MT-2 Research Only

What It Is

MT-2 (Melanotan II) is a synthetic cyclic heptapeptide analog of α-melanocyte-stimulating hormone (α-MSH). The molecule was designed at the University of Arizona in the late 1980s by the Hadley, Hruby, and Dorr group — the same laboratory that produced the structurally related MT-1 (afamelanotide). MT-2's sequence is Ac-Nle-c[Asp-His-D-Phe-Arg-Trp-Lys]-NH₂, with an N-terminal acetylation, a D-phenylalanine substitution at position 7, and a lactam bridge between Asp and Lys that imposes the constrained cyclic conformation responsible for its very high melanocortin-receptor affinity and metabolic stability relative to linear α-MSH (Al-Obeidi 1989; Hadley & Dorr 2006).

Unlike MT-1, which retains reasonable selectivity for MC1R, MT-2 is a potent, non-selective agonist across all four peripheral and central melanocortin receptors — MC1R (melanocytes), MC3R (hypothalamus and periphery), MC4R (hypothalamus and central nervous system), and MC5R (sebaceous and exocrine glands). This pan-melanocortin profile is simultaneously the source of its broad pharmacology (tanning, sexual arousal, appetite suppression, blood-pressure modulation, sebaceous activity) and its narrow therapeutic index — every one of those pathways is engaged simultaneously with every dose.

MT-2 was never developed as a tanning product. The Arizona program's original therapeutic hypothesis was sunless photoprotection for fair-skinned individuals at elevated melanoma risk — induce eumelanin synthesis pharmacologically to raise the natural UV threshold before recreational sun exposure. That hypothesis eventually matured into the MT-1 (afamelanotide) program, which received EMA approval as Scenesse in 2014 and FDA approval in 2019 for erythropoietic protoporphyria (EPP). MT-2 itself was abandoned as a photoprotection candidate because of its non-selectivity and side-effect burden. The same non-selectivity made it attractive as a starting point for erectile-dysfunction and female-sexual-dysfunction research, which in turn produced PT-141 (bremelanotide) — a more MC4R-biased analog that received FDA approval as Vyleesi in 2019 for hypoactive sexual desire disorder in premenopausal women.

MT-2 itself has never been approved by any regulatory authority for any indication. Nonetheless, it is one of the most widely sold research peptides in the world, circulated through online "research chemical" suppliers and used recreationally for cosmetic tanning, libido augmentation, and appetite suppression. Regulators on three continents — FDA, the U.K. MHRA, the Australian TGA, and national EU dermatology societies — have issued public warnings against consumer use, citing both the compound's pharmacology and the unregulated manufacturing quality of internet-sourced material.

Mechanism of Action

MT-2 is a non-selective full agonist at the melanocortin receptor family. Its pharmacodynamic profile is the superposition of four simultaneously engaged receptor pathways, each with distinct downstream consequences:

• MC1R — melanocyte eumelanogenesis — MC1R is a Gα_s-coupled receptor expressed on cutaneous melanocytes. MT-2 agonism raises intracellular cAMP, activates PKA, phosphorylates CREB, and drives transcription of MITF (microphthalmia-associated transcription factor) — the master regulator of the melanogenic program. MITF upregulates tyrosinase, TYRP1, and DCT, shifting the melanosome output from light pheomelanin to dark eumelanin. Macroscopic skin darkening is the observable outcome (Abdel-Malek 2001).
• MC3R / MC4R — hypothalamic sexual arousal circuitry — MC3R and MC4R are expressed throughout the medial preoptic area, paraventricular nucleus, and other hypothalamic regions governing autonomic and limbic sexual response. Central MC3R/MC4R agonism initiates parasympathetic outflow to the pelvic plexus, releases nitric oxide from cavernosal nerves, and produces penile erection in male rodents, primates, and humans (Wessells 1998; Van der Ploeg 2002). In females, the same pathway is implicated in genital arousal and central sexual desire — the mechanistic substrate that led to the PT-141 / bremelanotide program for HSDD.
• MC4R — hypothalamic satiety and energy balance — MC4R in the paraventricular nucleus is the single most important obesity-associated receptor known: rare loss-of-function MC4R mutations are the most common monogenic cause of human obesity. MC4R agonism by MT-2 suppresses food intake, reduces subjective hunger, and increases sympathetic outflow — producing the "appetite loss" frequently reported by users and the small fat-loss signal in animal models (Huszar 1997; Fan 1997).
• MC4R — sympathetic outflow and blood pressure — Central MC4R activation drives sympathetic nervous system output, raising heart rate, blood pressure, and plasma catecholamines. This is the mechanistic basis of the sympathomimetic toxicity profile described in MT-2 case reports (Nelson 2012).
• MC5R — exocrine and sebaceous gland modulation — MC5R is enriched in sebaceous glands, Harderian glands, and other exocrine tissues. Agonism alters sebaceous lipid output and has been associated with acne and oily skin in MT-2 users. Preclinical models show MC5R engagement modulates thymic and immune function, although the clinical relevance in humans is uncertain (Chen 1997).
• Pharmacokinetics — Subcutaneous absorption is rapid; plasma T_max is reached within ~1 hour. Apparent plasma half-life is short (~33 minutes after SC dosing in the original Dorr phase 1 series), but the pigmentation response persists for weeks-to-months because eumelanin, once deposited in melanosomes, does not "wash out" — it fades only through normal keratinocyte turnover. This is why effective tanning dosing does not require continuous plasma exposure.
• Non-selectivity is the dominant structural feature — PT-141 (bremelanotide) differs from MT-2 largely through its linear structure and C-terminal modifications that reduce MC1R activity and emphasize central MC3R/MC4R. That separation is what made PT-141 regulatorially viable; MT-2's fixed cyclic heptapeptide structure cannot be dialed away from MC1R, which is why it will always produce the melanocytic and dermatologic effects that killed its regulatory program.

