The short version of alpha-MSH analogue fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2026-05-25. Anything still debated is marked as such rather than presented as settled.
Structurally, Melanotan-2 retains the core recognition motif of alpha-melanocyte-stimulating hormone while adding a lactam bridge that links two side chains and constrains the molecule into a ring. This modification lowers susceptibility to enzymatic degradation. The compound acts as an agonist at melanocortin receptors, particularly subtypes associated with melanin production. Because the same receptor family influences several physiological processes, researchers note that its activity is not confined to pigmentation alone. Receptor selectivity continues to be examined in published studies.
Melanotan-2 is a synthetic cyclic heptapeptide designed as an analogue of alpha-melanocyte-stimulating hormone, a naturally occurring peptide involved in pigmentation signalling. Its sequence incorporates modified residues that increase potency and extend biological activity relative to the native hormone. The compound binds receptors of the melanocortin family and is examined mainly in laboratory research. It does not occur naturally and exists only as a manufactured chemical entity produced by solid-phase synthesis.
The peptide was developed during the 1980s by researchers investigating melanocortin signalling and skin pigmentation pathways. Early work focused on analogues of alpha-melanocyte-stimulating hormone that would resist enzymatic breakdown more effectively than the parent molecule. Melanotan-2 emerged from that programme as a shortened, cyclised variant. Reports describing its synthesis and receptor activity later appeared in the scientific literature. Commercial availability grew through unregulated channels rather than through pharmaceutical approval.
Regulatory treatment varies between countries. Several national medicines agencies have classified the peptide as unapproved, and customs authorities in some jurisdictions seize shipments on that basis. A few jurisdictions channel supply through prescription-only frameworks that do not list the substance by name. Because the material circulates mainly through online vendors, composition and purity are rarely verified before sale. Surveys of unapproved peptide products have reported labels that did not match measured content in a substantial fraction of samples.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C50H69N15O9 | Synthetic cyclic heptapeptide |
| Molecular mass | Approximately 1024 g/mol | Depends on counter-ion content |
| Appearance | White to off-white powder | Commonly supplied as a lyophilised solid |
| Solubility | Freely soluble in water | Also dissolves in common aqueous buffers |
| Typical storage | -20 degrees Celsius, desiccated | Protect from light and repeated freeze-thaw |
Two structural changes distinguish the synthetic peptide from the natural hormone. A norleucine residue replaces methionine at one position, and a D-configured phenylalanine replaces the natural L-form at another. Both substitutions slow enzymatic breakdown, which extends the molecule's persistence relative to the parent hormone. The lactam bridge further constrains the backbone into a stable conformation. These features are standard design strategies in peptide chemistry and are not unique to this compound; they appear across many research peptides built for improved stability.
The compound was developed in the late 1980s and early 1990s by academic researchers investigating melanocortin signaling and pigmentation. Early work explored whether synthetic analogs could reproduce effects of the natural hormone under controlled conditions. The molecule never advanced through the full regulatory pathway required for approval as a medicine. From the mid-2000s onward it appeared in unregulated consumer markets, often distributed through informal channels. That gap between research origins and commercial availability shapes how the compound is discussed today.
Melanotan-2 is a synthetic peptide designed as an analog of alpha-melanocyte-stimulating hormone, a signaling molecule produced in the pituitary and skin. Its structure is a linear chain of seven amino acids that folds into a ring through an internal lactam bridge joining two side chains. The compound is sometimes written as MT-II or MEL-2 in informal and commercial contexts. It belongs to the melanocortin peptide family, a group of short signaling molecules that share a conserved core sequence recognized by melanocortin receptors.
Melanotan II is a synthetic cyclic heptapeptide analog derived from the core sequence of alpha-melanocyte-stimulating hormone. Researchers at the University of Arizona synthesized it during the 1980s while studying pigmentation and appetite signaling. The compound is not an approved medicine in any major jurisdiction and appears mainly in laboratory and research-chemical settings. Its structure incorporates a lactam bridge between side chains, which constrains the ring and slows enzymatic breakdown relative to the natural hormone.
Melanotan II binds several melanocortin receptor subtypes rather than a single target. MC1R on melanocytes drives melanin synthesis, while MC3R and MC4R participate in energy balance, appetite, and sexual response pathways. This lack of selectivity explains why reported effects extend beyond skin darkening. Substitutions at positions four and seven, including norleucine and D-phenylalanine, increase potency and resistance to peptidases. Understanding which receptor mediates which effect remains an active area of investigation.
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 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.
Melanotan-2 is a synthetic cyclic heptapeptide designed as an analogue of alpha-melanocyte-stimulating hormone. Its sequence incorporates a lactam bridge that constrains the peptide into a ring, which increases resistance to enzymatic breakdown relative to the natural hormone. Researchers at the University of Arizona synthesised the compound in the late 1980s and early 1990s while studying pigmentation pathways. It has never received marketing approval from any national medicines regulator. In the scientific literature it is usually described as a laboratory research reagent rather than a therapeutic product.
