Melanotan II (MT-2): A Research Review of the Cyclic α-MSH Analog, Its Melanocortin Receptor Pharmacology and How It Differs from Melanotan I and PT-141

By Peptide Insider Research Team · 11 min read · Last updated 2026-09-08

Melanotan II (MT-2, MT-II) is a synthetic cyclic heptapeptide analog of α-melanocyte-stimulating hormone (α-MSH) created in 1989 at the University of Arizona by side-chain lactam cyclization of the potent [Nle⁴,D-Phe⁷]-α-MSH core. Unlike its linear predecessor Melanotan I, MT-II is a truncated, conformationally constrained molecule that activates four of the five melanocortin receptors with similar nanomolar affinity, which made it both a landmark pharmacological tool and, later, the parent molecule of the approved drug bremelanotide (PT-141). This review summarizes its design history, receptor pharmacology, the small body of human data, the safety literature, and how MT-II differs from Melanotan I and PT-141. All content is provided strictly for research reference.

Melanotan II at a glance

Attribute	Detail
Compound class	Cyclic α-MSH(4–10) analog; melanocortin receptor agonist
Sequence	Ac-Nle-c[Asp-His-D-Phe-Arg-Trp-Lys]-NH2 (7 residues; Asp5–Lys10 side-chain lactam) [2]
Origin	Designed by Al-Obeidi, Hadley and Hruby (University of Arizona, 1989) from molecular-dynamics modeling of α-MSH [2,13]
Receptor profile	Nanomolar agonist at MC1R, MC3R, MC4R, MC5R; inactive at MC2R [3,6]
Key analogs	Melanotan I (linear MT-1), PT-141/bremelanotide (free-acid metabolite), SHU9119 (D-Nal(2')7 antagonist) [4,5,12]
Human data	Pilot Phase I (n=3, 1996); two small double-blind crossover studies (1998, 2000); no pivotal trials [7,8,9]
Regulatory status	Not approved anywhere; subject to regulatory warnings on unregulated products [14,15,17]

Nomenclature: MT-2, MT2, MT-II, melanotan 2 and melanotan II

Few research peptides circulate under as many spellings. The variants below all refer to the same molecule; the table exists so that a reader who arrives via one alias can be certain which compound the literature is describing.

Alias	Where it appears	Refers to
Melanotan II, melanotan-II, MT-II	Primary literature (Hadley, Hruby, Dorr) [1,2,7]	The cyclic heptapeptide reviewed here
Melanotan 2, melanotan-2, MT-2, MT2, MT 2	Supplier catalogs, forums, regulatory notices	Same molecule; formatting only
Ac-Nle4-c[Asp5,D-Phe7,Lys10]-α-MSH(4–10)-NH2	Medicinal-chemistry papers [2,4]	Systematic name of MT-II
Melanotan I, MT-1, MT-I, afamelanotide, NDP-MSH	Literature and pharmacopeias	Different molecule: linear 13-residue analog [1,13]
PT-141, bremelanotide	Palatin Technologies literature, FDA labeling	Different molecule: MT-II with a C-terminal carboxylic acid [5,16]

In catalog and search usage the same molecule is written as MT2 peptide, MT-2 peptide, MT 2 peptide, MT-II peptide, melanotan 2 peptide or simply melanotan peptide. Plural forms — MT2 peptides, melanotan peptides, peptides melanotan 2, peptides MT2 — usually denote the melanotan family as a whole (Melanotan-1 and Melanotan-2) rather than one compound, and inverted index forms such as “peptide MT2,” “peptide melanotan,” “peptide melanotan II” and “peptide melanotan 2” are simply alphabetical catalog conventions. Whatever the spelling, the identity check is the same: a 1,024.2 Da cyclic species with the Asp5–Lys10 lactam, distinguishable by mass spectrometry from the 1,646.9 Da linear Melanotan I [2,13].

Introduction

The melanotan program began as a photoprotection idea. In the early 1980s Mac Hadley and Victor Hruby at the University of Arizona reasoned that a stable analog of α-MSH could induce eumelanin pigmentation without ultraviolet exposure, and set out to engineer one from the natural tridecapeptide [1]. Their first success, [Nle⁴,D-Phe⁷]-α-MSH (NDP-MSH, later Melanotan I), replaced the oxidation-prone methionine with norleucine and inverted the chirality of phenylalanine-7, yielding a molecule roughly 10- to 100-fold more potent than α-MSH with ultra-long activity in frog- and lizard-skin bioassays [13].

