Melanotan II Research Only

What It Is

Melanotan II (MT-II) is a synthetic cyclic heptapeptide analog of the endogenous neuropeptide α-melanocyte-stimulating hormone (α-MSH). It was designed and synthesized in the 1980s at the University of Arizona by Mac Hadley, Victor Hruby, and colleagues as part of a research program aimed at developing a "sunless tanning" drug to reduce reliance on UV exposure — the theory being that stimulating endogenous melanogenesis would allow protective melanin pigmentation without the DNA damage of ultraviolet light. The structure is Ac-Nle-cyclo(Asp-His-D-Phe-Arg-Trp-Lys)-NH₂, a lactam-bridged cyclic construct that resists proteolytic degradation and confers dramatically higher potency than native α-MSH.

The design succeeded pharmacologically — MT-II is orders of magnitude more potent than α-MSH at melanocortin receptors and produces robust cutaneous pigmentation in humans — but failed to achieve approval. The commercial rights were licensed to Competitive Technologies and development was pursued for years without crossing the regulatory finish line. In the process, the program spun off two successor molecules that did reach clinical use: afamelanotide (Melanotan I, brand name Scenesse), a linear α-MSH analog approved by the FDA in 2019 for erythropoietic protoporphyria, and bremelanotide (PT-141), a retuned MC4R-selective analog approved in 2019 for hypoactive sexual desire disorder in premenopausal women.

MT-II itself remained in research-chemical and gray-market channels. In those channels, it became one of the most popular non-approved peptides — used off-label for cosmetic tanning, appetite suppression, and both male erectile dysfunction and female sexual dysfunction. That history is largely responsible for its appearance in the Kalios database: it is widely used in community settings, has a genuinely substantial early-phase human research record, and carries serious safety signals (melanoma case reports, atypical nevus transformation, priapism, rhabdomyolysis) that are important to document honestly.

What separates Melanotan II from its successor PT-141 is receptor selectivity. MT-II is non-selective across the melanocortin family, binding MC1R (skin pigmentation), MC3R and MC4R (CNS, sexual function, appetite), and MC5R (exocrine, sebaceous function). PT-141 was engineered to be MC4R-biased, retaining the sexual-function effect while reducing MC1R-mediated pigmentation. Melanotan II's non-selectivity is simultaneously its feature and its liability — you get tanning, appetite suppression, and sexual-arousal effects together, along with the safety signals associated with chronic MC1R activation in users with significant nevus burden or melanoma risk.

Mechanism of Action

Melanotan II is a pan-melanocortin-receptor agonist. Its clinical effects reflect the integrated output of activity at MC1R, MC3R, MC4R, and MC5R across skin, CNS, and peripheral tissue.

• MC1R agonism (skin pigmentation — the primary effect) — MT-II activates MC1R on epidermal melanocytes, driving cAMP/PKA-mediated transcription of microphthalmia-associated transcription factor (MITF) and downstream expression of tyrosinase, TRP-1, and TRP-2. The net effect is increased eumelanin synthesis, darker skin pigmentation, and a modest UV-protective effect via increased epidermal melanin content (Dorr et al., 1996; PMID 8637402).
• MC4R agonism (central appetite + sexual function) — MC4R activation in hypothalamic paraventricular nucleus drives anorexigenic signaling (appetite suppression) and in preoptic/limbic circuits drives sexual arousal and pro-erectile output. This is the receptor bremelanotide was designed to target selectively; MT-II engages it non-selectively (Wessells et al., 2000; PMID 11035391).
• MC3R agonism (metabolism + energy balance) — MC3R in hypothalamic ventromedial nucleus and arcuate contributes to energy homeostasis, feeding regulation, and reward processing. Contribution to MT-II's clinical phenotype is harder to isolate.
• MC5R agonism (exocrine + sebaceous) — MC5R signals through sebaceous glands and exocrine tissue; chronic MT-II can exacerbate acne and seborrheic symptoms.
• Downstream dopaminergic tone — MC4R activation in medial preoptic area increases dopaminergic output in the mesolimbic pathway — the proximal neurochemistry of the pro-erectile and pro-libido effects.
• BP and HR (sympathetic outflow) — Transient ~5–15 mmHg systolic BP rise and modest HR increase within 1–4 hours of dose, reflecting sympathetic activation. Relevant to cardiovascular safety in predisposed users.
• Anorectic effect — Well-documented dose-dependent appetite suppression during the early phase of dosing, with partial tachyphylaxis over weeks.
• Pigmentation versus sexual effect timing — Pigmentation accumulates over weeks and persists after cessation (melanin is stable); the acute sexual/erectile effect is dose-dose, appearing within 1–2 hours and dissipating in 4–8 hours.
• α-MSH biological context — Endogenous α-MSH is derived from POMC cleavage and circulates at very low concentrations; MT-II achieves pharmacological levels orders of magnitude above physiologic α-MSH exposure, explaining the dramatic clinical effects absent from endogenous signaling.

