Alpha-MSH is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Updated 2026-06-04. Numbers and descriptions here follow the published literature rather than marketing material.
Melanotan-2, also written Melanotan II, is a synthetic cyclic heptapeptide designed as an analogue of alpha-melanocyte-stimulating hormone. Its sequence is Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-NH2, and the lactam bridge between the aspartate and lysine side chains constrains the peptide into a ring. This structural change increases receptor affinity and metabolic stability relative to the native hormone. The compound was created in the 1980s as a research tool for studying pigmentation biology.
Melanocytes are the pigment-producing cells of the skin, and they carry melanocortin-1 receptors on their surface. When the receptor is activated, cyclic adenosine monophosphate rises inside the cell and raises the activity of enzymes such as tyrosinase, which increases melanin output. Melanotan-2 binds melanocortin-1 receptors in vitro and in animal models, and this binding is generally described as the basis for the tanning effect. Other receptors account for different effects: melanocortin-4 receptors contribute to appetite and erectile signalling, while melanocortin-3 and melanocortin-5 receptors contribute to energy balance and exocrine function.
Melanotan II binds several melanocortin receptor subtypes rather than a single target. MC1R on melanocytes drives melanin synthesis, while MC3R and MC4R participate in energy balance, appetite, and sexual response pathways. This lack of selectivity explains why reported effects extend beyond skin darkening. Substitutions at positions four and seven, including norleucine and D-phenylalanine, increase potency and resistance to peptidases. Understanding which receptor mediates which effect remains an active area of investigation.
Published human data come mostly from small, short studies rather than large controlled trials. Reported outcomes include increased skin pigmentation and, in some reports, effects on appetite and libido, but sample sizes are small and follow-up is limited. Whether long-term use produces durable pigment changes or adverse effects is not established. Because products sold outside pharmacies are not standardized, the actual content of any given vial is often unknown. Independent testing of such material is uncommon.
Melanotan II is a synthetic cyclic heptapeptide analog derived from the core sequence of alpha-melanocyte-stimulating hormone. Researchers at the University of Arizona synthesized it during the 1980s while studying pigmentation and appetite signaling. The compound is not an approved medicine in any major jurisdiction and appears mainly in laboratory and research-chemical settings. Its structure incorporates a lactam bridge between side chains, which constrains the ring and slows enzymatic breakdown relative to the natural hormone.
| Property | Value | Notes |
|---|---|---|
| Compound class | Synthetic cyclic heptapeptide | Alpha-MSH analogue containing a D-phenylalanine residue |
| Molecular formula | C50H69N15O9 | Average molecular mass approximately 1024.2 g/mol |
| Appearance | White to off-white lyophilised powder | Normally supplied as a freeze-dried solid in a sealed vial |
| Solubility | Freely soluble in water and polar solvents | Dissolves readily in aqueous buffers and in alcohol-water mixtures |
| Receptor targets | MC1R, MC3R, MC4R, MC5R | Acts as a non-selective melanocortin receptor agonist |
No regulatory authority has approved melanotan-2 for human use, and several countries classify it as a prescription-only or controlled substance, which restricts lawful supply. Material sold online is generally labelled as a research chemical and is not required to meet pharmaceutical standards of identity or purity. Published human data consist mainly of small uncontrolled studies, case reports and adverse-event notifications, so the evidence base is descriptive rather than confirmatory. Whether repeated melanocyte stimulation alters long-term naevus behaviour remains an open question that no completed trial has resolved.
Melanotan-2 is a synthetic cyclic heptapeptide designed as a structural analogue of alpha-melanocyte-stimulating hormone, the endogenous tridecapeptide that regulates pigment production. Two modifications distinguish it from the natural hormone: norleucine replaces methionine at the N-terminus, which limits oxidation, and a D-phenylalanine substitution raises receptor affinity. The ring is closed through an aspartate-lysine lactam bridge, giving the molecule a constrained conformation. The free base has a molecular mass near 1024 daltons, and commercial material is usually supplied as an acetate salt. It appears in the literature as a research peptide rather than an approved therapeutic agent.
Receptor studies place melanotan-2 among non-selective melanocortin agonists, binding MC1R, MC3R, MC4R and MC5R rather than a single subtype. Activation of MC1R on cutaneous melanocytes raises tyrosinase activity and shifts pigment synthesis toward eumelanin, which is darker and more photostable than pheomelanin. Central receptors, particularly MC4R, are associated with appetite suppression and with reported effects on sexual function. Because subtype selectivity is low, the same molecule engages pigment, metabolic and vascular pathways at once, and this breadth is a common explanation offered for the range of adverse events described in user reports.
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 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.
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.
In Early June, German Forces (estimated at 9 divisions with tanks and artillery) began concentrating in the Lepel-Chashniki area. By June 10, the Germans had fortified the Lepel-Borisov Highway with Trenches and pillboxes every 100 meters, trapping the partisans. The Brigade was forced to retreat into the marshy terrains of Lake Palik. Under constant artillery fire and aerial bombardment, the partisans were pushed back into the forests, where they faced severe supply issues. Records indicate that during the height of the encirclement, the encircled partisans were suffering from extreme famine and were surviving on grass and animal hides.
