Peptides›Sexual / hormonal, Cosmetic›α-MSH (Alpha Melanocyte-Stimulating Hormone)

α-MSH (Alpha Melanocyte-Stimulating Hormone)

/ Endogenous tridecapeptide derived from POMC processing; native melanocortin receptor agonist

TIER 3 · PreclinicalN = 0 · TESTING PENDINGMW 1664.90 g·mol⁻¹

ALIAS · α-MSH · Alpha-MSH · α-melanocortin · Native α-melanocyte-stimulating hormone (1-13)

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Research use onlyAny dose figures below describe what specific cited studies used, reported factually. Nothing on this page is guidance for human use.READ FIRST →

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§ A · Identity

Primary sequenceAc-SYSMEHFRWGKPV-NH2

MW · 1664.90CLASS · Endogenous tridecapeptide derived from POMC processing; native melanocortin receptor agonistCATEGORY · Sexual / hormonal, Cosmetic

Tier 3. Native α-MSH is the foundational melanocortin peptide and the parent of clinically successful synthetic analogs (afamelanotide for erythropoietic protoporphyria; bremelanotide for HSDD). Native α-MSH itself has substantial preclinical pharmacology and Phase 1-style human pharmacology data but no FDA-approved therapeutic in its native form.

§ B · Mechanism of action

α-MSH is a tridecapeptide derived from proteolytic processing of pro-opiomelanocortin (POMC). It is a non-selective agonist at melanocortin receptors MC1R-MC5R, with highest affinity at MC1R. Pigmentary effects (skin and hair darkening) are mediated by MC1R on melanocytes; sexual-arousal effects emerge through MC4R signalling in CNS arousal circuits; metabolic and anti-inflammatory effects involve MC3R and MC5R.

§ C · Human clinical evidence

Tier 3. Foundational pharmacology with extensive rodent and primate literature dating to the 1960s. Synthetic stable analogs are the clinical translation: afamelanotide (Scenesse, Clinuvel) is FDA-approved for erythropoietic protoporphyria; bremelanotide (Vyleesi) is FDA-approved for HSDD in premenopausal women.

§ D · Primary literature

PubMed20852827Catania A et al. — The melanocortin system in control of inflammation · ScientificWorldJournal · reviewReviews the anti-inflammatory roles of alpha-MSH and the broader melanocortin system across MC1R-MC5R subtypes in systemic and local host reactions.Limitations: Narrative review; no original data; predominantly preclinical literature.2010

PubMed9078687Lipton JM et al. — Anti-inflammatory actions of the neuroimmunomodulator alpha-MSH · Immunology Today · reviewFoundational review establishing alpha-MSH as an endogenous anti-inflammatory peptide acting via central and peripheral melanocortin receptors.Limitations: Pre-2000 review; rodent and in-vitro data dominate the supporting literature.1997

PubMed11023702Wikberg JE et al. — New aspects on the melanocortins and their receptors · Pharmacological Research · reviewReviews structure, function, and tissue distribution of MC1R-MC5R and the actions of endogenous alpha-, beta-, and gamma-MSH ligands.Limitations: Narrative review; clinical translational data limited at time of publication.2000

§ F · Safety signal

Native α-MSH has very short plasma half-life and rapid clearance — therapeutic application requires the more stable synthetic analogs. Class concerns from melanocortin agonism include skin pigmentation, transient nausea, and (with MC4R-active agents) elevations in blood pressure.

§ H · Regulatory status

Regulatory status

FDA status:: Not FDA-approved

§ I · Notable gaps and controversies

The native peptide has been largely supplanted by synthetic analogs with longer half-life and selective receptor profiles. Vendor-sold 'α-MSH' is not the same molecule as afamelanotide or bremelanotide — those have additional substitutions and acetylation patterns conferring their pharmacokinetic and selectivity differences.