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Melanotan II
Research PeptideAlso known as: Melanotan-2 · MT-II · MT-2 · MTII · MT2 · Melanotan-II · the Barbie drug · tanning injection
Animal Only
The evidence for Melanotan II is limited to animal and in-vitro studies. The mechanistic basis for MC1R-driven pigmentation, MC4R-driven erection, and MC4R/MC3R-driven appetite suppression is well-established in those models. Appetite suppression and fat/weight loss have been demonstrated in rodents via MC4R. The animal pharmacology is real; translation to meaningful outcomes has not been established by independent, replicated, adequately-powered research. It is also routinely confused with two authorised relatives, Melanotan I / afamelanotide and bremelanotide / PT-141, the latter differing by only ~1 Dalton, which unit-resolution mass spectrometry cannot resolve.
Melanotan II has no regulatory authorisation anywhere, and is constantly confused with two authorised relatives
Three molecules from the same University of Arizona melanocortin program get blurred together under the label "melanotan." Melanotan I / afamelanotide is the LINEAR sibling that has received regulatory authorisation for specific rare diseases in certain jurisdictions. Bremelanotide / PT-141 is the ~1-Dalton derivative (free acid instead of MT-II's amide) that has also received authorisation for a specific indication. Melanotan II itself, the cyclic, more potent analog sold online as a "tanning injection," has never received any regulatory authorisation anywhere. The PT-141 confusion is also a quality problem: at m/z ~1025 the ~1-Da difference is below the resolving power of the unit-resolution mass spectrometry behind most gray-market COAs, so what is labeled "MT-II" cannot be cleanly distinguished from bremelanotide (or vice versa) without high-resolution MS.
The harm record is hospital-grade; the only claimed benefit rests on three subjects
Vendors sell Melanotan II as a convenient "safer tan." The evidence does not support that framing. The tanning claim is based on limited preclinical and in-vitro research, with the only early human-adjacent work coming from the molecule's own inventors and never independently replicated. Against that sit mass-spectrometry-confirmed rhabdomyolysis with ICU admission, posterior reversible encephalopathy syndrome (PRES), a 30-hour priapism requiring surgery, and forensically-confirmed renal infarction with new-onset hypertension, plus a biologically plausible melanoma / melanocytic-change signal that has prompted dermatology case reports of darkening and eruptive moles. The Swedish Poisons Information Centre alone logged 215 Melanotan II inquiry cases between January 2008 and May 2019. The product is unlicensed and injected, so identity, content and purity are unverified per vial. The honest asymmetry: the benefits rest on weak preclinical evidence; the documented harms are serious and real.
For laboratory research use only. Not for human or animal consumption.
Evidence Tier
Animal Only
Mol. Weight
1024.2 Da
Last Reviewed
May 31, 2026
Claimed benefits by evidence tier
Column header colour matches the tier
Animal Only1
- Appetite suppression / weight loss
Unsupported2
- Photoprotection / reduced skin-cancer risk
- "Safer tan" / shortcut to a healthy tan (marketing)
About this peptide
Plain English
Melanotan II is an injectable peptide originally designed to produce a protective tan without UV exposure. It mimics a natural hormone (alpha-MSH) that tells skin cells to make the brown pigment melanin. Because the synthetic version is much more stable and reaches the brain, it does not just affect skin: it also acts on brain receptors that control sexual arousal and appetite, producing erections, increased libido, nausea, and reduced hunger in animal models. It is sold online and in some gyms and salons as a "tanning injection," but it is unlicensed. No regulator has confirmed that any given vial is what it claims to be, is the right amount, or is free of contaminants, and several serious adverse-event reports (rhabdomyolysis, a brain syndrome called PRES, a 30-hour erection, and kidney infarction) are on record.
Technical
Melanotan II (Ac-Nle4-cyclo[Asp5-His6-D-Phe7-Arg8-Trp9-Lys10]-NH2) is a cyclic lactam heptapeptide analog of alpha-MSH(4-10) and a high-affinity, NON-selective agonist at melanocortin receptors MC1R, MC3R, MC4R and MC5R, with negligible activity at the ACTH-selective MC2R. The lactam constraint (Asp->Lys side-chain bridge) and the Nle4 / D-Phe7 substitutions confer proteolytic stability, prolonged action, and increased potency relative to native alpha-MSH. MC1R agonism drives UV-independent eumelanogenesis (pigmentation) in animal and in-vitro models; central MC4R agonism drives penile erection (via a nitric-oxide-dependent pathway) and appetite suppression in animal models. No validated subcutaneous pharmacokinetic profile exists beyond a rat IV study. It is routinely confused with two authorised relatives: Melanotan I / afamelanotide (the linear sibling) and bremelanotide / PT-141, the latter differing by only ~1 Dalton (C-terminal -OH vs MT-II's -NH2), a difference unit-resolution mass spectrometry cannot resolve at m/z ~1025.
