Melanotan 2

Cyclic melanocortin agonist · pigmentation & sexual health

Melanotan 2 is a synthetic, ring-shaped copy of α-MSH, the hormone the body uses to switch on pigment production. It is a non-selective agonist at the melanocortin receptors: acting on MC1R it drives melanin synthesis (tanning), and acting on MC4R it produces erectile and appetite effects. Small early human studies from the University of Arizona did show that it darkens skin and triggers erections, and it is the molecule from which the approved sexual-dysfunction drug bremelanotide (PT-141) was later derived — but Melanotan 2 itself is not approved for any use anywhere, and the only currently registered clinical trial is an early-stage vitiligo study with no results yet. What sets this compound apart from the rest of this catalog is its documented harm record: the medical literature contains case reports of new and darkening moles, of melanoma in users, and of rhabdomyolysis and priapism after overdose, and the US, UK, and Australian regulators have all issued public warnings against unlicensed melanotan injections. The popular framing of it as a 'safe tan' that protects against skin cancer is contradicted by that evidence. No validated human half-life has ever been published. This page documents the research and case literature only and makes no therapeutic or cosmetic recommendation.

The short version

Melanotan 2 is a lab-made, ring-shaped version of α-MSH — the natural hormone that tells your skin to make pigment. Because it switches on that pigment machinery, it darkens the skin; because it also hits a related receptor in the brain (MC4R), it can trigger erections and reduce appetite.

Those effects are real and were seen in small human studies in the 1990s. Melanotan 2 is also the chemical 'parent' of an actual approved drug, bremelanotide (PT-141), which was developed from it for sexual dysfunction. But Melanotan 2 itself was never approved for anything, and almost no controlled human research has been done on it since.

The reason this compound stands apart from everything else in this catalog is safety. The medical literature contains real case reports of people who developed new or darkening moles after using it, of melanoma diagnosed in users, and of serious reactions — muscle breakdown (rhabdomyolysis) and dangerously prolonged erections (priapism) — after overdoses. Health regulators in the US, UK, and Australia have all publicly warned against unlicensed melanotan tanning injections.

So the popular idea of Melanotan 2 as a 'safe tan' that also protects against skin cancer is not supported — the documented evidence points the other way. There is also no reliable published figure for how long it stays in the body. This page lays out the research and the case reports as they actually exist; it is not tanning advice and makes no health or cosmetic claim.

Molecular identity

Specs

Molecular weight: 1024.2 g/mol
Molecular formula: C50H69N15O9
Monoisotopic mass: 1023.5403 Da
CAS / UNII: 121062-08-6 · UPF5CJ93X7

Sequence: Ac-Nle-c[Asp-His-D-Phe-Arg-Trp-Lys]-NH2 (7 AA, cyclic lactam)PubChem CID 92432
Structure / class: Synthetic cyclic α-MSH analog (23-membered Asp–Lys lactam; N-acetyl, C-amide)PubChem CID 92432
Molecular target: Melanocortin receptors (non-selective: MC1R/MC3R/MC4R/MC5R)Research literature
Half-life: No validated human pharmacokinetics publishedNot established
Brand / approval: None — not approved anywhere; parent molecule of bremelanotide (PT-141/Vyleesi)Research literature
Regulatory status: Research chemical; not FDA-approved. FDA/MHRA/TGA have warned against unlicensed melanotan injectionsFDA / MHRA / TGA

Plain English

Mechanism

Melanotan 2 is a synthetic analog of α-melanocyte-stimulating hormone (α-MSH), one of the melanocortin peptides cleaved from pro-opiomelanocortin. It preserves the conserved His-Phe-Arg-Trp melanocortin pharmacophore (with the phenylalanine in its D-form) but closes the molecule into a ring: a lactam bridge between an aspartate side chain and a lysine side chain forms a 23-membered macrocycle, with the N-terminus acetylated and the C-terminus amidated. This cyclization and the D-Phe substitution make it dramatically more potent and more metabolically stable than native α-MSH.

