A practical reference on MC1R: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
Reviewed 2026-05-12. Anything still debated is marked as such rather than presented as settled.
The peptide was developed during the 1980s by researchers investigating melanocortin signalling and skin pigmentation pathways. Early work focused on analogues of alpha-melanocyte-stimulating hormone that would resist enzymatic breakdown more effectively than the parent molecule. Melanotan-2 emerged from that programme as a shortened, cyclised variant. Reports describing its synthesis and receptor activity later appeared in the scientific literature. Commercial availability grew through unregulated channels rather than through pharmaceutical approval.
Structurally, Melanotan-2 retains the core recognition motif of alpha-melanocyte-stimulating hormone while adding a lactam bridge that links two side chains and constrains the molecule into a ring. This modification lowers susceptibility to enzymatic degradation. The compound acts as an agonist at melanocortin receptors, particularly subtypes associated with melanin production. Because the same receptor family influences several physiological processes, researchers note that its activity is not confined to pigmentation alone. Receptor selectivity continues to be examined in published studies.
Melanotan-2 is a synthetic cyclic heptapeptide designed as an analogue of alpha-melanocyte-stimulating hormone, a naturally occurring peptide involved in pigmentation signalling. Its sequence incorporates modified residues that increase potency and extend biological activity relative to the native hormone. The compound binds receptors of the melanocortin family and is examined mainly in laboratory research. It does not occur naturally and exists only as a manufactured chemical entity produced by solid-phase synthesis.
Melanocortin receptors comprise five subtypes with distinct tissue distributions and functions. Melanotan-2 is described in the literature as a non-selective agonist that engages several of these subtypes, including MC1R, MC3R, MC4R, and MC5R. MC1R is the subtype most directly linked to melanin production in skin cells. Because the compound is not subtype-selective, its observed effects in experimental settings are generally attributed to activity across multiple receptor pathways rather than to a single target.
Melanotan-2 is a synthetic linear peptide built from seven amino acids arranged in a short chain. Its sequence is commonly written as Ac-Nle-Asp-His-D-Phe-Arg-Trp-Lys-NH2, which includes a modified N-terminus and an amidated C-terminus. The molecule belongs to the melanocortin family and acts as a receptor agonist. Structural features such as the D-phenylalanine residue and the Nle substitution are associated with increased stability against enzymatic degradation relative to the natural parent peptide.
The compound emerged from research programs in the 1980s that examined analogues of alpha-melanocyte-stimulating hormone for pigmentation and photoprotection. Investigators modified the native sequence to extend activity duration and potency. A related analogue, afamelanotide, was developed within the same broad line of inquiry and eventually gained approval in certain jurisdictions for a rare light-sensitivity condition. Melanotan-2 itself did not progress through the same regulatory route and has no approved therapeutic indication.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C50H69N15O9 | Synthetic cyclic heptapeptide |
| Molecular mass | Approximately 1024 g/mol | Depends on counter-ion content |
| Appearance | White to off-white powder | Commonly supplied as a lyophilised solid |
| Solubility | Freely soluble in water | Also dissolves in common aqueous buffers |
| Typical storage | -20 degrees Celsius, desiccated | Protect from light and repeated freeze-thaw |
Activity is attributed to agonism at melanocortin receptors, particularly MC1R and MC4R. Activation of MC1R on melanocytes increases melanin synthesis, which underlies the reported tanning effect. MC4R engagement in the central nervous system is linked to appetite suppression and to effects on sexual arousal reported in early clinical studies. Those studies were small and were not designed to establish efficacy or long-term safety. Receptor selectivity among the melanocortin subtypes is not absolute, which complicates attribution of any effect to a single pathway.
Regulatory treatment varies between countries. Several national medicines agencies have classified the peptide as unapproved, and customs authorities in some jurisdictions seize shipments on that basis. A few jurisdictions channel supply through prescription-only frameworks that do not list the substance by name. Because the material circulates mainly through online vendors, composition and purity are rarely verified before sale. Surveys of unapproved peptide products have reported labels that did not match measured content in a substantial fraction of samples.
