Human alpha-MSH
- Mature form
- 13-amino-acid N-acetylated, C-terminally amidated peptide
- Precursor gene
- POMC
- Sequence
- SYSMEHFRWGKPV-NH2
- Modifications
- Ser1 N-acetylation; Val13 C-terminal amidation
Signalling pathway
A source-bound map of mature human alpha-MSH, its MC1R, MC3R, MC4R and MC5R agonist relations, and separate human-target evidence for afamelanotide, bremelanotide and Melanotan II.
Updated: 2026-08-22
| Molecule | Type | Receptor / target | Relation | Evidence class | Sources |
|---|---|---|---|---|---|
| Human alpha-MSH | Endogenous ligand | MC1RMelanocortin 1 receptor | AgonistCanonical endogenous agonismGs → adenylyl cyclase → cAMP | Curated receptor pharmacology | 123 |
| Human alpha-MSH | Endogenous ligand | MC3RMelanocortin 3 receptor | AgonistCanonical endogenous agonismGs → adenylyl cyclase → cAMP | Curated receptor pharmacology | 123 |
| Human alpha-MSH | Endogenous ligand | MC4RMelanocortin 4 receptor | AgonistCanonical endogenous agonismGs → adenylyl cyclase → cAMP | Curated receptor pharmacology | 123 |
| Human alpha-MSH | Endogenous ligand | MC5RMelanocortin 5 receptor | AgonistCanonical endogenous agonismGs → adenylyl cyclase → cAMP | Curated receptor pharmacology | 123 |
Each edge below comes from an agent-specific source. Status and receptor pharmacology are verified separately.
| Molecule | Type | Receptor / target | Relation | Evidence class | Sources |
|---|---|---|---|---|---|
| Afamelanotide | Approved medicineStatus reviewed: 2026-08-22Status source 1 | MC1RMelanocortin 1 receptor | AgonistEngineered receptor agonism | Official product pharmacology | 1 |
| Afamelanotide | Approved medicineStatus reviewed: 2026-08-22Status source 1 | MC3RMelanocortin 3 receptor | AgonistEngineered receptor agonism | Official product pharmacology | 1 |
| Afamelanotide | Approved medicineStatus reviewed: 2026-08-22Status source 1 | MC4RMelanocortin 4 receptor | AgonistEngineered receptor agonism | Official product pharmacology | 1 |
| Afamelanotide | Approved medicineStatus reviewed: 2026-08-22Status source 1 | MC5RMelanocortin 5 receptor | AgonistEngineered receptor agonism | Official product pharmacology | 1 |
| Bremelanotide | Approved medicineStatus reviewed: 2026-08-22Status source 1 | MC1RMelanocortin 1 receptor | AgonistEngineered receptor agonism | Official product pharmacology | 1 |
| Bremelanotide | Approved medicineStatus reviewed: 2026-08-22Status source 1 | MC3RMelanocortin 3 receptor | AgonistEngineered receptor agonism | Official product pharmacology | 1 |
| Bremelanotide | Approved medicineStatus reviewed: 2026-08-22Status source 1 | MC4RMelanocortin 4 receptor | AgonistEngineered receptor agonism | Official product pharmacology | 1 |
| Bremelanotide | Approved medicineStatus reviewed: 2026-08-22Status source 1 | MC5RMelanocortin 5 receptor | AgonistEngineered receptor agonism | Official product pharmacology | 1 |
| Melanotan II | Research ligandStatus reviewed: 2026-08-22Status source 1Status source 2 | MC1RMelanocortin 1 receptor | AgonistEngineered receptor agonism | Curated research pharmacology | 1 |
| Melanotan II | Research ligandStatus reviewed: 2026-08-22Status source 1Status source 2 | MC3RMelanocortin 3 receptor | AgonistEngineered receptor agonism | Curated research pharmacology | 1 |
| Melanotan II | Research ligandStatus reviewed: 2026-08-22Status source 1Status source 2 | MC4RMelanocortin 4 receptor | AgonistEngineered receptor agonism | Curated research pharmacology | 1 |
| Melanotan II | Research ligandStatus reviewed: 2026-08-22Status source 1Status source 2 | MC5RMelanocortin 5 receptor | AgonistEngineered receptor agonism | Curated research pharmacology | 1 |
This page maps human receptor pharmacology, not pigmentation, appetite, sexual function or treatment. UniProt identifies human alpha-MSH as residues 138–150 of the 267-residue POMC precursor. The mature 13-residue peptide is N-acetylated at Ser1 and amidated at its C-terminal Val13; both modifications are part of the identity shown in the card.
POMC produces several processed peptides. Sharing a precursor does not make alpha-MSH interchangeable with ACTH, beta-MSH, beta-endorphin or another POMC product.
The reviewed human interaction records support alpha-MSH agonist edges at MC1R, MC3R, MC4R and MC5R. These are four separate human proteins with their own gene and UniProt identifiers.
MC2R is not added by family membership. This slice contains only the alpha-MSH relations directly present in the reviewed human interaction set; an omitted receptor edge is not inferred, and the omission is not a universal claim about every possible assay.
GtoPdb records Gs-family coupling → adenylyl cyclase stimulation as the primary transduction for each of the four mapped receptors. The table renders the shared compact route Gs → adenylyl cyclase → cAMP.
Each target also has secondary signalling annotations. The shared primary route therefore does not make the receptors interchangeable, and it does not imply identical potency, expression, receptor reserve or downstream biology.
Afamelanotide, bremelanotide and Melanotan II each have their own human-target records. GtoPdb reports agonism for all three at MC1R, MC3R, MC4R and MC5R, which supports four edges per agent. Those edges do not rank the agents or assign a clinical effect to any one receptor.
Afamelanotide and bremelanotide are labelled approved medicines because current US product information supports that status; approval remains product-, indication- and jurisdiction-specific. Melanotan II is labelled a research ligand from its curated ligand record and is kept separate from those medicines; the cited regulator warning is status/safety context, not receptor evidence.
Afamelanotide is linked to the wiki’s Melanotan I monograph, bremelanotide to PT-141, and MT-II to Melanotan II. Similar names and a shared receptor family do not make these molecules synonymous.
Target pharmacology, medicine approval and product quality are separate evidence axes. An approved medicine’s status does not validate a differently named research product, and a research ligand’s receptor activity does not create an approved use.
A melanocortin-receptor edge cannot by itself establish tanning, photoprotection, appetite change, sexual response, clinical benefit, safety, approval for a particular use or suitability for an individual. Such claims require their own product-specific, clinical and regulatory evidence. The linked monographs preserve those boundaries rather than letting whole-organism claims flow from a receptor table.