It is a non-selective agonist across the melanocortin receptor family — MC1R, MC3R, MC4R, and MC5R — with little activity at MC2R (the adrenal ACTH receptor). Two of those receptors account for its observed human effects: MC1R on melanocytes drives the synthesis of eumelanin, which is the basis of its skin-darkening (tanning) action; MC4R in the central nervous system mediates its effects on erectile function and appetite. (Specific receptor binding-affinity numbers circulated by vendors could not be traced to a primary radioligand-binding study and are deliberately not stated here.)

The human-relevant actions are pigmentation and erectile function, both demonstrated in early clinical work. The appetite/energy-balance effects of MC3R/MC4R signalling are characterized largely in animal models, and the broader melanocortin pharmacology of receptor subtype selectivity rests mostly on in-vitro and animal data — so the centrally mediated metabolic effects should be read as preclinical rather than established in humans.

An important identity point: Melanotan 2 is the structural parent of bremelanotide (PT-141), an FDA-approved drug for hypoactive sexual desire disorder. PT-141 is a derivative in which Melanotan 2's C-terminal carboxamide is replaced by a free carboxylic acid, shifting activity toward MC4R-mediated sexual function and away from pigmentation. Melanotan 2 is also distinct from afamelanotide (Scenesse), a different α-MSH analog that is the source of most legitimate human photoprotection data — the three are routinely conflated in marketing but are separate compounds with separate evidence and regulatory status.

Sources:PubChem CID 92432 PMID 9760697 PMID 8637402 PMID 9679884

Why people reach for it

Potential benefits

Melanotan 2 is reached for as a two-in-one melanocortin — tan plus libido — but it carries the heaviest documented harm record in this catalog, so the appeal and the risk sit side by side. Here's what draws people to it, read against that.

Tan plus libido from one compound — Its draw is breadth: as a non-selective melanocortin agonist it hits MC1R (pigmentation) and MC4R (sexual arousal), so early human studies showed both a deeper tan and erectile/desire effects from the same molecule.
A deep tan with less sun — Through MC1R it drives eumelanin synthesis, building pigment with less UV exposure — the effect that made it popular, though a tan is not meaningful sun protection and the molecule darkens moles.
An on-demand arousal effect — The MC4R activity produces a centrally-driven libido and erectile effect, shown in small early trials — which is why some use it situationally before activity rather than only for tanning.
Appetite blunting (mostly animal data) — MC3R/MC4R signaling reduces appetite in animal models; some users report the same, but this effect is largely preclinical and not established in humans.
The honest counterweight — it is approved nowhere, with a real harm record — The same broad receptor activity behind its appeal drives its documented downsides: case reports of new and darkening moles, melanoma in users, and overdose reactions (rhabdomyolysis, priapism). For the sexual effect specifically, the selective, FDA-approved PT-141 is the cleaner option — and Melanotan 1 is the approved, more pigment-focused tanning cousin.

Sources:PMID 8637402 PMID 9679884 PMID 11018622 PMID 24355990 PMID 19575725

What people reach for Melanotan 2 for, drawn from what the research and case literature report and how it's used — not proven outcomes or any cosmetic/medical recommendation; it is approved nowhere and carries a documented harm record.

Implied timing

Best time to dose

Implied best time

Evening

For the tanning/maintenance dose, most people inject Melanotan 2 in the evening so nausea passes during sleep; the libido use is timed situationally instead.

Nausea and flushing are the principal acute effects from the studies, and they're dose-dependent — taking the daily/maintenance pigmentation dose in the evening means they tend to pass while asleep rather than during waking hours.
The tanning effect is not clock-driven: pigment builds from MC1R activation plus the UV exposure that compounds it, not from the hour of the injection. So evening is about side-effect timing, not a pharmacologic optimum.
For the libido/erectile effect specifically, some dose situationally instead — taking it 1–2 hours before activity rather than on the evening pigmentation schedule. That's a secondary, occasion-based timing, separate from the daily tan dose.
There is no validated human half-life for Melanotan 2, so no PK figure refines this — a consistent evening habit for the maintenance dose is convention built on tolerability, nothing more.