What the Research Shows

Melanotan II has a modest but genuine early-clinical human evidence base from the Arizona and subsequent follow-on groups. It has never completed Phase 3 development for any indication and has never been FDA-approved.

• Phase 1 pilot (Dorr et al., Life Sci 1996; PMID 8637402) — 3 normal male volunteers; SubQ 0.01–0.03 mg/kg alternating-day dosing over 2 weeks. Increased pigmentation of face, upper body, and buttock. Side effects: "stretching and yawning complex" correlated with spontaneous penile erections 1–5 hours after dosing. First human demonstration that MT-II is orally bioactive for tanning at sub-mg/kg doses.
• Phase I/II erectile dysfunction (Wessells et al., J Urol 1998; PMID 9679884) — Double-blind placebo-controlled crossover in men with psychogenic ED. Erections achieved in responders without sexual stimulation; established proof-of-concept for melanocortin agonism in ED.
• Organic ED (Wessells et al., Urology 2000; PMID 11018622) — Men with organic ED. Increased erectile response plus increased sexual desire (68% of MT-II doses vs 19% placebo, p<0.01).
• Human sexual motivation review (Wessells, Int J Impot Res 2000; PMID 11035391) — 20 men with psychogenic and organic ED, double-blind placebo-controlled crossover. 17 of 20 achieved erection without sexual stimulation; mean 41 min Rigiscan tip rigidity >80%. At 0.025 mg/kg, 12.9% severe nausea.
• Discovery paper on sexual function (Hadley/Dorr, 2005; PMID 15996790) — Summarized the discovery arc — incidental observation of spontaneous erection in early α-MSH rat studies leading to the melanocortin-as-sexual-function drug-target hypothesis that produced MT-II, afamelanotide, and bremelanotide.
• UV + melanotropin synergy (Levine et al., 2004; PMID 15262693) — Superpotent melanotropin plus solar UV produced greater pigmentation than UV alone. Underpinned the "tan enhancer" positioning.
• Melanocortin agonists in sexual dysfunction review (King et al., 2014; PMID 25096243) — Comprehensive review of melanocortin agonists in male and female sexual dysfunction contexts, placing MT-II alongside bremelanotide.
• Melanoma/nevus case series (Cardones 2009; Nolte 2015; various dermatology case reports) — Multiple case reports describe atypical nevus transformation, dysplastic nevi, and melanoma-arising-from-mole following MT-II or Melanotan I use. The 2009 Cardones teenage FAMMM case remains the most-cited alarm publication (PMC3663356).
• Eruptive dysplastic nevi following Melanotan — Case series documenting rapid appearance of new atypical nevi during Melanotan use.
• Systemic toxicity case (Ellis et al., 2012; PMID 23121206) — Melanotan II injection resulting in systemic toxicity and rhabdomyolysis in a 39-year-old male after a 6 mg SubQ dose — one of the few published acute overdose reports.
• Priapism case reports (PMC7930850) — Melanotan tanning injection as cause of priapism requiring cavernosal aspiration, phenylephrine, and in one case operative penoscrotal decompression.
• Epidemiological review (Gorrie 2015) — "An unhealthy glow? A review of melanotan use and associated clinical outcomes" summarized the pattern of adverse events and cosmetic/sexual use.

Human Data

Small but real:

• Pilot Phase 1 tanning (Dorr 1996; N=3) — Foundational pigmentation demonstration.
• Phase 1/2 ED (Wessells 1998, 2000; N≈20) — Erectile response demonstrated.
• UV + MT-II combination (Levine 2004) — Additive tanning effect.
• Fitzpatrick skin type II/III characterization — Tanning response strongest in medium-fair skin types, weaker in very fair (Type I) and very dark (Type V/VI) individuals.
• Women with sexual dysfunction (preliminary) — Early studies of melanocortin agonists in female sexual dysfunction provided signal that ultimately led to bremelanotide's HSDD Phase 3 program.
• No Phase 3 — Development program never advanced to registrational trials for any indication.
• Case series (Gorrie 2015 and subsequent) — Multi-country case series documenting dermatologic adverse events and sexual/tanning misuse patterns.
• Poison control / MHRA registries — UK MHRA and equivalent bodies have accumulated case data on acute toxicity, supporting ongoing warnings against consumer use.

