This is a working overview of regulatory status, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-07-03 and is reviewed periodically as new material appears.
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controlled human data on melanotan-2 remain sparse, and much of what circulates online derives from small studies or unpublished reports.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.
The peer-reviewed record is dominated by small early-phase studies, case reports and pharmacovigilance summaries rather than large randomised trials. Papers typically examine tanning response, receptor selectivity or patterns of reported adverse events. Many note that participants obtained the peptide outside a clinical setting, which limits verification of composition and administered amount. Reported events vary widely, and causality is frequently unclear because the identity and purity of self-sourced material are unknown. Open questions include whether repeated melanocortin receptor stimulation produces cumulative effects, and how often label claims match actual content.
Identification in laboratories relies on reversed-phase liquid chromatography coupled with tandem mass spectrometry, with product-ion spectra compared against a certified reference standard. High-resolution mass spectrometry supplies accurate mass confirmation, and peptide mapping after enzymatic digestion separates melanotan II from closely related analogues. Quantitation of seized material is complicated by unknown counter-ions and residual trifluoroacetate left from purification. Immunoassays raised against alpha-melanocyte-stimulating hormone can cross-react, so chromatographic confirmation is normally required. Urinary detection windows are short, and reported limits of detection differ substantially between laboratories.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic cyclic heptapeptide | Alpha-MSH analogue with a lactam ring |
| Molecular formula | C50H69N15O9 | Commonly cited value for the neutral peptide |
| Molecular weight | 1024.18 g/mol | Calculated for the free molecule |
| Appearance | White to off-white powder | Typically supplied as a lyophilised solid |
| Solubility | Soluble in water, DMSO and ethanol | Dissolution in pure water is often slow |
Research interest has centred on photoprotection and pigmentation, with a smaller body of work on appetite and sexual function. Published human data remain limited to small, frequently uncontrolled studies, and the compound has never received marketing approval from a national medicines regulator. Most laboratory work treats it as a pharmacological tool for probing melanocortin signalling in cell culture or animal models. Whether pigmentation changes observed in people translate into measurable protection against ultraviolet-induced DNA damage remains an open question.
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.
Verification of a purchased sample requires documentation linking a batch to a certificate of analysis, and that document should be read for the methods used rather than the headline purity figure. A single chromatographic percentage does not establish identity. Independent laboratories can perform identity and content assays, but no such test establishes that a product is suitable for human use. Claims about efficacy rest largely on small, early studies rather than on replicated controlled trials, and that gap remains open.
