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Cyclic heptapeptide · melanocortin agonist
A cyclic lactam heptapeptide analogue of alpha-MSH, engineered to resist the proteases that clear the linear hormone. Supplied as a lyophilized powder for research purposes only.
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Tested lot by lot at ≥99% purity. The Janoshik certificate for your lot is emailed with the order.
Everything Valtrax Research ships is bench material for in-vitro work. None of it is a drug, a supplement, a cosmetic, or a medical device, and none of it is intended for human or animal use, ingestion, or administration. Placing an order is your confirmation that you are a qualified researcher buying for lawful research, under every Canadian law and regulation that applies to you.
Take the active core of α-MSH, shorten it, and close it into a lactam ring. The ring is the engineering: it defeats the proteases that take the linear hormone apart in minutes, and in doing so leaves a compact, durable agonist. Melanotan II does not pick a melanocortin subtype — it activates the receptor family broadly.
That lack of selectivity is, on the bench, the feature. MC1R governs pigmentation, MC4R sits in feeding and central circuits, MC3R falls between them — and a single stable agonist lets one preparation reach across several of those arms at once instead of needing a separate ligand for each.
Two distinct lines run side by side. One is pharmacological: the broad agonism itself, split between MC1R pigmentation and MC4R central effects on feeding and behaviour, the latter often probed by direct CNS microinjection. The other is synthetic: the cyclic scaffold treated as a model substrate to validate new macrocyclization and stapling chemistry.
Broad receptor activity is what makes MT-II useful as a multi-target probe: it engages MC1R, MC3R, MC4R, and MC5R rather than one. Pigmentation work routes through MC1R; the central studies — feeding behaviour, the accumbens microinjection experiments — route through MC4R.
Recent papers fall into two camps. On the chemistry side, Todorovic and Yue use MT-II as a substrate for new macrocyclization and stapling routes. On the pharmacology side, Eliason and Wekwejt track its central effects — appetite, memory — in rodent preparations.
The compound originated in Hadley and Hruby’s α-MSH analogue program at Arizona, where cyclizing the active core was the decisive step — it converted a fragile hormone into something stable and potent. From that lead two branches diverged: a selective, MC1R-leaning analogue (afamelanotide) and the broad agonist here.
What MT-II became is a reference point. It serves both as a fixture in melanocortin pharmacology and, increasingly, as a model substrate that synthetic-chemistry groups reach for when they need to test a new peptide-cyclization method.
In vitro and animal studies
Melanotan II is a cyclic lactam analogue of alpha-melanocyte-stimulating hormone, developed at the University of Arizona in a programme whose original goal was photoprotection. The reasoning was sound: if pigmentation could be induced without ultraviolet exposure, the DNA damage that drives skin cancer might be reduced while still producing the protective melanin.
It is a non-selective agonist, and that is the defining feature of its pharmacology. It binds MC1R, MC3R, MC4R and MC5R. MC1R activation on melanocytes stimulates eumelanin synthesis, which is the effect the compound was designed around and which preclinical work confirmed across species. MC3R and MC4R activation in the central nervous system produces the appetite suppression and sexual-function effects that were observed as side findings — and that side finding is what led directly to the development of PT-141 as a selective metabolite.
Animal work also documented effects on insulin sensitivity and energy homeostasis through central melanocortin signalling, consistent with the known role of MC4R in body weight regulation.
Human data, where it exists
Melanotan II has never been approved by any regulatory authority anywhere, and it did not complete clinical development. Early human work established that it produces tanning, and that effect is real and reproducible.
What exists instead of a trial record is a substantial case-report literature, which is unusual and worth taking seriously. Because the compound circulated widely outside medical supervision, dermatologists and emergency physicians have published documented case reports of adverse events in people using it. That literature is not a controlled dataset and cannot establish incidence rates, but it does establish that specific serious harms have actually occurred rather than being hypothetical.
Regulatory agencies in several countries, including the UK, Australia and elsewhere, have issued public warnings against its use. Health Canada has not approved it for any purpose.
A structurally related but distinct compound, afamelanotide, did complete development and holds approvals for erythropoietic protoporphyria. It is not the same molecule.
