This is a working overview of alpha-MSH analog, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-02-07. Anything still debated is marked as such rather than presented as settled.
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.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C50H69N15O9 | Free base; salt forms add to total mass |
| Molecular mass | About 1024 daltons | Calculated for the free base |
| Structural class | Cyclic heptapeptide | Contains D-phenylalanine and norleucine |
| Parent hormone | Alpha-melanocyte-stimulating hormone | Endogenous tridecapeptide of 13 residues |
| Receptor profile | Non-selective melanocortin agonist | Interacts with MC1R, MC3R, MC4R and MC5R |
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.
Early published reports described melanotan-2 as a tanning agent without sun protection, which means darkening is not the same as protection against ultraviolet radiation. Later studies explored the peptide in erectile dysfunction, hemorrhagic shock, and some skin conditions. No regulator in the United States or Europe has approved it for clinical use. Many products labelled melanotan-2 are sold without approval and their identity and purity are unverified. Its long-term safety in humans remains an open question.
Melanotan II is a synthetic cyclic heptapeptide that acts as an agonist at melanocortin receptors. It was designed as a structural analogue of alpha-melanocyte-stimulating hormone, the endogenous peptide involved in pigment production. The analogue carries a lactam bridge that constrains the ring and slows enzymatic breakdown relative to the native hormone. In research literature it appears under several abbreviations, and naming conventions are not fully standardized. Published descriptions usually place it within the broader melanocortin agonist family.
Receptor binding at MC1R on melanocytes raises intracellular cyclic AMP and increases expression of tyrosinase and related enzymes. The downstream result is greater synthesis of eumelanin, the dark pigment, without ultraviolet exposure acting as the trigger. The compound is not selective, however, and also engages MC3R, MC4R and MC5R, which are expressed in the central nervous system and elsewhere. That lack of selectivity is the explanation usually offered for effects reported outside pigmentation, including appetite suppression and nausea. Selectivity remains a central theme in comparative studies of related peptides.
Melanotan-2 is a synthetic cyclic heptapeptide designed as an analogue of alpha-melanocyte-stimulating hormone, the naturally occurring peptide involved in pigmentation signalling. Its sequence is conventionally written as Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-NH2, with a lactam bridge joining the aspartate side chain to the lysine side chain. The empirical formula is C50H69N15O9 and the monoisotopic mass lies near 1023.5 daltons. N-terminal acetylation and the D-configured phenylalanine both increase resistance to enzymatic breakdown compared with the parent hormone.
Pharmacologically, melanotan-2 behaves as a non-selective agonist across the melanocortin receptor family. Binding at MC1R on dermal melanocytes promotes eumelanin synthesis, which underlies the tanning response described in early human work. Activity at the centrally expressed MC4R receptor is associated with reported effects on appetite and erectile function. Because the peptide does not discriminate strongly among receptor subtypes, attributing any single observed effect to one receptor pathway is generally not possible without selective antagonists or receptor knockout models.
The peptide acts as a non-selective agonist at melanocortin receptors, showing affinity for MC1R, MC3R, MC4R and MC5R. Activation of MC1R on melanocytes drives the conversion of tyrosine into melanin and shifts production toward the darker eumelanin form. MC4R signalling in the central nervous system is linked to appetite and energy balance, which helps explain why reduced food intake appeared in early human studies. Effects on MC4R and on vascular tone also account for the erectile responses recorded as unexpected findings in those same trials.
Melanotan-2 is frequently confused with afamelanotide, a linear analogue authorised in the European Union for erythropoietic protoporphyria. The two compounds differ in chain length, ring structure and receptor selectivity, so findings for one cannot be transferred directly to the other. Published controlled human data on melanotan-2 remain sparse, and much of what circulates online derives from small studies or unpublished reports. Questions about effect size, dose-response behaviour and long-term safety therefore remain unresolved.
NAD(P)H quinone oxidoreductase 1 (Nqo1) is a prototypical NRF2 target protein which catalyzes the reduction and detoxification of highly reactive quinones that can cause redox cycling and oxidative stress. Glutamate-cysteine ligase catalytic subunit (GCLC) and glutamate-cysteine ligase regulatory subunit (GCLM) form a heterodimer, which is the rate-limiting step in the synthesis of glutathione (GSH), a very powerful endogenous antioxidant. Both Gclc and Gclm are characteristic NRF2 target genes, which establish NRF2 as a regulator of glutathione, one of the most important antioxidants in the body. Sulfiredoxin 1 (SRXN1) and Thioredoxin reductase 1 (TXNRD1) support the reduction and recovery of peroxiredoxins, proteins important in the detoxification of highly reactive peroxides, including hydrogen peroxide and peroxynitrite. Heme oxygenase-1 (HMOX1, HO-1) is an enzyme that catalyzes the breakdown of heme into the antioxidant biliverdin, the anti-inflammatory agent carbon monoxide, and iron. HO-1 is a NRF2 target gene that has been shown to protect from a variety of pathologies, including sepsis, hypertension, atherosclerosis, acute lung injury, kidney injury, and pain. Conversely, induction of HO-1 has been shown to exacerbate early brain injury after intracerebral hemorrhage. The glutathione S-transferase (GST) family includes cytosolic, mitochondrial, and microsomal enzymes that catalyze the conjugation of GSH with endogenous and xenobiotic electrophiles.