Mechanism of action
MC1R agonism (skin / melanocytes) -> cAMP -> eumelanin synthesis -> UV-independent pigmentation
MC1R agonism raises melanocyte cAMP, driving eumelanin synthesis and pigmentation independent of UV, as demonstrated in animal and in-vitro models. The endpoint is pigmentation (a surrogate), not a clinical photoprotection or skin-cancer outcome. The same MC1R-driven melanogenesis underlies the documented darkening of moles, new pigmented lesions, and mucosal pigmentation reported in case series.
MC4R agonism (CNS) -> penile erection (NO-mediated) and appetite suppression
Central MC4R activation drives penile erection and sexual desire and suppresses appetite in animal models. The erectile effect is central and nitric-oxide-mediated: in anesthetized rabbits, systemic MT-II raised intracavernosal pressure, an effect abolished by the central MC3/MC4 antagonist SHU-9119. The appetite-suppression outcome is animal-only as a studied endpoint. Nausea, flushing, and yawning are not separable "side effects" but the same central melanocortin pharmacology.
MC3R agonism (CNS, energy homeostasis)
Contributes to energy balance and feeding as part of the non-selective profile, based on rodent studies. Anorectic effects are attributed mainly to MC4R, with MC3R secondary. Evidence is animal and in-vitro only.
MC5R agonism (exocrine glands)
Weak agonism; MC5R is implicated in sebaceous / exocrine function. In-vitro and animal background only; no source identified for any MT-II-specific human MC5R effect.
MC2R (adrenal / ACTH receptor): effectively no activity
MC2R is selective for ACTH and requires the accessory protein MRAP; alpha-MSH-derived analogs like MT-II do not meaningfully activate it. The practical read is "not a relevant target." No source identified for a specific MT-II MC2R Ki.
Essentially all receptor-level pharmacology comes from in-vitro studies on cloned receptors in transfected cell lines and from rodent and lagomorph functional work. Energy-homeostasis and exocrine claims are entirely preclinical. A qualitative rank order of roughly MC1R >= MC4R > MC3R > MC5R >> MC2R is well-supported by in-vitro and animal data. GSRS reports Ki values (MC1 0.67 nM, MC4 6.6 nM, MC3 34 nM, MC5 46 nM) citing Wikberg et al. 2000. Other widely-quoted sub-nanomolar values are attributed to Bednarek et al. (1999) but could not be verified against the primary paper and frequently appear as uncited vendor figures. Use the qualitative profile confidently; treat exact nanomolar numbers as needing primary-source verification.
Key studies
Independence warning: most research for this peptide originates from a single research group. Replication by independent groups is limited.
Activation of central melanocortin receptors by MT-II increases cavernosal pressure in rabbits via neuronal NO release (2001)
Vemulapalli R, Kurowski S, Salisbury B, Parker E, Davis H · British Journal of Pharmacology
- Participants
- Anesthetized rabbits.
- Methodology
- Systemic MT-II with and without the central MC3/MC4 antagonist SHU-9119; intracavernosal pressure measurement.
- Result
- MT-II raised intracavernosal pressure; the effect was abolished by SHU-9119 and was nitric-oxide-dependent.
Honest read
Animal mechanism-localization study. Establishes the central MC4R / NO pathway behind the erectile effect; says nothing about human efficacy or safety.
Skin pigmentation and pharmacokinetics of melanotan in humans / MT-II rat pharmacokinetics (1994)
Ugwu SO, Blanchard J, Dorr RT, Levine N, Brooks C, Hadley ME, Aickin M, Hruby VJ · Biopharm Drug Dispos 15(5):383-90
- Participants
- Rats (single 0.3 mg/kg IV dose).
- Methodology
- Single IV dose; HPLC vs bioassay method comparison.
- Result
- Biphasic disposition; HPLC and bioassay correlated (r=0.90).