Melanotan II came next, and it was a more radical design. Instead of stabilizing the full-length sequence, Al-Obeidi, Castrucci, Hadley and Hruby truncated α-MSH to its 4–10 message core and locked that core into a bioactive shape with a lactam bridge between the side chains of aspartate-5 and lysine-10 [2]. The resulting compound was more potent than NDP-MSH and became the standard agonist for a receptor family that had not yet been cloned. When Mountjoy and Cone identified the melanocortin receptor genes in 1992 [3], MT-II was already on the shelf, ready to define what those receptors did. Much of what is known about MC4R in feeding and sexual function was learned with this molecule [6,10,11].

Biological background: the melanocortin system

Melanocortins are peptides cleaved from the pro-opiomelanocortin (POMC) precursor: α-, β- and γ-MSH and adrenocorticotropic hormone (ACTH). They act on five G protein-coupled receptors, MC1R through MC5R, all of which signal predominantly through G_s and adenylyl cyclase to raise intracellular cAMP [3,18]. Each receptor has a characteristic tissue distribution and function. MC1R on melanocytes drives the switch from pheomelanin to eumelanin synthesis; MC2R in the adrenal cortex responds only to ACTH; MC3R and MC4R in the hypothalamus and brainstem regulate energy homeostasis and autonomic outputs; MC5R is expressed in exocrine glands [18].

The system is unusual in having endogenous antagonists. Agouti protein antagonizes MC1R in skin, and agouti-related protein (AgRP) antagonizes MC3R and MC4R in the brain. The 1997 discovery that targeted disruption of MC4R produces hyperphagia and obesity in mice [11], together with the demonstration that the MT-II agonist suppresses feeding and the SHU9119 antagonist increases it [10], established MC4R as a central node in energy balance. MC4R signaling in spinal and hypothalamic circuits was later shown to modulate erectile and copulatory behavior in rodents [6]. Because α-MSH itself is degraded within minutes in plasma, stabilized analogs such as MT-II were essential for every one of these experiments.

Compound structure and mechanism of action

Structure. Melanotan II retains the His⁶-D-Phe⁷-Arg⁸-Trp⁹ pharmacophore that every melanocortin agonist shares, flanked by norleucine-4 at the N-terminus and the Asp⁵/Lys¹⁰ pair whose side chains are joined in a 23-membered lactam ring [2]. The N-terminus is acetylated and the C-terminus is a primary amide. Molecular-dynamics modeling predicted that this bridge would hold the message sequence in a β-turn resembling the receptor-bound conformation of α-MSH, and bioassays confirmed that the cyclized heptapeptide was both more potent and longer acting than its linear counterpart [2]. The D-configuration at position 7 contributes resistance to proteolysis and, as the antagonist series later showed, is the single most pharmacologically sensitive position in the scaffold [4].

Receptor pharmacology. Radioligand binding at cloned human receptors shows MT-II to be a high-affinity agonist at MC1R, MC3R, MC4R and MC5R with little discrimination between them; it does not activate MC2R [12,18]. This lack of subtype selectivity is the defining property of the molecule. It explains why MT-II produces pigmentary (MC1R), metabolic (MC3R/MC4R) and sexual-function (MC4R) effects simultaneously in animal models, and why medicinal chemists subsequently pursued selective ligands. Substituting D-Phe⁷ with the bulkier D-2′-naphthylalanine converts MT-II into SHU9119, a potent MC3R/MC4R antagonist that retains MC1R and MC5R agonism [4] — the agonist/antagonist pair that underpins the feeding literature [10].

Signaling and metabolism. At each receptor MT-II stimulates cAMP accumulation through G_s, with downstream PKA and CREB activation; MC4R additionally couples to MAPK pathways in some cell systems [18]. In vivo, the C-terminal amide of MT-II can be hydrolyzed to the free carboxylic acid. That metabolite, originally designated PT-141 and now known as bremelanotide, retains MC4R agonism with modestly reduced MC1R activity and was carried forward by Palatin Technologies into clinical development [5,16].

