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 2026-05-28 and is reviewed periodically as new material appears.
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.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Compound class | Synthetic cyclic heptapeptide | Alpha-MSH analogue containing a D-phenylalanine residue |
| Molecular formula | C50H69N15O9 | Average molecular mass approximately 1024.2 g/mol |
| Appearance | White to off-white lyophilised powder | Normally supplied as a freeze-dried solid in a sealed vial |
| Solubility | Freely soluble in water and polar solvents | Dissolves readily in aqueous buffers and in alcohol-water mixtures |
| Receptor targets | MC1R, MC3R, MC4R, MC5R | Acts as a non-selective melanocortin receptor agonist |
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.
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.
=== Growth Factors === Bioconjugation of TGF-β to iron oxide nanoparticles and its activation through magnetic hyperthermia in-vitro has been reported. This was done by using 1-(3-dimethylaminopropyl)ethylcarbodiimide combined with N-Hydroxysuccinimide to form primary amide bonds with the free primary amines on the growth factor. Carbon nanotubes have been successfully used in conjunction with bioconjugation to link TGF-β followed by an activation with near-infrared light. Typically, these reactions have involved the use of a crosslinker, but some of these add molecular space between the compound of interest and base material and in turn causes higher degrees of non-specific binding and unwanted reactivity.
is a surface integral. (Note that the concept that is here called "flux" is alternatively termed flux density in some literature, in which context "flux" denotes the surface integral of flux density. See the main article on Flux for details.)
=== History === The team first competed in the Victorian Junior Football League (later the AFL reserves) when the competition was established in 1919, and was known as Essendon Juniors until the end of 1922. The team enjoyed success in the form of eight premierships, including in the last year of the reserves competition in 1999. From 2000 until 2002, the club's reserves team competed in the Victorian Football League. At the end of 2002, the club dissolved its reserves team and established a reserves affiliation with the Bendigo Football Club in the VFL. The affiliation ran for ten years from 2003 until 2012, allowing reserves players from the Essendon list to play with Bendigo. For all but the final year of the affiliation, Bendigo was known as the Bendigo Bombers. The club re-established its reserves team in 2013, seeking greater developmental autonomy. The team plays its home games at Windy Hill. The team is made up of senior-listed AFL players and VFL-contracted players.
=== Depression === The evidence overall supports the effectiveness of bupropion over placebo for the treatment of depression. Evidence-based guidelines consistently recommend bupropion as a treatment option for adults with major depressive disorder; some support first-line use for major depressive disorder, but there is limited guidance for treatment-resistant depression. Some peer-reviewed studies suggest the quality of evidence is low. Some meta-analyses report that bupropion has an at-most small effect size for depression. Evidence suggests that the effectiveness of bupropion for depression is similar to that of other antidepressants. Over the autumn and winter months, bupropion can prevent the development of depression in those who have recurring seasonal affective disorder: 15% of participants on bupropion experienced a major depressive episode vs. 27% of those on placebo. Bupropion also improves depression in bipolar disorder, however the risk of an affective switch is similar to other antidepressants. Bupropion has several features that distinguish it from other antidepressants: for instance, unlike the majority of antidepressants, it does not usually cause sexual dysfunction, and the occurrence of sexual side effects is not different from placebo. Bupropion treatment is not associated with weight gain; on the contrary, the majority of studies observed significant weight loss in bupropion-treated participants. Bupropion treatment also is not associated with the sleepiness that may be produced by other antidepressants.