No study establishes an ideal time of day for Melanotan 2 — this is reasoned from its side-effect profile and how it's used. As a rule of thumb most peptide dosing lands in the midday-to-evening window; for Melanotan 2 the maintenance dose leans evening (so nausea passes during sleep), while the libido use is timed before activity instead.

How to run it

Dosing & protocol

MT-2 has a thin evidence base — a handful of small, early studies from one research group — and a documented harm record that makes dose discipline the most important practical fact on this page. The numbers below are community patterns drawn from the human studies in this file and the case literature; they are not a validated regimen, not an endorsement of use, and not a medical or cosmetic recommendation. Every published human study used subcutaneous injection (a shallow injection into the fat under the skin); MT-2 is not orally active.

Approved nowhere; documented harm record: new and darkening moles, melanoma reported in users, nausea, blood-pressure changes, priapism, and rhabdomyolysis after overdose. These are not theoretical risks — they are published case reports. Nothing in this section changes that. The companion page for the sexual effect with a cleaner, approved profile is PT-141 (bremelanotide).

Tiered dose ranges

The only hard number the literature provides is a danger ceiling, not a target. The ranges below are community convention; the overdose report defines where the ceiling sits.

Loading (pigmentation approach):: ~0.25–0.5 mg subcutaneously once daily for 1–2 weeks to build melanin — the community-reported starting pattern. The lower end (0.25 mg) is standard for first use to gauge tolerance. Note: this is anecdotal; no controlled study validates a tanning schedule.
Maintenance (pigmentation):: ~0.5–1 mg subcutaneously once or twice weekly, often paired with UV exposure, to maintain pigment once it is established. Community convention only.
Acute sexual-function approach:: ~0.025 mg/kg as a single subcutaneous dose taken acutely — the dose range used in the controlled erectile-function studies (Wessells 1998, 2000). For a 75 kg person, that is ~1.875 mg. This was a single research dose, not a standing daily regimen.
Danger ceiling — do not approach:: A single 6 mg subcutaneous dose produced systemic sympathomimetic toxicity and rhabdomyolysis (muscle breakdown with kidney injury). This is a published overdose, not a theoretical limit. The unregulated, self-injected nature of typical use makes dosing error a documented danger.

Subcutaneous administration

MT-2 is injected subcutaneously — the route used in every human study and the route the calculator is built for.

Injection site:: Abdomen (staying two inches clear of the navel), outer thigh, or love-handle area. Rotate sites between doses to prevent local irritation and lipohypertrophy (fatty lumps from repeated use of the same spot).
Measuring the dose:: Drawn on a U-100 insulin syringe from the reconstituted vial. At the standard mix (10 mg vial + 2 mL bacteriostatic water = 5,000 mcg/mL): 250 mcg = 5 IU · 500 mcg = 10 IU · 1,000 mcg = 20 IU. The on-page calculator covers any vial size.
Time of day:: Evening dosing is common for the pigmentation approach, so nausea (the principal acute effect from the studies) occurs during sleep rather than waking hours. Acute sexual-function use is timed to need — typically 1–2 hours before.
Food window:: Subcutaneous administration does not compete with food for absorption. Some users take it with food specifically to reduce nausea, though this has no pharmacokinetic basis.

Cycle & washout

Because MT-2 stimulates melanocytes throughout the body, prolonged continuous use increases the total melanocortin load on skin tissue — the same biology that underlies the mole-change case reports.