Large absence: randomized controlled trials at modern regulatory scale for any indication. What MT-II has instead is a relatively narrow early-phase database and a broader case-series signal of harm that never found a counter-weight in Phase 2/3 efficacy programs.

Dosing from the Literature

Doses below are drawn from the Phase 1 trials and aggregated community practice. MT-II is not approved; there is no labeled human dose.

Reconstitution & Storage

Melanotan II is supplied as lyophilized powder, typically in 10 mg vials. No pre-mixed clinical formulation exists.

• Reconstitution — Inject BAC water slowly down the vial wall at 45°. Swirl; do not shake. Clear, colorless solution.
• Storage — Unreconstituted: 2–8°C preferred; room temperature acceptable short-term. Reconstituted: 2–8°C, use within 21–28 days. Do not freeze.
• Injection sites — SubQ into abdomen (2" from navel) or thigh. Rotate sites.
• Timing — Evening dosing common to minimize awareness of nausea and flushing during waking hours; sexual-function timing anchors 30–60 minutes pre-activity.
• Inspection — Discard if cloudy, discolored, or contaminated.

→ Use the Kalios Peptide Calculator for exact syringe units

Side Effects & Risks

Melanotan II has one of the most important safety profiles to understand carefully in this database, because its side-effect signals are both common (nausea, flushing) and occasionally severe (melanoma transformation, priapism, rhabdomyolysis).

• Nausea and vomiting — Dose-dependent, most intense on first 1–3 doses. In Wessells 2000 at 0.025 mg/kg, severe nausea in 12.9%. Pre-dose ondansetron or ginger is common practice (not label).
• Facial flushing / warmth — Common within 30–60 minutes. Usually self-limited.
• Stretching / yawning complex — A characteristic MC4R-driven behavioral signature, noted since the original Dorr trial. Correlated with spontaneous erections.
• Appetite suppression — Real and often welcomed by users, but distinguishes MT-II from PT-141 (which is MC4R-selective and has less CNS appetite signature).
• Cardiovascular / BP elevation — Transient systolic rise (~5–15 mmHg), modest HR increase. Contraindicated in uncontrolled hypertension and significant cardiovascular disease.
• Hyperpigmentation — generalized and focal — Generalized skin darkening. Focal hyperpigmentation of face, nipples, gums, scars, and genitals is common and often persistent for months after cessation.
• Nevus darkening / atypical nevus transformation — Well-documented in case reports. Existing nevi darken, enlarge, and develop atypical features. In susceptible individuals (FAMMM, dysplastic nevus syndrome, significant nevus burden), transformation toward melanoma has been reported.
• Melanoma (case reports) — Multiple dermatology case reports describe melanoma arising during or after Melanotan I/II use, including cases confirmed histologically at 1 mm Breslow depth. Causal proof at population level is limited; mechanistic plausibility and accumulating case-series data are real.
• Priapism — Multiple case reports of ischemic priapism requiring emergent cavernosal aspiration, phenylephrine, and in some cases penoscrotal decompression. Combining MT-II with PDE5 inhibitors substantially amplifies this risk.
• Rhabdomyolysis (reported) — One published case of systemic toxicity with sympathomimetic excess and rhabdomyolysis after 6 mg SubQ in a 39-year-old male. Emergent medical care required.
• Acne and seborrhea exacerbation — MC5R-driven sebaceous activation.
• Gastrointestinal discomfort — Beyond acute nausea, some users report chronic mild GI changes.
• Gray-market purity — MT-II is particularly poorly synthesized in low-end supply channels. Oxidation of tryptophan and methionine residues is common; contamination with bacterial endotoxins has been documented in third-party testing of gray-market vials.
• Regulatory warnings — MHRA (UK), TGA (Australia), FDA, and several European agencies have issued formal consumer warnings against use.
• Contraindications — Personal or family history of melanoma; significant atypical nevus burden; dysplastic nevus syndrome; FAMMM (familial atypical multiple mole melanoma) syndrome; uncontrolled hypertension; active cardiovascular disease; pregnancy; lactation; concurrent PDE5-inhibitor use (priapism risk).

