Everything below concerns MC1R. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-05-06. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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-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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic cyclic heptapeptide | Belongs to the melanocortin agonist family |
| Key substitutions | Nle4 and D-Phe7 | Improve resistance to enzymatic degradation |
| Molecular formula | C50H69N15O9 | Approximately 1024 g/mol |
| Regulatory status | Not approved as a medicine | Distributed as a research chemical |
| Common synonyms | Melanotan II, MT-II, MT-2 | Spelling varies across sources |
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.
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.
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.
The modifications covered in this diagram have to do with carbon skeleton modifications of the original fentanyl molecular structure. These are organized into methyl acetate additions, which are most known for the fentanyl -> carfentanil conversion. Many analogues of great potency, such as ohmfentanyl and lofentanyl possess methyl acetate groups added to the 4-carbon (of the piperidine ring, in the para- position relative to the annular nitrogen). The methyl acetate is added here from the α-carbon of the acetate moiety as it is with ohm- and lofentanyl. The 4-carbon is not a chiral center in carfetnanil because of a lack of piperidinyl substituents, but this same carbon is a chiral center in both ohm- and lofentanyl because both of those analogues have piperidinyl substituents. The second group are organized into methyl additions, which are known for the fentanyl analogues such as α-methylfentanyl and cis-3-methylfentanyl. These analogues can possess a wide variety of modified pharmacological properties, including increased and decreased potency (receptor binding efficiency), increased or decreased half-life (metabolic binding efficiency) or other side effects on human physiology. Other substituents such as hydroxy, chloro, fluoro, and a wide variety of alkyl groups, are also substituted in place of these methylations to produce psychoactive analogues of fentanyl, but because they often use the same skeletal naming conventions as the simple methyl analogues, we did not reproduce them all in the image here.
flagellum (pl.) flagella A long, thin, hair-like appendage protruding from the surface of some cells, which serves locomotory functions by undulating in a way that propels the cell through its environment or by effecting the movement of extracellular fluids and solutes past the cell surface. Many unicellular organisms, including some bacteria, protozoa, and algae, bear one or more flagella, and certain cell types in multicellular organisms, namely sperm cells, also have flagella. Eukaryotic flagella are essentially just longer versions of cilia, often up to 150 micrometres (μm) in length, while bacterial flagella are typically smaller and completely different in structure and mechanism of action.
This group, named after the Ivuna meteorite (Tanzania), have chemical compositions that are close to that measured in the solar photosphere (aside from gaseous elements, and elements such as lithium which are underrepresented in the Sun's photosphere by comparison to their abundance in CI chondrites). In this sense, they are chemically the most primitive known meteorites. CI chondrites typically contain a high proportion of water (up to 22%), and organic matter in the form of amino acids and PAHs. Aqueous alteration promotes a composition of hydrous phyllosilicates, magnetite, and olivine crystals occurring in a black matrix, and a possible lack of chondrules. It is thought they have not been heated above 50 °C (122 °F), indicating that they condensed in the cooler outer portion of the solar nebula. Five CI chondrites have been observed to fall: Ivuna, Orgueil, Alais, Tonk, and Revelstoke. Four others have been found by Japanese field parties in Antarctica. In general, the extreme fragility of CI chondrites causes them to be highly susceptible to terrestrial weathering, and they do not survive on Earth's surface for long after they fall.
Sources: en.wikipedia.org
== Portrayal in the media == Woodroof’s life was the basis of the 2013 film Dallas Buyers Club. He was portrayed in the film by Matthew McConaughey, who won an Academy Award for Best Actor for his performance as Woodroof.
=== Dosing === Although doxycycline is approved to treat Lyme disease, the optimal dosing and duration of treatment for this condition is a topic of ongoing research. it can be used in adults and children. For treatment or prophylaxis of Lyme disease in children, it can be used for a duration of up to 21 days in children of any age. Doxycycline is specifically indicated to treat Lyme disease for patients presenting with erythema migrans. As for the optimal duration of treatment of this disease, guidelines vary, with some recommending a 10-day course of doxycycline, while others suggest a 14-day course; still, recent data suggest that even a 7-day course of doxycycline can be effective. Compared to other drugs, there are no significant differences in treatment response across antibiotic agents, doses, or durations when comparing 14 days versus 21 days; as such, the optimal duration of treatment of Lyme disease remains uncertain, as prolonged antibiotic courses have drawbacks, including diminishing returns in terms of patient outcomes, heightened risks of adverse events, superinfections, increased healthcare costs, and the potential for development of antibiotic resistance. Therefore, the consensus remains to treat patients with the shortest effective duration of antibiotics, as is the case with doxycycline for Lyme disease as well.