The peptide acts as a non-selective agonist at melanocortin receptors, showing affinity for MC1R, MC3R, MC4R and MC5R. Activation of MC1R on melanocytes drives the conversion of tyrosine into melanin and shifts production toward the darker eumelanin form. MC4R signalling in the central nervous system is linked to appetite and energy balance, which helps explain why reduced food intake appeared in early human studies. Effects on MC4R and on vascular tone also account for the erectile responses recorded as unexpected findings in those same trials.
Melanotan-2 is frequently confused with afamelanotide, a linear analogue authorised in the European Union for erythropoietic protoporphyria. The two compounds differ in chain length, ring structure and receptor selectivity, so findings for one cannot be transferred directly to the other. Published controlled human data on melanotan-2 remain sparse, and much of what circulates online derives from small studies or unpublished reports. Questions about effect size, dose-response behaviour and long-term safety therefore remain unresolved.
Selected-ion flow-tube mass spectrometry (SIFT-MS) is a quantitative mass spectrometry technique for trace gas analysis which involves the chemical ionization of trace volatile compounds by selected positive precursor ions during a well-defined time period along a flow tube. Absolute concentrations of trace compounds present in air, breath or the headspace of bottled liquid samples can be calculated in real time from the ratio of the precursor and product ion signal ratios, without the need for sample preparation or calibration with standard mixtures. The detection limit of commercially available SIFT-MS instruments extends to the single digit pptv range. The instrument is an extension of the selected ion flow tube, SIFT, technique, which was first described in 1976 by Adams and Smith. It is a fast flow tube/ion swarm method to react positive or negative ions with atoms and molecules under truly thermalised conditions over a wide range of temperatures. It has been used extensively to study ion-molecule reaction kinetics. Its application to ionospheric and interstellar ion chemistry over a 20-year period has been crucial to the advancement and understanding of these topics. SIFT-MS was initially developed for use in human breath analysis, and has shown great promise as a non-invasive tool for physiological monitoring and disease diagnosis. It has since shown potential for use across a wide variety of fields, particularly in the life sciences, such as agriculture and animal husbandry, environmental research and food technology.
== Veterinary == In horses, it is sometimes given by injection as an anxiety-relieving medication, though there are many negative common side effects and it is forbidden by many equestrian competition organizations.
In addition, a London wastewater analysis found that enobosarm was the most abundant "pharmaceutical drug" detected and was more prevalent than "classical" recreational drugs like MDMA and cocaine. Enobosarm is often used in these contexts at doses greatly exceeding those evaluated in clinical trials, with unknown effectiveness and safety. Many products sold online that are purported to be enobosarm either contain none or contain other unrelated substances. Social media has played an important role in facilitating the widespread non-medical use of SARMs.
== Cause == A diagnosis of iron-deficiency anemia requires further investigation into its cause. It can be caused by increased iron demand, increased iron loss, or decreased iron intake. Increased iron demand often occurs during periods of growth, such as in children and pregnant women. For example, during stages of rapid growth, babies and adolescents may outpace their dietary intake of iron, which can result in deficiency in the absence of disease or a grossly abnormal diet. Iron loss is typically from blood loss. One example of blood loss is by chronic gastrointestinal blood loss, which could be linked to a possible cancer. In women of childbearing age, heavy menstrual periods can be a source of blood loss, causing iron-deficiency anemia. People who do not consume much iron in their diet, such as vegans or vegetarians, are also at increased risk of developing iron deficiency anemia.
In 1958, Korolev upgraded the R-7 to be able to launch a 400-kilogram (880 lb) payload to the Moon. The Luna program began with three failed secret 1958 attempts to launch Luna E-1-class impactor probes. The fourth attempt, Luna 1, launched successfully on January 2, 1959, but missed the Moon. The fifth attempt on June 18 also failed at launch. The 390-kilogram (860 lb) Luna 2 successfully impacted the Moon on September 14, 1959. The 278.5-kilogram (614 lb) Luna 3 successfully flew by the Moon and sent back pictures of its far side on October 7, 1959. The US first embarked on the Pioneer program in 1958 by launching the first probe, albeit ending in failure. A subsequent probe named Pioneer 1 was launched with the intention of orbiting the Moon only to result in a partial mission success when it reached an apogee of 113,800 km before falling back to Earth. The missions of Pioneer 2 and Pioneer 3 failed whereas Pioneer 4 had one partially successful lunar flyby in March 1959.