Identity testing for a cyclic peptide of this size usually relies on reversed-phase high-performance liquid chromatography coupled to mass spectrometry. The mass spectrum confirms molecular weight, while the chromatographic trace indicates the proportion of related impurities. Tandem mass spectrometry can provide sequence-level information when fragmentation data are compared against a reference standard. Nuclear magnetic resonance is sometimes used to confirm the lactam bridge, although it requires more material and greater operator expertise than routine chromatographic methods.
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.
=== EC 1.3.1 With NAD+ or NADP+ as acceptor === EC 1.3.1.1: dihydrouracil dehydrogenase (NAD+) EC 1.3.1.2: dihydropyrimidine dehydrogenase (NADP+) EC 1.3.1.3: Δ4-3-oxosteroid 5β-reductase EC 1.3.1.4: transferred to EC 1.3.1.22, 3-oxo-5α-steroid 4-dehydrogenase (NADP+) EC 1.3.1.5: cucurbitacin Δ23-reductase EC 1.3.1.6: fumarate reductase (NADH) EC 1.3.1.7: meso-tartrate dehydrogenase EC 1.3.1.8: acyl-CoA dehydrogenase (NADP+) EC 1.3.1.9: enoyl-[acyl-carrier-protein] reductase (NADH) EC 1.3.1.10: enoyl-[acyl-carrier-protein] reductase (NADPH, Si-specific) EC 1.3.1.11: 2-coumarate reductase EC 1.3.1.12: prephenate dehydrogenase EC 1.3.1.13: prephenate dehydrogenase (NADP+) EC 1.3.1.14: dihydroorotate dehydrogenase (NAD+) EC 1.3.1.15: dihydroorotate dehydrogenase (NADP+) EC 1.3.1.16: β-nitroacrylate reductase EC 1.3.1.17: 3-methyleneoxindole reductase EC 1.3.1.18: kynurenate-7,8-dihydrodiol dehydrogenase EC 1.3.1.19: cis-1,2-dihydrobenzene-1,2-diol dehydrogenase EC 1.3.1.20: trans-1,2-dihydrobenzene-1,2-diol dehydrogenase EC 1.3.1.21: 7-dehydrocholesterol reductase EC 1.3.1.22: 3-oxo-5α-steroid 4-dehydrogenase (NADP+) EC 1.3.1.23: Identical to EC 1.3.1.3, Δ4-3-oxosteroid 5β-reductase EC 1.3.1.24: biliverdin reductase EC 1.3.1.25: 1,6-dihydroxycyclohexa-2,4-diene-1-carboxylate dehydrogenase EC 1.3.1.26: Now EC 1.17.1.8, 4-hydroxy-tetrahydrodipicolinate reductase EC 1.3.1.27: 2-hexadecenal reductase EC 1.3.1.28: 2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase EC 1.3.1.29: cis-1,2-dihydro-1,2-dihydroxynaphthalene dehydrogenase EC 1.3.1.30: transferred to EC 1.3.1.22, 3-oxo-5α-steroid 4-dehydrogenase (NADP+) EC 1.3.1.31: 2-enoate reductase EC 1.3.1.32: maleylacetate reductase EC 1.3.1.33: protochlorophyllide reductase EC 1.3.1.34: 2,4 Dienoyl-CoA reductase (NADPH) EC 1.3.1.35: Now EC 1.14.19.22, microsomal oleoyl-lipid 12-desaturase EC 1.3.1.36: geissoschizine dehydrogenase EC 1.3.1.37: cis-2-enoyl-CoA reductase (NADPH) EC 1.3.1.38: trans-2-enoyl-CoA reductase (NADPH) EC 1.3.1.39: trans-2-enoyl-CoA reductase (NADPH) EC 1.3.1.40: 2-hydroxy-6-oxo-6-phenylhexa-2,4-dienoate reductase EC 1.3.1.41: xanthommatin reductase EC 1.3.1.42: 12-oxophytodienoate reductase EC 1.3.1.43: arogenate dehydrogenase EC 1.3.1.44: trans-2-enoyl-CoA reductase (NAD+) EC 1.3.1.45: 2′-hydroxyisoflavone reductase EC 1.3.1.46: biochanin-A reductase EC 1.3.1.47: α-santonin 1,2-reductase EC 1.3.1.48: 13,14-dehydro-15-oxoprostaglandin 13-reductase EC 1.3.1.49: cis-3,4-dihydrophenanthrene-3,4-diol dehydrogenase EC 1.3.1.50: n Now EC 1.1.1.252 tetrahydroxynaphthalene reductase EC 1.3.1.51: 2′-hydroxydaidzein reductase EC 1.3.1.52: Now EC 1.3.8.5, 2-methyl-branched-chain-enoyl-CoA reductase EC 1.3.1.53: (3S,4R)-3,4-dihydroxycyclohexa-1,5-diene-1,4-dicarboxylate dehydrogenase EC 1.3.1.54: precorrin-6A reductase EC 1.3.1.55: identical to EC 1.3.1.25, 1,6-dihydroxycyclohexa-2,4-diene-1-carboxylate dehydrogenase EC 1.3.1.56: cis-2,3-dihydrobiphenyl-2,3-diol dehydrogenase EC 1.3.1.57: phloroglucinol reductase EC 1.3.1.58: 2,3-dihydroxy-2,3-dihydro-p-cumate dehydrogenase EC 1.3.1.59: There is no evidence that the enzyme exists EC 1.3.1.60: dibenzothiophene dihydrodiol dehydrogenase EC 1.3.1.61: identical to EC 1.3.1.53, (3S,4R)-3,4-dihydroxycyclohexa-1,5-diene-1,4-dicarboxylate dehydrogenase EC 1.3.1.62: pimeloyl-CoA dehydrogenase EC 1.3.1.63: Now EC 1.21.1.2, 