alpha-MSH comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Updated 2025-11-23. Numbers and descriptions here follow the published literature rather than marketing material.
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, 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.
| 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 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.
Research interest has centred on photoprotection and pigmentation, with a smaller body of work on appetite and sexual function. Published human data remain limited to small, frequently uncontrolled studies, and the compound has never received marketing approval from a national medicines regulator. Most laboratory work treats it as a pharmacological tool for probing melanocortin signalling in cell culture or animal models. Whether pigmentation changes observed in people translate into measurable protection against ultraviolet-induced DNA damage remains an open question.
Melanotan II is a synthetic peptide analog modeled on alpha-melanocyte-stimulating hormone, a naturally occurring signaling peptide involved in pigmentation. Its structure is a cyclic heptapeptide containing two non-natural substitutions, norleucine at position four and D-phenylalanine at position seven. These modifications resist enzymatic breakdown and extend the molecule's activity relative to the native hormone. The compound binds melanocortin receptors and is studied mainly as a pharmacological tool rather than a therapeutic product. It has never received approval as a medicine in any major jurisdiction.
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.
In November 2007, Merck agreed to pay $4.85 billion to settle most of the pending Vioxx lawsuits. The settlement required that claimants provide medical and pharmacy records confirming the occurrence of a heart attack, ischemic stroke, or sudden cardiac death; the receipt of at least 30 Vioxx pills within 60 days prior to the injury or death; and confirmation of Vioxx being used within 14 days of the Vioxx-related event. The settlement was generally viewed by industry analysts and investors as a victory for Merck, considering that original estimates of Merck's liability reached between $10 billion and $25 billion. As of mid-2008, when the plaintiff class had reached the threshold percentage required by Merck to go through with the settlement, plaintiffs had prevailed in only three of the twenty cases that had reached juries, all with relatively small awards. Merck has refused to consider compensation for Vioxx victims and their families outside the US. This is particularly true in the UK where there are at least 400 victims and the legal protection afforded to the victims and their families is particularly weak. According to internal e-mail traffic released at a later lawsuit, Merck had a list of doctors critical of Vioxx to be "neutralized" or "discredited". "We may need to seek them out and destroy them where they live," wrote an employee. A Stanford Medical School professor said that Merck was engaged in intimidation of researchers and infringement upon academic freedom.
=== Estrogens === The estrogen diethylstilbestrol (DES) is occasionally used to treat prostate cancer through suppression of testosterone production. It was previously used in the treatment of breast cancer, but has been replaced by more effective and less toxic agents. Estrace is an estrogen which was also formerly used for antiandrogen therapy of prostate cancer. Polyestradiol phosphate is a long-acting derivative of estradiol that is applied as an intramuscular injection.
=== Full table === The nuclide table below shows nuclides (often loosely called "isotopes", but this term properly refers to nuclides with the same atomic number, see above), including all with half-life of at least one day. They are arranged with increasing atomic numbers from left to right and increasing neutron numbers from top to bottom. Cell color denotes the half-life of each nuclide; if a border is present, its color indicates the half-life of the most stable nuclear isomer. In graphical browsers, each nuclide also has a tool tip indicating its half-life. Each color represents a certain range of length of half-life, and the color of the border indicates the half-life of its nuclear isomer state. Some nuclides have multiple nuclear isomers, and this table notes the one with the longest half-life. Dotted borders mean that a nuclide has a nuclear isomer with a half-life in the same range as the ground state nuclide. The dashed lines between several nuclides of the first few elements are the experimentally determined proton and neutron drip lines.
Sources: en.wikipedia.org
== See also == Bisbee Blue – Turquoise from copper mines near Bisbee, Arizona, with a deep blue color Lapis lazuli – Metamorphic rock containing lazurite, prized for its intense blue color, with a deep blue color Lazurite – Alumino-silicate mineral whose blue colour is due to a sulfide species and not copper, with a deep blue color List of minerals Variscite – Hydrated aluminium phosphate of pale green color due to trivalent chromium (Cr3+)
Leukotriene C4 (LTC4) is a leukotriene. LTC4 has been extensively studied in the context of allergy and asthma. In cells of myeloid origin such as mast cells, its biosynthesis is orchestrated by translocation to the nuclear envelope along with co-localization of cytosolic phospholipase A2 (cPLA2), arachidonate 5-lipoxygenase (5-LO), 5-lipoxygenase-activating protein (FLAP) and LTC4 synthase (LTC4S), which couples glutathione to an LTA4 intermediate. The MRP1 transporter then secretes cytosolic LTC4 and cell surface proteases further metabolize it by sequential cleavage of the γ-glutamyl and glycine residues off its glutathione segment, generating the more stable products LTD4 and LTE4. All three leukotrienes then bind at different affinities to two G-protein coupled receptors: CYSLTR1 and CYSLTR2, triggering pulmonary vasoconstriction and bronchoconstriction. In cells of non-haematopoietic lineage, endoplasmic reticulum (ER) stress and chemotherapy induce LTC4 biosynthesis by transcriptionally upregulating and activating the enzyme microsomal glutathione-S-transferase 2 (MGST2). ER stress and chemotherapy also trigger nuclear translocation of the two LTC4 receptors. Acting in an intracrine manner, LTC4 then elicits nuclear translocation of NADPH oxidase 4 (NOX4), ROS accumulation and oxidative DNA damage. Besides being a potent lipid mediator in asthma and inflammation, LTC4 was reported to be involved in several other diseases, such as allergic airway diseases, dermatological diseases, cardiovascular diseases, liver injury, atherosclerosis and colon cancer.
