Everything below concerns melanocortin receptor. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-08-01. Numbers and descriptions here follow the published literature rather than marketing material.
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 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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic cyclic heptapeptide | Belongs to the melanocortin agonist family |
| Key substitutions | Nle4 and D-Phe7 | Improve resistance to enzymatic degradation |
| Molecular formula | C50H69N15O9 | Approximately 1024 g/mol |
| Regulatory status | Not approved as a medicine | Distributed as a research chemical |
| Common synonyms | Melanotan II, MT-II, MT-2 | Spelling varies across sources |
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.
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.
== Isotherms == The adsorption of gases and solutes is usually described through isotherms, that is, the amount of adsorbate on the adsorbent as a function of its pressure (if gas) or concentration (for liquid phase solutes) at constant temperature. The quantity adsorbed is nearly always normalized by the mass of the adsorbent to allow comparison of different materials. A number of different isotherm models have been developed.
== Role in disease == Granzyme B has a normal concentration of 20-40 pg/ml in the blood plasma while retaining 70% activity and elevated concentrations of granzyme B are found in a number of disease states. Granzyme B can generate autoantigens by cleaving in disordered regions and linker regions of antigens exposing new epitopes and this can cause the development of autoimmune diseases. Granzyme B release with perforin from CD8+ T cells can cause heart and kidney transplant rejection through killing of allogeneic endothelial cells. The destruction of insulin producing β cells in pancreatic islets is mediated by T cells and granzyme B contributing to Type 1 Diabetes. Granzyme B can also mediate the death of cells after spinal cord injury and is found at elevated levels in rheumatoid arthritis. Chronic obstructive pulmonary disease (COPD) has been attributed to granzyme B secreted from NK and T cells causing the apoptosis of bronchial epithelial cells. Matrix destabilisation and remodelling by granzyme B is also linked to asthma pathogenesis. Granzyme B can kill melanocytes causing the skin condition vitiligo and granzyme B overexpression is found in contact dermatitis, lichen sclerosus and lichen planus cases. Cytotoxic cells expressing granzyme B have been identified close to hair follicles linking a possible role in hair loss. The ECM remodelling properties of granzyme B have also implicated its involvement in left ventricular remodelling, which increases the subsequent chances of myocardial infarction.
It mandates that "the use of artificial intelligence efforts should not compromise the integrity of nuclear safeguards, whether through the functionality of weapons systems, the validation of communications from command authorities, or the principle of requiring positive human actions in execution of decisions by the President with respect to the employment of nuclear weapons." In February 2026, the Trump Administration publicly reaffirmed that nuclear weapons decisions will remain subject to human control, with a senior Pentagon official reiterating the "Department's policy that there is a human in the loop on all decisions on whether to employ nuclear weapons". In September 2025, the French Center for AI Safety (CeSIA), The Future Society and the Center for Human-Compatible AI (CHAI) published a global call for AI red lines urging governments to reach a binding international agreement prohibiting unacceptable AI uses by the end of 2026. The declaration was initially signed by 200 prominent figures including 10 Nobel Prize winners, and was announced by Maria Ressa at the United Nations General Assembly. In December 2025, President Donald Trump signed an executive order to establish a "National Policy Framework for Artificial Intelligence". The executive order discouraged state governments from regulating AI, urging Congress to pass a law pre-empting such regulations. The White House cited economic and national security concerns as reasons for the measure, while some criticized Trump for creating uncertainty for AI regulation. On July 6, 2026, Illinois Governor J.B.
Sources: en.wikipedia.org
=== Provost of Queen's College, Oxford === As he approached the age of sixty, Florey faced mandatory retirement. He had to vacate the university house he had occupied since 1935, which was subsequently demolished, with a new school erected on the site. He bought a parcel of land in Marston, Oxford, and built a house on it. No sooner had they moved in than Florey accepted the position of Provost of The Queen's College, Oxford, to which he was elected on 25 June 1962, and he moved into the provost's lodgings. This meant relinquishing his chair at the Sir William Dunn School. He was succeeded by Henry Harris, a fellow Australian scientist who had been invited to study at the Sir William Dunn School by Florey in 1952 on an ANU scholarship. Florey was the first provost of Queen's College with no prior association with the college as an undergraduate, graduate researcher or fellow, and the first scientist. The role was closely associated with the academic establishment, of which he had been critical, but he could stay until 1971, the lodgings came with a housekeeper, and he could make use of its facilities to entertain visiting scientists and dignitaries. Florey had a lift installed to make it easier for Ethel and himself to reach the upstairs bedrooms.
