Everything below concerns alpha-MSH analog. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2025-09-19. Numbers and descriptions here follow the published literature rather than marketing material.
Melanotan-2 is a synthetic cyclic heptapeptide designed as a structural analogue of alpha-melanocyte-stimulating hormone, the endogenous tridecapeptide that regulates pigment production. Two modifications distinguish it from the natural hormone: norleucine replaces methionine at the N-terminus, which limits oxidation, and a D-phenylalanine substitution raises receptor affinity. The ring is closed through an aspartate-lysine lactam bridge, giving the molecule a constrained conformation. The free base has a molecular mass near 1024 daltons, and commercial material is usually supplied as an acetate salt. It appears in the literature as a research peptide rather than an approved therapeutic agent.
Receptor studies place melanotan-2 among non-selective melanocortin agonists, binding MC1R, MC3R, MC4R and MC5R rather than a single subtype. Activation of MC1R on cutaneous melanocytes raises tyrosinase activity and shifts pigment synthesis toward eumelanin, which is darker and more photostable than pheomelanin. Central receptors, particularly MC4R, are associated with appetite suppression and with reported effects on sexual function. Because subtype selectivity is low, the same molecule engages pigment, metabolic and vascular pathways at once, and this breadth is a common explanation offered for the range of adverse events described in user reports.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C50H69N15O9 | Free base; salt forms add to total mass |
| Molecular mass | About 1024 daltons | Calculated for the free base |
| Structural class | Cyclic heptapeptide | Contains D-phenylalanine and norleucine |
| Parent hormone | Alpha-melanocyte-stimulating hormone | Endogenous tridecapeptide of 13 residues |
| Receptor profile | Non-selective melanocortin agonist | Interacts with MC1R, MC3R, MC4R and MC5R |
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 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.
Melanotan-2 is a synthetic linear peptide built from seven amino acids arranged in a short chain. Its sequence is commonly written as Ac-Nle-Asp-His-D-Phe-Arg-Trp-Lys-NH2, which includes a modified N-terminus and an amidated C-terminus. The molecule belongs to the melanocortin family and acts as a receptor agonist. Structural features such as the D-phenylalanine residue and the Nle substitution are associated with increased stability against enzymatic degradation relative to the natural parent peptide.
The compound emerged from research programs in the 1980s that examined analogues of alpha-melanocyte-stimulating hormone for pigmentation and photoprotection. Investigators modified the native sequence to extend activity duration and potency. A related analogue, afamelanotide, was developed within the same broad line of inquiry and eventually gained approval in certain jurisdictions for a rare light-sensitivity condition. Melanotan-2 itself did not progress through the same regulatory route and has no approved therapeutic indication.
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.
On May 14, 1913, New York Governor William Sulzer approved a charter for the foundation with Junior becoming the first president. With its large-scale endowment, a large part of Senior's fortune was insulated from inheritance taxes. The first secretary of the foundation was Jerome Davis Greene, the former secretary of Harvard University, who wrote a "memorandum on principles and policies" for an early meeting of the trustees that established a rough framework for the foundation's work. It was initially located within the family office at Standard Oil's headquarters at 26 Broadway, later (in 1933) shifting to the GE Building (then RCA), along with the newly named family office, Room 5600, at Rockefeller Center; later it moved to the Time-Life Building in the center, before shifting to its current Fifth Avenue address. In 1914, the trustees set up a new Department of Industrial Relations, inviting William Lyon Mackenzie King to head it. He became a close and key advisor to Junior through the Ludlow Massacre, turning around his attitude to unions; however the foundation's involvement in IR was criticized for advancing the family's business interests. The foundation henceforth confined itself to funding responsible organizations involved in this and other controversial fields, which were beyond the control of the foundation itself.
=== 5S-GlcNAc === Ac45S-GlcNAc is converted intracellularly into UDP-5S-GlcNAc, a substrate analogue inhibitor of OGT. UDP-5S-GlcNAc is not efficiently utilized as a donor sugar by OGT, possibly due to distortion of the pyranose ring by replacement of oxygen with sulfur. As other glycosyltransferases utilize UDP-GlcNAc as a donor sugar, UDP-5S-GlcNAc has some non-specific effects on cell-surface glycosylation.
