetic GHRP (a GHRP-6 analog) studied for growth-hormone release and, separately, cardioprotective effects. ### What is the CD36 connection? Beyond GH release, hexarelin binds the CD36 receptor, through which preclinical studies report cardioprotective activity. ### How does it compare with ipamorelin? Both are GHRPs, but hexarelin is more potent and less selective; ipamorelin is valued for releasing GH with minimal cortisol or prolactin effect. ### Is it approved? No — it is a research compound. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/hexarelin Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Myostatin (GDF-8) > The body’s brake on muscle growth — a TGF-β-family growth factor whose inhibition is the leading strategy to preserve muscle, including during GLP-1 weight loss. - Also known as: GDF-8, Growth differentiation factor 8, MSTN - Class: Growth Hormone, Metabolic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/myostatin ## Overview Myostatin (GDF-8) is the molecule that limits how much muscle you build. A member of the TGF-β superfamily, it is a negative regulator of skeletal-muscle mass: secreted by muscle itself, it signals muscle to stop growing. That makes myostatin unusual in this catalog — the therapeutic interest is almost entirely in blocking it, not supplying it — and it has become a forward-looking target precisely because the GLP-1 era exposed a problem myostatin inhibition could solve. Myostatin is best understood by what happens when it is missing. Cattle breeds with loss-of-function mutations — the "double-muscled" Belgian Blue — are dramatically more muscular; so are myostatin-null mice, a strain of "bully whippets," and, in a well-documented 2004 case, a human child with a myostatin mutation born unusually strong. The lesson is consistent across species: myostatin is a brake, and releasing it builds muscle. That is why the drug development around it aims to inhibit the pathway — with antibodies, ligand traps, and receptor blockers — rather than administer the growth factor. The clinical targets were originally the diseases of muscle loss: muscular dystrophies, sarcopenia (age-related muscle wasting), and cachexia. Results have been mixed — blocking myostatin reliably adds muscle mass, but translating that into durable strength and function has proven harder — which is the honest state of the field. The forward-looking turn is metabolic. The GLP-1 and dual/triple-agonist drugs produce large weight loss, but a substantial fraction of that loss is lean muscle, not just fat — a growing concern about the *quality* of weight loss as these drugs scale. Myostatin-pathway inhibition is the leading strategy to preserve or build muscle alongside that fat loss, and combinations of incretin agonists with muscle-sparing agents are an active frontier. This is the real "next chapter" beyond first-generation GLP-1 fat loss: not just losing weight, but keeping the muscle. It is also a doping and hype target — "myostatin blockers" are marketed well ahead of the evidence, and the pathway is banned in sport. As a reference entry, myostatin is the target and the science; specific inhibitor drugs are described as research and investigational, not endorsements. ## Mechanism Synthesized as a precursor and processed to a disulfide-linked dimer that signals through the activin type II receptors (ActRIIB) and the Smad2/3 pathway to suppress muscle-fiber growth. Removing or blocking myostatin releases that brake, increasing muscle mass; follistatin is a natural antagonist of this signal. ## Chemistry | Property | Value | | --- | --- | | Molecular weight | 12400 Da | | UniProt | [O14793](https://www.uniprot.org/uniprotkb/O14793) | ## Research areas Studied in: Muscle growth, Body composition, Sarcopenia, Muscular dystrophy, GLP-1 muscle preservation. Guides on this site: - [Longevity & Aging](https://www.americanpeptide.com/research-areas/longevity-aging): Peptides studied across the aging axis — senescence, NAD+, and resilience. - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - Negative regulator of muscle — loss of myostatin (cattle, mice, dogs, a human case) produces dramatic muscle overgrowth. - Inhibition as the therapeutic angle — antibodies, ligand traps, and receptor blockers aim to release the brake, not supply the factor. - Muscle-wasting disease — studied in muscular dystrophy, sarcopenia, and cachexia; mass gains are more reliable than functional gains so far. - GLP-1 muscle preservation — a leading strategy to counter the lean-mass loss that accompanies incretin-driven weight loss (the forward-looking use). - ActRIIB/Smad signaling — myostatin acts through activin receptors; follistatin is its natural antagonist. - Not an approved drug — no myostatin-targeting therapy is broadly approved; agents remain investigational. ## Storage, handling & synthesis **Storage.** As a research protein, recombinant myostatin/GDF-8 is handled like other growth factors — stored frozen as lyophilized powder, kept cold and protected from repeated freeze–thaw once reconstituted. **Handling.** A disulfide-linked dimeric protein sensitive to heat, repeated freeze–thaw, and agitation, any of which can disrupt the dimer and reduce activity. **Synthesis.** Myostatin is a processed, disulfide-linked dimer of the TGF-β superfamily — not a solid-phase synthetic peptide. Its mature monomer is ~12.4 kDa and the active form is a ~25 kDa dimer; because it is produced and processed in cells (and is studied as a target rather than supplied as a drug), it has no single small-molecule formula. Most therapeutics in this space are antibodies or engineered receptor traps, which are biologic-grade products in their own right. ## FAQs ### What is myostatin? Myostatin (GDF-8) is a TGF-β-family growth factor that limits skeletal-muscle growth — the body’s brake on muscle mass. Most therapeutic interest is in blocking it to increase muscle, not in administering it. ### Why is myostatin relevant to GLP-1 weight loss? GLP-1 and related drugs cause large weight loss that includes significant muscle, not just fat. Inhibiting the myostatin pathway is the leading approach to preserve muscle during that weight loss — a major forward-looking direction. ### Do myostatin blockers work? Blocking myostatin reliably increases muscle mass in studies, but translating that into lasting strength and function has been inconsistent. No myostatin-targeting drug is broadly approved; they remain investigational. ### Is this medical advice? No — this is a research and educational reference. Myostatin-targeting agents are investigational and, as a pathway, are banned in sport. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/myostatin Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Follistatin > A natural myostatin and activin antagonist — by neutralizing the muscle brake it is one of the most potent pro-muscle factors studied, and a doping and gene-therapy flashpoint. - Also known as: FST, FS-288, FS-315, follistatin-344 - Class: Growth Hormone, Metabolic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/follistatin ## Overview Follistatin is the body’s own counterweight to myostatin. It is a secreted glycoprotein that binds and neutralizes TGF-β-superfamily ligands — most importantly myostatin and activin — and by mopping up the signals that restrain muscle, it becomes one of the most powerful pro-muscle factors in the research literature. If myostatin is the brake on muscle growth, follistatin takes the foot off it. Follistatin exists in the body precisely to oppose the activin/myostatin axis, and overexpressing it produces some of the most striking muscle-growth phenotypes in animal research — larger gains than knocking out myostatin alone, because follistatin blocks multiple inhibitory ligands at once. It occurs in several isoforms (the FS-288 and FS-315 forms differ in how tightly they bind to cell surfaces and heparan sulfate), and as a secreted glycoprotein it is a true biologic, not a synthetic peptide. Most of the serious work on follistatin has been as gene therapy: delivering a follistatin gene (often the FS-344 construct) to muscle has shown durable muscle growth in models and has been explored in early human trials for muscular dystrophies and inclusion-body myositis. That gene-therapy route — rather than injecting the protein — reflects both follistatin’s short half-life and the goal of sustained local expression. It shares the forward-looking metabolic angle with myostatin: as GLP-1-class drugs drive large weight loss that includes muscle, follistatin-based and myostatin-antagonist approaches are part of the strategy to protect lean mass and improve the *quality* of that weight loss. It is, equally, a doping and hype target — "follistatin" products are marketed far beyond the evidence, and the pathway is banned in sport. For a reference, follistatin is best framed honestly: a genuinely potent muscle-growth regulator with real promise in muscle-wasting disease and a real frontier role alongside metabolic drugs — but one whose most credible results come from gene therapy in research settings, not from the supplements and injectables sold under its name. ## Mechanism Binds activin and myostatin with high affinity and sequesters them from their receptors, blocking the ActRIIB/Smad2/3 signaling that suppresses muscle growth. The net effect is disinhibition of muscle-fiber growth, studied as both a protein and a gene-therapy payload. ## Chemistry | Property | Value | | --- | --- | | Molecular weight | 34000 Da | | UniProt | [P19883](https://www.uniprot.org/uniprotkb/P19883) | ## Research areas Studied in: Muscle growth, Muscular dystrophy, Sarcopenia, Body composition, GLP-1 muscle preservation. Guides on this site: - [Longevity & Aging](https://www.americanpeptide.com/research-areas/longevity-aging): Peptides studied across the aging axis — senescence, NAD+, and resilience. - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - Potent muscle growth — neutralizing activin and myostatin disinhibits muscle, often exceeding myostatin knockout alone. - Gene therapy — follistatin (FS-344) gene delivery has shown durable muscle growth in models and early human dystrophy/myositis trials. - Muscle-wasting disease — studied across muscular dystrophies, sarcopenia, and cachexia. - GLP-1 muscle preservation — part of the forward-looking strategy to protect lean mass during incretin-driven weight loss. - Multiple isoforms — FS-288 vs FS-315 differ in cell-surface binding and bioavailability. - Doping/hype caution — banned in sport; marketed products run well ahead of the evidence. ## Storage, handling & synthesis **Storage.** Recombinant follistatin is handled as a research glycoprotein — stored frozen as lyophilized powder, kept cold and protected from repeated freeze–thaw after reconstitution. **Handling.** A glycosylated protein sensitive to heat, freeze–thaw, and agitation, which can aggregate it and reduce activity. **Synthesis.