Everything below concerns alpha-MSH analog. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-01-31. Where a claim depends on a specific study, the study is described rather than over-claimed.
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, 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.
| 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 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.
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.
Modern kefir is made by adding kefir grains to milk typically at a proportion of 2–5% grains-to-milk. The mixture is then placed in a corrosion-resistant container, such as a glass jar, and stored preferably in the dark to prevent degradation of light-sensitive vitamins. After a period between 12 and 24 hours of fermentation at mild temperature, ideally 20–25 °C (68–77 °F), the grains are strained from the milk using a corrosion-resistant (stainless steel or plastic) utensil and kept to produce another batch. During the fermentation process the grains enlarge and eventually split forming new units. The resulting fermented liquid may be drunk, used in recipes, or kept aside in a sealed container for additional time to undergo a secondary fermentation. Because of its acidity the beverage should not be stored in reactive metal containers such as aluminium, copper, or zinc, as these may leach into it over time. The shelf life, unrefrigerated, is up to thirty days. The Russian method permits production of kefir on a larger scale and uses two fermentations. The first step is to prepare the cultures by inoculating milk with 2–3% grains as described. The grains are then removed by filtration and 1–3% of the resulting liquid mother culture is added to milk and fermented for 12 to 18 hours. Kefir can be made using freeze-dried cultures commonly available in powder form from health food stores. A portion of the resulting kefir can be saved to be used a number of times to propagate further fermentations but ultimately does not form grains.
The famous "Tajiri-go" bull was born from the "Atsuta tsuru," which is a descendant of the Shusuke tsuru. According to a survey conducted by the Japan Wagyu Registry Association, the pedigree was traced from a database of 718,969 Japanese black cattle mothers registered in Japan, and it was found that 718,330 or 99.9% of them are descended from the Tajiri-go. On the other hand, there are those who are concerned about the current situation in which only the Tajima cattle line represented by the Tajiri-go is spreading and genetic diversity is being lost from Wagyu, and the movement to revive the Takenotani tsuru has been attracting attention in recent years. In 1859, Japan opened the port of Yokohama in accordance with the demands of Western nations. At the same time, a foreign settlement was established in Yokohama. Foreign residents sought cattle for meat from neighboring villages but were refused, so cattle were imported from the U.S., China, and Korea, which gradually became unable to meet the demand. In 1865, before the Port of Kobe was opened, the Hyogo Port Opening Demand Incident occurred, in which nine warships from Britain, France, the Netherlands, and the United States invaded Hyogo Port demanding its opening. At that time, sailors negotiated with local cattle merchants for cattle, which were initially slaughtered on board, but as demand increased, it became necessary to slaughter them on land. 1866 saw the first slaughter of cattle by foreigners in the pine forests of Cape Wadamisaki.
=== Books === Predictably Irrational: The Hidden Forces That Shape Our Decisions (2008; second edition in 2012). HarperCollins. ISBN 9780061353239 The Upside of Irrationality (2010). HarperCollins. ISBN 9780062008565 The Honest Truth about Dishonesty: How We Lie to Everyone – Especially Ourselves (2012; second edition in 2013). HarperCollins. ISBN 9780062298553 Behavioral Economics Saved My Dog: Life Advice for the Imperfect Human (2015). Oneworld. ISBN 9781780748177 Irrationally Yours: On Missing Socks, Pick-up Lines, and Other Existential Puzzles (2015). HarperCollins. ISBN 9780062380012 Payoff: The Hidden Logic That Shapes Our Motivations (2016). Simon & Schuster / TED. ISBN 9781501120053 Dollars and Sense: How We Misthink Money and How to Spend Smarter (2017). Co-authored with Jeff Kreisler. HarperCollins. ISBN 9780062651228 Small Change: Money Mishaps and How to Avoid Them (2018). Co-authored with Jeff Kreisler. Pan Macmillan. ISBN 9781509889167 Amazing Decisions: The Illustrated Guide to Improving Business Deals and Family Meals (2019, illustrated by Matt R. Trower), Farrar, Straus and Giroux.ISBN 9781466899544 Misbelief: What Makes Rational People Believe Irrational Things (2023), Bonnier Books UK. ISBN 9781785120787 Professor D Takes Control (2026). Charlesbridge. ISBN 978-1-62354-792-9
Sources: en.wikipedia.org
Mimosa tenuiflora is an entheogen used by the Jurema Cult (O Culto da Jurema) in northeastern Brazil. Dried Mexican Mimosa tenuiflora root bark has been shown to have a dimethyltryptamine (DMT) content of about 1-1.7%. The stem bark has about 0.03% DMT. The parts of the tree are traditionally used in northeastern Brazil in a psychoactive decoction also called Jurema or Yurema. Analogously, the traditional Western Amazonian sacrament Ayahuasca is brewed from indigenous ayahuasca vines. However, to date no β-carbolines such as harmala alkaloids have been detected in Mimosa tenuiflora decoctions, yet the Jurema is used in combination with several plants. This presents challenges to the pharmacological understanding of how DMT from the plant is rendered orally active as an entheogen, because the psychoactivity of ingested DMT requires the presence of a monoamine oxidase inhibitor (MAOI), such as a β-carboline. If an MAOI is neither present in the plant nor added to the mixture, the enzyme monoamine oxidase (MAO) will metabolize DMT in the human gut, preventing the active molecule from entering the blood and brain. The plant is also used in clandestine manufacture of crystalline dimethyltryptamine (DMT). In this form, it is psychoactive by itself when vaporized and inhaled. The isolation of the chemical compound yuremamine from Mimosa tenuiflora as reported in 2005 represents a new class of phytoindoles, which may explain an apparent oral activity of DMT in Jurema.
