The short version of MC1R fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-03-30 and is reviewed periodically as new material appears.
Melanotan II is a synthetic cyclic heptapeptide that acts as an agonist at melanocortin receptors. It was designed as a structural analogue of alpha-melanocyte-stimulating hormone, the endogenous peptide involved in pigment production. The analogue carries a lactam bridge that constrains the ring and slows enzymatic breakdown relative to the native hormone. In research literature it appears under several abbreviations, and naming conventions are not fully standardized. Published descriptions usually place it within the broader melanocortin agonist family.
Receptor binding at MC1R on melanocytes raises intracellular cyclic AMP and increases expression of tyrosinase and related enzymes. The downstream result is greater synthesis of eumelanin, the dark pigment, without ultraviolet exposure acting as the trigger. The compound is not selective, however, and also engages MC3R, MC4R and MC5R, which are expressed in the central nervous system and elsewhere. That lack of selectivity is the explanation usually offered for effects reported outside pigmentation, including appetite suppression and nausea. Selectivity remains a central theme in comparative studies of related peptides.
Human data remain limited and mostly short-term. Reports describe small trials and observational accounts rather than large controlled studies, so questions about dose-response relationships and long-term effects on melanocytes stay open. Whether repeated exposure alters naevus behaviour is not settled in the published record. Researchers also note that self-administered use outside clinical settings makes actual exposure difficult to quantify. Statements about efficacy and safety should therefore be read as preliminary rather than established.
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.
No regulatory authority has approved melanotan-2 for human use, and several countries classify it as a prescription-only or controlled substance, which restricts lawful supply. Material sold online is generally labelled as a research chemical and is not required to meet pharmaceutical standards of identity or purity. Published human data consist mainly of small uncontrolled studies, case reports and adverse-event notifications, so the evidence base is descriptive rather than confirmatory. Whether repeated melanocyte stimulation alters long-term naevus behaviour remains an open question that no completed trial has resolved.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic cyclic heptapeptide | Melanocortin receptor agonist |
| Molecular formula | C50H69N15O9 | Neutral form, mass near 1024.2 g/mol |
| Primary targets | MC1R, MC3R, MC4R, MC5R | Binding is non-selective across subtypes |
| Related compounds | Alpha-MSH, melanotan I, afamelanotide | Structurally or functionally related peptides |
| Common abbreviations | MT-II, MT-2 | Naming in the literature is not uniform |
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.
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.
The International Brain Initiative was created in 2017, currently integrated by more than seven national-level brain research initiatives (US, Europe, Allen Institute, Japan, China, Australia, Canada, Korea, and Israel) spanning four continents.
Isoforms I, III, and VIII are also stimulated by Ca2+/calmodulin. Isoforms V and VI are inhibited by Ca2+ in a calmodulin-independent manner. Isoforms II, IV and IX are stimulated by alpha subunit of the G protein. Isoforms I, V and VI are most clearly inhibited by Gi, while other isoforms show less dual regulation by the inhibitory G protein. Soluble AC (sAC) is not a transmembrane form and is not regulated by G proteins or forskolin, instead acts as a bicarbonate/pH sensor. It is anchored at various locations within the cell and, with phosphodiesterases, forms local cAMP signalling domains. In neurons, calcium-sensitive adenylyl cyclases are located next to calcium ion channels for faster reaction to Ca2+ influx; they are suspected of playing an important role in learning processes. This is supported by the fact that adenylyl cyclases are coincidence detectors, meaning that they are activated only by several different signals occurring together. In peripheral cells and tissues adenylyl cyclases appear to form molecular complexes with specific receptors and other signaling proteins in an isoform-specific manner.
At low concentrations of TNP-ATP (≤1 μM), fluorescent intensity is proportional to the concentration of TNP added. However, at concentrations exceeding 1 μM, inner filter effects cause this relationship to no longer be linear. To correct this, researchers must determine the ratio of the predicted theoretical fluorescence intensity (assuming linearity) to the observed fluorescence intensity and then apply this correction factor. However, in most cases, researchers will try to keep the concentration of TNP to lower than 1 μM. To determine binding affinities, TNP-ATP is added to a solution and then titrated with protein. This produces a saturation curve from which the binding affinity can be determined. The number of binding sites may also be determined through this saturation curve by looking to see if there are sudden changes in slope. One can also titrate a fixed amount of protein with increasing additions of TNP-ATP to obtain a saturation curve. To do so, however, may get complicated due to the inner filter effects that will need to be corrected for. To determine dissociation constants, TNP-ATP can be competed off of a protein with ATP. The value of the dissociation constant Kd for a single-site binding can then be obtained by applying the Langmuir equation for a curve fit:
Sources: en.wikipedia.org
== Description == The cap is 1.5–4 centimetres (1⁄2–1+1⁄2 in) across, dry, at first hemispheric, expanding to campanulate or convex, with an incurved margin when young. Young caps start out light brown and fade to off-white or light gray at maturity, sometimes with yellowish or brownish tones. Often developing cracks in dry weather, slightly hygrophanous, turning greenish or blue where damaged. The gills are broadly adnate to adnexed, close, starting out gray and turning black as the spores mature. The gill faces have a mottled appearance and the edges are white. The spore print is black. The stipe is 6–12 cm long by 2 to 4 mm thick, equal to slightly enlarged at the base, pruinose, colored like the cap, staining somewhat blue where bruised. The taste and odor are farinaceous.
