Everything below concerns afamelanotide. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-08-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C50H69N15O9 | Cyclic heptapeptide, C-terminally amidated |
| Approximate molecular mass | 1024 Da | Monoisotopic mass of the free peptide |
| Appearance | White to off-white powder | Typically supplied as a lyophilised solid |
| Solubility class | Soluble in water and polar solvents | Also dissolves in neutral aqueous buffer |
| Common synonyms | Melanotan II, MT-II, MT-2 | Described as a melanocortin agonist in early literature |
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 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.
Acute myocardial infarction (heart attack) Heart failure (left ventricular systolic dysfunction) Kidney complications of diabetes mellitus (diabetic nephropathy) by means of decreasing the blood pressure and preventing glomerular hyperfiltration injury In treating high blood pressure, ACE inhibitors are a first-line initial drug choice. Age, frailty, and race can influence treatment choices and it is common to need more than one drug to obtain the desired improvement. All ACE inhibitors but enalapril, which can be given intravenously, are administered orally. Each one has different strengths with different starting dosages. Dosage should be adjusted according to the clinical response. Most ACE inhibitors can be dosed once daily with the exception of captopril. ACE inhibitors possess many common characteristics with another class of cardiovascular drugs, angiotensin II receptor antagonists, which are often used when patients are intolerant of the adverse effects produced by ACE inhibitors. ACE inhibitors do not completely prevent the formation of angiotensin II, as blockage is dose-dependent, so angiotensin II receptor antagonists may be useful because they act to prevent the action of angiotensin II at the AT1 receptor, leaving AT2 receptor unblocked; the latter may have consequences needing further study. There are fixed-dose combination drugs, such as ACE inhibitor and thiazide combinations. ACE inhibitors have also been used in chronic kidney failure and kidney involvement in systemic sclerosis (hardening of tissues, as scleroderma renal crisis).
Members of this family are found in birds, fish, reptiles and amphibians (mesotocin, isotocin, valitocin, glumitocin, aspargtocin, vasotocin, seritocin, asvatocin, phasvatocin), in worms (annetocin, nematocin), octopuses (cephalotocin, octopressin), insects (locupressin, inotocin) and in molluscs (conopressins G and S). Animals that lack a hormone from this family include fruit flies, and at least some mosquitos, silkworms, and honeybees.
Isopeptag is a 16-amino acid peptide tag (TDKDMTITFTNKKDAE) that can be genetically linked to proteins without interfering with protein folding. What makes the isopeptag different from other peptide tags is that it can bind its binding protein through a permanent and irreversible covalent bond. Other peptide tags generally bind their targets through weak non-covalent interactions, thus limiting their use in applications where molecules experience extreme forces. The isopeptag's covalent binding to its target overcomes these barriers and allows target proteins to be studied in harsher molecular environments.
Silver staining is the use of silver to stain histologic sections. This kind of staining is important in the demonstration of proteins (for example type III collagen) and DNA. It is used to show both substances inside and outside cells. Silver staining is also used in temperature gradient gel electrophoresis. Argentaffin cells reduce silver solution to metallic silver after formalin fixation. This method was discovered by Italian Camillo Golgi, by using a reaction between silver nitrate and potassium dichromate, thus precipitating silver chromate in some cells (see Golgi's method). Argyrophilic cells reduce silver solution to metallic silver after being exposed to the stain that contains a reductant. An example of this would be hydroquinone or formalin.
Homocysteine (symbol Hcy) is a non-proteinogenic α-amino acid. It is a homologue of the amino acid cysteine, differing by an additional methylene bridge (−CH2−). It is biosynthesized from methionine by the removal of its terminal Cε methyl group. Although the production of homocysteine is a normal part of the metabolism of methionine, an excess of homocysteine can be harmful. There are two primary ways for organisms such as humans to metabolize homocysteine: remethylation and transsulfuration. Remethylation adds a methyl group to the homocysteine molecule, converting homocysteine back into methionine. There are two known remethylation pathways. One pathway requires vitamin B9 (folate) and B12 (cobalamin), which drive the MTR (methionine synthase) and MTRR (methionine synthase reductase) enzymes. The other pathway uses TMG (trimethylglycine) to drive the BHMT (betaine-homocysteine methyltransferase) enzyme. Transsulfuration converts homocysteine to cystathionine. This pathway requires vitamin B6 to drive the CBS (cystathionine beta synthase) enzyme. Cystathionine is the immediate precursor of the amino acid cysteine, which (along with glutamate and glycine), is incorporated into the tripeptide glutathione, a major antioxidant in the human body. Homocysteine is therefore an important metabolic substrate. However, excessive levels of homocysteine can result in hyperhomocysteinemia, which is regarded as an indicator of cardiovascular disease risk. Homocysteine likely contributes to atherogenesis, which can result in ischemic injury.