Cycle length:: Community patterns: 4–6 weeks of loading, then drop to maintenance frequency or stop entirely. Longer continuous runs increase cumulative melanocyte stimulation — the biology behind the eruptive-nevi reports.
Washout:: A minimum 4–6 week break before any subsequent cycle. During and after any cycle: full-body skin and mole self-examination monthly; any new mole, change in existing mole, or unusual lesion — especially in combination with UV exposure — warrants prompt dermatologic review. This is not optional caution; it is the evidence-based mitigation.
No indefinite use:: There is no studied long-term-use schedule for MT-2. Indefinite continuous use is not supported by any evidence and compounds the melanocyte-stimulation exposure the case literature links to harm.

Reconstitution at a glance

The on-page calculator handles any vial size live; the quick reference for the standard 10 mg vial (calculator default):

Mixing:: 10 mg vial + 2 mL bacteriostatic water = 5,000 mcg per mL. On a 100-unit (1 mL) U-100 insulin syringe: 250 mcg = 5 IU · 500 mcg = 10 IU · 750 mcg = 15 IU · 1,000 mcg = 20 IU.
Why 2 mL:: Yields a 5,000 mcg/mL concentration that maps the typical MT-2 dose range (250–1,000 mcg) onto 5–20 IU — a measurable syringe range that reduces precision errors at lower doses.

Sources:PMID 8637402 PMID 9679884 PMID 11018622 PMID 23121206 PMID 23537392

Substrate the signal needs

Nutritional cofactor precision

MT-2 acts on two separate systems — melanocyte pigmentation (MC1R) and central sexual/appetite signalling (MC4R). Before the substrate and amplifier notes: the honest framing for this compound's 'cofactor' question is an absence, not a nutrient.

No supplement fixes Melanotan 2's actual problem. Its danger is that it is a non-selective melanocortin agonist with a documented harm record — mole changes, melanoma signal, nausea, blood-pressure effects, overdose toxicity. No vitamin, mineral, or amino acid changes that off-target safety profile. The real mitigation is awareness and monitoring, not a supplement stack.

Mitigate — skin and mole monitoring (the only meaningful mitigation)

The primary 'cofactor protocol' for MT-2 is dermatologic awareness, not a supplement. This is not a platitude — it is the direct evidence-based response to the published case literature.

Why monitoring is the mitigation:: MT-2 stimulates melanocytes across the entire body regardless of intent. The case reports of eruptive new moles and melanoma are the documented consequence of that non-selective MC1R agonism. No supplement buffers this. Monthly self-examination of all moles and any skin change is the actionable response.
When to act:: Any new mole, any existing mole that changes in size, shape, color, or border, or any unusual dark spot — particularly in the context of UV exposure — warrants prompt dermatologic review. This applies during any cycle and for weeks after it ends.
Medical awareness:: Nausea and flushing are expected acute effects (direct melanocortin activation, not allergy). Elevated blood pressure and cardiovascular symptoms are reported. A prolonged erection exceeding 4 hours is a urologic emergency. An overdose-like presentation (agitation, muscle pain, dark urine) requires emergency evaluation.

Supply — melanin substrate (L-tyrosine + copper)

If MT-2 is being used for the pigmentation effect, the melanin biosynthetic pathway has two nutritional inputs — this is textbook biochemistry, not a Melanotan-2 cofactor study.

Tyrosine (melanin precursor):: Eumelanin is synthesized from the amino acid L-tyrosine. The body makes tyrosine from phenylalanine; adequate dietary protein covers both. For most people on a normal diet, tyrosine is not a deficiency — supplementation only matters if total protein intake is low. Dose if used: 500–1,000 mg L-tyrosine daily on an empty stomach.
Copper (tyrosinase cofactor):: The enzyme that converts tyrosine to melanin — tyrosinase — requires copper as a cofactor. Deficiency would slow pigment formation; normal dietary copper (1–3 mg/day from nuts, seeds, shellfish) is typically sufficient. Supplement only if confirmed deficient. Note: high-dose zinc supplementation depletes copper — if running zinc alongside, ensure balance (e.g. 2 mg copper per 50 mg zinc).
UV as biology, not benefit:: Ultraviolet light activates MC1R in skin cells — the same receptor MT-2 agonizes — and is therefore required to trigger eumelanin production. Without UV exposure there is little pigmentary response. State this as biology and stop: a darker tan is not sun protection in the medical sense, and UV exposure while using a melanocyte-stimulating agent does not reduce skin-cancer risk.