Supportive Nutrition & Supplements

Skin health and melanogenesis depend on nutritional inputs. MT-II amplifies melanocyte output; the rest of the skin remains a general-health structure that requires its structural and micronutrient inputs.

• Vitamin D (target 40–60 ng/mL) — Paradoxical concern on MT-II: increased pigmentation reduces endogenous vitamin D production from UV. Supplementation becomes more important, not less. 2,000–5,000 IU/day with K2.
• Nicotinamide (500 mg BID) — ONTRAC trial (Chen NEJM 2015) reduced new non-melanoma skin cancers in high-risk adults. Compatible with any protocol that increases UV tolerance.
• Beta-carotene / carotenoids (dietary) — Dietary carotenoids contribute to a modest skin "glow" phenotype independent of melanin — 5–7 servings/day of colored vegetables demonstrably affect skin color over 6 weeks (Stephen et al., 2011).
• Omega-3 (2–3 g EPA/DHA) — Supports dermal barrier function and inflammation resolution.
• Astaxanthin (4–12 mg/day) — Carotenoid with substantial antioxidant activity in human skin trials; modest UV-protective effect.
• Polypodium leucotomos (240 mg BID) — Botanical with human data for reducing UV-induced erythema and DNA damage. Compatible adjunct in any melanogenic or high-UV-exposure protocol.
• Hydration + electrolytes — Tanning + heat + BP-modulating drug = real dehydration risk during the peak-UV portion of cycles.
• Protein (1.6–2.2 g/kg) — General skin-quality support; nothing MT-II-specific.
• Sun exposure timing — Modest UV exposure amplifies MT-II's tanning signal (Levine 2004 synergy). Burning UV exposure does not — and amplifies melanoma risk independent of MT-II.
• Things to avoid — Combining MT-II with PDE5 inhibitors (priapism risk), combining with high-dose stimulants (BP + sympathetic stacking), UV sunburn (combines MT-II's melanogenic stimulus with DNA damage), and use in anyone with significant nevus burden or melanoma family history.

What to Expect — Timeline

Individual response varies substantially by Fitzpatrick skin type, baseline nevus burden, sun exposure habits, and genetics. This synthesizes trial data and aggregated community reports.

• First dose — Nausea onset at 30–90 minutes is the most common first experience, often accompanied by facial flushing and the characteristic stretching/yawning complex. Spontaneous erection in many male users within 1–4 hours of dose. No visible pigmentation change yet.
• Day 3–5 — Nausea blunts substantially with repeated dosing. Appetite suppression often noted. Earliest darkening of existing freckles, moles, and genital skin often visible by day 5.
• Week 1–2 (loading) — Moderate skin darkening, particularly on face and areas exposed to sunlight. Freckles darken first. Nipples and genitals often among the first areas to visibly pigment.
• Week 3–4 — Generalized tan visible. Many users transition from loading (daily) to maintenance (1–2x/week). Appetite suppression partially tachyphylactic by this window.
• Week 6–8 — Peak pigmentation. The most common community-recommended window to pause for dermatologic reassessment — compare nevi to baseline photographs.
• Post-cycle (months 2–6 off) — Pigmentation fades over months as melanin-laden keratinocytes shed. Deep pigmentation of nipples, scars, and genitals can persist longer or permanently.
• If you notice a changing mole — ANY change (size, color, asymmetry, bleeding, itching) warrants urgent dermatology evaluation. This is the threshold where hesitation causes harm.
• Non-responders (tanning) — Very fair (Fitzpatrick Type I) users often achieve only modest tanning. Very dark (Type V/VI) users see minimal visible change because they are already maximally melanogenic.
• Sexual effect timing — Spontaneous erection in males is typically dose-dose; not a chronic effect. Lower doses taken specifically for sexual use (e.g., 250 mcg 30–60 min pre-activity) work for some but carry the same side-effect profile — nausea, flushing, BP rise.
• If you feel worse — Prolonged erection (>2 hours) → emergency care. Severe BP elevation, chest pain, muscle pain with dark urine, any persistent new skin lesion → stop and seek evaluation.

