Melanotan II is a synthetic cyclic heptapeptide analogue of α-melanocyte-stimulating hormone, formally acetyl-(Nle⁴, Asp⁵, D-Phe⁷, Lys¹⁰)-cyclo-α-MSH(4–10) amide. A side-chain lactam bridge between Asp² and Lys⁷ rigidifies the structure, and the D-phenylalanine substitution within the His-Phe-Arg-Trp message sequence increases metabolic stability relative to native α-MSH. It terminates in a carboxamide.

It is characterised as a non-selective agonist across melanocortin receptor subtypes, with reported activity at MC1R, MC3R, MC4R and MC5R. Engagement of MC1R on melanocytes drives eumelanin synthesis, which is the basis on which the compound has been examined in pigmentation and photoprotection research; MC3R and MC4R activity underlies its study in models of erectile function and feeding behaviour. Its lack of receptor selectivity is a defining pharmacological feature rather than an incidental one.

Two identity points matter here and both are frequently got wrong. Melanotan II is not PT-141 — PT-141 (bremelanotide) is the des-amido metabolite bearing a C-terminal free acid, a separate product with a distinct CAS, and the near-identical masses of 1024.2 and 1025.2 make transposition easy. Melanotan II is also not afamelanotide, sometimes called Melanotan-I, which is a linear α-MSH analogue approved by the FDA in October 2019 as Scenesse for erythropoietic protoporphyria. The similarity of the informal names does not carry over to regulatory status: Melanotan II is not an approved medicine in any jurisdiction, its human data are limited to small early-phase studies, and multiple national regulators have issued public warnings about unlicensed supply. Case reports in the dermatology literature describe changes in melanocytic naevi among people who obtained it outside medical supervision.