Evidence by research domain

Research domain	Typical models	Reported findings	Evidence maturity
Melanocortin receptor pharmacology	Cloned human MC1R–MC5R in HEK293/COS cells; frog and lizard skin bioassays	Nanomolar, non-selective agonism at MC1/3/4/5R; prolonged activity vs. α-MSH; basis for SHU9119 antagonist series [2,4,12]	Well replicated; foundational
Pigmentation	Amphibian/reptile skin; pilot human Phase I (n=3)	Increased eumelanin pigmentation; visible tanning in 2 of 3 subjects after repeated exposures [7]	Preliminary human; small n
Energy balance and feeding	Fasted, ob/ob, Ay and NPY-stimulated mice; MC4R knockout mice	ICV MT-II suppressed feeding in four hyperphagia models; effect blocked by SHU9119; MC4R KO mice obese [10,11]	Robust rodent mechanistic
Sexual function	Rats and mice (cavernous-nerve stimulation, copulatory behavior); two small double-blind human crossover studies	MC4R-dependent pro-erectile responses in rodents; erections vs. placebo in men with psychogenic and organic ED [6,8,9]	Rodent mechanistic; small human trials
Safety and toxicology	Case reports; national poison-center and regulatory data; dermatology reviews	Eruptive nevi, nevus darkening, melanoma in pre-existing lesions, sympathomimetic toxicity with rhabdomyolysis after high-dose self-injection [14,15,17]	Case-level; consistent signals

Receptor pharmacology and tool-compound use

MT-II’s first and most durable contribution is as a reference agonist. Schiöth and colleagues, comparing cyclic D-Phe⁷ and D-Nal⁷ analogs across the cloned receptor subtypes, found MT-II bound MC1R, MC3R, MC4R and MC5R with affinities in the low-nanomolar range and without meaningful selectivity [12]. Hruby’s group used the same scaffold to demonstrate that a single bulky aromatic substitution at position 7 flips MC3R/MC4R activity from agonism to antagonism [4]. The MT-II/SHU9119 pair remains the most cited pharmacological toolkit in melanocortin physiology [18].

Pigmentation

The only published human pigmentation study of MT-II is the 1996 Arizona pilot, a single-blind, placebo-controlled trial in three healthy men [7]. Two subjects showed measurable increases in facial and upper-body pigmentation by quantitative reflectance one week after a two-week exposure protocol. The same study recorded dose-limiting somnolence and fatigue, nausea, a stretching-and-yawning complex and spontaneous erections — observations that redirected the program toward sexual-function research [7,1].

Energy balance and feeding

Fan and colleagues’ 1997 Nature study is the classic demonstration. Intracerebroventricular MT-II inhibited feeding in fasted C57BL/6J mice, leptin-deficient ob/ob mice, agouti (A^y) mice and NPY-stimulated mice; co-administration of SHU9119 abolished the effect, and SHU9119 alone increased nocturnal feeding [10]. Together with the MC4R-knockout phenotype reported the same year [11], these data established melanocortin tone as a tonic inhibitory signal on food intake. In this literature MT-II is the probe, not the candidate: its non-selectivity and central side-effect profile made it unsuitable as a lead, and drug discovery moved to selective MC4R ligands.

Sexual function

Following the 1996 observations, Wessells and colleagues ran two double-blind, placebo-controlled crossover studies. In ten men with psychogenic erectile dysfunction, MT-II produced clinically apparent erections in eight, with mean duration of >80% tip rigidity of 38 minutes versus 3 minutes for placebo [8]; a second study extended the finding to men with organic erectile dysfunction [9]. Van der Ploeg and colleagues subsequently showed in PNAS that pro-erectile melanocortin effects are absent in Mc4r-null mice and localized MC4R expression to spinal, hypothalamic and penile sensory-nerve sites [6]. Development did not proceed with MT-II itself; the free-acid metabolite PT-141 was selected instead [5].

Safety and toxicology signals

Because MT-II was never approved, most human safety data come from case reports involving unregulated internet products. Cardones and Grichnik described eruptive melanocytic nevi after MT-II exposure [15]; Habbema and colleagues reviewed reports of nevus darkening, dysplastic nevi and melanoma arising in pre-existing lesions during or shortly after melanotan use, while noting causality remains unproven [17]. Nelson, Bryant and Aks reported sympathomimetic toxicity — tachycardia, diaphoresis, mydriasis — with rhabdomyolysis and acute kidney injury after a high self-injected dose of a product later confirmed as MT-II by mass spectrometry [14]. A 2009 BMJ analysis documented the spread of unlicensed melanotan I and II in the general population and the ensuing warnings from the UK MHRA and other regulators [16].