2,4-dichlorobenzoyl-CoA reductase EC 1.3.1.64: phthalate 4,5-cis-dihydrodiol dehydrogenase EC 1.3.1.65: 5,6-dihydroxy-3-methyl-2-oxo-1,2,5,6-tetrahydroquinoline dehydrogenase EC 1.3.1.66: cis-dihydroethylcatechol dehydrogenase EC 1.3.1.67: cis-1,2-dihydroxy-4-methylcyclohexa-3,5-diene-1-carboxylate dehydrogenase EC 1.3.1.68: 1,2-dihydroxy-6-methylcyclohexa-3,5-dienecarboxylate dehydrogenase EC 1.3.1.69: zeatin reductase EC 1.3.1.70: Δ14-sterol reductase EC 1.3.1.71: Δ24(241)-sterol reductase EC 1.3.1.72: Δ24-sterol reductase EC 1.3.1.73: 1,2-dihydrovomilenine reductase EC 1.3.1.74: 2-alkenal reductase [NAD(P)+] EC 1.3.1.75: 3,8-divinyl protochlorophyllide a 8-vinyl-reductase (NADPH) EC 1.3.1.76: precorrin-2 dehydrogenase EC 1.3.1.77: anthocyanidin reductase [(2R,3R)-flavan-3-ol-forming] EC 1.3.1.78: arogenate dehydrogenase (NADP+) EC 1.3.1.79: arogenate dehydrogenase (NAD(P)+) EC 1.3.1.80: Now classified as EC 1.3.7.12, red chlorophyll catabolite reductase EC 1.3.1.81: (+)-pulegone reductase EC 1.3.1.82: (-)-isopiperitenone reductase EC 1.3.1.83: geranylgeranyl diphosphate reductase EC 1.3.1.84: acrylyl-CoA reductase (NADPH) EC 1.3.1.85: crotonyl-CoA carboxylase/reductase EC 1.3.1.86: crotonyl-CoA reductase EC 1.3.1.87: 3-(cis-5,6-dihydroxycyclohexa-1,3-dien-1-yl)propanoate dehydrogenase EC 1.3.1.88: tRNA-dihydrouridine16/17 synthase (NAD(P)+) EC 1.3.1.89: tRNA-dihydrouridine47 synthase (NAD(P)+) EC 1.3.1.90: tRNA-dihydrouridine20a/20b synthase (NAD(P)+) EC 1.3.1.91: tRNA-dihydrouridine20 synthase (NAD(P)+) EC 1.3.1.92: artemisinic aldehyde Δ11(13)-reductase EC 1.3.1.93: very-long-chain enoyl-CoA reductase EC 1.3.1.94: polyprenol reductase EC 1.3.1.95: acrylyl-CoA reductase (NADH) EC 1.3.1.96: Botryococcus squalene synthase EC 1.3.1.97: botryococcene synthase EC 1.3.1.98: Now known to be catalyzed by two different enzymes, EC 1.3.1.122, (S)-8-oxocitronellyl enol synthase, and EC 5.5.1.34, (+)-cis,trans-nepetalactol synthase EC 1.3.1.100: chanoclavine-I aldehyde reductase EC 1.3.1.101: 2,3-bis-O-geranylgeranyl-sn-glycerol 1-phosphate reductase [NAD(P)H] EC 1.3.1.102: 2-alkenal reductase (NADP+) EC 1.3.1.103: 2-haloacrylate reductase EC 1.3.1.104: enoyl-[acyl-carrier-protein] reductase (NADPH) EC 1.3.1.105: 2-methylene-furan-3-one reductase EC 1.3.1.106: cobalt-precorrin-6A reductase EC 1.3.1.107: sanguinarine reductase EC 1.3.1.108: caffeoyl-CoA reductase EC 1.3.1.109: butanoyl-CoA dehydrogenase complex (NAD+, ferredoxin) EC 1.3.1.110: lactate dehydrogenase (NAD+,ferredoxin) EC 1.3.1.111: geranylgeranyl-bacteriochlorophyllide a reductase EC 1.3.1.112: anthocyanidin reductase [(2S)-flavan-3-ol-forming] EC 1.3.1.113: (4-alkanoyl-5-oxo-2,5-dihydrofuran-3-yl)methyl phosphate reductase EC 1.3.1.114: 3-dehydro-bile acid Δ4,6-reductase EC 1.3.1.115: 3-oxocholoyl-CoA 4-desaturase EC 1.3.1.116: 7β-hydroxy-3-oxochol-24-oyl-CoA 4-desaturase EC 1.3.1.117: hydroxycinnamoyl-CoA reductase EC 1.3.1.118: meromycolic acid enoyl-[acyl-carrier-protein] reductase EC 1.3.1.119: chlorobenzene dihydrodiol dehydrogenase EC 1.3.1.120: cyclohexane-1-carbonyl-CoA reductase NADP+) EC 1.3.1.121: 4-amino-4-deoxyprephenate dehydrogenase EC 1.3.1.122: (S)-8-oxocitronellyl enol synthase EC 1.3.1.123: 8-oxogeranial reductase EC 1.3.1.124: 2,4-dienoyl-CoA reductase [(3E)-enoyl-CoA-producing]
The dermatosparaxis and kyphoscoliosis types of EDS and some cases of the classic and hypermobility forms, are inherited in an autosomal recessive pattern. In autosomal recessive inheritance, two copies of the gene in each cell are altered. Most often, both parents of an individual with an autosomal recessive disorder are carriers of one copy of the altered gene but do not show signs and symptoms of the disorder.