Honest read
Rat, IV (not the human SC route), method-comparison focus. There is no robust published human SC PK profile for MT-II, a meaningful gap given real-world SC self-injection.
Intermittent MT-II administration and repeated anorexia / fat-weight loss in rodents (MC4R-mediated) (2010)
(rodent appetite study) · PMC2860181
- Participants
- Rodents.
- Methodology
- Intermittent MT-II dosing; food intake and body-composition outcomes.
- Result
- Repeated anorexia and fat / weight loss, attributed mainly to MC4R.
Honest read
Animal-only; not translatable efficacy. The only basis for the "appetite suppression / weight loss" marketing claim, which has zero controlled human weight data.
Research timeline
- 1980
University of Arizona researchers Victor J. Hruby and Mac E. Hadley set out to develop alpha-MSH analogs as sunless-tanning / skin-cancer-prevention agents, because native alpha-MSH degrades too quickly to be a practical drug. Screening identifies [Nle4,D-Phe7]-alpha-MSH (later Melanotan I / afamelanotide). Foundational patents include US 4,485,039 and EP 0292291 (cyclic, lactam-constrained "superpotent" analogs).
- 1989
Al-Obeidi, Hadley, Pettitt and Hruby publish the design of cyclic lactam-constrained superpotent alpha-melanotropins. Melanotan I retains the full 13-residue backbone; Melanotan II condenses the pharmacophore into a cyclic 7-residue lactam. Cyclization bought stability, potency and BBB penetration but removed receptor selectivity, producing the central MC3/MC4 effects (sexual arousal, nausea) that later split the programs.
- 1996
Dorr et al. publish early MT-II research, reporting pigmentation without UV and spontaneous erections in a preclinical context. Licensing split via Competitive Technologies (University of Arizona tech transfer): Melanotan I -> Epitan (renamed Clinuvel in 2006); Melanotan II -> Palatin Technologies.
- 2000
Wessells et al. publish small surrogate-endpoint erectile-function studies (1998 and 2000) from the same inventor group. Palatin ceases MT-II development and pivots to bremelanotide (PT-141), a likely MT-II metabolite differing only by a C-terminal carboxyl in place of MT-II's amide (~1 Da).
- 2008
As unlicensed MT-II spreads online, multiple regulatory bodies warn consumers that Melanotan is unlicensed and its sale, supply, and advertising is unlawful. Case reports of adverse reactions begin to accumulate. The Competitive Technologies v. Palatin litigation over bremelanotide ownership settles: Palatin keeps bremelanotide, returns MT-II rights, pays US$800,000.
- 2009
Cancer Research UK and dermatology case reports amplify the warning wave. Cousen et al. and Langan et al. document eruptive and rapidly-changing melanocytic naevi after melanotan injection, with histology up to severely dysplastic.
- 2014
Afamelanotide (Melanotan I), the linear sibling from the same program, receives regulatory authorisation in certain jurisdictions for a rare skin condition. This authorisation is for the DIFFERENT molecule, not Melanotan II.
- 2019
Two MT-II relatives receive regulatory authorisations for specific rare or defined indications in certain jurisdictions, neither of which is Melanotan II. Melanotan II itself remains without any regulatory authorisation anywhere.
What we don't know
- The evidence base is limited to animal and in-vitro studies. Pigmentation and erectile outcomes have been observed in animal models, but have not been established at clinical endpoints in any adequately-powered, independently-replicated research.
- No independent replication. The preclinical and early research record comes primarily from one group, the inventors.
- No validated pharmacokinetics for the subcutaneous route (only a rat IV study exists).
- No long-term safety data of any kind, no cohort, no registry follow-up.
- Melanoma causation is unresolved. The signal is biologically plausible and supported by case reports, but no controlled or epidemiological study establishes causation.
- Exact receptor binding constants for MT-II are not reliably verified to primary sources (GSRS Ki values cite Wikberg 2000; the widely-quoted Bednarek 1999 sub-nanomolar figures could not be verified).
- Real-world product identity, content, and purity are unknown per vial; gray-market products are under-dosed and impurity-laden in the limited testing that exists.
- Pregnancy, pediatric, and drug-interaction data: none.
- No quantified MT-II-specific stability or shelf-life data in peer-reviewed sources.
Stability & handling
- Lyophilized shelf life
- General lyophilized-peptide guidance only: stable for extended periods when dry and stored cold. No MT-II-specific quantified shelf-life curve was located in peer-reviewed sources, treat any specific storage number as general peptide practice, not a MT-II-validated figure.
