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Research use only
· 7 min read
The names sit one digit apart, so they get filed as a matched pair - a "1" and a "2" of the same thing. The molecules are not a matched pair. One is a thirteen-residue linear chain; the other is a six-residue ring with a tail. One leans toward a single melanocortin receptor subtype; the other hits the whole family. They share an ancestor in alpha-melanocyte-stimulating hormone (alpha-MSH) and almost nothing else about how they engage that receptor family. This page compares them strictly on melanocortin-receptor pharmacology and verified chemistry - not on any use. Everything below describes what published structural and receptor-binding studies have characterised, grouped by receptor selectivity, not any human or animal application. Kovalabs supplies Melanotan-1 and Melanotan-2 strictly as research reagents for laboratory and in-vitro research only.
Melanotan-1 (afamelanotide) is a linear analogue of alpha-MSH built on the full thirteen-residue active sequence rather than a truncated core. Its structure is Ac-Ser-Tyr-Ser-Nle-Glu-His-D-Phe-Arg-Trp-Gly-Lys-Pro-Val-NH2, which is the native alpha-MSH chain carrying two well-documented edits: the Met4 position is replaced with norleucine (Nle) and the L-Phe7 is replaced with its D-enantiomer (D-Phe). Those two substitutions are the same stabilising strategy that defines the reference research ligand NDP-alpha-MSH; they slow enzymatic clipping and lock the bioactive turn. PubChem lists it under CID 16197727 with the molecular formula C78H111N21O19 and a molecular weight of 1646.8 g/mol - a large, hydroxyl-rich, fully linear peptide. In receptor terms it is the comparatively MC1R-preferring member of this pair: the longer chain retains the alpha-MSH C-terminal segment that the binding literature ties to subtype discrimination.
Melanotan-2 throws away most of the chain and keeps a ring. It is a shorter, cyclic analogue with the structure Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-NH2 - a six-residue lactam macrocycle closed by an amide bridge between an aspartate side chain and a lysine side chain, with a single norleucine cap outside the ring. PubChem lists it under CID 92432 with the molecular formula C50H69N15O9 and a molecular weight of 1024.2 g/mol, roughly 620 daltons lighter than Melanotan-1. The lactam cyclisation is the defining feature: it rigidifies the His-D-Phe-Arg-Trp pharmacophore that every melanocortin ligand shares, but it does so without the alpha-MSH terminal residues that confer subtype preference. The consequence, characterised by Tomassi and colleagues, is that Melanotan-2 behaves as a potent and unselective agonist across the human melanocortin receptors - the broad, non-selective profile that distinguishes it pharmacologically from its linear counterpart.
| Property | Melanotan-1 (afamelanotide) | Melanotan-2 |
|---|---|---|
| Structure type | Linear (13-residue chain) | Cyclic (6-residue lactam macrocycle plus cap) |
| Sequence | Ac-Ser-Tyr-Ser-Nle-Glu-His-D-Phe-Arg-Trp-Gly-Lys-Pro-Val-NH2 | Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-NH2 |
| Melanocortin-receptor selectivity profile | Comparatively MC1R-preferring | Broad, non-selective MC1R / MC3R / MC4R / MC5R agonist |
| Molecular formula | C78H111N21O19 | C50H69N15O9 |
| Molecular weight | 1646.8 g/mol | 1024.2 g/mol |
| PubChem CID | 16197727 | 92432 |
| Shared lineage | alpha-MSH analogue | alpha-MSH analogue |
Both molecules descend from alpha-MSH, and both keep the His-Phe-Arg-Trp core that the entire melanocortin family reads as the message. The divergence is in everything wrapped around that core. The human melanocortin system runs five receptor subtypes - MC1R through MC5R - all class A G-protein-coupled receptors that share the core motif but discriminate ligands through their terminal and flanking residues. Schioth and colleagues mapped exactly this: working with the stabilised alpha-MSH scaffold (the same Nle/D-Phe design Melanotan-1 uses), they deleted and exchanged the N- and C-terminal segments and individually substituted the core residues, then measured binding across cells expressing the human MC1, MC3, MC4 and MC5 receptors. Their finding - that the C-terminal Gly-Lys-Pro-Val segment matters for binding to all four subtypes while the N-terminal segment discriminates between them - is the structural reason a full-length linear analogue can preserve subtype preference. This is a structure-activity binding study; no effect of the compound in any living organism is asserted.