Combinations + timing

Stacking notes + timing windows

MT-2 gets discussed alongside two melanocortin relatives. The honest version of these comparisons is not 'stack them' — it is 'here are the cleaner or more selective options for the same goal, and combining melanocortins stacks the harm, not just the benefit.'

These are mechanism-based comparisons, not combinations studied for safety or efficacy. Combining melanocortin-active compounds compounds the off-target effects — the pigmentary harm, the mole-change risk, the cardiovascular and erectile side effects. The comparisons below exist so the trade-off is visible, not as an endorsement of combination use.

Comparison: MT-2 vs. PT-141 (bremelanotide) — the approved sibling for the sexual effect

PT-141 is the molecule MT-2 was turned into when the University of Arizona research moved toward an approved drug. For the sexual effect specifically, PT-141 is the direct, better-characterized, FDA-approved alternative.

Why PT-141 is the cleaner option:: PT-141 (bremelanotide) differs from MT-2 by a single chemical change — the C-terminal amide is replaced by a free carboxylic acid — but that change shifted the receptor profile toward MC4R (the central sexual-desire receptor) and away from MC1R (the pigmentation receptor). PT-141 does not produce the skin-darkening effect and carries a published safety profile from FDA approval studies. MT-2 produces both effects but with documented mole-change and melanoma signals on top.
Protocol comparison:: PT-141: 1.25 mg intranasal or 1.75 mg subcutaneous, administered 45 minutes before — the approved doses. MT-2 for sexual effect: ~0.025 mg/kg subcutaneous (e.g. ~1.875 mg for 75 kg), acute, from the research studies. The approved, characterized option has concrete dosing with a regulatory-reviewed safety profile; the unapproved one does not.
Honest framing:: If the intended use is the sexual effect, PT-141 is the more selective, approved, better-safety-characterized option. Using MT-2 for that goal adds the full non-selective melanocortin profile — including the pigmentary harm record — without adding benefit for the primary goal.

Comparison: MT-2 vs. Melanotan 1 (afamelanotide) — the cousin that became an approved pigmentation drug

Melanotan-1 (afamelanotide, Scenesse) is the other α-MSH analog from the same University of Arizona research program. It took the pigmentation path all the way to regulatory approval; MT-2 did not.

Key differences:: Melanotan 1 is a linear (non-cyclic) α-MSH analog with a norleucine substitution, approved in the EU and Australia for erythropoietic protoporphyria (a rare photodermatosis) and carrying the bulk of the legitimate human photoprotection data in this class. It does not have MT-2's MC4R-mediated sexual and appetite effects — it is more selective toward MC1R. MT-2's broader receptor profile is the source of both its broader effects and its broader harm profile.
Why combining is not the answer:: Running MT-2 alongside any other melanocortin compound — whether Melanotan 1 or PT-141 — does not produce a cleaner profile. It stacks melanocortin receptor activation, compounding the cardiovascular effects, the nausea, and — critically — the melanocyte stimulation that underlies the mole-change case reports. More melanocortin agonism is not a mitigation; it is additive exposure.
Outcome framing:: The existence of approved melanocortin analogs with defined safety profiles (Melanotan 1 for photoprotection in a specific medical indication; PT-141 for sexual desire) is the clearest argument against using MT-2, not for combining it with them.