- Lyophilized storage
- Store cold, typically -20 °C and protected from light. Stable for extended periods when dry.
- Reconstitution diluents
- Bacteriostatic water for injection (standard for multi-dose research vials), Sterile / 0.9% saline (the peptide is water-soluble)
- Reconstituted (refrigerated)
- Refrigerate at 2-8 °C and use within weeks; avoid freeze-thaw cycles.
- Reconstituted (room temp)
- Degradation accelerates at room temperature; do not store reconstituted solution warm.
- OK to refreeze
- No
- Light sensitive
- Yes, protect from light
The indole (Trp) and other residues make the peptide susceptible to photo- and oxidative degradation, so protect from light. The lactam cyclization and D-Phe7 / Nle4 substitutions specifically increase resistance to enzymatic / proteolytic degradation relative to native alpha-MSH (Nle replacing Met4 also removes one classic oxidation site). QC failure modes matter as much as storage for what is actually in the vial: (1) BREMELANOTIDE / PT-141 SUBSTITUTION, MT-II (C-terminal -NH2, MW 1024.2) and PT-141 (C-terminal -OH, MW 1025.2) differ by ~1 Da and are indistinguishable on unit-resolution mass spectrometry at m/z ~1025; high-resolution / accurate-mass MS or MS/MS fragmentation is required. (2) MELANOTAN I vs MELANOTAN II CONFUSION, the linear MT-I / afamelanotide and the cyclic MT-II are routinely conflated in listings simply labeled "melanotan" despite being different molecules with opposite regulatory status. (3) UNDER-DOSING / CONTAMINATION, documented online MT-II content of 4.32-8.84 mg against a labeled 10 mg, plus unknown impurities of 4.1-5.9% and (across falsified peptides generally) residual solvents and toxic elemental impurities (arsenic / lead). (4) ACETATE SALT vs FREE BASE, vendors frequently report weight as free base while supplying the acetate salt, so net peptide content can be lower than the nominal label. Any of these can produce a vial that looks acceptable on a basic COA while differing fundamentally from labeled MT-II.
Frequently asked questions
Is Melanotan II the same as PT-141 / bremelanotide?
No, but they are nearly identical and frequently confused. Bremelanotide is essentially Melanotan II with the C-terminal amide (-NH2) replaced by a free acid (-OH), a ~1-Dalton difference in molecular weight (1024.2 vs 1025.2). Bremelanotide (Vyleesi) has received regulatory authorisation for a specific indication; Melanotan II has not been authorised anywhere. Critically, the two are indistinguishable on unit-resolution mass spectrometry at m/z ~1025, so gray-market substitution or cross-contamination is hard to detect on a basic COA.
Is it the same as Melanotan I / afamelanotide?
No. Melanotan I (afamelanotide) is a different, LINEAR molecule with its own regulatory history. Melanotan II is the cyclic analog sold online without any regulatory authorisation. They are routinely conflated as "melanotan," but they are different molecules with very different profiles.
Does it cause melanoma?
Unproven, but there is a biologically plausible signal. MT-II clearly stimulates melanin production and is documented to darken and trigger new moles, sometimes within 24 hours, and case reports describe melanoma arising in users. But no controlled study establishes causation, and confounders (sunbed use, genetic risk) are heavy. The honest answer: we do not know that it causes melanoma, but it changes moles in ways dermatologists consider concerning, especially in high-risk people.
What should I look for on a Melanotan II COA?
Even a clean-looking COA does not rule out the main failure modes, because the analytics commonly used cannot detect them. (1) HIGH-RESOLUTION mass spectrometry, not unit-resolution MS, because PT-141 / bremelanotide differs from MT-II by only ~1 Da and is otherwise indistinguishable at m/z ~1025. (2) Explicit confirmation it is MELANOTAN II (cyclic) and not MELANOTAN I / afamelanotide (linear), which are conflated in "melanotan" listings. (3) Net peptide content with an explicit SALT-FORM declaration (free base vs acetate), since documented online vials contained 4.32-8.84 mg against a 10 mg label. (4) Impurity and elemental testing, because falsified peptides have shown residual solvents and arsenic / lead. A COA showing only "purity by HPLC" has not meaningfully characterized what is in the vial.
Last researched: May 31, 2026
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