Everything below concerns alpha-MSH analog. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2025-07-29. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
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.
| 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 |
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.
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.
Center for Medicare (CM) Center for Medicaid and CHIP Services (CMCS) Center for Medicare and Medicaid Innovation (CMMI, a.k.a. the CMS Innovation Center) Center for Consumer Information and Insurance Oversight (CCIIO) Center for Program Integrity (CPI) Center for Clinical Standards and Quality (CCSQ) The regions:
He also serves on the scientific advisory board for seven additional companies (Eisai, Kemxtree, Quanta Therapeutics, Inc., Alkermes, Inc, Nutcracker Therapeutics, Inc., Hongene Biotech Corporation, Shouxin, and Sage Therapeutics) and has consulted for over twenty more, including presently at Bristol-Meyers-Squibb, Gilead, and BASF Corporation. In 2014, Baran began a partnership with IKA, a laboratory equipment manufacturer, to bring to market equipment designed to standardize electrochemical protocols and make electrochemistry accessible to the average organic chemist. Three years after the partnership began, the ElectraSyn was presented at the American Chemical Society annual meeting. In the seven years since, the ElectraSyn and subsequent ElectraSyn 2.0 have been adopted by the synthetic community and utilized towards hundreds of research articles and patents.
== Adverse effects == In September 2016, the US Food and Drug Administration (FDA) required a new warning to be added to the prescribing information related to a link between vilazodone and acute pancreatitis and sleep paralysis. In addition, other sleep disturbances such as hypnagogic hallucinations and sleep terrors can occur. Sleep paralysis is a state, during waking up or falling asleep, in which a person is conscious but experiences full-body paralysis. During an episode, the person may hallucinate (hear, feel, or see things that are not there), which often results in fear. A night terror, also called sleep terror, is a sleep disorder causing feelings of panic or dread. The rate of sleep paralysis adverse events was high enough to merit an FDA warning added to the Viibryd prescription label. In July 2021, the US Food and Drug Administration required a new warning to be added to the prescription label that vilazodone may cause sexual dysfunction. Per the FDA label, sexual dysfunction can include ejaculatory delay or failure, decreased libido, and erectile dysfunction in male patients. In female patients, sexual dysfunction can include decreased libido and delayed or absent orgasm. The most common adverse effects include nausea, diarrhea, vomiting, and insomnia. After a one-year, open-label study assessing the safety and tolerability of vilazodone in people with major depressive disorder, the most common adverse effects were diarrhea (35.7%), nausea (31.6%), and headache (20.0%); greater than 90% of these adverse effects were mild or moderate.
=== Asia === China: Introduced in the 1930s. Increasingly, it became more widespread after 1949. The majority were inoculated by 1979. South Korea, Singapore, Taiwan, and Malaysia. In these countries, BCG was given at birth and again at age 12. In Malaysia and Singapore from 2001, this policy was changed to once only at birth. South Korea stopped re-vaccination in 2008. Hong Kong: BCG is given to all newborns. Japan: In Japan, BCG was introduced in 1951, given typically at age 6. From 2005 it is administered between five and eight months after birth, and no later than a child's first birthday. BCG was administered no later than the fourth birthday until 2005, and no later than six months from birth from 2005 to 2012; the schedule was changed in 2012 due to reports of osteitis side effects from vaccinations at 3–4 months. Some municipalities recommend an earlier immunization schedule. Thailand: In Thailand, the BCG vaccine is given routinely at birth. India and Pakistan: India and Pakistan introduced BCG mass immunization in 1948, the first countries outside Europe to do so. In 2015, millions of infants were denied BCG vaccine in Pakistan for the first time due to shortage globally. Mongolia: All newborns are vaccinated with BCG. Previously, the vaccine was also given at ages 8 and 15, although this is no longer common practice. Philippines: BCG vaccine started in the Philippines in 1979 with the Expanded Program on Immunization. Sri Lanka: In Sri Lanka, The National Policy of Sri Lanka is to give BCG vaccination to all newborn babies immediately after birth.
== Licenses == As of 2025, a plurality (39%) of models released on Hugging Face used the permissive Apache 2.0 License. Some models, such as the source-available Llama 3, have licenses that grant some of the benefits of open-source licenses, but also contain legal restrictions that deter some companies from using those models, as the companies fear a future lawsuit or a change in the terms and conditions. Some of the same fears also exist in the large number of smaller models that do not specify a license.
Sources: en.wikipedia.org
Light therapy treatments for the skin usually involve exposure to ultraviolet light. The exposures can be to a small area of the skin or over the whole body surface, as in a tanning bed. The most common treatment is with narrowband UVB, which has a wavelength of approximately 311–313 nanometers. Full body phototherapy can be delivered at a doctor's office or at home using a large high-power UVB booth. Tanning beds, however, generate mostly UVA light, and only 4% to 10% of tanning-bed light is in the UVB spectrum.
Even though the half-lives of these nuclei are very short (on the order of seconds), the very existence of elements heavier than rutherfordium is indicative of stabilizing effects thought to be caused by closed shells; a model not considering such effects would forbid the existence of these elements due to rapid spontaneous fission. Flerovium, with the expected magic 114 protons, was first synthesized in 1998 at the Joint Institute for Nuclear Research in Dubna, Russia, by a group of physicists led by Yuri Oganessian. A single atom of element 114 was detected, with a lifetime of 30.4 seconds, and its decay products had half-lives measurable in minutes. Because the produced nuclei underwent alpha decay rather than fission, and the half-lives were several orders of magnitude longer than those previously predicted or observed for superheavy elements, this event was seen as a "textbook example" of a decay chain characteristic of the island of stability, providing strong evidence for the existence of the island of stability in this region. Even though the original 1998 chain was not observed again, and its assignment remains uncertain, further successful experiments in the next two decades led to the discovery of all elements up to oganesson, whose half-lives were found to exceed initially predicted values; these decay properties further support the presence of the island of stability.
