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Compound monograph

alpha-MSH

alpha-MSH is the endogenous thirteen-residue melanocortin peptide hormone from which several of the synthetic compounds in this library are derived.

Published: 2026-09-13Literature/identifier verification: 2026-09-13
α-MSHalpha-MSHalpha-melanotropinMelanotropin alphaMelanocortin receptor ligands

01

Identity & nomenclature

alpha-MSH is the endogenous thirteen-residue melanocortin peptide hormone from which several of the synthetic compounds in this library are derived.

This is the native hormone, not an analog. It is not afamelanotide: the parent retains Met4 and L-Phe7, and the analog's norleucine and D-phenylalanine substitutions must not migrate into the parent's identity fields. Nor is it simply 'ACTH(1-13)' — the N-acetyl and C-amide processing distinguish it from an uncapped fragment. KPV is its C-terminal tripeptide sequence and nothing more; see structuralNotes.

Declared aliases and development codes: α-MSH, alpha-MSH, alpha-melanotropin, Melanotropin alpha.

02

Molecular properties

Molecular formulaC77H109N21O19S
Molecular mass1664.91 Da
CAS Registry Number581-05-5
PubChem CID16133793
UNIIOVF025LA77
One-letter sequenceSYSMEHFRWGKPV
Three-letter sequenceAc–Ser–Tyr–Ser–Met–Glu–His–Phe–Arg–Trp–Gly–Lys–Pro–Val–NH2

Thirteen residues, all L, linear, N-terminally acetylated and C-terminally amidated. The 'Ac' is the acetyl cap, not amino-acid letters.

03

Structural characteristics

An agonist at MC1R, MC3R, MC4R and MC5R, with receptor-bound structures establishing MC1R and MC4R recognition; it is not the canonical agonist at MC2R, which responds to ACTH. One caution matters for this library specifically: a fragment of alpha-MSH does not inherit its receptor profile. Comparative work reports that the C-terminal tripeptide KPV retains an anti-inflammatory effect that was NOT blocked by the MC3/4R antagonist SHU9119 and did not raise cAMP, and concludes it likely acts through a mechanism other than the melanocortin receptors. Sequence ancestry is a structural relationship, not a pharmacological one.

Terminal features: N-terminal acetylation, C-terminal amide.

04

Molecular targets & mechanisms

05

Analytical considerations

Confirmation requires the thirteen-residue sequence, Met4, the N-acetyl cap and the C-terminal amide, plus a methionine-oxidation assessment. The parent must be distinguished from the Nle4/D-Phe7 analog: those differ compositionally and are separable by mass, but mass alone establishes no D/L configuration. Detecting KPV after hydrolysis or degradation does not show the intact parent was present.

06

Verified bibliography

  1. Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides.

    Getting SJ, Schiöth HB, Perretti M

    The Journal of pharmacology and experimental therapeutics · 2003-05-15 · Journal Article

    current
  2. Use of chimeric melanocortin-2 and -4 receptors to identify regions responsible for ligand specificity and dependence on melanocortin 2 receptor accessory protein.

    Hinkle PM, Serasinghe MN, Jakabowski A, Sebag JA, Wilson KR, Haskell-Luevano C

    European journal of pharmacology · 2011-01-03 · Journal Article

    current
  3. Structural mechanism of calcium-mediated hormone recognition and Gβ interaction by the human melanocortin-1 receptor.

    Ma S, Chen Y, Dai A, Yin W, Guo J, Yang D, Zhou F, Jiang Y, Wang MW, Xu HE

    Cell research · 2021-08-27 · Journal Article

    current
  4. Structural insights into ligand recognition and activation of the melanocortin-4 receptor.

    Zhang H, Chen LN, Yang D, Mao C, Shen Q, Feng W, Shen DD, Dai A, Xie S, Zhou Y, Qin J, Sun JP, Scharf DH, Hou T, Zhou T, Wang MW, Zhang Y

    Cell research · 2021-08-25 · Journal Article

    current

10

Methodology & citation verification

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