Quick Compare — Melanotan II vs PT-141 vs Afamelanotide vs Nicotinamide

The most relevant comparators for MT-II are its two molecular cousins (PT-141 for sexual function, afamelanotide for tanning/photoprotection) and the non-drug skin-cancer chemo-prevention benchmark (nicotinamide).

Practical interpretation:

• MT-II vs PT-141 — Same molecular family, different selectivity. For sexual function specifically, PT-141 is the cleaner choice — MC4R-biased, FDA-approved, labeled dosing, pharmacovigilance. MT-II's only advantage over PT-141 is combined tanning + sexual effect; that combination is the exact source of its risk.
• MT-II vs afamelanotide — For any medically-indicated melanogenic need (EPP, Hailey-Hailey, polymorphous light eruption under specialist care), afamelanotide is the approved pathway with dermatologic surveillance. MT-II is the unsupervised variant.
• Cosmetic tanning use case — There is no legitimate pharmaceutical pathway for cosmetic tanning. MT-II is what users pursue in that space; no regulator has approved any melanocortin agonist for cosmesis. The risk calculation is personal.
• Skin cancer prevention — Nicotinamide is a genuinely evidence-based, low-cost, low-risk adjunct in high-UV-exposure individuals. It does not interfere with MT-II; neither amplifies the other's risk or benefit meaningfully.
• Who should not use MT-II under any circumstance — Melanoma history (personal or family), significant nevus burden, dysplastic nevus syndrome, FAMMM, uncontrolled hypertension, active cardiovascular disease, pregnancy, lactation. These are hard "no."

→ See full PT-141 profile  •  → See Melanotan I / afamelanotide profile

Practical User Notes

• Dermatology first, peptide second — Do not dose MT-II without a documented baseline dermatologic exam. Any user with significant nevus burden or melanoma family history should not use under any circumstance.
• Photo-document every mole — Whole-body photography at baseline. Re-image monthly. Compare. Any change is a stop signal.
• Start low — 125–250 mcg — First dose, evening, after a small meal. Assess nausea response. Pre-dose ondansetron 4 mg or ginger 1 g 30 min before reduces the dominant side effect.
• Loading then maintenance — Daily 250–500 mcg for 1–2 weeks of loading; 1–2x/week for maintenance. Resist the temptation to stay on loading dose for months.
• Sun exposure is potentiating — Moderate UV amplifies the tanning signal. Burning UV amplifies melanoma risk. Do not tan in a bed or burn in the sun while on MT-II.
• Do not combine with PDE5 inhibitors — Priapism risk multiplies. If sexual function is the goal, use PT-141 (FDA-approved, monitored) instead.
• Watch BP — Baseline and on first several doses. Sustained rise warrants reduction or cessation.
• Cycle, do not run continuously — 4–8 weeks on, 8–12 weeks off is a defensible pattern. Continuous year-round MT-II is the highest-risk community protocol.
• Injection technique — 29–31G insulin syringe, SubQ 45° into abdomen or thigh. Rotate sites.
• Sourcing — Third-party HPLC + mass spec + endotoxin testing is the floor. This compound has some of the highest rates of purity failures in independent testing of any research peptide.
• Storage — 2–8°C refrigerated; reconstituted <28 days.
• Symptoms that require emergency care — Erection >2 hours (ischemic priapism), severe muscle pain with dark urine (rhabdomyolysis), severe sustained hypertension, chest pain, stroke-like symptoms. These are real documented MT-II adverse events, not theoretical risks.
• If a mole changes — stop and see a dermatologist same week — Do not continue dosing while awaiting evaluation.
• Honest framing — For cosmetic tanning, the risk/benefit on MT-II is unfavorable at a population level. The people for whom it works well are those without the risk factors that make it dangerous. Self-assessment on risk factors should be conservative.

Bloodwork & Monitoring

Given the dermatologic and cardiovascular signal profile, monitoring for MT-II skews dermatologic rather than endocrine.

• Baseline dermatologic exam — Full-skin exam with dermoscopy before initiation. Photographic documentation of all existing nevi. Essential — arguably the single most important MT-II monitoring step.
• Repeat derm exam at 3 and 6 months — Compare dermoscopy and photographs to baseline for asymmetry, border change, color change, diameter change, and evolution (ABCDE).
• Baseline BP and HR — Document; recheck during first several doses.
• CMP and CBC — Baseline; repeat with chronic use.
• CK / renal function — If any muscle symptoms or dark urine emerge, rhabdomyolysis is a documented possibility — check CK, BUN/Cr, urine myoglobin.
• Family history review — Melanoma, dysplastic nevus syndrome, FAMMM. Any of these moves MT-II to "do not use."
• Mental health check — CNS MC4R activation can produce mood changes; document baseline.
• Photo log of tan progression + nevi — Standardized monthly photos are the most objective way to track both benefit (pigmentation) and risk (nevus change).

