MC1R comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Updated 2025-12-10. Numbers and descriptions here follow the published literature rather than marketing material.
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 analogue of alpha-melanocyte-stimulating hormone, a naturally occurring peptide involved in pigmentation signalling. Its structure substitutes a lactam bridge between side chains to increase stability relative to the native hormone. The compound is also known by the shorthand MT-II and by several non-proprietary synonyms used in research catalogues. It is not an approved therapeutic product in any major jurisdiction; material sold under this name is typically offered as a laboratory reagent rather than as a medicine.
Identity testing for a cyclic peptide of this size usually relies on reversed-phase high-performance liquid chromatography coupled to mass spectrometry. The mass spectrum confirms molecular weight, while the chromatographic trace indicates the proportion of related impurities. Tandem mass spectrometry can provide sequence-level information when fragmentation data are compared against a reference standard. Nuclear magnetic resonance is sometimes used to confirm the lactam bridge, although it requires more material and greater operator expertise than routine chromatographic methods.
Lyophilised peptide powder is comparatively stable when kept dry, cold and protected from light. Once dissolved, the molecule is exposed to hydrolysis, oxidation and microbial growth, and degradation accelerates at higher temperatures and in alkaline solution. Repeated freeze-thaw cycles concentrate solutes and promote aggregation. Handling guidance for research peptides commonly clusters around freezer temperatures for powder and short refrigerated use for reconstituted solutions, with pH control and sterile technique applied throughout.
Verification of a purchased sample requires documentation linking a batch to a certificate of analysis, and that document should be read for the methods used rather than the headline purity figure. A single chromatographic percentage does not establish identity. Independent laboratories can perform identity and content assays, but no such test establishes that a product is suitable for human use. Claims about efficacy rest largely on small, early studies rather than on replicated controlled trials, and that gap remains open.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic cyclic heptapeptide | Analogue of alpha-melanocyte-stimulating hormone |
| Common synonyms | MT-II; melanotan 2 | No internationally accepted non-proprietary name |
| Typical presentation | Lyophilised powder in a sealed vial | Often supplied alongside a separate diluent |
| Regulatory status | Unapproved therapeutic substance | Customs seizure reported in several jurisdictions |
| Reported route in use | Subcutaneous injection | Self-administered outside clinical settings |
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.
Published pharmacokinetic information is limited and comes mainly from small studies rather than registrational trials. Plasma half-life is usually described as short, on the order of tens of minutes, followed by rapid tissue distribution and clearance of the intact peptide. Metabolites and low concentrations of parent compound have been reported in urine, a detail relevant to anti-doping and forensic testing. Whether repeated exposure changes receptor sensitivity or clearance over time remains an open question. Values differ noticeably between analytical assays, so published numbers should be read as approximate rather than definitive.
The peer-reviewed record is dominated by small early-phase studies, case reports and pharmacovigilance summaries rather than large randomised trials. Papers typically examine tanning response, receptor selectivity or patterns of reported adverse events. Many note that participants obtained the peptide outside a clinical setting, which limits verification of composition and administered amount. Reported events vary widely, and causality is frequently unclear because the identity and purity of self-sourced material are unknown. Open questions include whether repeated melanocortin receptor stimulation produces cumulative effects, and how often label claims match actual content.
Identification in laboratories relies on reversed-phase liquid chromatography coupled with tandem mass spectrometry, with product-ion spectra compared against a certified reference standard. High-resolution mass spectrometry supplies accurate mass confirmation, and peptide mapping after enzymatic digestion separates melanotan II from closely related analogues. Quantitation of seized material is complicated by unknown counter-ions and residual trifluoroacetate left from purification. Immunoassays raised against alpha-melanocyte-stimulating hormone can cross-react, so chromatographic confirmation is normally required. Urinary detection windows are short, and reported limits of detection differ substantially between laboratories.
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.
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.
