Everything below concerns alpha-MSH analogue. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-02-05. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Melanotan-2 is a synthetic cyclic heptapeptide designed as an analogue of alpha-melanocyte-stimulating hormone. Its sequence incorporates a lactam bridge that constrains the peptide into a ring, which increases resistance to enzymatic breakdown relative to the natural hormone. Researchers at the University of Arizona synthesised the compound in the late 1980s and early 1990s while studying pigmentation pathways. It has never received marketing approval from any national medicines regulator. In the scientific literature it is usually described as a laboratory research reagent rather than a therapeutic product.
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.
| 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 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.
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.
=== Radiology === Chest X-rays are useful in the follow-up routine of IPF patients. Plain chest X-rays are unfortunately not diagnostic but may reveal decreased lung volumes, typically with prominent reticular interstitial markings near the lung bases.
==== General election ==== On July 25, 2000, Bush surprised some observers when he selected Dick Cheney – a former White House chief of staff, U.S. representative, and secretary of defense – to be his running mate. At the time, Cheney was serving as head of Bush's vice presidential search committee. Soon after at the 2000 Republican National Convention, Bush and Cheney were officially nominated by the Republican Party. Bush continued to campaign across the country and touted his record as Governor of Texas. During his campaign, Bush criticized his Democratic opponent, incumbent vice president Al Gore, over gun control and taxation. When the election returns were tallied on November 7, Bush had won 29 states, including Florida. The closeness of the Florida outcome led to a recount. The initial recount also went to Bush, but the outcome was tied up in lower courts for a month until eventually reaching the U.S. Supreme Court. On December 9, in the controversial Bush v. Gore ruling, the Court reversed a Florida Supreme Court decision that had ordered a third count, and stopped an ordered statewide hand recount based on the argument that the use of different standards among Florida's counties violated the Equal Protection Clause of the Fourteenth Amendment. The machine recount showed that Bush had won the Florida vote by a margin of 537 votes out of six million casts.
== Further reading == Author I'm Not the Only One (2004) Mr Galloway Goes to Washington (2005) Fidel Castro Handbook (2006), MQ Publications. ISBN 1-84072-688-1 Respect: Documents of the Crisis (2008) with Salma Yaqoob and Alan Thornett Open Season: The Neil Lennon Story (2011) Miranda Media
Sources: en.wikipedia.org
Arrestins (abbreviated Arr) are a small family of proteins important for regulating signal transduction at G protein-coupled receptors. Arrestins were first discovered in the late '80s as a part of a conserved two-step mechanism for regulating the activity of G protein-coupled receptors (GPCRs) in the visual rhodopsin system by Hermann Kühn, Scott Hall, and Ursula Wilden and in the β-adrenergic system by Martin J. Lohse and co-workers.
At low concentrations of TNP-ATP (≤1 μM), fluorescent intensity is proportional to the concentration of TNP added. However, at concentrations exceeding 1 μM, inner filter effects cause this relationship to no longer be linear. To correct this, researchers must determine the ratio of the predicted theoretical fluorescence intensity (assuming linearity) to the observed fluorescence intensity and then apply this correction factor. However, in most cases, researchers will try to keep the concentration of TNP to lower than 1 μM. To determine binding affinities, TNP-ATP is added to a solution and then titrated with protein. This produces a saturation curve from which the binding affinity can be determined. The number of binding sites may also be determined through this saturation curve by looking to see if there are sudden changes in slope. One can also titrate a fixed amount of protein with increasing additions of TNP-ATP to obtain a saturation curve. To do so, however, may get complicated due to the inner filter effects that will need to be corrected for. To determine dissociation constants, TNP-ATP can be competed off of a protein with ATP. The value of the dissociation constant Kd for a single-site binding can then be obtained by applying the Langmuir equation for a curve fit:
== List of Russian drugs == Aceclidine (Glaucostat, Glaunorm, Glaudin) – parasympathomimetic miotic Acetomepregenol (ACM; mepregenol diacetate; Diamol) – progestin Adapromine (1-(1′-adamantyl)propylamine; Etandan) – adamantane, antiviral, psychostimulant, antidepressant Alafen (alaphen, alafena; amphetamine–β-alanine) – amphetamine derivative, antiserotonergic Arabinopyranosyl-N-methyl-N-nitrosourea (Aranose, Aranoza) – antineoplastic agent Bemethyl (bemitil) – actoprotector Bromantane (Ladasten) – psychostimulant, antidepressant, anxiolytic, adaptogen/actoprotector, immunostimulant Butagest – progestin Carubicin – anthracycline antineoplastic agent Cepentil (tsepentil, N-cyclopentyllysergamide, LCyP) – lysergamide antiserotonergic Chlodantane (chlodantan; ADK-910) – adamantane, adaptogen/actoprotector, immunostimulant Chloracyzine – tricyclic antidepressant, phenothiazine, coronary vasodilator, antianginal Cortifen (cortiphen, kortifen, fencoron) – glucocorticoid, antineoplastic agent Corvalol (corvalolum, Korvalol) – tranquilizer, based on phenobarbital and containing various natural ingredients. In Russia it is sold without prescription, despite the fact that ordinary phenobarbital tablets are sold strictly by doctor's prescription.
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.
It is a synthetic cyclic heptapeptide modelled on alpha-melanocyte-stimulating hormone. A lactam bridge links two side chains, forming a ring that stabilises the molecule against proteolysis. It belongs to the broader melanocortin peptide family.