The amplitude of an action potential is often thought to be independent of the amount of current that produced it. In other words, larger currents do not create larger action potentials. Therefore, action potentials are said to be all-or-none signals, since either they occur fully or they do not occur at all. This is in contrast to receptor potentials, whose amplitudes are dependent on the intensity of a stimulus. In both cases, the frequency of action potentials is correlated with the intensity of a stimulus. Despite the classical view of the action potential as a stereotyped, uniform signal having dominated the field of neuroscience for many decades, newer evidence does suggest that action potentials are more complex events indeed capable of transmitting information through not just their amplitude, but their duration and phase as well, sometimes even up to distances originally not thought to be possible.
Therapeutic, diagnostic and preventive monoclonal antibodies are clones of a single parent cell. When used as drugs, the International Nonproprietary Names (INNs) end in -mab. The remaining syllables of the INNs, as well as the column Source, are explained in Nomenclature of monoclonal antibodies.
Sources: en.wikipedia.org
Other experiments show that a single miRNA may repress the production of hundreds of proteins, but that this repression often is relatively mild (less than 2-fold). The effects of miRNA dysregulation of gene expression seem to be important in cancer. For instance, in gastrointestinal cancers, nine miRNAs have been identified as epigenetically altered and effective in down regulating DNA repair enzymes. The effects of miRNA dysregulation of gene expression also seem to be important in neuropsychiatric disorders, such as schizophrenia, bipolar disorder, major depression, Parkinson's disease, Alzheimer's disease and autism spectrum disorders.
Consequently, cellular bodies that form through liquid–liquid phase separation are a subset of biomolecular condensates, as are those where the physical origins of assembly are unknown. Historically, many cellular non-membrane bound compartments identified microscopically fall under the broad umbrella of biomolecular condensates. In physics, phase separation can be classified into the following types of colloid, of which biomolecular condensates are one example:
49 Squadron RAF in October 1956 in Operation Buffalo at Maralinga; Project Dazzle and its research on re-entry vehicles enabled the Mercury-Atlas 6 launch to happen in February 1962; the Australian government built four launch pads for the Blue Streak in 1959, but it was cancelled in 1960, the redesignated satellite launcher Blue Streak first launched on 5 June 1964, and satellites would be launched by 1966, but only WRESAT was launched in November 1967, on a Redstone rocket instead; Woomera launched over 4000 missiles and cost the Australian government £900m; the site was demolished by the Australian government at the end of the 1960s; part of the former site is now the secret Joint Defense Facility Nurrungar 17 September Not in the Stars, making mathematical models for predictions; Robert May, Baron May of Oxford of Imperial College; William Phillips and his 1949 MONIAC economic model; a British Airways 747 flight simulator; computer models of epidemics - the R number, and vaccination policies; the UK fishing industry had quotas imposed in 1983, due to mathematical models of fish stocks; John Shepherd of the Centre for Environment, Fisheries and Aquaculture Science (CEFAS) laboratory in Lowestoft; computer models of warfare were developed by the Defence Operational Analysis Establishment in West Byfleet with deputy director David Faddy, which closed six years later, superseded in function by CORDA (UK); Irving Mintzer of the World Resources Institute; the NASA Goddard Space Flight Center had developed computer models of the Earth's atmosphere, such as rainfall; the hole in the Ozone layer and phytoplankton, with Norman Myers; Ian Riley of the Economist Intelligence Unit. Narrated by Bob Peck. Written, produced and directed by Chris Haws, made by InCA 24 September Race for the Top, CERN versus Fermilab; in 1983 CERN discovered the W and Z bosons, it and Fermilab were looking for the top quark; Leon M. Lederman, director of Fermilab; Andy Parker of CERN; CERN had 80 scientists led by Luigi Di Lella on its UA2 experiment, and Fermilab had its Collider Detector at Fermilab (CDF); Roy Schwitters; Fermilab had discovered the bottom quark in 1977; John Ellis of CERN; each team prepared for an annual physics conference at La Thuile, Aosta Valley in