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Research comparison

Melanotan I vs Melanotan II

No two compounds in this library are confused with each other more often than Melanotan I and Melanotan II — and few pairs differ more in the ways that matter. The similar names hide different molecules, different receptor selectivity and close to opposite regulatory positions.

This page sets the two profiles side by side. The profiles carry the citations; nothing here is a claim about effects in people.

Melanotan IMelanotan II
CategoryPeptide analoguePeptide
Highest evidenceClinical — evidence level 4 of 4: Established clinical evidence

Findings come from adequately powered, replicated controlled trials in humans, generally supported by regulatory assessment or systematic review.

Early human — evidence level 3 of 4: Early human evidence

Findings come from small, early-phase or observational human studies. These are typically short, sparsely replicated, and designed to examine tolerability or signal rather than to establish effect.

UK regulatory statusPrescription only — UK regulatory status: Prescription-only medicine (UK)

A medicine that may lawfully be supplied in the UK only against a prescription from an appropriate practitioner.

Experimental — UK regulatory status: Experimental — not authorised for human use in the UK

A compound appearing in research literature that holds no UK authorisation for human use in any indication.

Research areasMelanocortin signalling; PhotobiologyMelanocortin signalling; Pigmentation research
Verified citations24

Melanotan I

The same molecule as afamelanotide, the active substance of an authorised medicine.

Melanotan I is a synthetic thirteen-residue analogue of alpha-melanocyte-stimulating hormone, made by replacing the methionine at position 4 with norleucine and switching the phenylalanine at position 7 to its mirror-image form. Those two changes make it far more resistant to breakdown than the natural hormone. It acts at melanocortin receptors, principally the type 1 receptor on pigment cells, where it drives synthesis of eumelanin. Eumelanin absorbs ultraviolet and visible light strongly and reduces oxidative stress, which is the basis of the authorised medicine’s photoprotective use.

Melanotan II

A non-selective melanocortin receptor agonist. The MHRA has repeatedly acted to remove products containing it from the UK market.

Melanotan II is a synthetic cyclic analogue of alpha-melanocyte-stimulating hormone acting as a non-selective agonist across melanocortin receptors. Activation of the MC1 receptor is the proposed basis for increased melanogenesis and skin darkening, while activity at the MC3 and MC4 receptors is the proposed basis for the effects on sexual arousal and appetite reported in early human work. Because it is non-selective its effects are diffuse, and the relative contribution of each receptor to any given effect in humans is not well characterised.

How the research differs

Different molecules, despite the names

Melanotan I is a linear thirteen-residue analogue of alpha-melanocyte-stimulating hormone with two stabilising substitutions. Melanotan II is a shorter cyclic analogue. The naming implies a series; chemically they took different routes from the same parent hormone.

Selective versus non-selective

The receptor story is the scientific heart of the difference. Melanotan I acts predominantly at the MC1 receptor, the receptor tied to melanogenesis. Melanotan II is a non-selective agonist across melanocortin receptors, including MC3 and MC4 — which is why its research literature spreads beyond pigmentation while Melanotan I’s stays close to it.

Opposite ends of the regulatory map

Melanotan I is the same molecule as afamelanotide, the active substance of an authorised medicine — its profile records prescription-only status in the UK. Melanotan II is not an authorised medicine anywhere, and the MHRA has repeatedly acted to remove products containing it from the UK market. The two pages state both positions with sources, and confusing the two names blurs exactly the distinction a careful reader needs.