Sources: en.wikipedia.org
== Sports == Maccabi Yavne is the city's major football club. During the 1980s the club played in the top division and in 1985 won the Toto Cup. Today they are in Liga Leumit. The basketball team, Elitzur Yavne, have also played in the Liga Leumit since 2007. Omri Casspi, the first Israeli to play in the National Basketball Association, grew up in the city and played for some of its teams.
Although many mechanisms have been proposed, no definite model accounts for the mechanisms of chronic arsenic poisoning. The prevailing events of toxicity and carcinogenicity might be quite tissue-specific. The current consensus on the mode of carcinogenesis is that it acts primarily as a tumor promoter. Its co-carcinogenicity has been demonstrated in several models. However, the finding of several studies that chronically arsenic-exposed Andean populations (as most extremely exposed to UV-light) do not develop skin cancer with chronic arsenic exposure, is puzzling.
Nylon 66 and related polyamides are condensation polymers forms from equal parts of diamine and dicarboxylic acids. In the first case, the "repeating unit" has the ABAB structure, as also seen in many polyesters and polyurethanes. Since each monomer in this copolymer has the same reactive group on both ends, the direction of the amide bond reverses between each monomer, unlike natural polyamide proteins, which have overall directionality: C terminal → N terminal. In the second case (so called AA), the repeating unit corresponds to the single monomer. Wallace Carothers at DuPont patented nylon 66. In the case of nylons that involve reaction of a diamine and a dicarboxylic acid, it is difficult to get the proportions exactly correct, and deviations can lead to chain termination at molecular weights less than a desirable 10,000 daltons. To overcome this problem, a crystalline, solid "nylon salt" can be formed at room temperature, using an exact 1:1 ratio of the acid and the base to neutralize each other. The salt is crystallized to purify it and obtain the desired precise stoichiometry. Heated to 285 °C (545 °F), the salt reacts to form nylon polymer with the production of water. Nylon 510, made from pentamethylene diamine and sebacic acid, was included in the Carothers patent to nylon 66 Nylon 610 is produced similarly using hexamethylene diamine. These materials are more expensive because of the relatively high cost of sebacic acid. Owing to the high hydrocarbon content, nylon 610 is more hydrophobic and finds applications suited for this property, such as bristles.
Erlich, "Enzymatic Amplification of β-globin Genomic Sequences and Restriction Site Analysis for Diagnosis of Sickle Cell Anemia"—the polymerase chain reaction invention (PCR)—was honored by a Citation for Chemical Breakthrough Award from the Division of History of Chemistry of the American Chemical Society in 2017. At the core of the PCR method is the use of a suitable DNA polymerase able to withstand the high temperatures of >90 °C (194 °F) required for separation of the two DNA strands in the DNA double helix after each replication cycle. The DNA polymerases initially employed for in vitro experiments presaging PCR were unable to withstand these high temperatures. So the early procedures for DNA replication were very inefficient and time-consuming, and required large amounts of DNA polymerase and continuous handling throughout the process. The discovery in 1976 of Taq polymerase—a DNA polymerase purified from the thermophilic bacterium, Thermus aquaticus in work co-authored by Alice Chien Chang—which naturally lives in hot (50 to 80 °C (122 to 176 °F)) environments such as hot springs—paved the way for dramatic improvements of the PCR method. The DNA polymerase isolated from T. aquaticus is stable at high temperatures remaining active even after DNA denaturation, thus obviating the need to add new DNA polymerase after each cycle. This allowed an automated thermocycler-based process for DNA amplification.