north-west Italy; UA2 had a meeting in July 1989 in Cambridge; the top quark would be discovered in 1995 with 175 GeV by Fermilab. Narrated by Carole Boyd, known for playing Lynda Snell in The Archers, joint production InCA and WGBH 1 October Walk on Wheels, a half-million disabled people have a wheelchair in the UK; NHS wheelchairs were made by Carter's; the quick-release axle was developed in World War II, for releasing munitions; the residential Treloar School in Alton, Hampshire, which was funded by individual LEAs, with charity funding as well; Bill Walmsley of the Department of Health's wheelchair research centre in Blackpool, now part of the Disability and Carers Service at DWP Peel Park at the end of the M55 motorway, on the A5230 in Westby-with-Plumptons. Narrated by John Hedges, produced by Jeremy Llewellyn-Jones, made by Chrysalis Television (North One Television) 8 October Invasion of the Body Scanners, a reference to the 1956 film Invasion of the Body Snatchers; X-rays were introduced in the 1890s, but it took fifty years to vastly improve the early crude techniques; CT was invented in the late 1960s - its inventor with Prince Philip, Duke of Edinburgh; Ian McDougall at a magnet technology company, who designed the first magnet, cooled with liquid helium in 1979; X-ray scans were a fairly crude process, but other types required computer image processing; Michael Boswell of GE Medical Systems; scans were taken in the coronal plane and sagittal plane; by 1989 the NHS only had four of these scanners - one was at Frenchay Hospital, made by GEC Medical (Picker International) - there were around 25 scanners in the whole UK; the Brockton Hospital; there were 1500 scanners in the US, with 39 in Massachusetts; Donald Longmore of the National Heart and Chest Hospitals, who performed the UK's first heart transplant on 3 May 1968; CT scanning had been performed for neuroradiology since the mid-1970s; radiology at Middlesex Hospital; medical ultrasound was a much safer technique than X-rays, and a new type deployed the Doppler effect, but medical ultrasound lacked cast-iron image definition; but scanners were hideously expensive, due to the convoluted enormous magnets that were required. Narrated by John Benson, produced by Mike Johnstone, directed by Ed Newstead, made by VATV (Video Arts) 15 October Wheels of War, about the early 1990s Leyland 4-tonne truck and defence procurement; James Adams, journalist; military historian Correlli Barnett; general service (GS) cargo vehicles, and a RE vehicle carrying a Medium Girder Bridge; a youthful-looking Mark Francois; the Austin Champ, designed in the 1950s; the British Aerospace Nimrod AEW3 was cancelled in 1986 at a cost of £860m; cost-plus contracts were replaced by competitive; Sir Peter Levine was brought in as Chief of Defence Procurement; the Leyland 4-tonne truck would replace the Bedford MK, made by Bedford Vehicles; journalist John Parsons; each vehicle would cost around £23,000 each; the Leyland 5-tonne was developed from its Comet and Roadrunner vehicles (developed into the DAF LF) under project director Stuart Hayes; the equivalent German vehicle, the MAN KAT1, had cost £75,000 each; the Panavia Tornado; Leyland design engineer Colin Ingram; the three vehicle prototypes were punishingly tested at the Royal Armament Research and Development Establishment (RARDE). Narrated by Anthony Valentine, produced by Patrick Uden made by Uden Associates 22 October Three Score Years and Then? 29 October Robotopia, advances of robotics in Japan, and bizarre contraptions; Frederik L. Schodt, author of the 1988 book Inside the Robot Kingdom - for hundreds of years until 1853, Japan was a fairly backward country; Joseph Engelberger, who developed the first industrial robot, Unimate, made by his company Unimation from 1961 - there were around 200,000 industrial robots, with around 130,000 of those in Japan; Japanese robot artist Hajime Sorayama, who drew lurid female robots; automated mannequins; nineteen universities in Japan were developing ungainly humanoid robots, notably Ichiro Kato at Waseda University; Seiuemon Inaba of FANUC, produced by Mike Wallington, made by Kai Productions 5 November Fly-by-wire, the new Airbus 320; software engineer Mike Hennell of the University of Liverpool; Roger Beteille, managing director of Airbus from 1967–85, and Henri Ziegler; John Knight of the University of Virginia; software engineer Bev Littlewood of City University; the A320 was the first fly-by-wire airliner; Blind Landing Experimental Unit testing at RAE Bedford in the 1960s, and developing the automatic pilot with a Vickers