== Career == From 1988 to 1989, Brayden worked as a research assistant at the University of Cambridge. He undertook a postdoctoral fellowship at Stanford University in 1989. In 2001, he joined UCD as an assistant professor and was promoted to associate professor in 2005, to professor in 2006, and to full professor in 2014. Between 2003 and 2006, Brayden was the co-founding chairperson of the UK–Ireland Chapter of the Controlled Release Society. He was employed as the Deputy Coordinator of an EU 7th Framework grant on oral nanomedicines, TRANS-INT. He holds the role of Co-lead principal Investigator at CÚRAM, the Research Ireland Centre for Medical Devices, and is the coordinator of the Horizon Europe Consortium, BUCCAL-PEP. He is the Field Chief Editor of Frontiers in Drug Delivery. Brayden was appointed to Ireland's National Research Ethics Committee for Clinical Trials by the Minister for Health in 2021, and in 2024 became chairperson of NREC-CT D. In 2026, he received the higher doctorate of Doctor of Science (DSc) from the National University of Ireland on the basis of his published work in pharmacology.
Bivalves and the gastropods in the family Juliidae have very similar shells. There are limpet-like forms in several lines of gastropods: "true" limpets, pulmonate siphonariid limpets and several lineages of pulmonate freshwater limpets. Cephalopod (like in octopuses and squid) and vertebrate eyes are both lens-camera eyes with much overall similarity, yet are very unrelated species. A closer examination reveals some differences including embryonic development, extraocular muscles, number of lens parts, and the lack of a retinal blindspot in the cephalopod eye. Swim bladders: buoyant bladders independently evolved in fishes, the tuberculate pelagic octopus, and siphonophores such as the Portuguese man o' war. Bivalves and brachiopods independently evolved paired hinged shells for protection. However, the anatomy of their soft parts is very dissimilar, which is why molluscs and brachiopods are put into different phyla. Jet propulsion in squids and in scallops: these two groups of mollusks have very different ways of squeezing water through their bodies in order to power rapid movement through a fluid. (Dragonfly larvae in the aquatic stage also use an anal jet to propel them, and jellyfish have used jet propulsion for a very long time.) Sea hares (gastropod molluscs) employ a similar means of jet propulsion, but without the sophisticated neurological machinery of cephalopods they navigate somewhat more clumsily. Tunicates (such as salps), and some jellyfish also employ jet propulsion.
Sources: en.wikipedia.org
An Alu polymorphism analysis by Mastana S (2007) using Sinhalese, Tamil, Bengali, Gujarati (Patel), and Punjabi as parental populations found the following proportions of genetic contribution. The Sinhalese sample size used was 121 individuals.:
== Enzyme mechanism == Cystathionase uses pyridoxal phosphate to facilitate the cleavage of the sulfur-gamma carbon bond of cystathionine, resulting in the release of cysteine. The lysine residue reforms the internal aldimine by kicking off α-iminobutyric acid. Afterwards the external ketimine is hydrolyzed, causing the formation of α-ketobutyrate. The amino group on cystathionine is deprotonated and undergoes a nucleophilic attack of the internal aldimine. An additional deprotonation by a general base results in the formation of the external aldimine and removal of the lysine residue. The basic lysine residue is then able to deprotonate the alpha carbon, pushing electron density into the nitrogen of the pyridine ring. Pyridoxal phosphate is necessary to stabilize this carbanionic intermediate; otherwise the proton's pKa would be too high. The beta carbon is then deprotonated, creating an alpha-beta unsaturation and pushing a lone pair onto the aldimine nitrogen. To reform the aldimine, this lone pair pushes back down, cleaving the sulfur-gamma carbon bond, resulting in the release of cysteine. A pyridoxamine derivative of vinyl glyoxylate remains after the gamma elimination. The lone pair from the pyridine nitrogen pushes electron density to the gamma carbon, which is protonated by lysine. Lysine then attacks the external aldimine, pushing electron density to the beta carbon, which is protonated by a general acid. The imine is then hydrolyzed to release α-ketobutyrate. Deprotonation of the lysine residue causes ammonia to leave, thus completing the catalytic cycle.
α-Methylthiofentanyl is an opioid analgesic that is an analogue of fentanyl. α-Methylthiofentanyl was sold briefly on the black market in the early 1980s, before the introduction of the Federal Analog Act which for the first time attempted to control entire families of drugs based on their structural similarity rather than scheduling each drug individually as they appeared. α-Methylthiofentanyl has similar effects to fentanyl. Side effects of fentanyl analogs are similar to those of fentanyl itself, which include itching, nausea and potentially serious respiratory depression, which can be life-threatening. Fentanyl analogs have killed hundreds of people throughout Europe and the former Soviet republics since the most recent resurgence in use began in Estonia in the early 2000s, and novel derivatives continue to appear.
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. It is a synthetic analogue carrying four amino acid changes, a lactam ring and an amidated C-terminus. The natural hormone is a linear thirteen-amino-acid peptide processed from proopiomelanocortin.