Prolactin also self-regulates through a counter-current flow in the hypophyseal pituitary portal system, which triggers the release of hypothalamic dopamine. This process also inhibits the pulsatile secretion of gonadotropin-releasing hormone (GnRH), thereby negatively influencing the secretion of pituitary hormones that regulate gonadal function. Estrogen promotes the growth of pituitary lactotroph cells, particularly during pregnancy. However, lactation is hindered by the elevated levels of estrogen and progesterone during this period. The rapid decline in estrogen and progesterone after childbirth enables lactation to begin. While breastfeeding, prolactin suppresses gonadotropin secretion, potentially delaying ovulation. Ovulation may resume before the return of menstruation during this time. Although hyperprolactinemia can result from normal physiological changes during pregnancy and breastfeeding, it can also be caused by other etiologies. For example, high prolactin levels could result from diseases affecting the hypothalamus and pituitary gland. Other organs, such as the liver and kidneys, could affect prolactin clearance and consequently, prolactin levels in the serum. The disruption of prolactin regulation could also be attributed to external sources such as medications. In the general population, the prevalence of hyperprolactinemia is 0.4%. The prevalence increases to as high as 17% in women with reproductive diseases, such as polyendocrine metabolic ovarian syndrome.
Sources: en.wikipedia.org
== Side effects == Cyclofenil is associated with a relatively high incidence of hepatotoxicity. Biochemical signs of undesirable liver changes have been observed in 35% or more of individuals and 1% of individuals experience overt hepatitis.
An aldehyde tag is a short peptide tag that can be further modified to add fluorophores, glycans, PEG (polyethylene glycol) chains, or reactive groups for further synthesis. A short, genetically-encoded peptide with a consensus sequence LCxPxR is introduced into fusion proteins, and by subsequent treatment with the formylglycine-generating enzyme (FGE), the cysteine of the tag is converted to a reactive aldehyde group. This electrophilic group can be targeted by an array of aldehyde-specific reagents, such as aminooxy- or hydrazide-functionalized compounds.
The amplitude of SHOC2-mediated ERK1/2 signals has been proposed to be regulated by differential regulation of RAF activation at the plasma membrane and internalized endosome compartment as well an alternative model proposing post-translational modifications. SHOC2 ubiquitination mediated by HUWE1 is triggered by growth factor activation of the ERK1/2 pathway and is a prerequisite for the subsequent ubiquitination of the RAF-1 kinase associated with SHOC2. However, the current data has yet to address how these ubiquitin modifications regulate the SHOC2 holophosphatase function to reduce the amplitude of RAF-ERK1/2 signals. It has been shown that activity that results in lipidation (specifically Myristoylation) of SHOC2 can cause Noonan syndrome. SHOC2 has been shown to interact with the catalytic phosphatase subunit PP1C and MRAS as well as canonical RAS isoforms (H/K/NRAS). The ternary complex SHOC2-RAS-PP1C functions to dephosphorylate an inhibitory phosphorylation site ('S259') on RAF family proteins to enable MAPK signaling.
Sources: en.wikipedia.org
It is a synthetic cyclic peptide designed as an analog of alpha-melanocyte-stimulating hormone. It acts on melanocortin receptors and is best known from research into pigmentation. It is not an approved pharmaceutical product.
No regulatory agency has approved it for any indication. It is encountered as a research chemical sold outside pharmaceutical supply chains. Products marketed this way are not subject to the manufacturing and labeling requirements that apply to approved drugs.
Reports describe increased skin pigmentation as well as side effects such as nausea, flushing, and changes to existing moles. Much of the evidence comes from small studies and case reports rather than large trials. The long-term safety profile is therefore uncertain.
It is a synthetic seven-amino-acid peptide modeled on alpha-melanocyte-stimulating hormone. It carries two non-natural substitutions and a cyclic bridge that increase its stability relative to the natural hormone. It circulates as a research chemical and is not an approved medicine.