Sources: en.wikipedia.org
Government Medical College, Patiala was proposed in October 1951 by the Patiala and East Punjab States Union government, under the First Five-Year Plan. The first batch was started on 29 September 1953. The classes initially started from the old building of the Rajindra Hospital, which later shifted to the Archives Department, about 2 kilometers from its current location. With the construction of the new Rajindra Hospital in 1953 the old hospital building was made available to house some of the offices of the PEPSU state. Currently the Archives Department is housed in the Rajindra Hospital, which was built in 1877 and opened in January 1883. The nearby Dufferin Hospital started construction in November 1888 and opened in October 1890. The Rajindra Hospital is named after Maharaja Sir Rajinder Singh and it receives a notable mention in 1908 by The Imperial Gazetteer of India as the Rajindra Hospital. The hospital was known as Rajindra Hospital in pre-independence era, was sometimes mentioned as Rajendra Hospital, and currently uses the name Rajindra Hospital. With its attached 1009-bed Rajindra Hospital + 121-bed TB hospital is one of the largest health institutions in the region. The attached central clinical laboratory with facilities for hematology, pathology, microbiology, biochemistry is known as Bhupindra Clinical Laboratory.
=== Acidity === The C9–H sites of the fluorene ring are weakly acidic (pKa = 22.6 in DMSO). Deprotonation gives the stable fluorenyl anion, nominally C13H−9, which is aromatic and has an intense orange colour. The anion is a nucleophile. Electrophiles react with it by adding to the 9-position. The purification of fluorene exploits its acidity and the low solubility of its sodium derivative in hydrocarbon solvents. Both protons can be removed from C9. For example, 9,9-fluorenyldipotassium can be obtained by treating fluorene with potassium metal in boiling dioxane.
== Interactions == Buprenorphine's sedating/narcotic effect is increased by other sedating substances, such as other opioids, benzodiazepines, first-generation antihistamines, alcohol, and antipsychotics. Opioids and especially benzodiazepines also increase the risk of potentially lethal respiratory depression. Strong inhibitors of the liver enzyme CYP3A4, such as ketoconazole, moderately increase buprenorphine concentrations; CYP3A4 inducers can theoretically decrease concentrations of buprenorphine.
Certain drugs that have been introduced for uses other than analgesics are also used in pain management. Both first-generation (such as amitriptyline) and newer antidepressants (such as duloxetine) are used alongside NSAIDs and opioids for pain involving nerve damage and similar problems. Other agents directly potentiate the effects of analgesics, such as using hydroxyzine, promethazine, carisoprodol, or tripelennamine to increase the pain-killing ability of a given dose of opioid analgesic. Adjuvant analgesics, also called atypical analgesics, include orphenadrine, mexiletine, pregabalin, gabapentin, cyclobenzaprine, hyoscine (scopolamine), and other drugs possessing anticonvulsant, anticholinergic, and/or antispasmodic properties, as well as many other drugs with CNS actions. These drugs are used along with analgesics to modulate and/or modify the action of opioids when used against pain, especially of neuropathic origin. Dextromethorphan has been noted to slow the development of and reverse tolerance to opioids, as well as to exert additional analgesia by acting upon NMDA receptors, as does ketamine. Some analgesics such as methadone and ketobemidone and perhaps piritramide have intrinsic NMDA action. The anticonvulsant carbamazepine is used to treat neuropathic pain. Similarly, the gabapentinoids gabapentin and pregabalin are prescribed for neuropathic pain, and phenibut is available without prescription. Gabapentinoids work as α2δ-subunit blockers of voltage-gated calcium channels, and tend to have other mechanisms of action as well.
Action – Far Cry 3 Artistic Achievement – Journey Audio Achievement – Journey Best Game – Dishonored British Game – The Room Debut Game – The Unfinished Swan Family – Lego Batman 2: DC Super Heroes Game Design – Journey Game Innovation – The Unfinished Swan Mobile & Handheld – The Walking Dead Online – Browser – SongPop Online Multiplayer – Journey Original Music – Journey Performer – Danny Wallace (as the narrator, Thomas Was Alone) Sports/Fitness – New Star Soccer Story – The Walking Dead Strategy – XCOM: Enemy Unknown BAFTA Ones to Watch Award (in association with Dare to Be Digital) – Starcrossed Academy Fellowship – Gabe Newell
Sources: en.wikipedia.org
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.
Afamelanotide is the linear analogue [Nle4-D-Phe7]-alpha-MSH, sometimes called melanotan I, while melanotan II is cyclic and carries three further substitutions. The two are distinct molecules and are not interchangeable in analytical testing.
Binding to the four melanocortin receptor subtypes is well documented in vitro. The relative contribution of each subtype to whole-body effects in humans is far less certain.
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.