Sources: en.wikipedia.org
Mkhedrioni relied on illegal sources of income (targeting gasoline supplies) and exploited connections with Moscow's Georgian underworld. Mkhedrioni members were often accused of criminal activity, extorting "protection money" from businesses in areas which they effectively controlled, operating roadblocks where drivers would be "fined", smuggling drugs and committing robberies. By 1991, the Mkhedrioni was claimed to have had about 1,000 fighters and 10,000 associate members – considerably more than the official state National Guard. Despite Gamsakhurdia and Ioseliani sharing a broadly similar nationalist outlook, the two men fell out badly shortly after Gamsakhurdia came to power in November 1990. In February 1991, Ioseliani was imprisoned without trial, along with many of his supporters, and the Mkhedrioni was banned. In August 1991, just after the Soviet coup attempt, Gamsakhurdia sacked Tengiz Kitovani, the commander of Georgia's National Guard, and his Prime Minister Tengiz Sigua resigned around the same time. Kitovani soon formed an anti-Gamsakhurdia alliance with Sigua and the imprisoned Ioseliani. In December 1991, Kitovani's supporters released Ioseliani from jail and launched a violent coup d'état against the Gamsakhurdia government in alliance with the Mkhedrioni. Intense gun battles took place in the streets of Tbilisi between the rebels and "Zviadists" holed up in the state parliament building during December 1991 – January 1992, which ended with Gamsakhurdia fleeing to the breakaway Russian republic of Chechnya. At least 100 people were killed in the fighting.
== Family == Convulxin is part of the snake venom C-type lectin family, a group of hemorrhagic toxins that disrupt body homeostasis. The name describes their similarity in structure to C-type lectins from other animals, proteins that bind calcium to induce various signalling pathways. Proteins of about 130 amino acids in length, C-type lectins contain at least a carbohydrate recognition domain (CRD), which mediates sugar and calcium binding. They are involved in various biological activities, ranging from cell-cell adhesion, serum glycoprotein turnover, to immune responses and cell apoptosis.
In 2022, he rejoined his former departments at Harvard and the Dana–Farber Cancer Institute. Cantley is married to Vicki Sato, herself a prominent figure in the pharmaceutical industry and a professor at Harvard University in both the Business and Medical Schools.
Puberty is the process of physical changes through which a child's body matures into an adult body capable of sexual reproduction. It is initiated by hormonal signals from the brain to the gonads: the ovaries in a female, the testicles in a male. In response to the signals, the gonads produce hormones that stimulate libido and the growth, function, and transformation of the brain, bones, muscle, blood, skin, hair, breasts, and sex organs. Physical growth—height and weight—accelerates in the first half of puberty and is completed when an adult body has been developed. Before puberty, the external sex organs, known as primary sexual characteristics, are sex characteristics that distinguish males and females. Puberty leads to sexual dimorphism through the development of the secondary sex characteristics, which further distinguish the sexes. On average, females begin puberty at age 10½ and complete puberty at ages 15–17; males begin at ages 11½–12 and complete puberty at ages 16–17. The major landmark of puberty for females is menarche, the onset of menstruation, which occurs on average around age 12½. For males, first ejaculation, spermarche, occurs on average at age 13. In the 21st century, the average age at which children, especially females, reach specific markers of puberty is lower compared to the 19th century, when it was 15 for females and 17 for males (with age at first periods for females and voice-breaks for males being used as examples).
Colonial administration records (migrated archives): Malaya at The National Archives (Pg. 52) The UK Statute Law Database: Federation of Malaya Independence Act 1957 (c. 60) United Nations Treaty Collection: No.10760: Agreement relating to Malaysia FEDERATION OF MALAYA AGREEMENT OF 5 AUGUST 1957 Media related to Federation of Malaya at Wikimedia Commons
Sources: en.wikipedia.org
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.
No approved regulatory indication exists in major markets. An approval exists for a different peptide, afamelanotide, which is used for a rare photosensitivity disorder called erythropoietic protoporphyria. Melanotan-2 itself remains a research compound with no cleared clinical role.
Melanocortin-1 receptors on melanocytes are the receptor most closely linked to pigment production. The peptide is not selective, however, and also activates melanocortin-3, melanocortin-4, and melanocortin-5 receptors. That lack of selectivity is the usual explanation offered for both its range of observed effects and its off-target effects.
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.