Melanotan II vs. Melanotan I, PT-141 and α-MSH

Feature	α-MSH (endogenous)	Melanotan I (afamelanotide)	Melanotan II (MT-2)	PT-141 (bremelanotide)
Structure	Linear 13-mer, Met4, L-Phe7	Linear 13-mer, Nle4, D-Phe7	Cyclic 7-mer (4–10), Asp5–Lys10 lactam, C-terminal amide	Same cyclic 7-mer, C-terminal carboxylic acid
Plasma stability	Minutes	Hours; prolonged bioassay activity	Prolonged; resistant to proteolysis	Prolonged
Receptor emphasis	MC1R, MC3R, MC4R, MC5R (physiological)	MC1R-biased in practice; peripheral	Non-selective MC1/3/4/5R agonist; central effects	MC4R (with MC1R); central effects
Development status	Endogenous hormone	Approved (Scenesse, 2014 EU / 2019 US) for a rare photodermatosis	Never approved; research reagent	Approved (Vyleesi, 2019 US) for a specific indication
Key references	[3,18]	[1,13]	[2,7,8,12]	[5,16]

Melanotan 2 vs. Melanotan 1

The two melanotans are frequently conflated, but they are structurally and pharmacologically distinct. MT-1 is a full-length linear analog whose activity in humans is dominated by MC1R-mediated pigmentation; it progressed through formal development as afamelanotide [1,13]. MT-2 is a truncated cyclic analog with strong MC4R agonism, which is why its human studies recorded central effects — nausea, yawning, appetite change, erections — that MT-1 studies did not [7,8]. For a detailed treatment of the linear analog see the Melanotan I research review.

Melanotan 2 vs. PT-141

PT-141 is MT-II minus one amide: hydrolysis of the C-terminal carboxamide produces bremelanotide, which was identified as an active metabolite during MT-II studies and then developed independently [5]. The change modestly reduces MC1R activity relative to MC4R and alters pharmacokinetics; clinically, bremelanotide completed Phase III trials and gained FDA approval in 2019 [16]. MT-II never entered pivotal trials. The PT-141 research review covers the successor molecule in depth.

Limitations and research considerations

• Tiny human evidence base. All published human data on MT-II come from three studies enrolling a combined total of fewer than 40 men, all conducted at a single institution in the 1990s [7,8,9]. No dose-ranging, long-term, or female-cohort data exist for MT-II itself.
• Non-selectivity confounds interpretation. Because MT-II activates four receptor subtypes, any in-vivo effect must be attributed by pairing with subtype-selective antagonists or knockout models [10,11]. Results with MT-II should not be extrapolated to selective MC1R or MC4R ligands.
• Product identity in case reports. Most safety reports involve unregulated internet products whose composition was rarely verified analytically; the Nelson case is a notable exception in confirming MT-II by mass spectrometry [14]. Contaminants and mislabeling cannot be excluded in the remainder [16,17].
• Melanocytic risk remains unresolved. Reports of nevus changes and melanoma are temporally associated with melanotan exposure but lack controlled denominators [15,17]. The mechanistic plausibility (MC1R-driven melanocyte proliferation) is clear; causality is not established.
• Species differences in MC receptor pharmacology. Frog- and lizard-skin bioassays, on which early potency claims rest, do not fully predict affinities at human receptors; comparisons should rely on cloned-receptor data [12,18].
• Regulatory context. MT-II is not approved for any use in any jurisdiction and has been the subject of import alerts and consumer warnings [16,17]. Laboratory work should be conducted under research-use-only conditions.

Where to source for research

Melanotan II is offered as a lyophilized research-grade peptide by several suppliers serving the laboratory market. For in-vitro receptor-binding, cAMP or analytical work the relevant criteria are batch-specific HPLC purity, mass-spectrometry confirmation of the 1,024.2 Da cyclic species, documented peptide content and salt form, and unambiguous research-use-only labeling. Short Chain Aminos lists melanocortin analogs including MT-2 with lot-level certificates of analysis; BioPep supplies research peptides with third-party testing documentation; Catalyst Research carries cyclic and linear α-MSH analogs for comparative assay work; and Apex Research Services provides research compounds with published analytical data. Given the documented prevalence of mislabeled melanotan products in unregulated channels [16,17], independent identity verification is especially important for this compound. See the supplier evaluation guide and the suppliers directory for methodology.

Frequently asked research questions

What is MT-2 peptide (Melanotan II)?

Melanotan II (MT-2, MT-II, MT2) is a synthetic cyclic heptapeptide analog of α-melanocyte-stimulating hormone, Ac-Nle4-cyclo[Asp5,D-Phe7,Lys10]-α-MSH(4–10)-NH2. Designed at the University of Arizona in 1989 by lactam cyclization of the NDP-MSH core, it is a potent, non-selective agonist at MC1, MC3, MC4 and MC5 receptors and is studied strictly as a research compound.