** Follistatin is a secreted glycoprotein (isoforms ~31–38 kDa with glycosylation), produced recombinantly in eukaryotic cells rather than by solid-phase synthesis; its mass varies with isoform and glycosylation, so it has no single molecular formula. Much of the credible therapeutic work uses follistatin gene delivery, characterized as a gene-therapy product, with the expressed protein verified by glycoprotein-grade analytics. ## FAQs ### What is follistatin? A secreted glycoprotein that binds and neutralizes myostatin and activin, removing the brakes on muscle growth. It is one of the most potent pro-muscle factors in research, studied mainly as a gene therapy. ### How is follistatin different from myostatin? Myostatin restrains muscle growth; follistatin blocks myostatin (and activin), so it does the opposite. Follistatin can exceed the muscle gains of removing myostatin alone because it neutralizes several inhibitory signals. ### Does follistatin build muscle in humans? The most credible results come from follistatin gene therapy in research and early trials, not from injectable proteins or supplements sold as "follistatin," which run ahead of the evidence. No follistatin therapy is broadly approved. ### Is this medical advice? No — this is a research and educational reference. Follistatin-based approaches are investigational and the pathway is banned in sport. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/follistatin Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Apitegromab > A monoclonal antibody that selectively blocks pro/latent myostatin — the muscle brake — studied to preserve lean mass during GLP-1 weight loss. - Also known as: SRK-015, SRK-439 - Class: Growth Hormone, Metabolic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/apitegromab ## Overview Apitegromab is a fully human monoclonal antibody (Scholar Rock) and the first of the anti-myostatin biologics in this catalog. Where myostatin is the growth factor that brakes muscle and follistatin is the body’s natural antagonist, apitegromab is an engineered antagonist: an antibody that binds the inactive precursor forms of myostatin (pro- and latent myostatin) and prevents their activation. Its selectivity for those precursors — rather than mature myostatin or the related GDF11/activins — is its defining design feature. Apitegromab’s lead program is in spinal muscular atrophy (SMA), where it is added on top of SMN-targeted therapy to build motor-relevant muscle. The same mechanism underlies its forward-looking metabolic use: in the Phase 2 EMBRAZE study, adding apitegromab to tirzepatide preserved lean mass during weight loss compared with tirzepatide alone, and its precursor-selectivity was framed as a potential tolerability advantage over broader myostatin/activin blockers. As a biologic it sits a full step beyond the protein hormones elsewhere in this catalog: it is an antibody (~150 kDa), produced in mammalian cells, designed to deplete a specific target. It is investigational — not an approved drug — and is included here as the antibody arm of the myostatin axis that myostatin and follistatin introduce. ## Mechanism Binds pro-myostatin and latent myostatin, blocking the proteolytic activation that releases mature, active myostatin. Lowering active myostatin disinhibits muscle growth via the ActRIIB/Smad pathway. ## Chemistry | Property | Value | | --- | --- | | Molecular weight | 150000 Da | ## Research areas Studied in: Spinal muscular atrophy, Muscle preservation, GLP-1 muscle preservation, Body composition. Guides on this site: - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - Precursor-selective — binds pro/latent myostatin rather than mature myostatin or GDF11/activins, the basis of its selectivity claim. - SMA — the lead clinical program, building muscle on top of SMN-directed therapy. - GLP-1 muscle preservation — Phase 2 EMBRAZE preserved lean mass when added to tirzepatide. - Antibody biologic — a ~150 kDa monoclonal antibody, the far end of the biologic spectrum from synthetic peptides. - Investigational — not FDA-approved. ## Storage, handling & synthesis **Storage.** Monoclonal antibodies are stored refrigerated (2–8 °C), protected from light and freezing, and never shaken. Investigational handling follows the trial protocol. **Handling.** A large folded, glycosylated antibody — sensitive to freezing, heat, and agitation, which can aggregate it. Aggregation is an immunogenicity concern. **Synthesis.** Apitegromab is a recombinant monoclonal antibody (~150 kDa) produced in mammalian cell culture — the most complex biologic class in this catalog, far removed from solid-phase peptide synthesis. Characterization is antibody-grade: glycan and charge-variant profiling, identity by mass spectrometry, and target-binding/cell-based potency, with host-cell-protein and endotoxin limits. ## FAQs ### What is apitegromab? A monoclonal antibody that selectively blocks the precursor forms of myostatin, the growth factor that limits muscle. It is studied in spinal muscular atrophy and, in combination with GLP-1/GIP drugs, to preserve muscle during weight loss. ### How is it different from blocking mature myostatin? Apitegromab targets pro- and latent (inactive) myostatin before it is activated, rather than the mature protein — a selectivity intended to avoid hitting related factors and improve tolerability. ### Is this medical advice? No — this is a research and educational reference. Apitegromab is an investigational antibody, not an approved drug. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/apitegromab Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Trevogrumab > An anti-myostatin antibody (Regeneron) now studied in obesity combinations to cut lean-mass loss and deepen fat loss alongside semaglutide. - Also known as: REGN1033 - Class: Growth Hormone, Metabolic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/trevogrumab ## Overview Trevogrumab is a monoclonal antibody from Regeneron that neutralizes mature myostatin. After an earlier life in sarcopenia research, it has re-emerged squarely in the GLP-1 era: as a muscle-sparing add-on to incretin weight-loss drugs, and as one leg of a triple combination designed to maximize fat loss while protecting muscle. Trevogrumab is the clearest worked example of the muscle-preservation thesis. In trial data, semaglutide alone reduced both fat (~−15.7%) and lean mass (~−6.5%); adding trevogrumab roughly halved the lean-mass loss (to ~−3.3 to −3.8%) while increasing fat loss (up to ~−19.1%). The triple combination of semaglutide + trevogrumab + garetosmab (an anti-activin-A antibody) produced the most favorable body-composition profile of all — heavy fat loss with minimal lean loss — and is being tested in the COURAGE program expected to read out in late 2026. It is a monoclonal antibody (~150 kDa) and an investigational agent. Its inclusion rounds out the myostatin axis with a mature-myostatin neutralizer, complementing apitegromab’s precursor-selective approach. ## Mechanism Binds and neutralizes mature myostatin (GDF-8), removing its brake on muscle growth via the ActRIIB/Smad pathway. Used to offset the lean-mass loss that accompanies large GLP-1-driven weight loss. ## Chemistry | Property | Value | | --- | --- | | Molecular weight | 150000 Da | ## Research areas Studied in: Obesity, Muscle preservation, GLP-1 muscle preservation, Body composition. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - GLP-1 muscle preservation — roughly halved semaglutide-associated lean-mass loss while deepening fat loss in trial data. - Triple combination — semaglutide + trevogrumab + garetosmab gave the best body-composition profile; COURAGE trial expected to complete late 2026. - Mature-myostatin neutralizer — binds active myostatin, complementing precursor-selective antibodies. - Sarcopenia origins — earlier studied for age-related muscle loss before the obesity pivot. - Investigational — not FDA-approved. ## Storage, handling & synthesis **Storage.** Stored refrigerated (2–8 °C), protected from light and freezing, not shaken; investigational handling per trial protocol. **Handling.** A large glycosylated antibody sensitive to freezing, heat, and agitation, which can cause aggregation. **Synthesis.** Trevogrumab is a recombinant monoclonal antibody (~150 kDa) made in mammalian cell culture, characterized with antibody-grade analytics (glycan/charge-variant profiling, mass spectrometry, binding/potency bioassay) — not a synthetic peptide. ## FAQs ### What is trevogrumab? A Regeneron monoclonal antibody that neutralizes myostatin, studied as a muscle-sparing add-on to GLP-1 weight-loss drugs and in a triple combination with semaglutide and garetosmab. ### What does adding it to semaglutide do? In trial data it roughly halved the lean-mass loss seen with semaglutide alone while increasing fat loss — the core "quality of weight loss" idea. ### Is this medical advice? No — this is a research and educational reference. Trevogrumab is an investigational antibody, not an approved drug. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/trevogrumab Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Emugrobart > A "sweeping" anti-myostatin antibody (Roche/Chugai) that not only blocks but actively clears myostatin — a cautionary case after its rare-disease trials failed. - Also known as: GYM-329, RG6237, RG-70240 - Class: Growth Hormone, Metabolic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/emugrobart ## Overview Emugrobart is a humanized IgG1 monoclonal antibody developed by Chugai and Roche, and it is the most mechanistically distinctive entry on the myostatin axis. Beyond binding pro- and latent myostatin to block their activation, it uses a "sweeping antibody" design: pH-dependent binding that ferries captured myostatin into cells for degradation and then releases it, recycling the antibody to capture more. The intent is not just to block myostatin but to actively lower its levels. Emugrobart is also the catalog’s clearest honest-evidence cautionary tale. Its lead muscular-disease programs failed: in March 2026, Roche/Genentech discontinued development in spinal muscular atrophy (SMA) and facioscapulohumeral muscular dystrophy (FSHD) after the MANATEE trial showed no consistent benefit over risdiplam monotherapy. Notably, the company stated that the scientific rationale in obesity remained, and the Phase 2 obesity program was set to continue. That split — a failed rare-disease readout but a continuing metabolic program — is exactly the kind of nuance a credible reference should carry, against the marketing that treats every "myostatin antibody" as a guaranteed muscle-builder. Emugrobart is an investigational antibody (~150 kDa); its sweeping-clearance design is its scientific signature. ## Mechanism Binds pro/latent myostatin to prevent activation, and via pH-dependent (recycling/sweeping) engineering accelerates clearance of bound myostatin — reducing the circulating pool rather than only neutralizing it in place. ## Chemistry | Property | Value | | --- | --- | | Molecular weight | 150000 Da | ## Research areas Studied in: Spinal muscular atrophy, FSHD, Obesity, Muscle preservation. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. ## Key research - Sweeping/recycling design — pH-dependent binding actively clears myostatin rather than only blocking it. - MANATEE failure — discontinued in SMA and FSHD (March 2026) after no consistent benefit over risdiplam. - Obesity program continued — the metabolic rationale was retained even as rare-disease use was dropped. - Pro/latent myostatin target — binds the inactive precursor forms. - Investigational — not FDA-approved. ## Storage, handling & synthesis **Storage.** Stored refrigerated (2–8 °C), protected from light and freezing, not shaken; investigational handling per trial protocol. **Handling.** A large glycosylated antibody sensitive to freezing, heat, and agitation, which can cause aggregation. **Synthesis.