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.05 mL
Doses per vial: 40
Concentration: 5 mg/mL

One vial lasts

Daily: 40 days
Every other day: 80 days
5×/week: 56 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

Melanotan 2 has the most substantial documented harm record of any compound in this catalog, and that evidence — not the marketing — is what defines its safety profile. The acute effects reported in studies and case series include nausea, facial flushing, yawning, and spontaneous (sometimes prolonged) erections. These are direct melanocortin effects, not idiosyncratic reactions.

The most serious documented concern is dermatological. Because Melanotan 2 stimulates melanocytes throughout the body, the case literature describes the eruption of new melanocytic naevi (moles) and the darkening and enlargement of existing moles — in one report within 24 hours of a single dose. Beyond benign mole changes, there are published case reports of melanoma in Melanotan 2 users, including a report of oral mucosal melanoma associated with a Melanotan II nasal spray. A causal role is not established by case reports alone, but the pattern is the direct opposite of the 'protects against skin cancer' claim and is treated here as a serious documented signal.

Systemic toxicity is also on record: a subcutaneous overdose produced rhabdomyolysis (muscle breakdown) with renal (kidney) dysfunction and sympathomimetic symptoms (the racing-heart, agitated 'fight-or-flight' pattern), and a separate overdose report describes priapism (a prolonged, often painful erection). These illustrate that the dose-response is not benign and that the unregulated, self-injected nature of typical use compounds the risk.

Regulatory status reinforces the picture: Melanotan 2 is not an approved drug for tanning — or for anything — in the United States, the United Kingdom, the European Union, or Australia. The US FDA, the UK's MHRA, and Australia's TGA have all issued public warnings against unlicensed melanotan tanning products, and the peer-reviewed literature has flagged unregulated Melanotan 2 as a public-health concern. This page presents the research and case literature only and makes no therapeutic or cosmetic claim; the documented harms above are the reason that framing matters.

Sources:PMID 19575725 PMID 24334249 PMID 24355990 PMID 40210573 PMID 23121206 PMID 23537392 PMID 28905366

As reported in literature

Research dosing ranges

These are the doses actually used in the published human studies and case reports — the evidence the practical figures above lean on, shown separately so research data is never mistaken for a dosing recommendation, and this page makes no therapeutic, cosmetic, or how-to claim. Every human study used the subcutaneous route (injection into the fat just under the skin). Two cautions frame the table. First, the efficacy studies are small, early (1990s–2000s), and from a single research group, so the doses describe historical research rather than a validated regimen. Second — and unusually for this catalog — the table includes a documented overdose: a single 6 mg subcutaneous dose produced systemic toxicity and rhabdomyolysis (muscle breakdown), a direct illustration of why the 'more is better' framing around this compound is dangerous. Vendor tanning 'protocols' are anecdotal and are not presented here as established.

Dose	Route	Model	Outcome	Sources:
Escalating subcutaneous doses (Phase-I)	Subcutaneous	Human — healthy volunteers (Phase-I safety)	Established dose-tolerability and pigmentary response; principal adverse effect was nausea	PMID 8637402
~0.025 mg/kg	Subcutaneous	Human — psychogenic erectile dysfunction (double-blind crossover, small n)	Produced erections vs placebo	PMID 9679884
Subcutaneous course	Subcutaneous	Human — organic erectile dysfunction (crossover, small n)	Erectogenic effect plus increased sexual desire	PMID 11018622
6 mg (single overdose)	Subcutaneous	Human — case report (toxicity)	Systemic sympathomimetic toxicity with rhabdomyolysis and renal dysfunction	PMID 23121206
Melanotan II (as marketed)	Subcutaneous	Human — case report (toxicity)	Priapism following overdose	PMID 23537392

Quick answers

Frequently asked

What is Melanotan 2?

Melanotan 2 (MT-2) is a synthetic, ring-shaped analog of α-MSH, the hormone that switches on skin-pigment production. It is a non-selective melanocortin-receptor agonist: through MC1R it darkens skin (tanning), and through MC4R it affects erectile function and appetite. It is not an approved drug for any use, and it is sold as a research chemical.