The predecessor of the Parliament of South Africa, before the 1910 Union of South Africa, was the bicameral Parliament of the Cape of Good Hope. This was composed of the House of Assembly (the lower house) and the Legislative Council (the upper house). This predecessor dated back to the beginnings of Cape independence in 1853 and was elected according to the multi-racial Cape Qualified Franchise system, whereby suffrage qualifications were applied equally to all males, regardless of race. The buildings of the Cape Parliament went on to house the Parliament of South Africa, after union.
While artesunate is used primarily as treatment for malaria, there is some evidence that it may also have some beneficial effects in Schistosoma haematobium infection, but has not been evaluated in large randomized trials. Artesunate is used as the treatment of choice for severe malaria by the World Health Organization (WHO) over quinine.
Sources: en.wikipedia.org
Trigger finger, also known as stenosing tenosynovitis, is a disorder characterized by catching or locking of the involved finger in full or near full flexion, typically when the hand is closed with force. There may be tenderness in the palm of the hand near the last skin crease (distal palmar crease). The ring finger and thumb are the most common digits. The problem is generally idiopathic (no known cause). People with diabetes might be relatively prone to trigger finger. The pathophysiology is enlargement of the flexor tendon and the A1 pulley of the tendon sheath. While often referred to as a type of stenosing tenosynovitis (which implies inflammation) the pathology is mucoid degeneration. Mucoid degeneration refers to changes in fibrous tissue, such as tendon, to have less organized collagen, more abundant extracellular matrix, and changes in the cells (fibrocytes) so as to act and look more like cartilage cells (chondroid metaplasia). Diagnosis is typically based on symptoms and signs after excluding other possible causes. Trigger digits can resolve without treatment. Treatment options that are disease modifying include steroid injections and surgery. Splinting immobilization of the finger may or may not be disease modifying.
== Cause == While the exact cause is unknown, the genetic predisposition to GPS involves the human leukocyte antigen (HLA) system, specifically HLA-DR15. In addition to genetic susceptibility, an initial environmental insult to the pulmonary vasculature is needed to allow the anti-glomerular basement membrane (anti-GBM) antibodies to reach the alveolar capillaries. Examples of such an insult include: exposure to organic solvents (e.g. chloroform) or hydrocarbons, exposure to tobacco smoke, infection (such as influenza A), cocaine inhalation, metal dust inhalation, bacteremia, sepsis, high-oxygen environments, and antilymphocyte therapies (especially with monoclonal antibodies). Exposure to dry cleaning chemicals and paraquat herbicide have also been implicated as potential insults. In GPS, anti-GBM antibodies are produced and circulated throughout the bloodstream, damaging the membranes lining the lungs and kidneys as well as targeting their capillaries.
=== Epidermal barrier === Necrobiosis, mainly affecting dermis and subcutaneous tissue, can also impact the epidermis. TNF-α and IFN-γ impair keratinocyte function, inhibiting keratinocyte proliferation and migration, two processes essential for reepithelialization and wound closure. Chronic keratinocyte dysfunction can lead to tissue atrophy. Furthermore, inflammatory signaling may downregulate key cell-cell adhesion molecules such as E-cadherin and β-catenin, compromising epidermal tight junctions and leading to skin barrier dysfunction. All of these factors impact the epidermal integrity and barrier.
== Types and uses == Animal glue was the most common woodworking glue for thousands of years until the advent of synthetic glues, such as polyvinyl acetate (PVA) and other resin glues, in the 20th century. Today it is used primarily in specialty applications, such as lutherie, pipe organ building, piano repairs, and antique restoration. Glass artists take advantage of hide glue's ability to bond with glass. As the glue hardens it shrinks, chipping the glass. It has several advantages and disadvantages compared to other glues. The glue is applied hot, typically with a brush or spatula. Glue is kept hot in a glue pot, which may be an electric unit built for the purpose, a double boiler, or simply a saucepan or crock pot to provide a warm water bath for the container of glue. Most animal glues are soluble in water, useful for joints which may at some time need to be separated. Alcohol is sometimes applied to such joints to dehydrate the glue, making it more brittle and easier to crack apart. Steam can also be used to soften glue and separate joints. Specific types include hide glue, bone glue, fish glue, and rabbit-skin glue.
Sources: en.wikipedia.org
It is a synthetic cyclic heptapeptide and a non-selective melanocortin receptor agonist. Structurally it is modelled on alpha-melanocyte-stimulating hormone, a peptide that occurs naturally in the body.
Activation of MC1R increases pigment synthesis independently of ultraviolet exposure, which is the mechanism usually cited for darkening without sun exposure. Ultraviolet light still influences skin response through separate biological pathways.
Because the peptide binds several melanocortin receptor subtypes, its effects are not confined to pigmentation. This complicates interpretation of both intended and unintended outcomes reported in studies.
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.