This is a working overview of Melanotan II, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-05-21 and is reviewed periodically as new material appears.
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.
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.
Melanotan-2 is a synthetic linear peptide built from seven amino acids arranged in a short chain. Its sequence is commonly written as Ac-Nle-Asp-His-D-Phe-Arg-Trp-Lys-NH2, which includes a modified N-terminus and an amidated C-terminus. The molecule belongs to the melanocortin family and acts as a receptor agonist. Structural features such as the D-phenylalanine residue and the Nle substitution are associated with increased stability against enzymatic degradation relative to the natural parent peptide.
The compound emerged from research programs in the 1980s that examined analogues of alpha-melanocyte-stimulating hormone for pigmentation and photoprotection. Investigators modified the native sequence to extend activity duration and potency. A related analogue, afamelanotide, was developed within the same broad line of inquiry and eventually gained approval in certain jurisdictions for a rare light-sensitivity condition. Melanotan-2 itself did not progress through the same regulatory route and has no approved therapeutic indication.
| 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 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.
The compound was developed in the late 1980s and 1990s by academic researchers investigating photoprotection. The rationale held that stimulating melanin production might reduce ultraviolet damage to skin and lower skin cancer risk. Early work examined receptor binding, pigment response, and short-term tolerability in small studies. That program did not produce an approved drug, and formal development stalled after early-phase trials. Whether induced pigmentation confers meaningful photoprotection remains an open question.
Outside regulated medicine, melanotan II circulates through online vendors as a research chemical, often marketed for tanning. Products sold this way vary widely in purity, concentration, and labeling accuracy, and independent testing has documented discrepancies. Published reports describe both pigment effects and adverse reactions, including nausea, flushing, and darkening of existing moles. Long-term safety data are sparse, and no large controlled trial has established a risk profile. Questions about cumulative effects on melanocytes remain unresolved in the literature.
Multivariate stepwise regression analysis reveals that, in combination with other placental hormones, leptin, tumor necrosis factor alpha, and resistin are involved in the decrease in insulin sensitivity occurring during pregnancy, with tumor necrosis factor alpha named as the strongest independent predictor of insulin sensitivity in pregnancy. An inverse correlation with the changes in insulin sensitivity from the time before conception through late gestation accounts for about half of the variance in the decrease in insulin sensitivity during gestation: in other words, low levels or alteration of TNF alpha factors correspond with a greater chance of, or predisposition to, insulin resistance or sensitivity. It is unclear why some women are unable to balance insulin needs and develop GDM; however, several explanations have been given, similar to those in type 2 diabetes: autoimmunity, single gene mutations, obesity, along with other mechanisms. Though the clinical presentation of gestational diabetes is well characterized, the biochemical mechanism behind the disease is not well known. One proposed biochemical mechanism involves insulin-producing β-cell adaptation controlled by the HGF/c-MET signaling pathway. β-cell adaptation refers to the change that pancreatic islet cells undergo during pregnancy in response to maternal hormones to compensate for the increased physiological needs of the mother and baby. These changes in the β-cells cause increased insulin secretion due to increased β-cell proliferation.
Tertiary structure — domains The tertiary structure is formed by two domains known as the large and the small, which are separated by a cleft centred around the location of the bond with ATP-ADP+Pi. Below this there is a deeper notch called a "groove". In the native state, despite their names, both have a comparable depth. The normal convention in topological studies means that a protein is shown with the biggest domain on the left-hand side and the smallest domain on the right-hand side. In this position the smaller domain is in turn divided into two: subdomain I (lower position, residues 1–32, 70–144, and 338–374) and subdomain II (upper position, residues 33–69). The larger domain is also divided in two: subdomain III (lower, residues 145–180 and 270–337) and subdomain IV (higher, residues 181–269). The exposed areas of subdomains I and III are referred to as the "barbed" ends, while the exposed areas of domains II and IV are termed the "pointed" ends. This nomenclature refers to the fact that, due to the small mass of subdomain II actin is polar; the importance of this will be discussed below in the discussion on assembly dynamics. Some authors call the subdomains Ia, Ib, IIa, and IIb, respectively.
== Origin == The term was coined by Joseph Marius DallaValle in his book Micromeritics: The Technology of Fine Particles (1948). It was derived from the Greek words Greek: μικρο, romanized: micro meaning "small" and Greek: μέρος, romanized: méros meaning "part". The size range which he covered in the book was from 100 nm to 100 mm. Anything smaller than this but bigger than a molecule was referred to at the time as a colloid but is now often referred to as a nanoparticle. Applications included soil physics, mineral physics, chemical engineering, geology, and hydrology. Characteristics discussed included particle size and shape, packing, electrical, optical, chemical and surface science.
Sources: en.wikipedia.org
RNAi Atlas: a database of RNAi libraries and their target analysis results miRSearch Archived 2012-12-04 at the Wayback Machine: Tool for finding microRNAs that target mRNA How mRNA is coded?: YouTube video What is mRNA?: theconversation.com
A chest radiograph, chest X-ray (CXR), or chest film is a projection radiograph of the chest used to diagnose conditions affecting the chest, its contents, and nearby structures. Chest radiographs are the most common film taken in medicine. Like all methods of radiography, chest radiography employs ionizing radiation in the form of X-rays to generate images of the chest. The mean radiation dose to an adult from a chest radiograph is around 0.02 mSv (2 mrem) for a front view (PA, or posteroanterior) and 0.08 mSv (8 mrem) for a side view (LL, or latero-lateral). Together, this corresponds to a background radiation equivalent time of about 10 days.
The unsanitary conditions engendered by the war, severe overcrowding in barracks, wartime propaganda interfering with public health warnings, and migration of so many soldiers around the world helped the outbreak become a pandemic. Ultimately, World War I created a decisive break with the old world order that had emerged after the Napoleonic Wars, which was modified by the mid-19th century's nationalistic revolutions. The results of World War I would be important factors in the development of World War II approximately 20 years later.
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. Melanotan-2 is manufactured synthetically. The naturally occurring peptide in the same family is alpha-melanocyte-stimulating hormone, which the body produces as part of normal endocrine and neural signalling.