In the widely used Couinaud system, the functional lobes are further divided into a total of eight subsegments based on a transverse plane through the bifurcation of the main portal vein. The caudate lobe is a separate structure that receives blood flow from both the right- and left-sided vascular branches. The Couinaud classification divides the liver into eight functionally independent liver segments. Each segment has its own vascular inflow, outflow and biliary drainage. In the centre of each segment are branches of the portal vein, hepatic artery, and bile duct. In the periphery of each segment is vascular outflow through the hepatic veins. The classification system uses the vascular supply in the liver to separate the functional units (numbered I to VIII) with unit 1, the caudate lobe, receiving its supply from both the right and the left branches of the portal vein. It contains one or more hepatic veins which drain directly into the inferior vena cava. The remainder of the units (II to VIII) are numbered in a clockwise fashion:
molal concentration Also molality. A measure of the concentration of a solute in a solution in terms of the amount of solute per unit mass of solvent. Molality is typically expressed in units of moles per kilogram (mol/kg); a solution with a concentration of exactly 1 mol/kg is sometimes said to be 1 molal. Contrast molarity.
Sources: en.wikipedia.org
== Mechanism == CD8+ T cells play a key role in killing Plasmodium developing in the liver. Mice or monkeys which received monoclonal antibody to the CD8 lost protection by this type of vaccine. Once the antibody application was stopped, the protection was returned. Plasmodium is injected by infected mosquito into the bloodstream of the host in the form of sporozoites, which travel to the liver and invade liver cells, where sporozoites divide and produce tens of thousands merozoites per one cell. RTS,S is prepared to stop malaria in the phase after the injection. The PfSPZ vaccine is made of attenuated sporozites, which are active and travel to liver cells, where CD8+ T cells producing IFNγ are activated. Frequencies of PfSPZ-specific CD3+CD4+, CD3+CD8+, CD3+γδ T cells are dose-dependent. PfSPZ-specific CD3+CD8+ T cells were found in 7 of 12 protected subjects in a human volunteer trial. These cells are required for protection in most individuals and are primarily situated in the liver because of the persistence of parasite antigens and retained as tissue memory cells.
DiCaprio rejected a role in Boogie Nights (1997) to star opposite Kate Winslet in James Cameron's Titanic as members of different social classes who fall in love aboard RMS Titanic. DiCaprio had doubts, but was encouraged by Cameron to pursue the part. With a production budget of more than $200 million, Titanic was the most expensive in history at the time. It became the highest-grossing film at the time, earning more than $2.1 billion in box-office receipts worldwide. It won 11 Academy Awards—the most wins for any film—including Best Picture; DiCaprio's failure to gain a nomination led to a protest against the Academy of Motion Picture Arts and Sciences by more than 200 fans. He was nominated for other high-profile awards, including a Golden Globe Award for Best Actor.
Although previous studies proposed that Komodo dragon saliva contains a variety of highly septic bacteria that would help to bring down prey, research in 2013 suggested that the bacteria in the mouths of Komodo dragons are ordinary and similar to those found in other carnivores. Komodo dragons have good mouth hygiene. To quote Bryan Fry: "After they are done feeding, they will spend 10 to 15 minutes lip-licking and rubbing their head in the leaves to clean their mouth ... Unlike people have been led to believe, they do not have chunks of rotting flesh from their meals on their teeth, cultivating bacteria." They do have a slashing bite, which normally includes a dose of their neurotoxic venom and anticoagulant saliva. Komodo dragons do not wait for prey to die and track it at a distance, as vipers do; observations of them hunting deer, boar and in some cases buffalo reveal that they kill prey in less than half an hour during successful hunts, and usually in a matter of a few minutes, similar to large mammalian carnivores. The observation of prey dying of sepsis is instead likely based on misinterpretations of failed predation attempts caused by the natural instinct of water buffalo, which are not native to the islands where the Komodo dragon lives, to run into water after escaping an attack. The warm, faeces-filled water would then cause the infections. The study used samples from 16 captive dragons (10 adults and six neonates) from three US zoos.
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.
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.