== See also == Breast-feeding Breastfeeding and fertility Epileptic seizure Hyperprolactinaemia Hypothalamic–pituitary–prolactin axis Male lactation Prolactin modulator Prolactin receptor Prolactin-releasing hormone Prolactinoma Weaning
== Human homologue == Agouti signaling protein (ASP) is the human homologue of murine agouti. It is encoded by the human agouti gene on chromosome 20 and is a protein consisting of 132 amino acids. It is expressed much more broadly than murine agouti and is found in adipose tissue, pancreas, testes, and ovaries, whereas murine agouti is solely expressed in melanocytes. ASP has 85% similarity to the murine form of agouti. As ectopic expression of murine agouti leads to the development of the yellow obese syndrome, this is expected to be consistent in humans. The yellow obese syndrome increases the development of many chronic diseases, including obesity, type II diabetes mellitus and tumorigenesis. ASP has similar pharmacological activation to murine agouti, as melanocortin receptors are inhibited through competitive antagonism. Inhibition of melanocortin by ASP can also be through non-competitive methods, broadening its range of effects. The function of ASP differs to murine agouti. ASP effects the quality of hair pigmentation whereas murine agouti controls the distribution of pigments that determine coat color. ASP has neuroendocrine functions consistent with murine agouti, as it agonizes via AgRP neurons in the hypothalamus and antagonizes MSH at MC4Rs which reduce satiety signals. AgRP acts as an appetite stimulator and increases appetite while decreasing metabolism. Because of these mechanisms, AgRP may be linked to increased body mass and obesity in both humans and mice.
== Ene-reductases: enzymatic promiscuity == In recent studies, flavin-dependent ERs have demonstrated a remarkable catalytic promiscuity, in particular in photo-ene-reductases catalysis. The non-natural reactions that can be performed can be divided in hydride-dependent and hydride-independent reactions:
Sources: en.wikipedia.org
AMP deaminase deficiency (formally known as myoadenylate deaminase deficiency or MADD) is a metabolic myopathy which results in excessive AMP buildup brought on by exercise. AMP deaminase is needed to convert AMP into IMP in the purine nucleotide cycle. Without this enzyme, the excessive AMP buildup is initially due to the adenylate kinase (myokinase) reaction which occurs after a muscle contraction. However, AMP is also used to allosterically regulate the enzyme myophosphorylase (see Glycogen phosphorylase § Regulation), so the initial buildup of AMP triggers the enzyme myophosphorylase to release muscle glycogen into glucose-1-P (glycogen→glucose-1-P), which eventually depletes the muscle glycogen, which in turn triggers protein metabolism, which then produces even more AMP. In AMP deaminase deficiency, excess adenosine is converted into uric acid in the following reaction:
Sir Bernard Rawdon Reilly (1 April 1937 – 24 October 1940) John Hathorn Hall (24 October 1940 – 1 January 1945) (From 2 December 1940, Sir John Hathorn Hall) Reginald Stuart Champion (1 January 1945 – 1950) (From 1 January 1946, Sir Reginald Stuart Champion) William Allmond Codrington Goode (1950 – April 1951) (Acting) Sir Tom Hickinbotham (April 1951 – 13 July 1956) Sir William Luce (13 July 1956 – 23 October 1960) Sir Charles Johnston (23 October 1960 – 18 January 1963)
The epididymis (; pl.: epididymides or ) is an elongated tubular genital organ attached to the posterior side of each one of the two male reproductive glands, the testicles. It is a single, narrow, tightly coiled tube which, in adult humans, is about 6 to 7 centimetres (2.4 to 2.8 in) in length; uncoiled, the tube would be approximately 6 m (20 feet) long. The epididymis connects the testicle to the vas deferens in the male reproductive system. The epididymis serves as an interconnection between the multiple efferent ducts at the rear of a testicle (proximally), and the vas deferens (distally). Its primary function is the storage, maturation, and transport of sperm.
Sources: en.wikipedia.org
No. No major regulatory agency has granted a marketing authorisation for melanotan II as a medicine. Products sold under this name are generally presented as laboratory reagents and are not subject to the batch-release testing applied to approved drugs.
It was developed in the 1980s by researchers investigating analogues of alpha-melanocyte-stimulating hormone for pigmentation and related endpoints. Early work included small human studies during the 1990s. Development did not progress to licensing, and the compound remained a research and grey-market item.
Peptides are prone to truncation, oxidation and aggregation during synthesis and handling. Without independent testing, a buyer cannot confirm the identity or the content of a vial. Analytical surveys of unapproved peptide products have repeatedly found discrepancies between label claims and measured composition.
Mass spectrometry combined with liquid chromatography provides both molecular weight confirmation and a measure of related impurities. Tandem mass spectrometry adds sequence information. A purity percentage reported without a mass measurement does not confirm what the material is.