Melanotan II is a synthetic cyclic heptapeptide with the sequence Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-NH2, corresponding to a molecular formula of C50H69N15O9 and a monoisotopic mass near 1024 daltons. It was designed as a structural analogue of alpha-melanocyte-stimulating hormone, a peptide hormone produced by cleavage of proopiomelanocortin. A lactam bridge between the aspartate and lysine side chains closes the ring, and the C-terminal amide removes a free carboxyl group. Both modifications increase resistance to enzymatic degradation compared with the linear parent hormone. Four substitutions distinguish it from afamelanotide, the linear analogue studied under the name melanotan I.
Receptor-binding studies classify melanotan II as a non-selective melanocortin agonist. It interacts with MC1R, MC3R, MC4R and MC5R, with reported affinities in the low nanomolar range and no strong subtype preference. Activation of MC1R on dermal melanocytes shifts pigment synthesis toward eumelanin, the dark polymer deposited in melanosomes and transferred to keratinocytes. Because the same peptide engages MC4R in the hypothalamus, it also appears in animal work on food intake and erectile response, which is why it is discussed in both pigment and metabolic research. Which receptor populations dominate after systemic exposure in humans is not fully established.
Two structural changes distinguish the synthetic peptide from the natural hormone. A norleucine residue replaces methionine at one position, and a D-configured phenylalanine replaces the natural L-form at another. Both substitutions slow enzymatic breakdown, which extends the molecule's persistence relative to the parent hormone. The lactam bridge further constrains the backbone into a stable conformation. These features are standard design strategies in peptide chemistry and are not unique to this compound; they appear across many research peptides built for improved stability.
The compound was developed in the late 1980s and early 1990s by academic researchers investigating melanocortin signaling and pigmentation. Early work explored whether synthetic analogs could reproduce effects of the natural hormone under controlled conditions. The molecule never advanced through the full regulatory pathway required for approval as a medicine. From the mid-2000s onward it appeared in unregulated consumer markets, often distributed through informal channels. That gap between research origins and commercial availability shapes how the compound is discussed today.
Melanotan-2 is a synthetic peptide designed as an analog of alpha-melanocyte-stimulating hormone, a signaling molecule produced in the pituitary and skin. Its structure is a linear chain of seven amino acids that folds into a ring through an internal lactam bridge joining two side chains. The compound is sometimes written as MT-II or MEL-2 in informal and commercial contexts. It belongs to the melanocortin peptide family, a group of short signaling molecules that share a conserved core sequence recognized by melanocortin receptors.
By the mid-1980s, over 65 papers on the topic of coupling reactions involving tin had been published, continuing to explore the substrate scope of this reaction. While initial research in the field focused on the coupling of alkyl groups, most future work involved the much more synthetically useful coupling of vinyl, alkenyl, aryl, and allyl organostannanes to halides. Due to these organotin reagent's stability to air and their ease of synthesis, the Stille reaction became common in organic synthesis.
Portal is a 2007 puzzle-platform game developed and published by Valve. It was originally released in a bundle, The Orange Box, for Windows, Xbox 360 and PlayStation 3, and has been ported to other systems, including Mac OS X, Linux, Android (via Nvidia Shield), and Nintendo Switch. Portal is a first person game. It consists primarily of a series of puzzles that must be solved by teleporting the player's character and simple objects using the "Aperture Science Handheld Portal Device", also referred to as the "portal gun", a device that can create portals between locations in the puzzles. The player character, Chell, is challenged and taunted by an artificial intelligence construct named GLaDOS (Genetic Lifeform and Disk Operating System) to complete each puzzle in the Aperture Science Enrichment Center using the portal gun with the promise of receiving cake when all the puzzles are completed. The Source engine's physics system allows kinetic energy to be retained through portals, requiring creative use of portals to maneuver through the test chambers. This gameplay element is based on a similar concept from the game Narbacular Drop; many of the team members from the DigiPen Institute of Technology who worked on Narbacular Drop were hired by Valve for the creation of Portal. Portal was acclaimed as one of the most original games of 2007, despite some criticism for its short duration. It received praise for its originality, unique gameplay, dark story and sense of comedy.
