Everything below concerns alpha-MSH analogue. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-05-13. 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 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 |
|---|---|---|
| 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-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.
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.
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.
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 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.
7.3.2.1 ABC-type phosphate transporter The expected taxonomic range for this enzyme is: Eukaryota, Bacteria. A bacterial enzyme that interacts with an extracytoplasmic substrate binding protein and mediates the high affinity uptake of phosphate anions. Unlike P-type ATPases, it does not undergo phosphorylation during the transport process. ATP + H2O + phosphate [phosphate - binding protein][side 1] = ADP + phosphate + phosphate [side 2] + [phosphate - binding protein][side 1] 7.3.2.2 ABC-type phosphonate transporter The enzyme, found in bacteria, interacts with an extracytoplasmic substrate binding protein and mediates the import of phosphonate and organophosphate anions. ATP + H2O + phosphonate [phosphonate-binding protein][side 1] = ADP + phosphate + phosphonate [side 2] + [phosphonate- binding protein][side 1] 7.3.2.3 ABC-type sulfate transporter The expected taxonomic range for this enzyme is: Eukaryota, Bacteria. The enzyme from Escherichia coli can interact with either of two periplasmic binding proteins and mediates the high affinity uptake of sulfate and thiosulfate. May also be involved in the uptake of selenite, selenate and possibly molybdate. Does not undergo phosphorylation during the transport. ATP + H2O + sulfate [sulfate - binding protein] [side 1] = ADP + phosphate + sulfate [side 2] + [sulfate - binding protein][side 1] 7.3.2.4 ABC-type nitrate transporter The expected taxonomic range for this enzyme is: Eukaryota, Bacteria.
== BOLD-100 derivatives == BOLD-100 is sodium trans-[tetrachlorobis (1H-indazole) ruthenate(III)] with cesium as an intermediate salt form. BOLD-100 was developed from KP1339 (also known as IT-139 or NKP-1339) which is also sodium trans-[tetrachlorobis (1H-indazole) ruthenate(III)], but has different manufacturing methods and purity profiles. The names are often used interchangeably. The precursor to BOLD-100 is KP1019, which is the indazole salt equivalent. KP1019 previously entered Phase 1 clinical trials but development was halted due to low solubility in water, leading to the development of KP1339 and BOLD-100 which are readily soluble in water. KP1019 and KP1339 were invented by Dr. Keppler at the University of Vienna.
Compounding involves preparing drugs in forms that are different from the generic prescription standard. This may include altering the strength, ingredients, or dosage form. Compounding is a way to create custom drugs for patients who may not be able to take the medication in its standard form, such as due to an allergy or difficulty swallowing. Compounding is necessary for these patients to still be able to properly get the prescriptions they need. One area of compounding is preparing drugs in new dosage forms. For example, if a drug manufacturer only provides a drug as a tablet, a compounding pharmacist might make a medicated lollipop that contains the drug. Patients who have difficulty swallowing the tablet may prefer to suck the medicated lollipop instead. Another form of compounding is by mixing different strengths (g, mg, mcg) of capsules or tablets to yield the desired amount of medication indicated by the physician, physician assistant, nurse practitioner, or clinical pharmacist practitioner. This form of compounding is found at community or hospital pharmacies or in-home administration therapy. Compounding pharmacies specialize in compounding, although many also dispense the same non-compounded drugs that patients can obtain from community pharmacies.
Sources: en.wikipedia.org
=== Fatty liver disease === Studies in mice have shown that activation of FFAR3 by short-chain fatty acids (SC-FAs) suppresses liver lipid synthesis, reduces triglyceride accumulation, and decreases liver weight in models of diet-induced obesity. Mice lacking the Ffar3 gene fail to exhibit these protective effects, suggesting a critical role for FFAR3 in preventing excessive hepatic fat accumulation. These findings support further research to determine whether FFAR3 functions similarly in humans and whether FFAR3 activators could be developed as potential treatments for human fatty liver diseases, including non-alcoholic fatty liver disease.Koh A, De Vadder F, Kovatcheva-Datchary P, Bäckhed F (June 2016). "From Dietary Fiber to Host Physiology: Short-Chain Fatty Acids as Key Bacterial Metabolites". Cell. 165 (6): 1332–1345. doi:10.1016/j.cell.2016.05.041. PMID 27259147. S2CID 8562345.
== Branches == Physical chemistry – study of the physical and fundamental basis of chemical systems and processes. In particular, the energetics and dynamics of such systems and processes are of interest to physical chemists. Important areas of study include chemical thermodynamics, chemical kinetics, electrochemistry, statistical mechanics, spectroscopy, and more recently, astrochemistry. Physical chemistry has large overlap with molecular physics. Physical chemistry involves the use of infinitesimal calculus in deriving equations. It is usually associated with quantum chemistry and theoretical chemistry. Physical chemistry is a distinct discipline from chemical physics, but again, there is very strong overlap. Chemical kinetics – study of rates of chemical processes. Chemical physics – investigates physicochemical phenomena using techniques from atomic and molecular physics and condensed matter physics; it is the branch of physics that studies chemical processes. Electrochemistry – branch of chemistry that studies chemical reactions which take place in a solution at the interface of an electron conductor (the electrode: a metal or a semiconductor) and an ionic conductor (the electrolyte), and which involve electron transfer between the electrode and the electrolyte or species in solution. Femtochemistry – area of physical chemistry that studies chemical reactions on extremely short timescales, approximately 10−15 seconds (one femtosecond). Geochemistry – chemical study of the mechanisms behind major systems studied in geology.
== V == Lauri Vaska (1925–2015), Estonian/American chemist Louis Nicolas Vauquelin (1763–1829), French pharmacist and chemist, discovered the elements beryllium and chromium Vincent du Vigneaud (1901–1978), 1955 Nobel Prize in Chemistry Artturi Ilmari Virtanen (1895–1973), chemist, Nobel Prize laureate Max Volmer, Germany (1885–1965) Alessandro Volta (1745–1827), Italian electrochemist, invented the voltaic cell Alexander Vinogradov (1895-1975), Soviet geochemist
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.
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.