Is Melanotan 2 the same as PT-141 or as the tanning drug Scenesse?

No — these are three different compounds that are often confused. PT-141 (bremelanotide) is a derivative of Melanotan 2 (its C-terminal amide is replaced by a free acid), developed and FDA-approved for a sexual-desire disorder. Afamelanotide (Scenesse) is a separate α-MSH analog approved for a rare light-sensitivity condition and is the source of most legitimate human photoprotection data. Melanotan 2 itself is not approved for anything.

Is Melanotan 2 a safe way to tan?

The documented evidence does not support that. The medical literature contains case reports of new and darkening moles, and of melanoma, in Melanotan 2 users, and regulators in the US, UK, and Australia have warned against unlicensed melanotan injections. The popular 'safe tan that protects against skin cancer' claim runs contrary to this case literature, which is why this page foregrounds the harm record rather than the cosmetic appeal.

What are the documented risks of Melanotan 2?

Reported acute effects include nausea, flushing, yawning, and prolonged erections. The case literature documents eruptive and darkening moles (sometimes within 24 hours of a dose), melanoma in users, and — after overdose — rhabdomyolysis with kidney injury and priapism. Because it is typically self-injected and unregulated, dosing errors are a real and documented danger.

Has Melanotan 2 been proven to work in proper clinical trials?

Its tanning and erectile effects were shown in small, early human studies from one research group (University of Arizona) in the 1990s–2000s. There has been very little controlled human research since; the only currently registered clinical trial is an early-stage study in vitiligo, with no results posted. Most claims beyond those early findings are extrapolation.

What is Melanotan 2's half-life?

No validated human pharmacokinetics or half-life has been published for Melanotan 2. The human pharmacokinetic data in this area are for the related compound melanotan-I/afamelanotide, not for Melanotan 2. The specific half-life numbers quoted online are not traceable to a primary study.

Primary sources

References

PubChem CID 92432PubChem CID 92432 (Melanotan II; formula, mass, sequence, CAS 121062-08-6)
PMID 9760697Hadley & Dorr, Pharm Biotechnol 1998 (discovery & development of Melanotan-I and -II at U. Arizona)
PMID 8637402Dorr et al., Life Sci 1996 (Phase-I human safety/tolerability; subcutaneous dosing; pigmentary response)
PMID 9679884Wessells et al., J Urol 1998 (Melanotan II in psychogenic erectile dysfunction; double-blind crossover)
PMID 11018622Wessells et al., Urology 2000 (Melanotan II in organic erectile dysfunction; crossover)
PMID 11035391Wessells et al., Int J Impot Res 2000 (human Melanotan II erectile-dysfunction study; double-blind crossover, RigiScan)
PMID 19575725Cousen et al., Br J Dermatol 2009 (eruptive melanocytic naevi after melanotan injection)
PMID 24334249Schulze et al., Eur J Dermatol 2014 (eruptive naevi + darkening of existing naevi after a single dose)
PMID 24355990Hjuler & Lorentzen, Dermatology 2014 (melanoma associated with Melanotan-II use)
PMID 40210573Yassin Alsabbagh et al., Int J Oral Maxillofac Surg 2025 (oral mucosal melanoma associated with Melanotan II nasal spray)
PMID 23121206Nelson et al., Clin Toxicol 2012 (systemic toxicity + rhabdomyolysis after 6 mg subcutaneous overdose)
PMID 23537392Devlin et al., Clin Toxicol 2013 (priapism after Melanotan II overdose)
PMID 28905366Adler et al., Australas J Dermatol 2017 (unregulated Melanotan II as a public-health concern)
NCT07437560Melanotan II as adjunct to NB-UVB for vitiligo repigmentation (Phase 2, recruiting; no results posted)

Research use only · Not medical advice · Updated 2026-06-01