Sources: en.wikipedia.org
Some of the earliest ancient human civilisations in South Asia originated from areas encompassing present-day Pakistan. The earliest known stone tools in the region, dating to the Lower Palaeolithic (~2 million years ago), were discovered in the Soan Valley of northern Pakistan. The Indus plain region, which covers most of the present-day Pakistan, was the site of several successive ancient cultures including the Neolithic (7000–4300 BCE) site of Mehrgarh, and the 5,000-year history of urban life in South Asia to the various sites of the Indus Valley Civilisation, including Mohenjo-daro and Harappa. Following the decline of the Indus Valley Civilisation, semi-nomadic Indo-European Aryans migrated into the Indian subcontinent around 2000 BCE, perhaps by way of the Khyber Pass. They fused with the indigenous Harappan culture of the Indus Valley, and elements of the pre-Aryan spiritual traditions were assimilated into the developing Vedic tradition. This cultural milieu shaped the Gandhara Civilisation, which flourished at the crossroads of India, Central Asia, and the Middle East, connecting trade routes and absorbing cultural influences from diverse civilisations. By the early Vedic period, parts of the Indus region in present-day Pakistan were populated by numerous tribes that were beginning to coalesce into chieftain-led clans and early kingdoms. During this period, the Vedas, the oldest scriptures of Hinduism, were composed.
=== Allied with Venezuela === The Washington Post wrote in October that Maduro had written to Russia's Vladimir Putin, asking for help with "defensive radars, military aircraft repairs and potentially missiles", and that Maduro had contacted "China and Iran, soliciting military assistance and equipment to strengthen the country's defenses". According to The Wall Street Journal, China and Russia are "Maduro's two most powerful allies" and they have "previously provided military equipment, maintenance and training, say analysts, along with economic assistance", but along with Maduro's other traditional allies of Cuba and Iran, they are unlikely to lend significant support help beyond words of support.
When two drugs have the same bioavailability, they are said to be biological equivalents or bioequivalents. The concept of bioequivalence is important since it is currently used as a yardstick in the authorization of generic drugs in many countries.
== Mechanism of action == Quinupristin and dalfopristin are protein synthesis inhibitors in a synergistic manner. While each of the two is only a bacteriostatic agent, the combination shows bactericidal activity.
Sources: en.wikipedia.org
=== Branched polymers === A monomer with functionality of 3 or more will introduce branching in a polymer and will ultimately form a cross-linked macrostructure or network even at low fractional conversion. The point at which a tree-like topology transits to a network is known as the gel point because it is signalled by an abrupt change in viscosity. One of the earliest so-called thermosets is known as Bakelite. It is not always water that is released in step-growth polymerization: in acyclic diene metathesis or ADMET, dienes polymerize with loss of ethene.
Skeletal advancement to physically increase the pharyngeal airspace is often an option for craniofacial patients with upper airway obstruction and small lower jaws (mandibles). These syndromes include Treacher Collins syndrome and Pierre Robin sequence. Mandibular advancement surgery is one of the modifications needed to improve the airway; others may include reduction of the tongue, tonsillectomy, or modified uvulopalatoplasty.
== Research == Oral administration of LGD-4033 to cynomolgus monkeys at daily doses varying from 0 to 75 mg/kg over 13 weeks demonstrated significant body weight gain in both males and females. After 48 days, the 75 mg/kg dose testing was halted due to toxicity concerns, but this did not negatively impact development of the drug as this dose is significantly higher than the doses being utilized in a phase 2 clinical trial. Two phase 1 clinical trials of LGD-4033 have been conducted and reported. The first was a single-dose study published as a conference abstract in 2010 and the second was a multi-dose study published as a journal article in 2013. The multi-dose phase 1 trial published in 2013 reported that LGD-4033 dose-dependently improved lean body mass and muscle strength in 76 healthy young men over 21 days. It was generally well-tolerated in this study, with no significant adverse effects reported. A phase 2 clinical trial, initiated on 3 November 2016, consisted of 108 women and men recovering from hip fracture surgery. The randomized study participants received either placebo or varying doses of LGD-4033 over a period of 12 weeks, with improved lean body mass as the primary endpoint. Other endpoints included satisfactory results in terms of quality of life, safety, and pharmacokinetics. This study was completed and results reported in 2017 and 2018. In the trial, LGD-4033 dose-dependently improved lean body mass and muscle strength and was reported to be safe and well-tolerated.
Sources: en.wikipedia.org
It is a synthetic cyclic heptapeptide and an analogue of alpha-melanocyte-stimulating hormone. The molecule is produced by chemical synthesis rather than extracted from a biological source.
It is shorter than the native hormone and carries a cyclic constraint that improves stability. These changes raise receptor potency and slow breakdown relative to the naturally occurring peptide.
Published accounts date its development to the 1980s, when researchers were generating analogues of melanocyte-stimulating hormone. That work aimed to produce more stable compounds for studying pigmentation biology.
No. No major regulatory agency has granted a marketing authorisation for melanotan II as a medicine. Products sold under this name are generally presented as laboratory reagents and are not subject to the batch-release testing applied to approved drugs.