Mescaline is biosynthesized from tyrosine, which, in turn, is derived from phenylalanine by the enzyme phenylalanine hydroxylase. In Lophophora williamsii (peyote), dopamine converts into mescaline in a biosynthetic pathway involving m-O-methylation and aromatic hydroxylation. Tyrosine and phenylalanine serve as metabolic precursors towards the synthesis of mescaline. Tyrosine can either undergo a decarboxylation via tyrosine decarboxylase to generate tyramine and subsequently undergo an oxidation at carbon 3 by a monophenol hydroxylase or first be hydroxylated by tyrosine hydroxylase to form L-DOPA and decarboxylated by DOPA decarboxylase. These create dopamine, which then experiences methylation by a catechol-O-methyltransferase (COMT) by an S-adenosyl methionine (SAM)-dependent mechanism. The resulting intermediate is then oxidized again by a hydroxylase enzyme, likely monophenol hydroxylase again, at carbon 5, and methylated by COMT. The product, methylated at the two meta positions with respect to the alkyl substituent, experiences a final methylation at the 4 carbon by a guaiacol-O-methyltransferase, which also operates by a SAM-dependent mechanism. This final methylation step results in the production of mescaline. Phenylalanine serves as a precursor by first being converted to L-tyrosine by L-amino acid hydroxylase. Once converted, it follows the same pathway as described above.
=== Executive committee === The management of the Society is vested in an Executive Committee made up of Officers and General Members, they also act as Trustees of the Society. There are currently 10 officers of the Society namely the Chair, Vice-Chair, Treasurer, General Secretary, Meetings Secretary, Papers Secretary, Education Officer, Publicity Secretary, Special Interest Group Co-ordinator, and Digital Communications Officer.
Sources: en.wikipedia.org
== Evaluation == A 2024 quasi-experimental study published in JMIR Public Health and Surveillance examined 21 clinical laboratories in Côte d'Ivoire and found that laboratory data timeliness and completeness improved following implementation of OpenELIS. A 2022 study examined the system's development and national-scale sustainability over its first 13 years in the country, and a 2016 study examined its implementation and host-country ownership in Vietnam.
== German Mass Spectrometry Society (Deutsche Gesellschaft für Massenspektrometrie, DGMS) == The major awards of the German Mass Spectrometry Society (Deutsche Gesellschaft für Massenspektrometrie, DGMS) are the Mattauch-Herzog Award for Mass Spectrometry, Wolfgang Paul Lecture, Mass Spectrometry in the Life Sciences Award, and Life Science Prize.
Commission D2: Refrigerated Transport The IIR's Commission D2 on Refrigerated Transport is extremely active. In addition to the IIR's four-yearly congress, Commission D2 participates in the IIR Conference on Sustainability and the Cold Chain, held out of synchronisation with the congress. Every year, Commission D2 CERTE test engineers meet in a European country to discuss refrigerated transport technology and testing issues. This group subsequently advises the United Nations working party on transport of perishable foodstuffs held each year in Geneva. Commission D2 is currently addressing the “Cold Chain for Pharmaceutical Products” and will add this to regular transport discussion and advisory topics. Commission D2 also helps to produce Informatory Notes to assist in areas of technical or regulatory difficulty. The IIR is recognised, for its contributions to refrigerated transport, particularly through the work of its Commission D2. The commission's research addresses food waste reduction and emissions mitigation.
Sources: en.wikipedia.org
Premature menopause Gonadal dysgenesis, Turner syndrome, Klinefelter syndrome Castration Swyer syndrome Polyendocrine metabolic ovarian syndrome Certain forms of congenital adrenal hyperplasia Testicular failure Pregnancy – BetaHCG can mimic LH so tests may show elevated LH Note: A medical drug for inhibiting luteinizing hormone secretion is butinazocine.
In ancient times, one highly abrasive depilatory paste consisted of an admixture of slaked lime, water, wood-ash and yellow orpiment (arsenic trisulfide); In rural India and Iran, where this mixture is called vajibt, it is still commonly used to remove pubic hair. In other cultures, oil extracted from unripe olives (which had not reached one-third of their natural stage of ripeness) was used to remove body hair. During the medieval period, Catholic women were expected to let their hair grow long as a display of femininity, whilst keeping the hair concealed by wearing a wimple headdress in public places. The face was the only area where hair growth was considered unsightly; 14th-century ladies would also pick off hair from their foreheads to recede the hairline and give their face a more oval form. From the mid-16th century, it is said when Queen Elizabeth I came to power, she made eyebrow removal fashionable. By the 18th century, body hair removal was still considered a non-necessity by European and American women. But in 1760, when the first safety straight razor appeared for men to safely shave their beard and not inadvertently cut themselves, some women allegedly used this safety razor too. It was invented in Paris by the French master cutler Jean-Jacques Perret, author of La pogonotomie, ou L'art d'apprendre à se raser soi-même (Pogonotomy, or The Art of Learning to Shave). It was not until the late 19th century that women in Europe and America started to make hair removal a component of their personal care regime.
=== In the Indian Ocean === In the Makran Trench, a subduction zone along the northeastern margin of the Gulf of Oman adjacent to the southwestern coast of Pakistan and the southeastern coast of Iran, compression of an accretionary wedge has resulted in the formation of cold seeps and mud volcanoes.
Sources: en.wikipedia.org
No regulatory agency has authorised melanotan-2 as a medicine for any indication. It circulates mainly as a research chemical or through unregulated channels. As a result, identity, purity and content are not independently guaranteed.
Melanotan-1, also called afamelanotide, is a linear analogue with greater selectivity for MC1R and has received approval in some jurisdictions for a specific photosensitivity disorder. Melanotan-2 is cyclic, less selective, and reaches central receptors more readily. The two are often confused in online discussion despite different pharmacology and regulatory status.
Alpha-MSH is an endogenous tridecapeptide derived from pro-opiomelanocortin. Melanotan-2 reproduces its core receptor-binding sequence inside a shortened, stabilised ring. The result is a molecule with a longer effective half-life and higher potency than the parent hormone.
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.