==== United States ==== The first approved PSMA imaging agent was indium-111 (111In) capromab pendetide (branded Prostascint). It received Food and Drug Administration (FDA) approval in 1996. However, the agent had poor sensitivity and saw little widespread use. The first PET PSMA imaging agent, 68Ga-PSMA-11, was approved by the FDA in 2020. Listed indications include suspected metastasis prior to initial treatment, and recurrence of prostate cancer (based on elevated serum prostate-specific antigen (PSA) level). This was followed by two further 68Ga-PSMA-11 agents in 2021 and 2022 (branded Illucix and Locametz). Listed indications for Lucametz additionally includes selection of patients prior to 177Lu-PSMA radionuclide therapy. An 18F-PSMA agent (18F-DCFPyL) (branded Pylarify) was approved by the FDA in 2021. Indications are as for 68Ga-PSMA-11. Another 18F-PSMA agent (18F-rhPSMA-7.3) (branded Posluma) was approved by the FDA in 2023.
Competence stimulating peptides are a subset of proteins that promote quorum sensing in numerous bacterial genera including Streptococcus and Bacillus. Quorum sensing contributes to regulation of specific gene expressions in response to cell population density fluctuations. Streptococcus pneumonia, a highly studied gram-positive bacterium, is capable of quorum sensing and can release autoinducers, chemical signals that increase as concentration based on density. CSPs are part of a unique form of regulation involved in DNA processing. The form of DNA processing starts abruptly and at the same time in all cells when in a constantly or exponentially growing culture, and then growth rapidly decreases after about 12 minutes of exponential growth.
Mahathir criticised the awarding of import permits for foreign cars, which he claimed were causing Proton's domestic sales to suffer, and attacked Abdullah for cancelling the construction of a second causeway between Malaysia and Singapore. Mahathir complained that his views were not getting sufficient airing by the Malaysian press. In response, he began writing a column for Malaysiakini and starting his own blog. He unsuccessfully sought election from his local party division to be a delegate to UMNO's general assembly in 2006, where he planned to initiate a challenge to Abdullah's leadership. Mahathir had previously missed the UMNO General Assembly twice since 2006 for health reasons. After the 2008 election, in which UMNO lost its two-thirds majority in parliament, Mahathir resigned from the party. When Abdullah was replaced by his deputy Najib Razak in 2009, Mahathir re-joined the party and urged all former members to follow his move. Before the 2013 general election, Mahathir promised to keep the government in check and ensure it fulfilled its manifesto promises, vowing to protest and fight against it if it failed.
Sources: en.wikipedia.org
Furthermore, Oxgr1 gene knockout mice drinking sodium bicarbonate-rich water developed metabolic alkalosis (body tissue pH levels higher than normal) that was associated with blood bicarbonate levels significantly higher and blood chloride levels significantly lower than those in control mice drinking the sodium bicarbonate-rich water. Several other studies confirmed these findings and reported that cells in the proximal tubules of mice synthesize α-ketoglutarate and either broke it down thereby reducing its urine levels or secreted it into the tubules' lumens thereby increasing its urine levels. Another study showed that a) In silico computer simulations strongly suggested that α-ketoglutarate bound to mouse OXGPR1; b) suspensions of canal duct cells isolated from the collecting ducts, loops of Henle, vasa recta, and interstitium of mouse kidneys raised their cytosolic ionic calcium, i.e., Ca2+ levels in response to α-ketoglutarate but this response (which is an indicator of cell activation) was blocked by pretreating the cells with montelukast; and c) compared to mice not treated with streptozotocin, streptozotocin-induced diabetic mice (an animal disease model of diabetes) urinated only a small amount of the ionic sodium (Na+) that they drank or received by intravenous injections; montelukast reversed this defect in the streptozotocin-pretreated mice.
1993/3173) Education (Individual Pupils' Achievements) (Information) Regulations 1993 (S.I. 1993/3182) Education (European Economic Area) (Amendment) Regulations 1993 (S.I. 1993/3183) Education (European Economic Area) (Scotland) Regulations 1993 (S.I. 1993/3184) Liquor Licensing (Fees) (Scotland) Order 1993 (S.I. 1993/3185) Advice and Assistance (Assistance by Way of Representation) (Scotland) Amendment (No. 2) Regulations 1993 (S.I. 1993/3186) Advice and Assistance (Financial Limit) (Scotland) Regulations 1993 (S.I. 1993/3187) Education (Grant–maintained Schools) (Initial Sponsor Governors) Regulations 1993 (S.I. 1993/3188) Education (Acquisition of Grant-maintained Status) (Ballot Information) Regulations 1993 (S.I. 1993/3189) Supreme Court Fees (Amendment) Order 1993 (S.I. 1993/3191) Cod and Saithe (Specified Sea Areas) (Prohibition of Fishing) Order 1993 (S.I. 1993/3192) Haddock, Hake, Nephrops, Plaice and Sole (Specified Sea Areas) (Prohibition of Fishing) Order 1993 (S.I. 1993/3193) Social Security (Severe Disablement Allowance) Amendment Regulations 1993 (S.I. 1993/3194) Doncaster Borough Council (North Bridge Relief Road) (Crossing of Navigable Waterway (Sheffield and South Yorkshire Navigation River Don New Cut)) Scheme 1991 Confirmation Instrument 1993 (S.I. 1993/3195) Education (Distribution by Schools of Information about Further Education Institutions) (England) Regulations 1993 (S.I. 1993/3197) Nitrate Sensitive Areas (Designation) (Amendment) Order 1993 (S.I. 1993/3198) Broadcasting (Restrictions on the Holding of Licences) (Amendment) Order 1993 (S.I.
