This is a working overview of cyclic heptapeptide, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-04-24. Anything still debated is marked as such rather than presented as settled.
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.
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.
| 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 |
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.
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.
=== General references === Daxer, Albert; Misof, Klaus; Grabner, Barbara; Ettl, Armin; Fratzl, Peter (1998). "Collagen fibrils in the human corneal stroma: Structure and aging". Investigative Ophthalmology & Visual Science. 39 (3): 644–8. PMID 9501878. Daxer, Albert; Fratzl, Peter (1997). "Collagen fibril orientation in the human corneal stroma and its implication in keratoconus". Investigative Ophthalmology & Visual Science. 38 (1): 121–9. PMID 9008637. Fratzl, Peter; Daxer, Albert (1993). "Structural transformation of collagen fibrils in corneal stroma during drying. An x-ray scattering study". Biophysical Journal. 64 (4): 1210–4. Bibcode:1993BpJ....64.1210F. doi:10.1016/S0006-3495(93)81487-5. PMC 1262438. PMID 8494978.
Preliminary 2021 calculations predicted that flerovium should have melting point −73 °C (lower than mercury at −39 °C and copernicium, predicted 10 ± 11 °C) and boiling point 107 °C, which would make it a liquid metal. Like mercury, radon, and copernicium, but not lead and oganesson (eka-radon), flerovium is calculated to have no electron affinity. A 2010 study published calculations predicting a hexagonal close-packed crystal structure for flerovium due to spin–orbit coupling effects, and a density of 9.928 g/cm3, though this was noted to be probably slightly too low. Newer calculations published in 2017 expected flerovium to crystallize in face-centred cubic crystal structure like its lighter congener lead, and calculations published in 2022 predicted a density of 11.4 ± 0.3 g/cm3, similar to lead (11.34 g/cm3). These calculations found that the face-centred cubic and hexagonal close-packed structures should have nearly the same energy, a phenomenon reminiscent of the noble gases. These calculations predict that hexagonal close-packed flerovium should be a semiconductor, with a band gap of 0.8 ± 0.3 eV. (Copernicium is also predicted to be a semiconductor.) These calculations predict that the cohesive energy of flerovium should be around −0.5 ± 0.1 eV; this is similar to that predicted for oganesson (−0.45 eV), larger than that predicted for copernicium (−0.38 eV), but smaller than that of mercury (−0.79 eV).
=== Ehrlichman interview === A former Nixon aide suggested that the war on drugs was racially and politically motivated.The Nixon campaign in 1968, and the Nixon White House after that, had two enemies: the antiwar left and black people. You understand what I'm saying? We knew we couldn't make it illegal to be either against the war or black, but by getting the public to associate the hippies with marijuana and blacks with heroin, and then criminalizing both heavily, we could disrupt those communities. We could arrest their leaders, raid their homes, break up their meetings, and vilify them night after night on the evening news. Did we know we were lying about the drugs? Of course we did. However, because he may have been disillusioned with the Nixon administration following the Watergate scandal, the validity of Ehrlichman's claim has been disputed.
== Second Ministry == On 22 February 2001, following the 2001 election, a ministry of 19 cabinet ministers and 5 parliamentary secretaries was sworn in. It served until the reconstitution of the Ministry on 12 February 2004 following the 2004 election.
=== Redox cycling === Many aromatic compounds are enzymatically reduced to form free radicals that contain one more electron than their parent compounds. In general, the electron donor is a flavoenzyme or one of its coenzymes. Once formed, these anion free radicals reduce molecular oxygen to superoxide and regenerate the unchanged parent compound. The net reaction is the oxidation of the flavoenzyme's coenzymes and the reduction of molecular oxygen to form superoxide. This catalytic behavior has been described as a futile cycle or redox cycling.
Sources: en.wikipedia.org
=== Substance use disorder === Uncontrolled and continuous use of a substance, drugs or alcohol, is known as substance use disorder. Substances can interfere with neuronal signaling and potentially disrupt the brain circuit. Addiction to these substances impairs thinking, behavior, and other biological functions. Intranasal delivery of insulin is associated with improvement in brain metabolic activities and alleviate impulsivity. Opioid addiction is prevalent and associated with many substance abuse deaths. A study observed high biodistribution in the brain and reduction in opioid overdose in rats administered with naloxone-loaded lipid nanoparticles.
He developed a method for chemical modification of the GLA residues in 1982 and studied it using various metal ims and prothrombin fragments binding to phospholipid surfaces. These studies were recognized in Hiskey's National Heart, Lung and Blood Institute's Merit Award for the period 1986 to 1996. The study was extended to include various models containing tris-phosphates and peptides containing several GLA residues. Hiskey's interest in peptide synthesis resulted in membership on the Organization Committee of the American Peptide Symposium from 1978 to 1983, as well as from 1988 to 1990, and co-chairman of the 1982 Gordon Research Conference on the Chemistry and Biology of Peptides. Hiskey also received and accepted an invitation to visit Japan as a Japan Society for the Promotion of Science Fellow as a result of his work on peptide synthesis. Finally, the American Peptide Society presented Hiskey with the Society's Annual Award in June 1996. In that same year, Hiskey retired from the University of North Carolina as Alumni Distinguished Professor Emeritus.
Traditional approaches in treating patients with DDD-resultant herniated discs oftentimes include discectomy—which, in essence, is a spine-related surgical procedure involving the removal of damaged intervertebral discs (either whole removal, or partially-based). The former of these two discectomy techniques involved in open discectomy is known as Subtotal Discectomy (SD; or, aggressive discectomy) and the latter, Limited Discectomy (LD; or, conservative discectomy). However, with either technique, the probability of post-operative reherniation exists and at a considerably high maximum of 21%, prompting patients to potentially undergo recurrent disk surgery. New treatments are emerging that are still in the beginning clinical trial phases. Glucosamine injections may offer pain relief for some without precluding the use of more aggressive treatment options. Adult stem cell or cell transplantation therapies for disc regeneration are in their infancy of development, but initial clinical trials have shown cell transplantation to be safe and initial observations suggest some beneficial effects for associated pain and disability. An optimal cell type, transplantation method, cell density, carrier, or patient indication remains to be determined. Investigation into mesenchymal stem cell therapy knife-less fusion of vertebrae in the United States began in 2006 and a DiscGenics nucleus pulposus progenitor cell transplantation clinical trial has started as of 2018 in the United States and Japan.
== Animal dentin == Elephant ivory is solid dentin. The structure of the dentinal tubules contributes to both its porosity and its elasticity. Elephant tusks are formed with a thin cap of enamel, which soon wears away, leaving the dentin exposed. Exposed dentin in humans causes the symptom of sensitive teeth. Dentin is best known for its occurrence in teeth, but in early vertebrates, it was an important part of the dermal skeleton that covered most of the body, and it persists today in a few taxa such as the coelacanth. Because dentin is less mineralized than enamel, it wears away more quickly than enamel. Some mammalian teeth exploit this phenomenon, especially herbivores such as horses, deer or elephants. In many herbivores, the occlusal (biting) surface of the tooth is composed of alternating areas of dentin and enamel. Differential wearing causes sharp ridges of enamel to be formed on the surface of the tooth (typically a molar), and to remain during the working life of the tooth. Herbivores grind their molars together as they chew (masticate), and the ridges help to shred tough plant material. In xenarthrans, enamel is generally absent, with the tooth instead consisting of alternating orthodentine and vasodentine. A material similar to dentin forms the hard material that makes up dermal denticles in sharks and other cartilaginous fish.
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.
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.