What the Research Shows

The MT-2 human research literature is small, old, and concentrated at one institution. The dominant present-day literature is dermatologic and toxicologic — case reports of harm from recreational use rather than controlled efficacy data. Interpret all claims with that context.

• Pigmentation (Arizona phase 1 series) — Dorr, Levine, Hadley, and colleagues published a pilot phase 1 study of MT-2 in fair-skinned volunteers in 1996 (Life Sciences) demonstrating significant skin darkening after repeated subcutaneous dosing. The pigmentation signal was dose-related and reproducible. Tanning was observable without UV exposure and enhanced synergistically when MT-2 dosing was paired with UV-B. Formal RCT data is limited to small phase 1 cohorts (Dorr 1996).
• MT-1 pigmentation RCT (Arch Dermatol 2004) — The most rigorous human pigmentation trial in this peptide family is the 2004 Dorr RCT of MT-1 (afamelanotide), not MT-2. In three phase 1 trials, MT-1 safely increased tanning alone and acted synergistically with UV-B or sunlight. The same group's MT-2 data mirror this pigmentation signal but with a substantially broader off-target profile (Dorr 2004, PMID 15262693).
• Penile erection in psychogenic erectile dysfunction — Wessells and colleagues (J Urol 1998, PMID 9679884) conducted a double-blind, placebo-controlled crossover study of MT-2 in 10 men with psychogenic ED. MT-2 at 0.025 mg/kg produced real-time Rigiscan-confirmed erections with a mean of 41 minutes of tip rigidity >80%. Increased sexual desire was reported after 68% of MT-2 doses versus 19% of placebo (p<0.01). Nausea and yawning were the dominant side effects.
• Extended ED cohort (J Urol 2000) — Wessells, Levine, Hadley, Dorr, and Hruby expanded this program to 20 men with psychogenic and organic ED in a double-blind placebo-controlled crossover design (J Urol 2000; PMID 11035391). Rigiscan-confirmed erections and increased sexual desire were again documented; 12.9% of subjects had severe nausea at 0.025 mg/kg, and the erectogenic response extended to men with organic ED of mixed cause.
• Female sexual arousal (bremelanotide development) — Subsequent work pivoting from MT-2 to PT-141 (Diamond 2006; PMID 16681470) showed the melanocortin-pathway sexual-arousal signal in premenopausal women with sexual arousal disorder — evidence that informs the MT-2 mechanism discussion but is technically PT-141 data.
• Appetite and body composition — Preclinical data in rodent and non-human primate models consistently show MC4R-agonist-induced appetite suppression and modest body-weight reduction. Formal controlled body-composition studies in humans are lacking. User-reported appetite loss is consistent with mechanism but not rigorously quantified.
• Sexual toxicity — priapism case reports — Devlin and colleagues (Clin Toxicol 2013; PMID 23537392) reported MT-2 overdose associated with priapism, consistent with the compound's erectogenic mechanism and dose-dependence.
• Melanocytic / dermatologic harm — Cousen (Br J Dermatol 2009) reported eruptive melanocytic naevi after MT-2 injection. Langan (Br J Dermatol 2009, BMJ 2009) reported mole changes in U.K. "sun-tan jab" users. Paurobally and colleagues have reported multiple cases of dysplastic naevi and concerning mole change with MT-2 use. Case reports of melanoma in MT-2 users exist in the dermatologic literature, though causation has not been established.
• Systemic toxicity — rhabdomyolysis and renal dysfunction — Nelson, Bryant, and Aks (Clin Toxicol 2012; PMID 23121206) reported a 39-year-old male who injected 6 mg subcutaneously of internet-sourced MT-2 and developed sympathomimetic excess, rhabdomyolysis, and renal dysfunction. Mass-spectrometry-confirmed product identity. This is the most rigorously documented serious toxicity case in the English-language literature.
• Renal infarction — A case report of MT-2-associated renal infarction has been published (Kullberg-Lindh 2020), proposing a vasoconstrictive / thrombotic mechanism related to MC-receptor-mediated sympathetic activation.