ω (omega) is the angle in the chain Cα − C' − N − Cα, φ (phi) is the angle in the chain C' − N − Cα − C' ψ (psi) is the angle in the chain N − Cα − C' − N (called φ′ by Ramachandran) The figure at right illustrates the location of each of these angles (but it does not show correctly the way they are defined). The planarity of the peptide bond usually restricts ω to be 180° (the typical trans case) or 0° (the rare cis case). The distance between the Cα atoms in the trans and cis isomers is approximately 3.8 and 2.9 Å, respectively. The vast majority of the peptide bonds in proteins are trans, though the peptide bond to the nitrogen of proline has an increased prevalence of cis compared to other amino-acid pairs. The side chain dihedral angles are designated with χn (chi-n). They tend to cluster near 180°, 60°, and −60°, which are called the trans, gauche−, and gauche+ conformations. The stability of certain sidechain dihedral angles is affected by the values φ and ψ. For instance, there are direct steric interactions between the Cγ of the side chain in the gauche+ rotamer and the backbone nitrogen of the next residue when ψ is near −60°. This is evident from statistical distributions in backbone-dependent rotamer libraries.
Sources: en.wikipedia.org
=== Subdivision === Traditionally Rhodiola was divided into subgenera, sections and series, based on plant characteristics. Four subgenera were recognised; Rhodiola, Primuloides, Crassipedes and Clementsia. However molecular studies have failed to demonstrate monophyly of these subtaxa.
== External links == NAS Report: The Health Effects of Perchlorate Ingestion NRDC's criticism of NAS report Environment California report Archived 2010-06-09 at the Wayback Machine (Executive Summary with link to full text) Macho Moms: Perchlorate pollutant masculinizes fish: Science News Online, August 12, 2006 Archived February 20, 2008, at the Wayback Machine New Scientist Space Blog: Phoenix discovery may be bad for Mars life State Threatening to Sue Military over Water Pollution Archived 2005-11-09 at the Wayback Machine, Associated Press, May 19, 2003. Health Effects of Perchlorate from Spent Rocket, SpaceDaily.com, July 11, 2002. Dept of Defense, Dept of Energy, and US Environmental Protection Agency's Strategic Environmental Research and Development Program, Elimination of Perchlorate Oxidizers from Pyrotechnic Flare Compositions, 2009 Archived 2007-08-06 at the Wayback Machine
== Clinical significance == AST is similar to alanine transaminase (ALT) in that both enzymes are associated with liver parenchymal cells. The difference is that ALT is found predominantly in the liver, with clinically negligible quantities found in the kidneys, heart, and skeletal muscle, while AST is found in the liver, heart (cardiac muscle), skeletal muscle, kidneys, brain, and red blood cells. As a result, ALT is a more specific indicator of liver inflammation than AST, as AST may be elevated also in diseases affecting other organs, such as myocardial infarction, acute pancreatitis, acute hemolytic anemia, severe burns, acute renal disease, musculoskeletal diseases, and trauma. The elevated AST level in hemorrhagic fever caused by crimean-congo hemorrhagic fever virus is associated with high mortality rate. AST was defined as a biochemical marker for the diagnosis of acute myocardial infarction in 1954. However, the use of AST for such a diagnosis is now redundant and has been superseded by the cardiac troponins. Laboratory tests should always be interpreted using the reference range from the laboratory that performed the test. Example reference ranges are shown below:
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. It is a laboratory-made peptide, while the natural hormone is alpha-melanocyte-stimulating hormone, a longer peptide produced by the pituitary gland and by skin cells. Melanotan-2 mimics only a short active region of that hormone and contains non-natural residues such as D-phenylalanine.