Commonly Stacked With

→ Check compound compatibility in the Stack Builder

Regulatory Status

Related Compounds

The two approved melanocortin children and the other peptides users reach for instead of MT-II.

Next Steps

Key References

1. 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: 8637402.
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. Wessells H, Gralnek D, Dorr R, Hruby VJ, Hadley ME, Levine N. Effect of an alpha-melanocyte stimulating hormone analog on penile erection and sexual desire in men with organic erectile dysfunction. Urology. 2000;56(4):641-646. PMID: 11018622.
4. 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.
5. Hadley ME, Dorr RT. Melanocortin peptide therapeutics: historical milestones, clinical studies and commercialization. Peptides. 2006;27(4):921-930. PMID: 16412534.
6. Wessells H, Hruby VJ, Hackett J, Han G, Balse-Srinivasan P, Vanderah TW. Ac-Nle-c[Asp-His-D-Phe-Arg-Trp-Lys]-NH2 induces penile erection via brain and spinal melanocortin receptors. Neuroscience. 2003;118(3):755-762. PMID: 12710982.
7. Levine N, Dorr RT, Ertl GA, Brooks C, 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(9):1126-1129. PMID: 15262693.
8. Cardones AR, Grichnik JM. Alpha-melanocyte-stimulating hormone-induced eruptive nevi. Arch Dermatol. 2009;145(4):441-444. PMID: 19380665.
9. Paurobally D, Jason F, Dezfoulian B, Nikkels AF. Melanotan-associated melanoma. Br J Dermatol. 2011;164(6):1403-1405. PMID: 21457222.
10. Nolte E, Lim AM, Mills P, Pfeiffer L. Changes of melanocytic lesions induced by Melanotan injections and sun bed use in a teenage patient with FAMMM syndrome. Dermatol Pract Concept. 2012;2(3):10. PMC3663356.
11. 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: 20545686.
12. Ellis R, Lahiri R, Chandler J, Mohamed MB. Melanotan II injection resulting in systemic toxicity and rhabdomyolysis. Clin Toxicol (Phila). 2012;50(8):729-730. PMID: 23121206.
13. Melanotan tanning injection: a rare cause of priapism. Case report. 2021. PMC7930850.
14. Gorrie S, Elwes R, Hardman G, Stratigos AJ. An unhealthy glow? A review of melanotan use and associated clinical outcomes. Australas J Dermatol. 2015;56(3):e66-e71.
15. Hadley ME. Discovery that a melanocortin regulates sexual functions in male and female humans. Peptides. 2005;26(10):1687-1689. PMID: 15996790.
16. King SH, Mayorov AV, Balse-Srinivasan P, Hruby VJ, Vanderah TW, Wessells H. Melanocortin receptors, melanotropic peptides and penile erection. Curr Top Med Chem. 2007;7(11):1098-1106. PMC2694735.
17. Rössler E, Salih V, Lee N, Bolz S, Pellacani G, Raposio E, Hönigsmann H. Melanocortin receptor agonists in the treatment of male and female sexual dysfunctions: results from basic research and clinical studies. Curr Top Med Chem. 2014;14(23):2670-2683. PMID: 25096243.
18. Lengyel I. Melanotan-II (MT-II): a safety perspective on an unlicensed product. Drug Test Anal. 2015;7(11-12):989-994.
19. Chen AC, Martin AJ, Choy B, Fernandez-Penas P, Dalziell RA, McKenzie CA, Scolyer RA, Dhillon HM, Vardy JL, Kricker A, St George G, Chinniah N, Halliday GM, Damian DL. A phase 3 randomized trial of nicotinamide for skin-cancer chemoprevention (ONTRAC). N Engl J Med. 2015;373(17):1618-1626. PMID: 26488693. (Comparator reference — nicotinamide NMSC chemoprevention.)
20. MHRA. Unlicensed Melanotan products warning. UK Medicines and Healthcare products Regulatory Agency advisories.