** Emugrobart is a humanized IgG1 monoclonal antibody (~150 kDa) produced in mammalian cell culture, engineered for pH-dependent recycling. Characterization is antibody-grade (glycan/charge-variant profiling, mass spectrometry, binding/potency bioassay) — not a synthetic peptide. ## FAQs ### What is emugrobart? A Roche/Chugai anti-myostatin antibody (GYM-329) with a "sweeping" design that actively clears myostatin. It was studied in muscular diseases and obesity. ### What happened in its trials? Its spinal muscular atrophy and FSHD programs were discontinued in March 2026 after the MANATEE trial showed no consistent benefit over standard therapy; the obesity program was reported to be continuing. ### Is this medical advice? No — this is a research and educational reference. Emugrobart is an investigational antibody, not an approved drug. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/emugrobart Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Garetosmab > An anti-activin-A antibody (Regeneron) — closest to approval of the axis (FOP), and a partner in obesity muscle-preservation combinations. - Also known as: REGN2477 - Class: Growth Hormone, Metabolic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/garetosmab ## Overview Garetosmab is a monoclonal antibody from Regeneron that neutralizes activin A — a TGF-β-superfamily ligand that, like myostatin, signals through the activin type II receptors. Blocking activin A widens the axis beyond myostatin alone, and garetosmab plays two roles in this catalog: it is the most clinically advanced agent here, and it is the third leg of the triple obesity combination. Garetosmab’s lead indication is fibrodysplasia ossificans progressiva (FOP) — an ultra-rare disease in which soft tissue turns to bone, driven by activin A. Its Phase 3 OPTIMA trial was positive (roughly 90–94% reduction in new heterotopic bone lesions), and its FDA Biologics License Application was accepted for Priority Review with a decision target around August 2026 — making it the closest-to-approval molecule on this axis, albeit for a rare bone disease rather than obesity. Its metabolic role is as the activin-A arm of the semaglutide + trevogrumab + garetosmab triple combination, which produced the best body-composition profile in early data. As an anti-activin-A antibody (~150 kDa), it illustrates that the "myostatin axis" is really a broader activin/ActRII network with multiple blockable nodes. ## Mechanism Binds and neutralizes activin A, blocking its signaling through ActRII. In bone disease this prevents activin-A-driven abnormal ossification; in the metabolic setting, adding activin-A blockade to myostatin blockade and incretin therapy further shifts body composition toward fat loss with preserved muscle. ## Chemistry | Property | Value | | --- | --- | | Molecular weight | 150000 Da | ## Research areas Studied in: Fibrodysplasia ossificans progressiva, Obesity, Body composition, Muscle preservation. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - FOP — positive Phase 3 OPTIMA (~90–94% reduction in new abnormal bone lesions); the lead indication. - Regulatory status — BLA accepted for FDA Priority Review (target decision ~Aug 2026), the most advanced agent on this axis. - Anti-activin A — widens muscle/fat modulation beyond myostatin by blocking a related ActRII ligand. - Triple combination — the activin-A leg of semaglutide + trevogrumab + garetosmab for body composition. - Investigational in obesity — its metabolic use is not approved. ## Storage, handling & synthesis **Storage.** Stored refrigerated (2–8 °C), protected from light and freezing, not shaken; investigational handling per trial protocol. **Handling.** A large glycosylated antibody sensitive to freezing, heat, and agitation, which can cause aggregation. **Synthesis.** Garetosmab is a recombinant monoclonal antibody (~150 kDa) produced in mammalian cell culture, characterized with antibody-grade analytics (glycan/charge-variant profiling, mass spectrometry, binding/potency bioassay) — not a synthetic peptide. ## FAQs ### What is garetosmab? A Regeneron monoclonal antibody that neutralizes activin A. Its lead use is the rare bone disease FOP, and it is also a component of an obesity triple-combination aimed at preserving muscle. ### Why does an FOP drug appear alongside obesity compounds? Activin A signals through the same ActRII receptors as myostatin. Blocking it both prevents abnormal bone formation in FOP and, combined with myostatin blockade and a GLP-1 drug, shifts weight loss toward fat while sparing muscle. ### Is this medical advice? No — this is a research and educational reference. Garetosmab’s obesity use is investigational; its FOP application was under FDA review. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/garetosmab Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Bimagrumab > An antibody that blocks the activin type II receptor itself — shutting off myostatin AND activin signaling at once; famous for adding muscle while cutting fat. - Also known as: BYM338 - Class: Growth Hormone, Metabolic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/bimagrumab ## Overview Bimagrumab is a fully human monoclonal antibody that blocks the activin type II receptors (ActRIIA/ActRIIB) — the receptor every ligand on this axis must use. By acting at the receptor rather than on a single ligand, it shuts down myostatin and activin signaling simultaneously, which is why it produces the axis’s most striking body-composition effect: in trials it has both reduced fat and increased lean mass, an unusual combination for a weight-affecting drug. Bimagrumab’s history maps the whole field. It was developed (as BYM338, Novartis) for muscle-wasting conditions — sporadic inclusion body myositis (where its pivotal trial failed), sarcopenia, and COPD-related wasting — before a notable Phase 2 in type 2 diabetes showed it cut fat mass substantially while adding lean mass. That fat-down/muscle-up profile made it a centerpiece of the obesity muscle-preservation thesis: Versanis advanced it, and Eli Lilly acquired Versanis for roughly $2 billion in 2023 to pair it with tirzepatide. The honest update is that the path has not been smooth: a combination Phase 2 with semaglutide showed weight loss with preserved/added lean mass, but Lilly subsequently terminated a mid-stage obesity study pairing bimagrumab with its own incretin therapy. As the receptor-level blocker of the axis, bimagrumab is the broadest-acting and the most-watched — and a reminder that even the most mechanistically compelling agent has to clear real trials. It is investigational for these uses. ## Mechanism Binds ActRIIA/ActRIIB and prevents their natural ligands (myostatin, activins, and related factors) from signaling. Blocking the shared receptor disinhibits muscle growth broadly while reducing fat mass. ## Chemistry | Property | Value | | --- | --- | | Molecular weight | 150000 Da | ## Research areas Studied in: Obesity, Type 2 diabetes, Muscle wasting, Body composition. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. - [Growth Hormone & Body Composition](https://www.americanpeptide.com/research-areas/growth-hormone-axis): Secretagogues studied for GH release, IGF-1, and body composition. ## Key research - Receptor-level blockade — targets ActRIIA/B, blocking myostatin and activin signaling together (broadest mechanism on the axis). - Fat down, muscle up — Phase 2 in type 2 diabetes reduced fat mass while increasing lean mass, an unusual profile. - GLP-1 combination — bimagrumab + semaglutide preserved/added lean mass alongside weight loss in Phase 2. - Commercial bet and setback — Lilly acquired Versanis (~$2B, 2023) but later terminated a mid-stage obesity combination study. - Muscle-wasting origins — earlier developed for inclusion body myositis (pivotal trial failed), sarcopenia, and COPD. ## Storage, handling & synthesis **Storage.** Stored refrigerated (2–8 °C), protected from light and freezing, not shaken; investigational handling per trial protocol. **Handling.** A large glycosylated antibody sensitive to freezing, heat, and agitation, which can cause aggregation. **Synthesis.** Bimagrumab is a fully human recombinant monoclonal antibody (~150 kDa) produced in mammalian cell culture, characterized with antibody-grade analytics (glycan/charge-variant profiling, mass spectrometry, receptor-binding/cell-based potency) — not a synthetic peptide. ## FAQs ### What is bimagrumab? A monoclonal antibody that blocks the activin type II receptor, shutting off both myostatin and activin signaling. It is notable for reducing fat while increasing muscle mass, and has been studied in obesity and type 2 diabetes. ### How is it different from the myostatin antibodies? The myostatin antibodies neutralize a ligand; bimagrumab blocks the shared receptor those ligands use, so it acts more broadly across the whole activin/myostatin axis. ### Is bimagrumab approved for obesity? No. Despite encouraging body-composition data and a major acquisition, it remains investigational, and at least one mid-stage obesity combination study was terminated. ### Is this medical advice? No — this is a research and educational reference. Bimagrumab is an investigational antibody, not an approved drug. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/bimagrumab Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # MOTS-c > Mitochondrially-encoded peptide with reported insulin-sensitizing activity. - Class: Mitochondrial, Longevity, Metabolic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/mots-c ## Overview MOTS-c is a 16-amino-acid peptide encoded within the mitochondrial 12S rRNA region. Preclinical studies report improved insulin sensitivity, AMPK activation, and exercise capacity. MOTS-c is a mitochondria-derived peptide: a 16-amino-acid sequence encoded within the mitochondrial 12S rRNA gene rather than the nuclear genome. It is one of a small family of peptides that the mitochondrion itself produces as signaling molecules. Preclinical research reports that MOTS-c activates the cellular energy sensor AMPK and influences the folate–methionine cycle, with downstream effects on insulin sensitivity and exercise capacity. Its expression declines with age, fueling interest in metabolic and aging research. ## Mechanism AMPK activation; modulation of folate / methionine cycle. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C101H152N28O22S2 | | Molecular weight | 2174.6 Da | | PubChem CID | [146675088](https://pubchem.ncbi.nlm.nih.gov/compound/146675088) | ## Sequence ``` MRWQEMGYIFYPRKLR ``` ## Research areas Studied in: Metabolic disease, Exercise physiology, Aging biology. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. - [Longevity & Aging](https://www.americanpeptide.com/research-areas/longevity-aging): Peptides studied across the aging axis — senescence, NAD+, and resilience. - [Mitochondrial & Bioenergetics](https://www.americanpeptide.com/research-areas/mitochondrial): Mitochondria-targeted peptides studied for bioenergetics and cardiolipin. ## Key research - AMPK activation — studied as a regulator of cellular energy metabolism. - Insulin sensitivity — reported improvements in metabolic models. - Exercise physiology — examined for exercise capacity and metabolic flexibility. - Aging biology — expression declines with age, a focus of longevity research. - Preclinical — not FDA-approved. ## FAQs ### What is MOTS-c? MOTS-c is a mitochondria-derived peptide encoded in mitochondrial DNA, studied for effects on energy metabolism, insulin sensitivity, and exercise capacity. ### What does "mitochondria-derived" mean? Unlike most peptides, which are encoded by the nuclear genome, MOTS-c is encoded within the mitochondrial genome and acts as a signaling molecule. ### What is it studied for? Research focuses on AMPK activation, insulin sensitivity, exercise physiology, and aging biology, largely in preclinical models. ### Is it approved? No — it is a research compound. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/mots-c Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # SS-31 > Mitochondria-targeted cardiolipin-binding tetrapeptide. - Also known as: Elamipretide, Bendavia - Class: Mitochondrial, Longevity - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/ss-31 ## Overview SS-31 (elamipretide) is a synthetic tetrapeptide that concentrates in the inner mitochondrial membrane and binds cardiolipin, stabilizing electron transport chain organization in clinical trials for primary mitochondrial myopathy and Barth syndrome. SS-31 (elamipretide, formerly Bendavia) is a synthetic tetrapeptide engineered to concentrate in the inner mitochondrial membrane, where it binds the phospholipid cardiolipin. Cardiolipin is essential to the organization of the electron-transport chain, and stabilizing it is the peptide’s proposed mechanism. Unlike many catalogued peptides, SS-31 has advanced into clinical trials — for primary mitochondrial myopathy, Barth syndrome, and heart failure — though it has not received FDA approval. It is among the most clinically studied mitochondria-targeted compounds. ## Mechanism Cardiolipin binding; preservation of cristae architecture and ETC efficiency. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C32H49N9O5 | | Molecular weight | 639.8 Da | | CAS number | 736992-21-5 | | PubChem CID | [11764719](https://pubchem.ncbi.nlm.nih.gov/compound/11764719) | ## Sequence ``` D-Arg-Dmt-Lys-Phe-NH2 ``` ## Research areas Studied in: Mitochondrial myopathy, Barth syndrome, Heart failure. Guides on this site: - [Mitochondrial & Bioenergetics](https://www.americanpeptide.com/research-areas/mitochondrial): Mitochondria-targeted peptides studied for bioenergetics and cardiolipin. ## Key research - Cardiolipin binding — concentrates in the inner mitochondrial membrane to stabilize cristae. - ETC efficiency — studied for preserved electron-transport-chain function. - Mitochondrial myopathy & Barth syndrome — clinical-trial contexts. - Heart failure — examined for cardiac energetics. - Investigational — in clinical trials, not FDA-approved. ## FAQs ### What is SS-31? SS-31 (elamipretide) is a mitochondria-targeted tetrapeptide that binds cardiolipin to stabilize the inner mitochondrial membrane, studied in mitochondrial disease and heart failure. ### What is elamipretide? Elamipretide is the development name for SS-31; both refer to the same cardiolipin-binding peptide. ### What is it studied for? Clinical research contexts include primary mitochondrial myopathy, Barth syndrome, and heart failure. ### Is it approved? No — it remains investigational despite clinical trials. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/ss-31 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Epitalon > Synthetic tetrapeptide investigated for telomerase activity and circadian effects. - Also known as: Epithalon, Epithalamin fragment - Class: Longevity - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/epitalon ## Overview Epitalon is a synthetic four-amino-acid peptide derived from the pineal peptide epithalamin. Russian-led clinical work has reported effects on melatonin secretion and lifespan endpoints in rodent models. Epitalon (epithalon) is a synthetic four-amino-acid peptide modeled on epithalamin, a peptide extract of the pineal gland. It emerged from Russian gerontology research, where the pineal axis is studied as a regulator of aging and circadian rhythm. Russian-led studies have reported effects on melatonin secretion, telomerase activity, and lifespan endpoints in animal models. The evidence base is concentrated in that research tradition, independent replication is limited, and Epitalon is not FDA-approved. ## Mechanism Reported telomerase upregulation; pineal-axis modulation. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C14H22N4O9 | | Molecular weight | 390.4 Da | | CAS number | 307297-39-8 | | PubChem CID | [219042](https://pubchem.ncbi.nlm.nih.gov/compound/219042) | ## Sequence ``` AEDG ``` ## Research areas Studied in: Aging biology, Circadian biology, Pineal function. Guides on this site: - [Sleep & Circadian Rhythm](https://www.americanpeptide.com/research-areas/sleep-circadian): Peptides studied for sleep architecture and circadian regulation. - [Longevity & Aging](https://www.americanpeptide.com/research-areas/longevity-aging): Peptides studied across the aging axis — senescence, NAD+, and resilience. ## Key research - Telomerase upregulation — studies report increased expression of the telomerase catalytic subunit and telomere elongation in human somatic cells (Khavinson, Bondarev & Butyugov, 2003). - Replicative lifespan — the originating study extended human fetal fibroblast lifespan beyond the Hayflick limit without signs of malignant transformation. - Circadian / pineal function — examined for effects on melatonin secretion via the pineal axis. - Compared to other longevity peptides — a distinct mechanism: Epitalon targets telomere maintenance, where thymosin α-1 works through immune modulation and MOTS-c through mitochondrial / metabolic regulation. - Evidence quality — concentrated in a single research tradition (the Khavinson group); large independent Western RCTs are not available. ## FAQs ### What is Epitalon? Epitalon is a synthetic tetrapeptide derived from a pineal extract (epithalamin), studied in aging and circadian research, largely in animal models. ### What is it studied for? Reported effects include telomerase activity, melatonin regulation, and lifespan endpoints, primarily in Russian-led preclinical work. ### How strong is the evidence? It is concentrated in a specific research tradition with limited independent replication, so findings should be treated as preliminary. ### Is it approved? No — it is a research compound. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/epitalon Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Semax > Russian synthetic ACTH(4-10) analog studied for nootropic and neuroprotective effects. - Class: Cognitive - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/semax ## Overview Semax is a heptapeptide analog of ACTH(4-10) developed in Russia, used clinically there for stroke and cognitive disorders. Preclinical studies report BDNF / NGF upregulation. Semax is a synthetic heptapeptide based on a fragment of adrenocorticotropic hormone, ACTH(4-10), modified for stability. It was developed in Russia, where it is used clinically for stroke and cognitive disorders. Unlike full ACTH, Semax does not activate the stress (HPA) axis; instead, preclinical research focuses on its reported induction of neurotrophic factors such as BDNF and NGF. Outside Russia it is not FDA-approved and the controlled-trial base is limited. ## Mechanism BDNF / NGF induction; melanocortin signaling without HPA activation. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C37H51N9O10S | | Molecular weight | 813.9 Da | | CAS number | 80714-61-0 | | PubChem CID | [9811102](https://pubchem.ncbi.nlm.nih.gov/compound/9811102) | ## Sequence ``` MEHFPGP ``` ## Research areas Studied in: Ischemic stroke recovery, Cognition, Neuroprotection. Guides on this site: - [Cognition & Neuroprotection](https://www.americanpeptide.com/research-areas/cognition-neuroprotection): Nootropic and neurotrophic peptides studied for cognition and recovery. ## Key research - Neurotrophic induction — reported to increase BDNF protein and trkB phosphorylation in the rat hippocampus and basal forebrain (Dolotov et al., 2006). - Monoaminergic modulation — studied for enhancing dopaminergic and serotonergic signaling, alongside melanocortin activity, without activating the HPA stress axis. - Ischemic stroke & cognition — approved in Russia for stroke, cognitive impairment, and optic-nerve disease; studied for attention and memory. - Compared to Selank — both Russian neuropeptides, but Semax is oriented toward focus / cognition / neuroprotection where Selank targets anxiety; the two are often paired. - Evidence quality — most controlled data are Russian-language; Western peer-reviewed replication is limited. ## FAQs ### What is Semax? Semax is a synthetic ACTH(4-10) analog studied for nootropic and neuroprotective effects, used clinically in Russia for stroke and cognitive disorders. ### How does it work? Research points to induction of neurotrophic factors (BDNF, NGF) and melanocortin signaling, without activating the stress axis. ### Is Semax FDA-approved? No — it is approved and used in Russia but is a research compound elsewhere. This page is a research and educational reference. ### What is it studied for? Ischemic stroke recovery, cognition, and neuroprotection, with most controlled data from Russian clinical use. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/semax Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Selank > Synthetic heptapeptide analog of tuftsin investigated as an anxiolytic. - Class: Cognitive - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/selank ## Overview Selank is a synthetic analog of the immunomodulatory peptide tuftsin, developed in Russia. Reported activity includes anxiolytic effects without sedation or dependence in clinical and preclinical work. Selank is a synthetic heptapeptide based on tuftsin, an immunomodulatory peptide fragment. Like Semax, it was developed in Russia, where it is used clinically as an anxiolytic. Research interest centers on achieving anxiolytic and mild cognitive effects without the sedation, dependence, or withdrawal associated with benzodiazepines. Proposed mechanisms include modulation of GABAergic and serotonergic signaling and inhibition of enkephalin breakdown. It is not FDA-approved. ## Mechanism Modulation of GABAergic and serotonergic systems; enkephalinase inhibition. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C33H57N11O9 | | Molecular weight | 751.9 Da | | CAS number | 129954-34-3 | | PubChem CID | [11765600](https://pubchem.ncbi.nlm.nih.gov/compound/11765600) | ## Sequence ``` TKPRPGP ``` ## Research areas Studied in: Generalized anxiety, Cognitive performance. Guides on this site: - [Cognition & Neuroprotection](https://www.americanpeptide.com/research-areas/cognition-neuroprotection): Nootropic and neurotrophic peptides studied for cognition and recovery. - [Anxiety, Mood & Stress](https://www.americanpeptide.com/research-areas/anxiety-mood): Regulatory peptides studied for anxiolysis and stress-axis modulation. ## Key research - Anxiolytic activity — clinical studies report an anxiolytic effect comparable to benzodiazepines but without sedation or dependence. - GABAergic modulation — alters expression of genes in GABAergic neurotransmission and modulates GABA-A complexes allosterically, without binding the benzodiazepine site directly (Front Pharmacol, 2017). - Serotonergic & enkephalin effects — also modulates serotonin metabolism and inhibits enkephalin breakdown — a multi-system rather than single-receptor profile. - Compared to Semax — the same Russian neuropeptide lineage, but Selank soothes (anxiety) where Semax sharpens (cognition). - Evidence quality — approved and used in Russia; not FDA-approved, and Western replication is limited. ## FAQs ### What is Selank? Selank is a synthetic tuftsin analog studied as an anxiolytic, used clinically in Russia, with reported calming effects without sedation or dependence. ### How does it differ from benzodiazepines? Research interest is in anxiolytic effects without the sedation, tolerance, and withdrawal characteristic of benzodiazepines, via different proposed mechanisms. ### Is Selank approved? It is approved and used in Russia but is a research compound elsewhere; it is not FDA-approved. This page is a research and educational reference. ### What is it studied for? Generalized anxiety and cognitive performance. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/selank Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # DSIP > Endogenous nonapeptide first isolated for its sleep-promoting properties. - Also known as: Delta Sleep-Inducing Peptide - Class: Cognitive - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/dsip ## Overview DSIP is a nine-amino-acid neuropeptide first isolated from rabbit cerebral venous blood. Reported effects span sleep architecture, stress response, and circadian rhythm modulation. DSIP (Delta Sleep-Inducing Peptide) is a naturally occurring nine-amino-acid neuropeptide, first isolated in the 1970s from the blood of rabbits during induced sleep. Its name reflects the early observation that it promoted slow-wave (delta) sleep. Decades of research have linked DSIP to sleep architecture, stress-response regulation, and circadian rhythm, but its precise mechanism and receptor remain incompletely characterized. It is a research compound and is not FDA-approved. ## Mechanism Mechanism remains incompletely characterized; likely multimodal CNS modulation. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C35H48N10O15 | | Molecular weight | 848.8 Da | | CAS number | 62568-57-4 | | PubChem CID | [68816](https://pubchem.ncbi.nlm.nih.gov/compound/68816) | ## Sequence ``` WAGGDASGE ``` ## Research areas Studied in: Sleep biology, Stress physiology. Guides on this site: - [Anxiety, Mood & Stress](https://www.americanpeptide.com/research-areas/anxiety-mood): Regulatory peptides studied for anxiolysis and stress-axis modulation. - [Sleep & Circadian Rhythm](https://www.americanpeptide.com/research-areas/sleep-circadian): Peptides studied for sleep architecture and circadian regulation. ## Key research - Sleep architecture — studied for effects on slow-wave (delta) sleep. - Stress physiology — examined for interactions with the stress axis. - Circadian rhythm — investigated as a modulator of biological timing. - Uncharacterized mechanism — receptor and pathway not fully established. - Not FDA-approved — research compound. ## FAQs ### What is DSIP? DSIP (Delta Sleep-Inducing Peptide) is a naturally occurring neuropeptide first isolated for its sleep-promoting properties, studied in sleep and stress research. ### How does DSIP work? Its mechanism is not fully characterized; it is thought to act through multiple central nervous system pathways rather than a single identified receptor. ### What is it studied for? Sleep architecture, stress physiology, and circadian rhythm modulation. ### Is it approved? No — it is a research compound. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/dsip Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Melanotan II > Synthetic cyclic analog of α-MSH; non-selective melanocortin receptor agonist. - Also known as: MT-2, MT-II - Class: Cosmetic, Reproductive - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/melanotan-2 ## Overview Melanotan II is a cyclic heptapeptide α-MSH analog developed at the University of Arizona. Acts as a non-selective agonist across MC1R, MC3R, MC4R, and MC5R — pigmentation and sexual-response effects have both been documented. Melanotan II is a synthetic cyclic analog of α-melanocyte-stimulating hormone (α-MSH), developed at the University of Arizona. It is a non-selective agonist across the melanocortin receptors MC1R through MC5R. Through MC1R it stimulates melanin production (pigmentation); through MC4R it influences central sexual-response pathways. Both effects are documented in research, but its non-selectivity also drives side effects, and it is not FDA-approved. ## Mechanism Non-selective melanocortin receptor (MC1-5R) agonism. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C50H69N15O9 | | Molecular weight | 1024.2 Da | | CAS number | 121062-08-6 | | PubChem CID | [92432](https://pubchem.ncbi.nlm.nih.gov/compound/92432) | ## Research areas Studied in: Pigmentation biology, Sexual dysfunction, Photoprotection. Guides on this site: - [Skin & Hair](https://www.americanpeptide.com/research-areas/skin-hair): Peptides studied for skin aging, pigmentation, and hair follicle biology. - [Sexual & Reproductive Health](https://www.americanpeptide.com/research-areas/sexual-reproductive): Peptides studied across the HPG axis and CNS sexual-response pathways. ## Key research - Pigmentation — MC1R agonism stimulates eumelanin production via Gs-coupled cAMP signaling. - Central sexual response — MC4R activation drives arousal effects; the same MC4R activity also produces the nausea, flushing, and spontaneous erections documented in human studies. - Compared to Melanotan I (afamelanotide) — MT-II is a truncated, non-selective MC1–5R agonist, whereas afamelanotide is highly MC1R-selective and FDA-approved (Scenesse) for photoprotection in erythropoietic protoporphyria. - Relationship to PT-141 — PT-141 (bremelanotide) is a metabolite refined toward MC4R / sexual response and away from pigmentation. - Not FDA-approved — its non-selectivity drives off-target effects; research compound. ## FAQs ### What is Melanotan II? Melanotan II is a synthetic, non-selective melanocortin-receptor agonist (an α-MSH analog) studied for pigmentation and sexual-response effects. ### How is it related to PT-141? PT-141 (bremelanotide) is a melanocortin agonist with preferential MC4R activity studied for sexual function; Melanotan II is non-selective and also drives pigmentation. ### Is it approved? No — Melanotan II is not FDA-approved. This page is a research and educational reference, not a usage recommendation. ### What receptors does it act on? It activates melanocortin receptors MC1R through MC5R without selectivity. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/melanotan-2 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Afamelanotide > MC1R-selective α-MSH analog; FDA-approved (Scenesse) for photoprotection in erythropoietic protoporphyria. - Also known as: Melanotan I, Melanotan-1, MT-I, MT-1, CUV1647, Scenesse - Class: Cosmetic - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/melanotan-1 ## Overview Afamelanotide (Melanotan I) is a 13-amino-acid linear analog of α-melanocyte-stimulating hormone (α-MSH), highly selective for the melanocortin-1 receptor (MC1R). It is FDA-approved as Scenesse — delivered as a controlled-release subcutaneous implant — to increase pain-free light exposure in adults with a history of phototoxic reactions from erythropoietic protoporphyria (EPP). Afamelanotide is the [Nle4, D-Phe7] analog of α-MSH — substitutions that confer metabolic stability and high MC1R selectivity (roughly three orders of magnitude lower affinity for MC3R/MC4R than for MC1R). Unlike the non-selective Melanotan II, afamelanotide’s MC1R selectivity keeps its action largely confined to pigmentation/photoprotection, which is what allowed it to reach approval. It is administered as a controlled-release subcutaneous implant (Scenesse) rather than by injection. ## Mechanism MC1R-selective melanocortin agonism, driving eumelanin synthesis (photoprotection) via Gs-coupled cAMP signaling. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C78H111N21O19 | | Molecular weight | 1646.8 Da | | PubChem CID | [16197727](https://pubchem.ncbi.nlm.nih.gov/compound/16197727) | ## Research areas Studied in: Photoprotection, Pigmentation biology. Guides on this site: - [Skin & Hair](https://www.americanpeptide.com/research-areas/skin-hair): Peptides studied for skin aging, pigmentation, and hair follicle biology. ## Key research - FDA-approved as Scenesse (2019) for photoprotection in erythropoietic protoporphyria (EPP) — the first approved treatment for the condition. - MC1R-selective — ~1000-fold lower affinity for MC3R/MC4R, so it drives eumelanin production without the MC4R-mediated sexual-response and nausea effects of non-selective analogs. - Studied beyond EPP in solar urticaria, nonsegmental vitiligo (with narrow-band UVB), and xeroderma pigmentosum. - Compared to Melanotan II — afamelanotide is linear, MC1R-selective, and approved; Melanotan II is cyclic, non-selective (MC1–5R), and unapproved. ## FAQs ### What is afamelanotide? Afamelanotide (Melanotan I) is an MC1R-selective α-MSH analog, FDA-approved as Scenesse for photoprotection in erythropoietic protoporphyria. ### How is it different from Melanotan II? Afamelanotide is MC1R-selective and FDA-approved; Melanotan II is non-selective across MC1–5R (including the MC4R activity that drives side effects) and is not approved. ### How is it administered? As a controlled-release subcutaneous implant (Scenesse), not a self-administered injection. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/melanotan-1 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # PT-141 > Melanocortin-4 receptor agonist FDA-approved for HSDD in premenopausal women. - Also known as: Bremelanotide, Vyleesi - Class: Reproductive - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/pt-141 ## Overview Bremelanotide (PT-141) is a cyclic heptapeptide melanocortin agonist with preferential activity at MC4R. Approved by the FDA in 2019 for hypoactive sexual desire disorder in premenopausal women. PT-141 (bremelanotide) is a cyclic heptapeptide melanocortin agonist with preferential activity at the MC4R receptor. It is a metabolite of Melanotan II, refined away from pigmentation toward central sexual-response pathways. Unlike vascular treatments for sexual dysfunction, PT-141 acts in the central nervous system on the circuits that govern desire and arousal. It is FDA-approved (Vyleesi, 2019) for hypoactive sexual desire disorder (HSDD) in premenopausal women. ## Mechanism MC4R-preferential melanocortin agonism in CNS sexual-response circuits. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C50H68N14O10 | | Molecular weight | 1025.2 Da | | CAS number | 189691-06-3 | | PubChem CID | [9941379](https://pubchem.ncbi.nlm.nih.gov/compound/9941379) | ## Research areas Studied in: HSDD, CNS sexual response, Ischemia models. Guides on this site: - [Sexual & Reproductive Health](https://www.americanpeptide.com/research-areas/sexual-reproductive): Peptides studied across the HPG axis and CNS sexual-response pathways. ## Key research - Central arousal mechanism — a cyclic α-MSH analog acting on melanocortin MC3R / MC4R in the hypothalamus to drive sexual desire independent of the reproductive hormone axis (Molinoff / Diamond et al., 2003). - HSDD — FDA-approved (Vyleesi, 2019) for hypoactive sexual desire disorder in premenopausal women. - Distinct from vascular agents — acts on central desire circuits rather than on blood flow. - Compared to kisspeptin — PT-141 produces acute central arousal via melanocortin receptors, while kisspeptin acts upstream on the GnRH hormone axis; they address different research questions. - FDA-approved (Vyleesi) — for a specific indication. ## FAQs ### What is PT-141? PT-141 (bremelanotide) is a melanocortin MC4R agonist FDA-approved (Vyleesi) for hypoactive sexual desire disorder in premenopausal women. ### How does it differ from erectile-dysfunction medications? Those act on blood flow; PT-141 acts centrally, on the brain circuits that govern sexual desire and arousal. ### How is it related to Melanotan II? PT-141 is a metabolite of Melanotan II, refined toward MC4R and sexual-response activity and away from pigmentation. ### Is this medical advice? No — this page is a research and educational reference, not medical advice. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/pt-141 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Kisspeptin-10 > C-terminal decapeptide fragment of kisspeptin; potent GnRH secretagogue. - Class: Reproductive - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/kisspeptin-10 ## Overview Kisspeptin-10 (KP-10) is the minimum bioactive fragment of kisspeptin, encoded by KISS1. Administration stimulates hypothalamic GnRH release and downstream LH / FSH secretion. Kisspeptin-10 is the shortest fully active fragment of kisspeptin, the neuropeptide encoded by the KISS1 gene that sits at the top of the reproductive hormone cascade. It signals through the KISS1R (GPR54) receptor on hypothalamic GnRH neurons. By stimulating GnRH release, kisspeptin drives downstream secretion of LH and FSH — making it a research tool for probing and potentially restoring reproductive-axis function. It is investigational and not FDA-approved. ## Mechanism KISS1R (GPR54) agonism on hypothalamic GnRH neurons. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C63H83N17O14 | | Molecular weight | 1302.4 Da | | PubChem CID | [25240297](https://pubchem.ncbi.nlm.nih.gov/compound/25240297) | ## Sequence ``` YNWNSFGLRF-NH2 ``` ## Research areas Studied in: Reproductive endocrinology, Hypothalamic amenorrhea, Puberty. Guides on this site: - [Sexual & Reproductive Health](https://www.americanpeptide.com/research-areas/sexual-reproductive): Peptides studied across the HPG axis and CNS sexual-response pathways. ## Key research - GnRH stimulation — KISS1R (GPR54) agonism on hypothalamic GnRH neurons increases GnRH pulsatility and downstream LH / FSH and sex-steroid secretion. - Reproductive-axis probe — studied for restoring signaling in hypothalamic amenorrhea and as a physiologic trigger of LH / FSH in fertility research. - Puberty & limbic effects — a key regulator of pubertal onset; KISS1R is also expressed in limbic areas, enabling direct central sexual-motivation effects. - Compared to PT-141 — kisspeptin acts upstream on the hormonal axis (GnRH → LH / FSH), where PT-141 produces acute central arousal via melanocortin receptors. - Investigational — not FDA-approved. ## FAQs ### What is Kisspeptin-10? Kisspeptin-10 is the active fragment of kisspeptin, a neuropeptide that triggers GnRH release at the top of the reproductive hormone axis. ### What is the HPG-axis connection? Kisspeptin is the upstream regulator of the hypothalamic-pituitary-gonadal axis, stimulating GnRH and downstream LH and FSH. ### What is it studied for? Reproductive endocrinology, hypothalamic amenorrhea, puberty, and fertility research. ### Is it approved? No — it is investigational. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/kisspeptin-10 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # HCG > A heterodimeric glycoprotein hormone — two different glycosylated subunits — that mimics the LH surge; the pregnancy hormone, also the subject of a debunked diet. - Also known as: Human chorionic gonadotropin, Choriogonadotropin alfa, Ovidrel, Pregnyl, Novarel - Class: Reproductive - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/hcg ## Overview Human chorionic gonadotropin is the most structurally complex hormone in this catalog. It is not a single chain but a non-covalent heterodimer of two different subunits — a 92-amino-acid alpha subunit (shared with LH, FSH, and TSH) and a 145-amino-acid beta subunit that is specific to hCG — each heavily decorated with sugar chains. That glycosylation is not decoration: it is essential to the hormone’s long circulating half-life and biological activity, and it makes hCG a true glycoprotein biologic, roughly 36–40 kDa, that cannot be captured as a simple amino-acid formula. hCG’s biology is defined by its architecture. The alpha subunit is common to the whole glycoprotein-hormone family (LH, FSH, TSH); specificity comes entirely from the beta subunit and the way the two fold together. Because the subunits are made and then assembled — and because the sugar chains are added by the producing cell — hCG is a genuine glycoprotein: recombinant versions (choriogonadotropin alfa) are made in mammalian (CHO) cells precisely so that human-like glycosylation can occur, while older products are purified from the urine of pregnant women. This is biology that bacterial synthesis cannot reproduce. In medicine it is well established: it triggers ovulation in assisted reproduction, supports early-pregnancy progesterone, and is used in male hypogonadism and to preserve testicular function and fertility — including alongside testosterone therapy, where it keeps the testes signaled. It is also, famously, the hormone that pregnancy tests detect. The drama is the HCG diet. In the 1950s a British physician, Albert Simeons, claimed hCG injections plus a 500-calorie diet caused targeted fat loss. The diet was repeatedly debunked — the weight loss comes from near-starvation, not the hormone — yet it resurfaces continually, and the FDA has explicitly warned that over-the-counter "homeopathic" hCG weight-loss products are illegal and ineffective. A second, quieter misunderstanding surrounds its use in performance and TRT communities. Both make hCG a clean example of a legitimate, well-characterized hormone whose public reputation is dominated by uses it was never validated for. ## Mechanism Acts as an agonist at the LH/CG receptor, reproducing the luteinizing-hormone signal: in women it triggers ovulation and sustains the corpus luteum’s progesterone; in men it stimulates Leydig-cell testosterone production. Its long half-life, conferred by glycosylation, lets a single dose mimic the natural LH surge. ## Chemistry | Property | Value | | --- | --- | | Molecular weight | 36700 Da | | CAS number | 9002-61-3 | ## Research areas Studied in: Ovulation induction, Assisted reproduction, Male hypogonadism, Fertility preservation. ## Key research - Ovulation induction & ART — the approved use, supplying the LH-like trigger for egg release and luteal support. - Male hypogonadism — stimulates endogenous testosterone via the LH/CG receptor; used to maintain testicular function. - Glycoprotein structure — a heterodimer whose shared alpha + specific beta subunits and glycosylation define its activity and half-life. - The HCG diet — repeatedly debunked; the FDA warns OTC homeopathic hCG weight-loss products are illegal and ineffective. - Pregnancy detection — the hormone measured by home and clinical pregnancy tests. ## Storage, handling & synthesis **Storage.** Depending on the product, hCG is stored refrigerated (2–8 °C) and, once reconstituted, used within the label’s window; it must not be frozen. Glycoprotein integrity is sensitive to heat and freeze–thaw. **Handling.** A glycosylated heterodimer sensitive to heat, freezing, and agitation, any of which can dissociate the subunits or aggregate the protein and reduce potency. **Synthesis.** hCG is either purified from the urine of pregnant women or, as choriogonadotropin alfa, produced recombinantly in mammalian (CHO) cells so that the essential glycosylation is human-like. Its molecular weight (~36–40 kDa) is approximate and varies with glycosylation, so it is not represented by a single molecular formula. Characterization includes subunit identity, glycan profiling, and bioassay potency — glycoprotein-grade analytics well beyond an HPLC purity number. ## FAQs ### What is HCG? Human chorionic gonadotropin — a glycoprotein hormone made of two different glycosylated subunits that mimics luteinizing hormone. It triggers ovulation, supports early pregnancy, and stimulates testosterone in men. It is also the hormone pregnancy tests detect. ### Why is HCG a glycoprotein rather than a simple peptide? It is a two-subunit protein heavily modified with sugar chains that are essential to its half-life and activity. Recombinant hCG is made in mammalian cells so that human-like glycosylation can occur — something bacterial peptide synthesis cannot do. ### Does the HCG diet work? No. The HCG diet has been repeatedly debunked — any weight loss comes from the extreme calorie restriction, not the hormone — and the FDA has warned that OTC homeopathic hCG weight-loss products are illegal and ineffective. ### Is this medical advice? No — this is a research and educational reference. hCG is a prescription hormone with specific approved indications. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/hcg Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Oxytocin > A 9-amino-acid cyclic hormone of labor and bonding — historically the first peptide hormone ever chemically synthesized, and the most over-marketed "love hormone." - Also known as: Pitocin, Syntocinon, the love hormone - Class: Reproductive, Cognitive - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/oxytocin ## Overview Oxytocin is a tiny but pivotal hormone: a 9-amino-acid cyclic peptide, closed by a single disulfide bridge, released from the posterior pituitary. It drives uterine contractions in labor and milk letdown in nursing, and it acts in the brain on social behavior — the source of its "love hormone" fame. It also holds a place in scientific history: in 1953 Vincent du Vigneaud synthesized it, the first polypeptide hormone ever made in the lab, a feat that won the 1955 Nobel Prize in Chemistry and opened the door to synthetic peptide therapeutics. Oxytocin’s established medicine is obstetric. As Pitocin it is one of the most widely used drugs in childbirth — to induce or augment labor and to control bleeding afterward — and it mediates the milk-ejection reflex during breastfeeding. Structurally it is almost a twin of vasopressin, differing in only two residues, which is why the two hormones’ effects sometimes overlap. Its fame, though, comes from the brain. Animal and early human work tied oxytocin to pair-bonding, maternal behavior, trust, and social affiliation, and the popular press crowned it the "love hormone" or "cuddle chemical." That framing drove a wave of intranasal-oxytocin research and products promising better social functioning — in autism, social anxiety, even relationship enhancement. The honest reckoning is more sober. Rigorous, larger trials of intranasal oxytocin — including in autism — have largely failed to reproduce the early promise, and there are real questions about how much intranasal oxytocin even reaches the brain. Oxytocin is a genuine, important hormone whose behavioral marketing ran far ahead of the evidence — a textbook case of a misunderstood molecule, which is exactly why it belongs in an honest reference. ## Mechanism Agonist at the oxytocin receptor (a G-protein-coupled receptor). Peripherally it contracts uterine smooth muscle and the mammary myoepithelium; centrally it modulates circuits involved in social bonding, trust, and stress, which is the basis of its behavioral research. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C43H66N12O12S2 | | Molecular weight | 1007.19 Da | | CAS number | 50-56-6 | ## Sequence ``` CYIQNCPLG-NH2 ``` ## Research areas Studied in: Labor induction, Lactation, Social bonding, Anxiety and stress. Guides on this site: - [Anxiety, Mood & Stress](https://www.americanpeptide.com/research-areas/anxiety-mood): Regulatory peptides studied for anxiolysis and stress-axis modulation. ## Key research - Labor and delivery — induction/augmentation of labor and control of postpartum bleeding (the core approved use). - Lactation — mediates the milk-ejection (letdown) reflex. - Social neuroscience — studied for bonding, trust, and stress modulation; the basis of the "love hormone" label. - Intranasal hype vs evidence — larger trials (including autism) have largely not confirmed early behavioral claims. - A historic first — the first peptide hormone chemically synthesized (du Vigneaud, 1953; Nobel Prize 1955). ## Storage, handling & synthesis **Storage.** Oxytocin injection is stored refrigerated (2–8 °C) per most labels; the cyclic disulfide peptide is sensitive to heat over time. Nasal/compounded forms follow their own storage. **Handling.** A small disulfide-bridged peptide; protect from heat and prolonged storage in solution to preserve potency. **Synthesis.** Oxytocin is a 9-residue cyclic peptide with a single intramolecular disulfide bond, made by solid-phase peptide synthesis — fittingly, since its 1953 chemical synthesis was the historical proof that peptide hormones could be built in the lab at all. Its small size and defined structure make it straightforward to characterize by mass spectrometry and HPLC, unlike the large folded biologics elsewhere in this catalog. ## FAQs ### What is oxytocin? A 9-amino-acid cyclic hormone from the posterior pituitary that drives uterine contractions and milk letdown, and acts in the brain on social behavior. As a drug (Pitocin) it is used in labor. ### Is oxytocin really the "love hormone"? It does play a role in bonding and social behavior, but the "love hormone" label is overstated. Rigorous trials of intranasal oxytocin for social conditions, including autism, have largely failed to confirm the early hype. ### Why is oxytocin historically important? It was the first peptide hormone ever chemically synthesized (Vincent du Vigneaud, 1953), which won the 1955 Nobel Prize in Chemistry and helped launch the field of synthetic peptide therapeutics. ### Is this medical advice? No — this is a research and educational reference, not dosing guidance. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/oxytocin Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # FSH (Follitropin) > A heterodimeric glycoprotein gonadotropin that drives follicle growth and spermatogenesis — the workhorse of IVF stimulation, and a sister molecule to HCG and LH. - Also known as: Follicle-stimulating hormone, Follitropin alfa, Gonal-f, Follistim, Puregon - Class: Reproductive - FDA approved: Yes - Canonical page: https://www.americanpeptide.com/catalog/fsh ## Overview Follicle-stimulating hormone is one of the three pituitary glycoprotein gonadotropins, and like its siblings LH and HCG it is built from a shared alpha subunit paired with a hormone-specific beta subunit, heavily glycosylated. FSH is the signal that recruits and grows ovarian follicles in women and supports sperm production in men, which makes recombinant FSH (follitropin) the central tool of assisted reproduction — the drug that drives controlled ovarian stimulation in IVF. FSH completes the gonadotropin picture alongside HCG and LH in this catalog: the same alpha subunit, a distinct beta subunit, and obligatory glycosylation that makes it a true glycoprotein hormone rather than a simple peptide. Its job is the front half of the reproductive cycle — recruiting and maturing ovarian follicles — where LH and the LH-mimicking HCG handle the ovulatory trigger that follows. Therapeutically, recombinant FSH (follitropin alfa, Gonal-f; follitropin beta, Follistim) is produced in mammalian cells so its glycosylation is human-like, and it is the backbone of controlled ovarian stimulation in IVF — driving the development of multiple follicles in a cycle — as well as treatment for anovulation and certain male infertility. Older urine-derived gonadotropin products (menotropins) supplied FSH and LH activity together; recombinant versions allow precise, consistent dosing. FSH is less surrounded by pop-culture drama than oxytocin or HCG, but it carries the same molecular lesson: glycoprotein hormones are assembled, glycosylated biologics whose sugar chains are part of the drug, which is why they are grown in cells and characterized by glycan and bioassay analytics rather than a simple purity figure. ## Mechanism Binds the FSH receptor on ovarian granulosa cells (driving follicle maturation and estrogen production) and on testicular Sertoli cells (supporting spermatogenesis). Its glycosylation governs its circulating half-life and activity. ## Chemistry | Property | Value | | --- | --- | | Molecular weight | 30000 Da | | UniProt | [P01225](https://www.uniprot.org/uniprotkb/P01225) | ## Research areas Studied in: Ovarian stimulation, IVF / assisted reproduction, Anovulation, Male infertility. ## Key research - Controlled ovarian stimulation — the core use; drives multi-follicle development for IVF. - Anovulation — used to induce follicle growth when ovulation fails. - Male infertility — supports spermatogenesis via Sertoli-cell FSH receptors. - Gonadotropin family — shares an alpha subunit with LH, HCG, and TSH; specificity is in the beta subunit. - Recombinant vs urinary — recombinant follitropin allows precise dosing vs older urine-derived menotropins. ## Storage, handling & synthesis **Storage.** Recombinant FSH products are refrigerated (2–8 °C) and protected from light and freezing; reconstituted/in-use pens follow the label’s window. Glycoprotein integrity is sensitive to heat and freeze–thaw. **Handling.** A glycosylated heterodimer sensitive to heat, freezing, and agitation, which can dissociate the subunits or aggregate the protein and reduce potency. **Synthesis.** Recombinant follitropin is produced in mammalian (CHO) cells so its essential glycosylation is human-like; its ~30 kDa mass is approximate and varies with glycosylation, so it has no single molecular formula. Characterization is glycoprotein-grade — subunit identity, glycan/isoform profiling, and bioassay potency — well beyond an HPLC purity number. ## FAQs ### What does FSH do? Follicle-stimulating hormone drives the growth of ovarian follicles in women and supports sperm production in men. As recombinant follitropin it is the main drug used to stimulate the ovaries in IVF. ### How is FSH related to HCG and LH? They are all glycoprotein gonadotropins sharing the same alpha subunit; their unique beta subunits give them different jobs. FSH grows follicles, while LH and the LH-mimicking HCG trigger ovulation. ### Why is FSH a glycoprotein biologic? It is a two-subunit, heavily glycosylated protein whose sugar chains are essential to its activity and half-life. It is made in mammalian cells so glycosylation is human-like — not by peptide synthesis. ### Is this medical advice? No — this is a research and educational reference, not dosing guidance. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/fsh Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # Thymosin Alpha-1 > Thymus-derived 28-amino-acid peptide approved in many countries as an immunomodulator. - Also known as: Tα1, Thymalfasin, Zadaxin - Class: Immune - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/thymosin-alpha-1 ## Overview Thymosin α1 is a 28-amino-acid peptide originally isolated from thymic tissue. Approved in numerous countries as adjunctive therapy in chronic hepatitis B / C and as an immune-system modulator. Thymosin alpha-1 (Tα1, thymalfasin) is a 28-amino-acid peptide originally isolated from the thymus, the organ where T cells mature. It acts as an immune modulator, helping to restore and direct T-cell responses. Unlike most catalogued peptides, Tα1 is approved in many countries (marketed as Zadaxin) as an adjunct in chronic hepatitis B and C and in other immune contexts, though it is not FDA-approved in the United States. It is among the most clinically studied immunomodulatory peptides. ## Mechanism TLR9-mediated DC activation; Th1 immune polarization. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C129H215N33O55 | | Molecular weight | 3108.3 Da | | CAS number | 62304-98-7 | | PubChem CID | [16130571](https://pubchem.ncbi.nlm.nih.gov/compound/16130571) | ## Sequence ``` SDAAVDTSSEITTKDLKEKKEVVEEAEN ``` ## Research areas Studied in: Chronic viral hepatitis, Sepsis adjunct, Oncology adjunct. Guides on this site: - [Immune & Inflammation](https://www.americanpeptide.com/research-areas/immune-inflammation): Thymic and host-defense peptides studied for immune modulation. ## Key research - T-cell modulation — TLR9-mediated dendritic-cell activation and Th1 polarization. - Chronic viral hepatitis — adjunctive use studied and approved in many countries. - Sepsis — examined as an immune-restoring adjunct. - Oncology — studied as an adjunct to support immune response. - Approved abroad — marketed as Zadaxin; not FDA-approved in the US. ## FAQs ### What is Thymosin alpha-1? Thymosin alpha-1 is a thymus-derived immunomodulatory peptide (Zadaxin) used in many countries as an adjunct in chronic hepatitis and other immune conditions. ### How does it work? It supports and directs T-cell responses, in part through TLR9-mediated dendritic-cell activation and a shift toward Th1 immunity. ### Is it FDA-approved? It is approved in numerous countries but not by the US FDA. This page is a research and educational reference. ### What is it studied for? Chronic viral hepatitis, and as an immune-supporting adjunct in sepsis and oncology research. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/thymosin-alpha-1 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # LL-37 > Human cathelicidin antimicrobial peptide active across bacteria, fungi, and viruses. - Also known as: Cathelicidin, hCAP-18 fragment - Class: Immune, Healing & Repair - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/ll-37 ## Overview LL-37 is the C-terminal 37-residue fragment of human cathelicidin hCAP-18 and the only cathelicidin expressed in humans. Roles span direct antimicrobial activity, chemotaxis, and wound healing. LL-37 is the only cathelicidin antimicrobial peptide expressed in humans — a 37-residue fragment released from the precursor protein hCAP-18. It is a frontline component of innate immunity, found in neutrophils, epithelial cells, and skin. Beyond directly disrupting the membranes of bacteria, fungi, and some viruses, LL-37 also acts as a signaling molecule that recruits immune cells and supports wound healing. Interest has grown as antibiotic resistance renews attention on host-defense peptides. It is studied as a research compound. ## Mechanism Membrane disruption of pathogens; immunomodulatory signaling via FPRL1. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C205H340N60O53 | | Molecular weight | 4493.3 Da | | CAS number | 154947-66-7 | | PubChem CID | [16198951](https://pubchem.ncbi.nlm.nih.gov/compound/16198951) | ## Research areas Studied in: Antimicrobial resistance, Chronic wound healing, Innate immunity. Guides on this site: - [Wound Healing & Tissue Repair](https://www.americanpeptide.com/research-areas/wound-healing): Regenerative peptides studied for soft-tissue, tendon, and vascular repair. - [Immune & Inflammation](https://www.americanpeptide.com/research-areas/immune-inflammation): Thymic and host-defense peptides studied for immune modulation. ## Key research - Broad antimicrobial activity — membrane disruption across bacteria, fungi, and viruses. - Antimicrobial resistance — host-defense peptides studied as an alternative strategy. - Wound healing — chemotaxis and tissue-repair signaling. - Immunomodulation — signaling via the FPRL1 receptor. - Research compound — not an approved medicine. ## FAQs ### What is LL-37? LL-37 is the only human cathelicidin antimicrobial peptide, part of innate immunity, with direct antimicrobial and wound-healing roles. ### Why is it of interest for antibiotic resistance? As a host-defense peptide that disrupts microbial membranes, it represents a mechanism distinct from conventional antibiotics, of growing interest as resistance spreads. ### What is it studied for? Antimicrobial-resistance research, chronic wound healing, and innate immunity. ### Is it approved? No — it is a research compound. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/ll-37 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # KPV > Anti-inflammatory C-terminal tripeptide of α-MSH. - Class: Immune, Healing & Repair - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/kpv ## Overview KPV (Lys-Pro-Val) is the C-terminal tripeptide of α-MSH and retains much of α-MSH's anti-inflammatory activity without pigmentary effects. Preclinical work in colitis and skin inflammation models. KPV is the C-terminal tripeptide (lysine-proline-valine) of α-melanocyte-stimulating hormone (α-MSH). It retains much of the parent hormone’s anti-inflammatory activity while shedding its pigmentary effects, making it a focused research tool for inflammation. Preclinical studies report that KPV reduces pro-inflammatory signaling — in part by interfering with the NF-κB pathway — in models of colitis, skin inflammation, and oral inflammation. It is a research compound and is not FDA-approved. ## Mechanism NF-κB pathway inhibition; reduction of pro-inflammatory cytokines. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C16H30N4O4 | | Molecular weight | 342.4 Da | | PubChem CID | [125672](https://pubchem.ncbi.nlm.nih.gov/compound/125672) | ## Sequence ``` KPV ``` ## Research areas Studied in: IBD models, Atopic dermatitis, Oral inflammation. Guides on this site: - [Immune & Inflammation](https://www.americanpeptide.com/research-areas/immune-inflammation): Thymic and host-defense peptides studied for immune modulation. ## Key research - Anti-inflammatory signaling — NF-κB pathway inhibition reducing cytokine output. - Inflammatory bowel disease — studied in colitis models. - Skin inflammation — examined in atopic-dermatitis models. - No pigmentary effect — retains α-MSH anti-inflammation without tanning. - Preclinical — not FDA-approved. ## FAQs ### What is KPV? KPV is the anti-inflammatory C-terminal tripeptide of α-MSH, studied in preclinical models of colitis and skin inflammation. ### How is it related to α-MSH? KPV is the final three residues of α-MSH and keeps much of its anti-inflammatory activity without the pigmentation effect. ### What is it studied for? Inflammatory bowel disease, atopic dermatitis, and oral inflammation, primarily in preclinical models. ### Is it approved? No — it is a research compound. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/kpv Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # AOD-9604 > C-terminal hGH fragment (177–191) historically investigated for lipolysis. - Class: Metabolic - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/aod-9604 ## Overview AOD-9604 is a 16-amino-acid synthetic peptide derived from the lipolytic C-terminal domain of human growth hormone. Reached Phase IIb obesity trials without meeting weight-loss endpoints; later repositioned to cartilage / joint research. AOD-9604 is a 16-amino-acid synthetic peptide corresponding to the lipolytic C-terminal region (residues 177–191) of human growth hormone. It was designed to reproduce GH’s fat-metabolizing effect without the growth-promoting or glucose effects of the full hormone. It advanced into Phase IIb obesity trials but did not meet its weight-loss endpoints, after which research interest shifted toward cartilage and joint applications. It is not FDA-approved as a therapeutic. ## Mechanism Putative β3-adrenergic mediated lipolysis without GH receptor binding. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C78H123N23O23S2 | | Molecular weight | 1815.1 Da | | PubChem CID | [71300630](https://pubchem.ncbi.nlm.nih.gov/compound/71300630) | ## Research areas Studied in: Obesity (historical), Cartilage repair. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. - [Wound Healing & Tissue Repair](https://www.americanpeptide.com/research-areas/wound-healing): Regenerative peptides studied for soft-tissue, tendon, and vascular repair. ## Key research - Lipolysis — the GH fragment studied for fat metabolism without GH-receptor binding. - Obesity trials — reached Phase IIb but did not meet weight-loss endpoints. - Cartilage repair — repositioned toward joint research. - Mechanism — proposed β3-adrenergic-mediated lipolysis. - Not FDA-approved — did not meet clinical endpoints for obesity. ## FAQs ### What is AOD-9604? AOD-9604 is a fragment of human growth hormone (residues 177–191) studied for fat metabolism (lipolysis) without GH’s other effects. ### Did it work for weight loss? It reached Phase IIb obesity trials but did not meet its weight-loss endpoints; research later shifted toward cartilage and joint applications. ### How does it differ from full GH? It is designed to reproduce GH’s lipolytic effect without binding the GH receptor or driving growth and glucose effects. ### Is it approved? No — it is not FDA-approved as a therapeutic. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/aod-9604 Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # 5-Amino-1MQ > Small-molecule NNMT inhibitor (often catalogued alongside peptides). - Class: Metabolic, Longevity - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/5-amino-1mq ## Overview 5-Amino-1MQ is a selective inhibitor of nicotinamide N-methyltransferase (NNMT). Preclinical work links NNMT inhibition to improvements in adipose tissue metabolism and skeletal muscle aging. 5-Amino-1MQ is a small molecule — not a peptide — that is frequently catalogued alongside research peptides because of its metabolic focus. It selectively inhibits the enzyme nicotinamide N-methyltransferase (NNMT). NNMT consumes methyl groups and influences cellular NAD+ and SAM pools; inhibiting it is studied in preclinical work for improved adipose-tissue metabolism and muscle aging. It is a research compound and is not FDA-approved. ## Mechanism NNMT inhibition → preserved cellular NAD+ / SAM pools. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C10H11N2+ | | Molecular weight | 159.21 Da | | CAS number | 209783-80-2 | | PubChem CID | [950107](https://pubchem.ncbi.nlm.nih.gov/compound/950107) | ## Research areas Studied in: Obesity, Sarcopenia, NAD+ biology. Guides on this site: - [Weight Loss & Metabolic Health](https://www.americanpeptide.com/research-areas/weight-loss): Incretin and metabolic peptides studied for glycemic control and fat loss. - [Longevity & Aging](https://www.americanpeptide.com/research-areas/longevity-aging): Peptides studied across the aging axis — senescence, NAD+, and resilience. ## Key research - NNMT inhibition — selectively blocks nicotinamide N-methyltransferase. - Adipose metabolism — studied for effects on fat-tissue energy handling. - Sarcopenia — examined for skeletal-muscle aging. - NAD+ / SAM pools — NNMT inhibition linked to preserved methyl-donor and NAD+ metabolism. - Small molecule — not a peptide; not FDA-approved. ## FAQs ### What is 5-Amino-1MQ? 5-Amino-1MQ is a small-molecule inhibitor of the enzyme NNMT, studied in metabolic and aging research; it is catalogued here alongside peptides for its metabolic relevance. ### Is it a peptide? No — it is a small molecule, not a peptide, but it is grouped with metabolic research compounds. ### What is it studied for? Obesity, sarcopenia (muscle aging), and NAD+ biology, primarily in preclinical models. ### Is it approved? No — it is a research compound. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/5-amino-1mq Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice. # NAD+ > Essential redox cofactor central to mitochondrial bioenergetics and sirtuin activity. - Also known as: Nicotinamide Adenine Dinucleotide - Class: Mitochondrial, Longevity - FDA approved: No - Canonical page: https://www.americanpeptide.com/catalog/nad-plus ## Overview NAD+ is a ubiquitous coenzyme required for electron transport, sirtuin activity, and PARP-mediated DNA repair. Often supplied as a research reagent and increasingly as an investigational therapeutic. NAD+ (nicotinamide adenine dinucleotide) is not a peptide but a universal coenzyme, included here for its central place in metabolic and longevity research. Every cell uses it to carry electrons through energy metabolism and to power signaling enzymes. Two enzyme families make NAD+ a focus of aging research: sirtuins, which depend on it to regulate gene expression and stress resistance, and PARPs, which use it for DNA repair. Cellular NAD+ declines with age, and restoring it — directly or via precursors — is widely studied. ## Mechanism Cofactor for hundreds of redox and signaling enzymes including sirtuins and PARPs. ## Chemistry | Property | Value | | --- | --- | | Molecular formula | C21H27N7O14P2 | | Molecular weight | 663.4 Da | | CAS number | 53-84-9 | | PubChem CID | [5893](https://pubchem.ncbi.nlm.nih.gov/compound/5893) | ## Research areas Studied in: Aging biology, Mitochondrial dysfunction, Neurodegeneration. Guides on this site: - [Cognition & Neuroprotection](https://www.americanpeptide.com/research-areas/cognition-neuroprotection): Nootropic and neurotrophic peptides studied for cognition and recovery. - [Longevity & Aging](https://www.americanpeptide.com/research-areas/longevity-aging): Peptides studied across the aging axis — senescence, NAD+, and resilience. - [Mitochondrial & Bioenergetics](https://www.americanpeptide.com/research-areas/mitochondrial): Mitochondria-targeted peptides studied for bioenergetics and cardiolipin. ## Key research - Energy metabolism — essential electron carrier in the mitochondrial electron-transport chain. - Sirtuin activity — required cofactor for sirtuin-mediated longevity signaling. - DNA repair — consumed by PARP enzymes during repair. - Age-related decline — NAD+ falls with age, a central theme in longevity research. - Cofactor / reagent — supplied as a research reagent and investigational therapeutic. ## FAQs ### What is NAD+? NAD+ (nicotinamide adenine dinucleotide) is an essential coenzyme central to energy metabolism, sirtuin activity, and DNA repair — a major focus of aging research. ### Is NAD+ a peptide? No — it is a coenzyme (a dinucleotide), included in the catalog for its central role in mitochondrial and longevity research. ### Why does NAD+ matter for aging? Cellular NAD+ declines with age, and the sirtuin and PARP enzymes that depend on it govern stress resistance and DNA repair, so restoring NAD+ is widely studied. ### Is it approved? NAD+ is used as a research reagent and studied as an investigational therapeutic. This page is a research and educational reference. --- Source: AmericanPeptide.com — https://www.americanpeptide.com/catalog/nad-plus Data license: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Attribution: AmericanPeptide.com. Research reference only — computational and educational content, not medical advice.