== Life and career == Green was born in Brooklyn, New York, the son of Jennie (née Marrow) and Hyman Levy Green, a garment manufacturer. His parents were Jewish immigrants from Russia and Germany. He was awarded a degree in biology from New York University. He then moved to England and worked for eight years at the University of Cambridge under the supervision of Malcolm Dixon, on redox reactions in biological systems. He received his PhD under Dixon in 1934 with a thesis entitled The Application of Oxidation-Reduction Potentials to Biological Systems. At the outbreak of the Second World War, Green moved back to America and established himself in a laboratory at Columbia University. Here he studied the metabolism of amino acids and the citric acid cycle. In 1948, Green moved to the University of Wisconsin–Madison and set up the Institute for Enzyme Research, making vital contributions to studies on oxidative phosphorylation, the electron transport chain and beta oxidation. He was married to English-born Doris Cribb. He is the father of biochemist Rowena Green Matthews and grandfather of Wisconsin Senator Tammy Baldwin.
Cocaine is sometimes used in otorhinolaryngology as a topical anesthetic and vasoconstrictor to help control pain and bleeding during surgery of the nose, mouth, throat, or lacrimal duct. It is also used for topical airway anaesthesia for procedures such as awake fibreoptic bronchoscopy or intubation. Although some absorption and systemic effects may occur, the use of cocaine as a topical anesthetic and vasoconstrictor is generally safe, rarely causing cardiovascular toxicity, glaucoma, and pupil dilation. Occasionally, cocaine is mixed with adrenaline and sodium bicarbonate and used topically for surgery, a formulation called Moffett's solution. It is occasionally used in surgeries involving the pharynx or nasopharynx to reduce pain, bleeding, and vocal cord spasm. Nasal solution cocaine hydrochloride (Goprelto), an ester used for intranasal application, was approved for medical use in the United States in December 2017, and is indicated for the introduction of topical anesthesia of the mucous membranes for diagnostic procedures and surgeries on or through the nasal cavities of adults. Cocaine hydrochloride (Numbrino) was approved for medical use in the United States in January 2020. Headache and epistaxis are the most frequently reported adverse reactions with Goprelto, while hypertension and tachycardia-including sinus tachycardia-are most common with Numbrino.
RNA editing through the addition and deletion of uracil has been found in kinetoplasts from the mitochondria of Trypanosoma brucei. Because this may involve a large fraction of the sites in a gene, it is sometimes called "pan-editing" to distinguish it from topical editing of one or a few sites. Pan-editing starts with the base-pairing of the unedited primary transcript with a guide RNA (gRNA), which contains complementary sequences to the regions around the insertion/deletion points. The newly formed double-stranded region is then enveloped by an editosome, a large multi-protein complex that catalyzes the editing. The editosome opens the transcript at the first mismatched nucleotide and starts inserting uridines. The inserted uridines will base-pair with the guide RNA, and insertion will continue as long as A or G is present in the guide RNA and will stop when a C or U is encountered. The inserted nucleotides cause a frameshift, and result in a translated protein that differs from its gene. The mechanism of the editosome involves an endonucleolytic cut at the mismatch point between the guide RNA and the unedited transcript. The next step is catalyzed by one of the enzymes in the complex, a terminal U-transferase, which adds Us from UTP at the 3' end of the mRNA. The opened ends are held in place by other proteins in the complex. Another enzyme, a U-specific exoribonuclease, removes the unpaired Us. After editing has made mRNA complementary to gRNA, an RNA ligase rejoins the ends of the edited mRNA transcript.
Sources: en.wikipedia.org
No. It is a laboratory-made peptide, while the natural hormone is alpha-melanocyte-stimulating hormone, a longer peptide produced by the pituitary gland and by skin cells. Melanotan-2 mimics only a short active region of that hormone and contains non-natural residues such as D-phenylalanine.
No approved regulatory indication exists in major markets. An approval exists for a different peptide, afamelanotide, which is used for a rare photosensitivity disorder called erythropoietic protoporphyria. Melanotan-2 itself remains a research compound with no cleared clinical role.
Melanocortin-1 receptors on melanocytes are the receptor most closely linked to pigment production. The peptide is not selective, however, and also activates melanocortin-3, melanocortin-4, and melanocortin-5 receptors. That lack of selectivity is the usual explanation offered for both its range of observed effects and its off-target effects.
No regulator in a major market has approved it for human use. It appears in research settings and in products marketed outside pharmacy channels. Legal status for personal possession varies by country.