Actinium (89Ac) has no stable isotopes and no characteristic terrestrial isotopic composition, thus a standard atomic weight cannot be given. There are 34 known isotopes, from 203Ac to 236Ac, and 9 isomers. Three isotopes are found in nature, 225Ac, 227Ac and 228Ac, as intermediate decay products of, respectively, 237Np, 235U, and 232Th. 228Ac and 225Ac are extremely rare, so almost all natural actinium is 227Ac. The most stable isotopes are 227Ac with a half-life of 21.772 years, 225Ac with a half-life of 9.919 days, and 226Ac with a half-life of 29.37 hours. All other isotopes have half-lives under seven hours, and most under a minute. The shortest-lived known isotope is 217Ac with a half-life of 69 ns. Purified 227Ac comes into equilibrium with its decay products (mainly 227Th and 223Ra) after 185 days.
=== Cystic fibrosis === The human lung and saliva contain a wide range of antimicrobial compound including lactoperoxidase system, producing hypothiocyanite and lactoferrin, with hypothiocyanite missing in cystic fibrosis patients. Lactoferrin, a component of innate immunity, prevents bacterial biofilm development. The loss of microbicidal activity and increased formation of biofilm due to decreased lactoferrin activity is observed in patients with cystic fibrosis. In cystic fibrosis, antibiotic susceptibility may be modified by lactoferrin. These findings demonstrate the important role of lactoferrin in human host defense and especially in lung. Lactoferrin with hypothiocyanite has been granted orphan drug status by the EMEA and the FDA.
Sources: en.wikipedia.org
== Life and career == Jack Donald Lennart Bergagård was born in Öckerö on 13 February 1936. In the late 1950s Bergagård was employed as a pastor in the Pentecostal congregation Elim in Örebro. After visiting Aage Samuelsen's Maran Ata meetings in Oslo in 1959, he resolved to spread the movement in Sweden, becoming one of the founders of the Maranata movement there. He founded the first Swedish Maranata congregation in Örebro in 1960. He was one of the founders of Maran Ata in Oslo, where he was also a pastor from 2001 to 2004. Later that year, he moved to the United States. Bergagård wrote the Swedish text to the song där rosor aldrig dör/Till en stad jag är på vandring, dit där rosor aldrig dör. The tune was written by Jack & Jim Elsie, under the original title I am going to a city, where the roses never fade. In March 1963, Bergagård led a Maran Ata meeting in Jönköping, where a 13-year-old boy with diabetes was prayed for. His parents withdrew his insulin shots; the boy died a week later, drawing media attention. Bergagård died on 29 September 2026, at the age of 90.
Extracellular polymeric substances (EPS) are natural polymers of high molecular weight secreted by microorganisms into their environment. EPS establish the functional and structural integrity of biofilms, and are considered the fundamental component that determines the physicochemical properties of a biofilm. EPS in the matrix of biofilms provides compositional support and protection of microbial communities from the harsh environments. Components of EPS can be of different classes of polysaccharides, lipids, nucleic acids, proteins, lipopolysaccharides, and minerals.
A large group of primarily lichenized fungi (the subclass Ostropomycetidae) apparently lost the ability to form lichens early in its history, reverting to a saprotrophic lifestyle. Later, some descendants regained a photobiont and lichenized again. This finding contradicts older assumptions that once a fungus became obligately lichenized it could never revert. Lineages with complex thalli, especially those bearing cyanobacterial cephalodia, show higher estimated extinction rates: they diversify rapidly but are more prone to die out, perhaps because of ecological specialization. Such large-scale studies now link geological and climatic shifts, for example, the spread of angiosperm forests in the Late Cretaceous–Early Paleogene, to bursts of lichen diversification, revealing a more intricate evolutionary history. In simple terms, this means lichens diversified in bursts when new habitats (like forests with lots of new tree bark) became available. New high-throughput techniques are also solving smaller-scale questions once thought intractable. 'Museomics' now retrieves DNA from old, fragmented specimens. For instance, Leavitt and colleagues (2019) shotgun-sequenced decades-old historical type specimens of the Rhizoplaca melanophthalma group. From three crustose thalli they recovered more than a thousand gene regions, sufficient to position each specimen in a phylogenomic tree and match them with modern material. The data showed one specimen was the distinct species R.
Sources: en.wikipedia.org
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.
No regulatory agency has approved it for any indication. It is encountered as a research chemical sold outside pharmaceutical supply chains. Products marketed this way are not subject to the manufacturing and labeling requirements that apply to approved drugs.
Reports describe increased skin pigmentation as well as side effects such as nausea, flushing, and changes to existing moles. Much of the evidence comes from small studies and case reports rather than large trials. The long-term safety profile is therefore uncertain.
No regulator in a major market has approved it for human use. It appears in research settings and in products marketed outside pharmacy channels. Legal status for personal possession varies by country.