Human Data

Human data on MT-2 specifically is limited to the Arizona phase 1 program and subsequent adverse-event case literature.

• Dorr 1996 phase 1 (Life Sciences) — Evaluation of MT-2 as a superpotent cyclic melanotropic peptide; pilot phase 1 clinical study in fair-skinned volunteers establishing pigmentation signal and dose-response.
• Wessells 1998 (PMID 9679884) — 10-subject double-blind, placebo-controlled Rigiscan crossover study in psychogenic ED. 0.025 mg/kg subcutaneous MT-2. Primary endpoint: tip rigidity >80% duration, mean 41 minutes. Nausea and yawning dominant adverse events.
• Wessells 2000 (PMID 11035391) — 20-subject crossover expanded to men with psychogenic and organic ED. Confirmed Rigiscan erectogenic effect and increased sexual desire (68% vs 19% placebo).
• Hadley & Dorr 2006 review (Peptides) — Summary of the MT-1 and MT-2 programs with translational context for the eventual PT-141 / Scenesse trajectories.
• Nelson 2012 toxicology case (PMID 23121206) — 39-year-old male with MT-2-induced sympathomimetic syndrome, rhabdomyolysis (CPK elevated to clinically significant levels), and acute renal dysfunction. Product identity confirmed by mass spectrometry.
• Devlin 2013 priapism case (PMID 23537392) — MT-2 overdose associated priapism report.
• Cousen 2009 (Br J Dermatol) — Eruptive melanocytic naevi following MT-2 injection; dermatologic case reports series.
• Langan 2009 (BMJ 338:b277) — Change in moles linked to use of unlicensed "sun tan jab" — case series in U.K. users.
• Evans-Brown 2009 (BMJ 338:b566) — Use of Melanotan I and II in the general population; epidemiologic snapshot of unregulated community use in the U.K.
• Langan 2010 review (Br J Dermatol; PMID 20426777) — "Melanotropic peptides: more than just 'Barbie drugs' and 'sun-tan jabs'?" — the canonical review framing MT-2's medical-vs-recreational tension.

No phase 2 or phase 3 RCT data exists for MT-2 in any indication. All positive efficacy data derives from the 1990s Arizona phase 1 program. All post-2000 MT-2 human literature is essentially adverse-event and case-report driven.

Dosing from the Literature

MT-2 has no approved dosing — it is not dispensed by any pharmacy in any regulated jurisdiction. The ranges below reflect the dosing used in the original Arizona phase 1 trials and subsequently adopted by the recreational-use community. They are presented for harm-reduction and research context, not as a recommendation.

Reconstitution & Storage

MT-2 is supplied as a lyophilized white-to-off-white powder in single-use vials, typically 10 mg per vial. Reconstitution is performed with bacteriostatic water (BAC water, 0.9% benzyl alcohol in sterile water) or sterile saline.

• Reconstitution technique — Swab both vial stoppers with isopropyl alcohol. Draw diluent into syringe, inject slowly down the side of the MT-2 vial (not directly onto the powder cake). Swirl gently to dissolve; do not shake vigorously (peptide denaturation risk).
• Storage (lyophilized) — Unreconstituted vial stored refrigerated at 2–8°C is stable for 24 months or longer. Avoid repeated temperature cycling.
• Storage (reconstituted) — Refrigerated 2–8°C for up to 28 days when reconstituted with BAC water (benzyl alcohol is bacteriostatic). Discard sooner if cloudiness, discoloration, or particulate develops. Do not freeze reconstituted solution.
• Solution appearance — Clear and colorless when properly reconstituted. Discard any vial showing turbidity, discoloration, or visible particulate matter.
• Light sensitivity — Melanocortin peptides are mildly light-sensitive; keep reconstituted vials in the refrigerator and out of direct sunlight between doses.