Similarly, ethylene oxide is detected by the bright pink color of the indicator when passing air through aqueous solutions of some salts of sodium or potassium (chlorides, iodides, thiosulfates, etc.) with the addition of phenolphthalein:
Naftali Loewenthal, member of the Chabad Hasidic community; main area of study is Hasidism and Jewish Mysticism; professor in the Department of Hebrew and Jewish Studies at University College London; director of the Chabad Research Unit, a division of the Chabad-Lubavitch movement in United Kingdom; author of Communicating the Infinite: The Emergence of the Habad School (1990); also authored Hasidism Beyond Modernity: Essays in Habad Thought and History (2019) as well as many scholarly articles and publications on the Chabad mysticism; also extensively written on history of Chabad Hasidic women. Nick Lowles, founder of Hope Not Hate and former editor of the anti-fascist Searchlight (magazine), backed by various politicians and celebrities several trade unions. Knowles is the author of a number of books on football violence, right wing groups and antisemitism in Britain. He was a freelance investigative journalist, working in television, including on BBC Panorama, World in Action, Channel Four Dispatches and MacIntyre Undercover. Moshé Machover (Hebrew: משה מחובר; born 1936) is a mathematician, philosopher, pro Palestinian socialist anti-Zionist activist and author, noted for his writings critical of Israel and Zionism. David Magarshack (23 December 1899 – 26 October 1977); author, translator and biographer of Russian authors, best remembered for his translations of Dostoevsky, Chekhov and Nikolai Gogol; of Russian Jewish ancestry. Miriam Margolyes (born 18 May 1941) is a British and Australian actress.
== Types == Anisocytosis may be assessed using the red blood cell distribution width (RDW), while the average size of red blood cells is measured by the mean corpuscular volume (MCV). Based on the MCV, anisocytosis may be associated with microcytic, macrocytic, or normocytic red blood cells. Anisocytosis with microcytosis may occur in conditions such as iron-deficiency anemia and sickle cell disease. Anisocytosis with macrocytosis may occur in folate deficiency, vitamin B12 deficiency, autoimmune hemolytic anemia, following cytotoxic chemotherapy, and in chronic liver disease or myelodysplastic syndrome. Anisocytosis with a normal MCV may be seen in early iron, vitamin B12, or folate deficiency, as well as in dimorphic anemia, sickle cell disease, chronic liver disease, and myelodysplastic syndrome. The RDW is typically increased in iron-deficiency anemia, whereas it may be normal or only mildly increased in some forms of thalassemia, including thalassemia major (Cooley anemia) and thalassemia intermedia.
Sources: en.wikipedia.org
== Formation and structure == β-Endorphin is found in neurons of the hypothalamus, as well as the pituitary gland. It is derived from β-lipotropin, which is produced in the pituitary gland from a larger peptide precursor, proopiomelanocortin (POMC). POMC is cleaved into two neuropeptides, adrenocorticotropic hormone (ACTH) and β-lipotropin. The formation of β-endorphin is then the result of cleavage of the C-terminal region of β-lipotropin, producing a 31 amino acid-long neuropeptide with an alpha-helical secondary structure. However, POMC also gives rise to other peptide hormones, including α- and γ-melanocyte-stimulating hormone (MSH), resulting from intracellular processing by internal enzymes known as prohormone convertases. A significant factor that differentiates β-endorphin from other endogenous opioids is its high affinity for and lasting effect on μ-opioid receptors. The structure of β-endorphin in part accounts for this through its resistance to proteolytic enzymes, as its secondary structure makes it less vulnerable to degradation.