Melanotan-1 keeps that full terminal apparatus and is, on this basis, comparatively MC1R-preferring. Melanotan-2 keeps the core but folds it into a six-residue lactam and discards the discriminating terminal residues altogether. Tomassi and colleagues describe the parent Melanotan-2 lactam as a potent and unselective agonist of the human melanocortin receptors, then showed that swapping the lactam bridge for different thioether linkers shifts the affinity profile - including one analogue that recovers selectivity toward MC1R. That is the cleanest available demonstration of the central point: the cyclisation chemistry, not the shared core, is what collapses subtype discrimination. The contrast is geometric, not mystical. A flexible linear chain can present its terminal residues to a receptor pocket; a rigid ring that lacks those residues binds the conserved core promiscuously across the family.
The chemistry is the well-established tier: the sequences, the linear-versus-cyclic distinction, the molecular formulae and the PubChem CIDs are reproducible and cross-checkable, and the alpha-MSH lineage of both molecules is not in dispute. The middle tier is the receptor pharmacology - the binding and functional data from Schioth and from Tomassi are real, but they are in-vitro measurements in transfected cells and biochemical assays. A receptor-binding curve in a dish describes how tightly a molecule binds its target; it is not a statement about a living body. The weakest tier is human evidence, and the honest answer is that neither molecule has an established, peer-reviewed human evidence base that would support any defined outcome. Both are research compounds. Kovalabs does not supply either compound as a medicine or for any human or animal use, and neither has been shown to produce defined outcomes in humans.
One regulatory fact belongs on this page because it is exactly that - a fact, not an inference. The Medicines and Healthcare products Regulatory Agency (MHRA), the UK regulator, has publicly warned against human use of Melanotan-2. That warning is a matter of public record and is reported here as regulatory context, not as commentary on what the molecule does. Under MHRA Guidance Note 8, the framework that governs the borderline between a research chemical and an unlicensed medicine, the determining factor is how a product is presented: a claim, not a molecule, is what converts a reagent into a medicine. Nothing on this page presents either compound for any human or animal use, and neither has been assessed by the MHRA for safety or efficacy in humans or animals. The afamelanotide INN is associated with a separately authorised medicinal product; that authorisation is not Kovalabs' product, presentation or indication, and nothing here is offered for medical use.
Structure and receptor selectivity. Melanotan-1 (afamelanotide) is a linear thirteen-residue alpha-MSH analogue (Ac-Ser-Tyr-Ser-Nle-Glu-His-D-Phe-Arg-Trp-Gly-Lys-Pro-Val-NH2, C78H111N21O19, 1646.8 g/mol, PubChem CID 16197727) that is comparatively MC1R-preferring. Melanotan-2 is a shorter cyclic analogue (Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-NH2, C50H69N15O9, 1024.2 g/mol, PubChem CID 92432) characterised as a broad, non-selective agonist across the melanocortin receptor subtypes. Both derive from alpha-MSH.
Yes. Melanotan-1 is a linear peptide chain that retains the full alpha-MSH terminal residues. Melanotan-2 is built on a six-residue lactam macrocycle - a ring closed by an amide bridge between an aspartate and a lysine side chain - capped by a single norleucine. The cyclic geometry rigidifies the shared His-D-Phe-Arg-Trp core and is the documented structural basis for its non-selective melanocortin-receptor profile.
Because it keeps the conserved melanocortin core but discards the alpha-MSH terminal residues that the binding literature associates with subtype discrimination. Tomassi and colleagues (2022) describe the parent Melanotan-2 lactam as a potent and unselective agonist of the human melanocortin receptors (MC1R, MC3R, MC4R and MC5R), whereas the full-length linear Melanotan-1 retains the terminal apparatus that confers comparative MC1R preference.
Neither compound is supplied for any human or animal use. Kovalabs supplies both strictly as research reagents for laboratory and in-vitro research only, with no dose, route, schedule or outcome described anywhere on this page.
Melanotan-1 and Melanotan-2 are supplied by Kovalabs for laboratory and in-vitro research only. They are not medicines, not supplements, and not for human or veterinary use, and nothing on this page describes a dose, a route, a schedule or an outcome. They are research compounds that have not been evaluated by the MHRA or any comparable regulator for safety or efficacy in humans or animals, and the MHRA has publicly warned against human use of Melanotan-2. Every batch is third-party tested with a certificate of analysis. See the full research disclaimer for terms.