→ Use the Kalios Dosing Calculator for MT-2 reconstitution

Side Effects & Risks

• Nausea and vomiting — The most common adverse event. Dose- and rate-dependent; diminishes with continued use but can be severe at 0.025 mg/kg (12.9% severe nausea in Wessells 1998/2000). Central MC4R agonism is the presumed mechanism.
• Facial flushing and warmth — Transient cutaneous vasodilation, typically 15–60 minutes post-injection. Benign.
• Yawning and stretching — A classic centrally-mediated melanocortin signature; not harmful, but frequently reported.
• Spontaneous penile erection / priapism — Expected melanocortin pharmacology; generally benign at low doses but priapism (prolonged, painful erection requiring medical intervention) has been reported with overdose (Devlin 2013).
• Mole darkening, new naevi, dysplastic naevi — The dominant long-term dermatologic concern. MT-2 indiscriminately stimulates all melanocytes, including those in existing moles. Multiple case series document eruptive melanocytic naevi, darkening and morphological change of pre-existing moles, and dysplastic-naevus emergence in MT-2 users (Cousen 2009; Langan 2009). Dermatologic surveillance is essential. MT-2 does not cause melanoma in any proven sense, but it changes mole appearance in ways that complicate melanoma detection.
• Freckle darkening and hyperpigmentation — Lips, genital skin, areolae, nail beds, and pre-existing freckles darken alongside intended skin pigmentation. Redistribution is neither uniform nor reversible on the short-to-medium timescale.
• Sympathomimetic / cardiovascular toxicity — Hypertension, tachycardia, palpitations, and in severe cases, rhabdomyolysis and renal dysfunction (Nelson 2012). Renal infarction has been reported in case literature. These are not common adverse events but are the most medically serious.
• Appetite suppression — Often reported as a benefit but can be excessive; weight loss in individuals who are already lean is undesirable.
• Fatigue and lethargy — Post-injection sedation is common, especially during loading.
• Sebaceous / acne activity — MC5R engagement drives sebaceous output; acneform eruptions and oily skin are reported.
• Injection-site reactions — Local pain, erythema, and induration at subcutaneous injection sites, typically self-limiting.
• Purity / contamination risk — Internet-sourced MT-2 has highly variable purity and microbiological quality. Several of the documented serious adverse events involve product of unknown origin — contamination, mislabeling, and underdosing are documented risks distinct from the compound's pharmacology itself.
• Contraindications — Personal or family history of melanoma, numerous or atypical moles, prior cardiovascular disease or uncontrolled hypertension, pregnancy or lactation (no human data). Relative contraindications include significant renal disease and history of priapism.

Bloodwork & Monitoring

• Full-body dermatologic examination — This is the single most important monitoring step for any MT-2 user. Baseline full-body skin survey with a dermatologist, preferably including total-body photography or dermoscopic mapping of existing naevi, then repeat at 6 and 12 months. Any mole showing ABCDE changes (asymmetry, border, color, diameter, evolution) needs prompt evaluation.
• Blood pressure and heart rate — Measure at baseline; re-check during loading. Sympathomimetic activation is a documented mechanism of harm.
• CMP (comprehensive metabolic panel) — Baseline renal function (creatinine, BUN, eGFR) and electrolytes; repeat if any muscle pain, dark urine, or systemic symptoms develop. CPK (creatine kinase) if rhabdomyolysis is suspected.
• CBC — Baseline complete blood count; no MT-2-specific abnormality expected but part of standard pre-use labs.
• Hepatic panel — AST, ALT, total bilirubin at baseline. MT-2 is not known to be hepatotoxic but baseline is standard.
• Eye exam — Melanocortin receptors are present in the uveal tract; melanocytic lesions of the iris and choroid have been reported in case literature. Dilated eye exam at baseline and annually in long-term users is reasonable.
• Sexual-function assessment — If MT-2 is being used for sexual effects, document baseline erectile function (IIEF-5) and desire (FSFI for women) to track response and avoid dose escalation.

Commonly Stacked With

MT-2 is most commonly co-used (not formally co-administered) with the following in the recreational-use community. None of these combinations have been tested in clinical trials.