1,2-Diarylethylamines exert their primary effects as uncompetitive antagonists of the N-methyl-D-aspartate receptor (NMDAR), similar to phencyclidine (PCP) and ketamine. This mechanism is believed to underlie their characteristic dissociative, hallucinogenic, and anesthetic properties. Compounds such as diphenidine, methoxphenidine (MXP), and ephenidine display high to moderate affinity for the NMDAR PCP-binding site (e.g., diphenidine Ki ≈ 18–39 nM). Additionally, some members of this class exhibit secondary interactions with monoamine transporters, including the dopamine and norepinephrine transporters (DAT and NET), as well as modest binding to sigma-1 and sigma-2 receptors, serotonin 5-HT2A receptors, alpha-adrenergic receptors, and the kappa opioid receptor. Despite potent NMDAR binding, several compounds exhibit reduced in vivo potency, potentially due to pharmacokinetic factors.
=== Specific === Acetylcysteine Atropine Calcium gluconate Methylthioninium chloride (methylene blue) Naloxone Penicillamine Potassium ferric hexacyano-ferrate(II) -2H2O (prussian blue) Sodium nitrite Sodium thiosulfate Complementary:
Paper chromatography is a technique that involves placing a small dot or line of sample solution onto a strip of chromatography paper. The paper is placed in a container with a shallow layer of solvent and sealed. As the solvent rises through the paper, it meets the sample mixture, which starts to travel up the paper with the solvent. This paper is made of cellulose, a polar substance, and the compounds within the mixture travel further if they are less polar. More polar substances bond with the cellulose paper more quickly, and therefore do not travel as far.
Sources: en.wikipedia.org
== History == In 1986 a Research Resource Facility Satellite Meeting was held in conjunction with the Sixth International Conference on Methods in Protein Sequence Analysis. The next year protein sequencing and amino acid samples were sent to survey 103 core facilities. By 1989 the ABRF was formally organized and incorporated. Each year an annual meeting was held as a satellite meeting of the Protein Society until 1996 when separate meetings began.
=== Interactions === It should not be used concomitantly with medications known to prolong the QTc interval (e.g., 5-HT3 antagonists, tricyclic antidepressants, citalopram, etc.) as this may lead to an increased risk of QTc interval prolongation. Neither should it be given concurrently with lithium (medication) as it may increase the risk of lithium toxicity and neuroleptic malignant syndrome. It should not be given concurrently with other antipsychotics due to the potential for this to increase the risk of side effects, especially neurological side effects such as neuroleptic malignant syndrome. It should be avoided in patients on CNS depressants such as opioids, alcohol and barbiturates.
=== Presence in ecstasy === In his 1993 book E for Ecstasy examining the uses of the street drug ecstasy in the United Kingdom, the writer, activist, and ecstasy advocate Nicholas Saunders highlighted test results showing that certain consignments of the drug also contained selegiline. Consignments of ecstasy known as "Strawberry" contained what Saunders described as a "potentially dangerous combination of ketamine, ephedrine and selegiline," as did a consignment of "Sitting Duck" Ecstasy tablets.
Sources: en.wikipedia.org
It is a synthetic cyclic heptapeptide and an analogue of alpha-melanocyte-stimulating hormone. The molecule is produced by chemical synthesis rather than extracted from a biological source.
It is shorter than the native hormone and carries a cyclic constraint that improves stability. These changes raise receptor potency and slow breakdown relative to the naturally occurring peptide.
Published accounts date its development to the 1980s, when researchers were generating analogues of melanocyte-stimulating hormone. That work aimed to produce more stable compounds for studying pigmentation biology.
No. Melanotan-2 is manufactured synthetically. The naturally occurring peptide in the same family is alpha-melanocyte-stimulating hormone, which the body produces as part of normal endocrine and neural signalling.