Is MT2 the same as Melanotan 2 and Melanotan II?

Yes. “MT2,” “MT-2,” “MT-II,” “melanotan 2,” “melanotan-2” and “melanotan II” all denote the same cyclic lactam heptapeptide (CAS 121062-08-6). Supplier catalogs vary only in formatting. The one alias that is a different molecule is “Melanotan I” (MT-1, afamelanotide), a linear 13-residue analog with a distinct receptor profile.

What is the difference between Melanotan 2 and Melanotan 1?

Melanotan I is the linear [Nle4,D-Phe7]-α-MSH tridecapeptide with MC1R-biased pharmacology; Melanotan II is a truncated, side-chain-cyclized heptapeptide with roughly equal high affinity at MC1, MC3, MC4 and MC5 receptors. The MC4R activity explains why MT-II, but not MT-I, produced central effects such as altered feeding and erectile responses in published studies.

How is PT-141 (bremelanotide) related to Melanotan II?

PT-141 (bremelanotide) is the C-terminal free-acid form of Melanotan II — the same cyclic sequence with a carboxylic acid instead of the amide. It was identified as an active metabolite during MT-II development and later became an FDA-approved medicine (Vyleesi, 2019) for a specific indication. MT-II itself was never approved and remains a research reagent.

Which melanocortin receptors does Melanotan II activate?

Radioligand studies report MT-II binding to human MC1, MC3, MC4 and MC5 receptors with nanomolar affinity and little selectivity among them; it does not act at MC2R, the ACTH receptor. This broad agonism made MT-II a standard pharmacological tool, paired with the antagonist SHU9119, for mapping melanocortin functions in feeding, pigmentation and sexual-function research.

What did the early clinical studies of MT-II report?

A 1996 University of Arizona pilot Phase I study in three volunteers reported increased skin pigmentation, along with nausea, somnolence, stretching-yawning and spontaneous erections. Two later double-blind crossover studies (1998, 2000) in men with erectile dysfunction reported erectile responses versus placebo. These small trials were not followed by pivotal development of MT-II itself.

What safety signals have been documented for Melanotan II?

Published case reports and reviews describe eruptive melanocytic nevi, darkening of existing nevi, melanoma arising in pre-existing lesions, and one case of sympathomimetic toxicity with rhabdomyolysis after a high self-injected dose of an internet-sourced product. Regulators in the UK, EU, US and Australia have issued warnings about unregulated melanotan products.

How should lyophilized MT-2 be handled in a laboratory setting?

Research suppliers ship Melanotan II as a lyophilized acetate or TFA salt. Standard peptide practice applies: store sealed vials cold and protected from light and moisture, confirm identity and purity by HPLC and mass spectrometry, and reconstitute only in solvents appropriate to the planned in-vitro assay. This is handling guidance for laboratory material, not use guidance.