Insulin (e.g. intravenous injection of 10 units of regular insulin along with 50 mL of 50% dextrose to prevent the blood sugar from dropping too low) leads to a shift of potassium ions into cells, secondary to increased activity of the sodium-potassium ATPase. Its effects last a few hours, so it sometimes must be repeated while other measures are taken to suppress potassium levels more permanently. The insulin is usually given with an appropriate amount of glucose to help prevent hypoglycemia following the insulin administration, though hypoglycaemia remains common especially in the context of acute or chronic renal impairment and capillary blood glucose measurements should be taken regularly after administration to identify this. Salbutamol (albuterol), a β2-selective catecholamine, is administered by nebuliser (e.g. 10–20 mg). This medication also lowers blood levels of K+ by promoting its movement into cells, and will work within 30 minutes. It is recommended to use 20 mg for maximum potassium lowering effect, but to use lower doses if the patient is tachycardic or has ischaemic heart disease. Note that 12-40% of patients do not respond to salbutamol therapy for reasons unknown, especially if on beta-blockers, so it should not be used as monotherapy Sodium bicarbonate may be used with the above measures if it is believed the person has metabolic acidosis, though time to effectiveness is longer and its use is controversial.
Sources: en.wikipedia.org
MVT-602 (other developmental code names RVT-602, TAK-448) is a kisspeptin receptor agonist which is under development for the treatment of female infertility and hypogonadism. It has been found to increase luteinizing hormone levels in premenopausal women. As of March 2021, MVT-602 is in phase 2 clinical trials for the treatment of female infertility and hypogonadism. It was also under development for the treatment of prostate cancer, but development for this indication was discontinued.
== Pathology == When initially identified, camptocormia was classified as a psychogenic disease. Although the condition is sometimes a psychogenic manifestation, camptocormia typically originates from either muscular or neurological diseases. However, due to the wide variety of pathologies resulting in camptocormia, there is no singular cause that is most influential for the condition.
1993/2854) Birmingham City Council (Grand Union Canal Bridge) Scheme 1992 Confirmation Instrument 1993 (S.I. 1993/2855) Mid Essex Community and Mental Health National Health Service Trust (Establishment) Order 1993 (S.I. 1993/2856) Wigan and Leigh Health Services National Health Service Trust (Transfer of Trust Property) Order 1993 (S.I. 1993/2857) Public Airport Companies (Capital Finance) (Fourth Amendment) Order 1993 (S.I. 1993/2875) Conservation of Seals (England) Order 1993 (S.I. 1993/2876) Motor Vehicles Tyres (Safety) (Amendment) Regulations 1993 (S.I. 1993/2877) Local Government Reorganisation (Capital Money) (Greater London) (Amendment) Order 1993 (S.I. 1993/2878) Redbridge and Waltham Forest (London Borough Boundaries) Order 1993 (S.I. 1993/2881) Local Government (Compensation for Premature Retirement) (Amendment) Regulations 1993 (S.I. 1993/2890) Local Government Act 1988 (Defined Activities) (Exemption) (Wales) (No. 2) Order 1993 (S.I. 1993/2894) Protection of Wrecks (Designation No. 3) Order 1993 (S.I. 1993/2895) Community Health Sheffield National Health Service Trust (Establishment) Order 1993 (S.I. 1993/2896) Public Telecommunication System Designation (Scottish Power Telecommunications Limited) Order 1993 (S.I. 1993/2897) Public Telecommunication System Designation (Torch Communications Limited) Order 1993 (S.I. 1993/2898) Public Telecommunication System Designation (MFS Communications Limited) Order 1993 (S.I. 1993/2899)
Sources: en.wikipedia.org
No regulatory agency has authorised melanotan-2 as a medicine for any indication. It circulates mainly as a research chemical or through unregulated channels. As a result, identity, purity and content are not independently guaranteed.
Melanotan-1, also called afamelanotide, is a linear analogue with greater selectivity for MC1R and has received approval in some jurisdictions for a specific photosensitivity disorder. Melanotan-2 is cyclic, less selective, and reaches central receptors more readily. The two are often confused in online discussion despite different pharmacology and regulatory status.
Alpha-MSH is an endogenous tridecapeptide derived from pro-opiomelanocortin. Melanotan-2 reproduces its core receptor-binding sequence inside a shortened, stabilised ring. The result is a molecule with a longer effective half-life and higher potency than the parent hormone.
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.