Common assertions, and what the record supports
The claim that Melanotan II produces tanning is true and well established. Almost every other claim attached to it requires qualification.
The photoprotection rationale is the most interesting case. Inducing melanin plausibly reduces UV damage, and that was the design premise. But the compound also stimulates melanocytes — the cell type that gives rise to melanoma — and it has never been demonstrated in humans that net skin cancer risk falls. The published case reports of changing and new melanocytic lesions point in the opposite direction. The claim is not merely unproven; the mechanism cuts both ways.
The framing of Melanotan II as a cosmetic convenience underplays that it is a non-selective agonist at a receptor family regulating pigmentation, appetite, sexual function, inflammation and cardiovascular tone simultaneously. Non-selectivity is not a minor caveat here; it is the compound's central pharmacological property.
Against the compounds it is most often confused with
Against PT-141, this is the parent-metabolite relationship and the clearest illustration of what selectivity buys. PT-141 was developed precisely to retain Melanotan II's central sexual-function activity while shedding the pigmentary and broader melanocortin effects, and it went on to complete trials and gain approval. Melanotan II did neither.
Against KPV, the contrast is the mirror image. KPV is an alpha-MSH fragment that keeps the anti-inflammatory activity and drops the pigmentary action. Melanotan II keeps the pigmentary action and adds everything else. Between them they show how differently fragments and analogues of one hormone can behave.
Against GHK-Cu on the skin shelf, both are studied in dermatological contexts but through unrelated mechanisms: GHK-Cu drives collagen synthesis and matrix remodelling in the dermis, while Melanotan II acts on melanocyte pigment production.
Adverse findings, toxicology gaps, material hazards
Melanotan II has the most concrete documented harm profile of anything in this catalogue, and the published case reports should be read directly rather than summarised away.
Dermatological: new and changing melanocytic naevi, darkening and enlargement of existing moles, and case reports of melanoma diagnosed in users. Because the compound stimulates the exact cell lineage from which melanoma arises, and because it can darken lesions and thereby obscure the visual changes used for early detection, this is the most serious concern attached to it.
Systemic: case reports of rhabdomyolysis, some severe. Priapism, a urological emergency, is documented and follows directly from melanocortin sexual-function activity. Nausea, flushing, and spontaneous erections are commonly reported.
Cardiovascular effects follow from melanocortin receptor distribution, including blood pressure changes.
Additional risk arises from the supply route: material of unverified identity, non-sterile preparation, and shared injection practice have all featured in published case reports of harm.
Bench practice for this compound
Melanotan II ships lyophilized as a cyclic peptide and dissolves readily. Introduce bacteriostatic water against the vial wall and swirl gently; avoid shaking.
Protect from light with particular care — this compound's chromophore chemistry makes light exposure a real degradation route. Store reconstituted material at 2–8 °C in the dark, observe the stated working window, and keep unopened lyophilized powder frozen for long-term storage.
This summary describes published research. It is not a protocol, not a recommendation, and not a statement that this compound is safe or effective for any use. Not for human or animal use.
Liu, H. et al. (2024). Therapeutic Strategies Against Metabolic Imbalance in a Male Mouse Model With 5-HT2CR Loss-of-Function.
PubMedTodorovic, M. et al. (2024). 5-Hydroxypyrroloindoline Affords Tryptathionine and 2,2′-bis-Indole Peptide Staples: Application to Melanotan-II.
PubMedWekwejt, P. et al. (2023). Melanotan-II reverses memory impairment induced by a short-term HF diet.
PubMedEliason, N.L. et al. (2022). Melanocortin receptor agonist melanotan-II microinjected in the nucleus accumbens decreases appetitive and consumptive responding for food.
PubMedYue, W.K. et al. (2023). Targeting Melanocortin Receptors Using SNAr-Type Macrocyclization: A Doubly Orthogonal Route to Cyclic Peptide Conjugates.
PubMedIndependent testing lot by lot: identity, purity, net content.
Janoshik Analytical, a laboratory Valtrax does not own, runs the testing — identity by mass spectrometry, purity by RP-HPLC at ≥99%, on the lot you receive.
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