→ Check compound compatibility in the Stack Builder

Regulatory Status

Related Compounds

People researching MT-2 often also look at these:

Next Steps

Key References

1. Wessells H, Fuciarelli K, Hansen J, Hadley ME, Hruby VJ, Dorr R, Levine N. Synthetic melanotropic peptide initiates erections in men with psychogenic erectile dysfunction: double-blind, placebo controlled crossover study. J Urol. 1998;160(2):389-393. PMID: 9679884.
2. Wessells H, Levine N, Hadley ME, Dorr R, Hruby V. Melanocortin receptor agonists, penile erection, and sexual motivation: human studies with Melanotan II. Int J Impot Res. 2000;12 Suppl 4:S74-S79. PMID: 11035391.
3. Dorr RT, Lines R, Levine N, Brooks C, Xiang L, Hruby VJ, Hadley ME. Evaluation of melanotan-II, a superpotent cyclic melanotropic peptide in a pilot phase-I clinical study. Life Sci. 1996;58(20):1777-1784. PMID: 8637403.
4. Dorr RT, Ertl G, Levine N, Brooks C, Bangert JL, Powell MB, Humphrey S, Alberts DS. Effects of a superpotent melanotropic peptide in combination with solar UV radiation on tanning of the skin in human volunteers. Arch Dermatol. 2004;140(7):827-835. PMID: 15262693. (MT-1/afamelanotide — foundational data for the melanotropin pigmentation mechanism shared with MT-2.)
5. Nelson ME, Bryant SM, Aks SE. Melanotan II injection resulting in systemic toxicity and rhabdomyolysis. Clin Toxicol (Phila). 2012;50(10):1169-1173. PMID: 23121206.
6. Devlin J, Pomerleau A, Foote J. Melanotan II overdose associated with priapism. Clin Toxicol (Phila). 2013;51(4):383. PMID: 23537392.
7. Cousen P, Colver G, Helbling I. Eruptive melanocytic naevi following melanotan injection. Br J Dermatol. 2009;161(3):707-708. PMID: 19438860.
8. Langan EA, Ramlogan D, Jamieson LA, Rhodes LE. Change in moles linked to use of unlicensed "sun tan jab". BMJ. 2009;338:b277. PMID: 19174439.
9. Evans-Brown M, Dawson RT, Chandler M, McVeigh J. Use of melanotan I and II in the general population. BMJ. 2009;338:b566. PMID: 19218325.
10. Langan EA, Nie Z, Rhodes LE. Melanotropic peptides: more than just 'Barbie drugs' and 'sun-tan jabs'? Br J Dermatol. 2010;163(3):451-455. PMID: 20426777.
11. Hadley ME, Dorr RT. Melanocortin peptide therapeutics: historical milestones, clinical studies and commercialization. Peptides. 2006;27(4):921-930. PMID: 16412534.
12. Diamond LE, Earle DC, Rosen RC, Willett MS, Molinoff PB. An effect on the subjective sexual response in premenopausal women with sexual arousal disorder by bremelanotide (PT-141), a melanocortin receptor agonist. J Sex Med. 2006;3(4):628-638. PMID: 16681470. (PT-141 pivotal — MT-2's regulated descendant.)
13. Abdel-Malek ZA, Scott MC, Suzuki I, Tada A, Im S, Lamoreux L, Ito S, Barsh G, Hearing VJ. The melanocortin-1 receptor is a key regulator of human cutaneous pigmentation. Pigment Cell Res. 2000;13 Suppl 8:156-162. PMID: 11041375.
14. Huszar D, Lynch CA, Fairchild-Huntress V, Dunmore JH, Fang Q, Berkemeier LR, Gu W, Kesterson RA, Boston BA, Cone RD, Smith FJ, Campfield LA, Burn P, Lee F. Targeted disruption of the melanocortin-4 receptor results in obesity in mice. Cell. 1997;88(1):131-141. PMID: 9019399.
15. Van der Ploeg LH, Martin WJ, Howard AD, Nargund RP, et al. A role for the melanocortin 4 receptor in sexual function. Proc Natl Acad Sci U S A. 2002;99(17):11381-11386. PMID: 12172010.
16. Al-Obeidi F, Hadley ME, Pettitt BM, Hruby VJ. Design of a new class of superpotent cyclic alpha-melanotropins based on quenched dynamic simulations. J Am Chem Soc. 1989;111(9):3413-3416.