Valetta; testing Concorde in a wind tunnel; the Apollo project had depended on computers - it couldn't be done otherwise; Paul Ceruzzi of the Air and Space Museum; Philip Felleman of the Draper Laboratory; testing the F-16 in the early 1970s; Joe Sutter, head of Boeing from 1981–86; Boeing introduced flight management systems, so not needing a flight engineer; David Learmount of Flight International, and how Airbus had more commercial need to be innovative; the A300 was the first two-engined wide body aircraft; the A310 had electrical hydraulics and electronic control of some flight surfaces; John Cullyer of the University of Warwick; the A320 had five master computers; Gordon Corps, the Airbus test pilot, later to fly on Thai Airways International Flight 311 in 1992; Gilles Pichon, chief engineer of the A320; Jacques Troyes, head of Flight Control at Airbus; there was emergency mechanical control to the rudder and tail trim; the June 1988 Air France Flight 296Q - Michel Asseline, the pilot, said the aircraft had tried to land, when he tried to raise the aircraft; Alain Monnier of the DGAC said it was pilot error; Greg Holt of the FAA and Brian Perry of the CAA; the four-engined A330 would be manufactured from 1992; a prototype fly-by-wire relaxed stability Saab JAS 39 Gripen tumbles on 2 February 1989 at Linköping/Saab Airport, piloted by Lars Rådeström. Narrated by James Bellini, produced by Ben Shephard (historian), directed by John Longley, made by Box Television with WGBH 12 November Deadly Force, aerial shots of Miami; the WINZ Miami broadcaster; the Miami SWAT response team; the 1980 Miami riots; Sgt Louis Battle, Bernie Gonzalez and the Heckler & Koch MP5; Tom Salerno and the Remington Model 870 pump action shotgun, the M1911 pistol and Beretta M9; Ted Bradley; a WSVN news broadcast with Jane Akre; two thirds of Miami's population were Latin-American, and had many exiled citizens; the 1980 Mariel boatlift, from Cuba, added to the population and much to the crime; Miami had two murders a day in the 1980s; Robert Waller; Edna Buchanan of the Miami Herald; severed limbs washed up on Miami beach; the Colt Python; the Beretta 92; the Colt AR-15 semi-automatic rifle; 80% of SWAT call-outs were connected to the drug trade; two thirds of illegal drugs went through Miami; Sgt Louis Philips and negotiation techniques; SWAT negotiator Eric Caspener; 95% of SWAT negotiations work. Produced by David Jones, directed by Catherine Bailey, made by Buffalo Pictures 19 November Faster than a Speeding Bullet, and the quest for supersonic flight, eventually resulting in Concorde. The programme features former Concorde pilot Christopher Orlebar, who wrote The Concorde Story. The history of supersonic research dates back to the 18th Century, but supersonic flight only became achievable after the development of the jet engine. Featured aircraft include: the wartime Messerschmitt Me 262; the innovative de Havilland DH 108; the Messerschmitt Me 163 Komet; the Fairey Delta 2, the Bell X1 and numerous experimental "X Planes". After the war, the world's fastest non-experimental aircraft was the Lockheed SR-71 Blackbird, which could fly at 95,000 ft at 2,300 mph. The programme interviews key figures in the development of supersonic military aircraft and second generation SST (Supersonic Transport) aircraft. Narrated by Tony Anholt, written, produced and directed by Chris Haws, made by InCA
== Awards and recognition == Eberlin was named among the Forbes "30 Under 30" list in 2015. She won the Marion Milligan Mason Award of the American Association for the Advancement of Science in 2016. The award is given every two years to promising young female researchers in chemistry. She won the MacArthur "Genius" Fellowship from the John D. and Catherine T. MacArthur Foundation in 2018 for her research on the use of mass spectrometry "to differentiate more quickly and accurately diseased from healthy tissues during surgery". She is the first UT Austin professor to win MacArthur grant this century. The award consists of a $625,000 no-strings-attached grant. According to the foundation, this award goes to "extraordinarily talented and creative individuals as an investment in their potential". She also won the Moore Inventor Fellowship in 2018. She received the 2020 Curt Brunnée Award from the International Mass Spectrometry Foundation. She was named on the Power List by the Analytical Scientist in 2014, 2018, 2019, 2021, 2022, 2023, and 2024. She received the 2024 Norman Hackerman Award from the Welch Foundation and the Biemann Medal from the American Society for Mass Spectrometry in 2025.