Works Cited

1. Hadley ME, Dorr RT. “Melanocortin peptide therapeutics: historical milestones, clinical studies and commercialization.” Peptides. 2006;27(4):921–930. PMID: 16412534. DOI: 10.1016/j.peptides.2005.01.029.
2. Al-Obeidi F, Castrucci AM, Hadley ME, Hruby VJ. “Potent and prolonged acting cyclic lactam analogues of alpha-melanotropin: design based on molecular dynamics.” Journal of Medicinal Chemistry. 1989;32(12):2555–2561. PMID: 2555512. DOI: 10.1021/jm00132a010.
3. Mountjoy KG, Robbins LS, Mortrud MT, Cone RD. “The cloning of a family of genes that encode the melanocortin receptors.” Science. 1992;257(5074):1248–1251. PMID: 1325670. DOI: 10.1126/science.1325670.
4. Hruby VJ, Lu D, Sharma SD, et al. “Cyclic lactam alpha-melanotropin analogues of Ac-Nle4-cyclo[Asp5,D-Phe7,Lys10]alpha-MSH(4-10)-NH2 with bulky aromatic amino acids at position 7 show high antagonist potency and selectivity at specific melanocortin receptors.” Journal of Medicinal Chemistry. 1995;38(18):3454–3461. PMID: 7658432. DOI: 10.1021/jm00018a005.
5. Molinoff PB, Shadiack AM, Earle D, Diamond LE, Quon CY. “PT-141: a melanocortin agonist for the treatment of sexual dysfunction.” Annals of the New York Academy of Sciences. 2003;994:96–102. PMID: 12851303. DOI: 10.1111/j.1749-6632.2003.tb03167.x.
6. Van der Ploeg LH, Martin WJ, Howard AD, et al. “A role for the melanocortin 4 receptor in sexual function.” Proceedings of the National Academy of Sciences USA. 2002;99(17):11381–11386. PMID: 12172010. DOI: 10.1073/pnas.172378699.
7. Dorr RT, Lines R, Levine N, et al. “Evaluation of melanotan-II, a superpotent cyclic melanotropic peptide in a pilot phase-I clinical study.” Life Sciences. 1996;58(20):1777–1784. PMID: 8637402. DOI: 10.1016/0024-3205(96)00160-9.
8. Wessells H, Fuciarelli K, Hansen J, et al. “Synthetic melanotropic peptide initiates erections in men with psychogenic erectile dysfunction: double-blind, placebo controlled crossover study.” Journal of Urology. 1998;160(2):389–393. PMID: 9679884. DOI: 10.1016/S0022-5347(01)62903-3.
9. 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. DOI: 10.1016/S0090-4295(00)00680-4.
10. Fan W, Boston BA, Kesterson RA, Hruby VJ, Cone RD. “Role of melanocortinergic neurons in feeding and the agouti obesity syndrome.” Nature. 1997;385(6612):165–168. PMID: 8990120. DOI: 10.1038/385165a0.
11. Huszar D, Lynch CA, Fairchild-Huntress V, et al. “Targeted disruption of the melanocortin-4 receptor results in obesity in mice.” Cell. 1997;88(1):131–141. PMID: 9019399. DOI: 10.1016/S0092-8674(00)81865-6.
12. Schiöth HB, Muceniece R, Mutulis F, et al. “Selectivity of cyclic [D-Nal7] and [D-Phe7] substituted MSH analogues for the melanocortin receptor subtypes.” Peptides. 1997;18(7):1009–1013. PMID: 9357059. DOI: 10.1016/S0196-9781(97)00079-X.
13. Sawyer TK, Sanfilippo PJ, Hruby VJ, et al. “4-Norleucine, 7-D-phenylalanine-alpha-melanocyte-stimulating hormone: a highly potent alpha-melanotropin with ultralong biological activity.” Proceedings of the National Academy of Sciences USA. 1980;77(10):5754–5758. PMID: 6777774. DOI: 10.1073/pnas.77.10.5754.
14. Nelson ME, Bryant SM, Aks SE. “Melanotan II injection resulting in systemic toxicity and rhabdomyolysis.” Clinical Toxicology. 2012;50(10):1169–1173. PMID: 23121206. DOI: 10.3109/15563650.2012.740637.
15. Cardones AR, Grichnik JM. “alpha-Melanocyte-stimulating hormone-induced eruptive nevi.” Archives of Dermatology. 2009;145(4):441–444. PMID: 19380666. DOI: 10.1001/archdermatol.2008.623.
16. Evans-Brown M, Dawson RT, Chandler M, McVeigh J. “Use of melanotan I and II in the general population.” BMJ. 2009;338:b566. PMID: 19211584. DOI: 10.1136/bmj.b566. See also: Kingsberg SA, Clayton AH, Portman D, et al. “Bremelanotide for the treatment of hypoactive sexual desire disorder: two randomized phase 3 trials.” Obstetrics & Gynecology. 2019;134(5):899–908. PMID: 31599840.
17. Habbema L, Halk AB, Neumann M, Bergman W. “Risks of unregulated use of alpha-melanocyte-stimulating hormone analogues: a review.” International Journal of Dermatology. 2017;56(10):975–980. PMID: 28266027. DOI: 10.1111/ijd.13585.
18. Ericson MD, Lensing CJ, Fleming KA, Schlasner KN, Doering SR, Haskell-Luevano C. “Bench-top to clinical therapies: A review of melanocortin ligands from 1954 to 2016.” Biochimica et Biophysica Acta – Molecular Basis of Disease. 2017;1863(10 Pt A):2414–2435. PMCID: PMC5600687. DOI: 10.1016/j.bbadis.2017.03.020.

Research Use Only. The information above summarizes published preclinical literature, small early-phase studies and case reports for laboratory reference. It is not medical advice and does not describe or endorse any human or veterinary use, dosing, or administration. Melanotan II is not an approved medicine and is intended solely for in-vitro and research applications. All content strictly for research reference; not for human or veterinary use.

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