Famotidine, sold under the brand name Pepcid among others, is a histamine H2 receptor antagonist medication that decreases stomach acid production. It is used to treat peptic ulcer disease, gastroesophageal reflux disease, and Zollinger–Ellison syndrome. It is taken by mouth or by injection into a vein. It begins working within an hour. Common side effects include headache, abdominal pain, diarrhea or constipation, and dizziness. Serious side effects may include pneumonia and seizures. Use in pregnancy appears safe but has not been well studied, while use during breastfeeding is not recommended. Famotidine was patented in 1979 and came into medical use in 1985. It is available as a generic medication. In 2023, it was the 33rd most commonly prescribed medication in the United States, with more than 16 million prescriptions.
Sources: en.wikipedia.org
== History == Harith Rajagopalan, MD, PhD, and Jay Caplan established Fractyl Health, initially named Fractyl Laboratories, in 2010. The company's Revita device gained CE marking in April 2016 and became commercially available in the UK in January 2020. In April 2021, the US Food and Drug Administration (FDA) gave Revita breakthrough device designation to treat type 2 diabetes. The company changed its name to Fractyl Health in June 2021. In April 2022, the FDA approved an investigational device exemption trial for Revita. It became available commercially in Germany in early 2023. The FDA issued additional breakthrough device designation to Revita in July 2024 for weight maintenance in certain people with type 2 diabetes or obesity. Fractyl had an initial public offering on the Nasdaq in February 2024. As of February 2025, the company's REMAIN-1 study is evaluating Revita for patients with obesity to support weight maintenance after use of a GLP-1 drug. In January 2025, Fractyl announced it would focus research for Revita on obesity and people on GLP-1s, citing rising demand driven by the popularity of GLP-1s. The company also laid off some employees focused on type 2 diabetes treatment.
=== Macrocyclic chiral stationary phases === Macrocyclic chiral stationary phases consist of a silica support, on which macrocyclic antibiotic molecules are bonded. The commonly used macrocyclic antibiotics include rifamycin, glycopeptides (for example, avoparcin, teicoplanin, ristocetin A, vancomycin, and their analogs), polypeptide antibiotic thiostrepton, and aminoglycosides (for example, fradiomycin, kanamycin, and streptomycin). The macrocyclic antibiotics interact with the analyte through hydrogen bonds, dipole-dipole interactions with the polar groups of the analyte, ionic interactions and π-π interactions.
Biology is the study of life and its processes. Biologists study all aspects of living things, including all of the many life forms on earth and the processes in them that enable life. These basic processes include the harnessing of energy, the synthesis and duplication of the materials that make up the body, the reproduction of the organism and many other functions. Biology, along with chemistry and physics is one of the major disciplines of natural science.
== History == 3,4-DMA was first described in the scientific literature by Gordon Alles by 1932. Its effects in humans were first described by Mahlon David Fairchild by 1963. Subsequently, the drug was described in greater detail by Alexander Shulgin in his book PiHKAL (Phenethylamines I Have Known and Loved) in 1991.
Julian Voss-Andreae, a German-born artist specializing in "protein sculptures", created sculptures based on the structure of GFP, including the 1.70 metres (5 feet 7 inches) tall "Green Fluorescent Protein" (2004) and the 1.40 metres (4 feet 7 inches) tall "Steel Jellyfish" (2006). The latter sculpture is located at the place of GFP's discovery by Shimomura in 1962, the University of Washington's Friday Harbor Laboratories.
Sources: en.wikipedia.org
It is a synthetic cyclic heptapeptide modelled on alpha-melanocyte-stimulating hormone. A lactam bridge links two side chains, forming a ring that stabilises the molecule against proteolysis. It belongs to the broader melanocortin peptide family.
No national medicines agency has approved melanotan-2 for clinical use. Afamelanotide, a related but distinct peptide, holds a marketing authorisation in the European Union for a rare photosensitivity disorder. Melanotan-2 itself is handled as a laboratory chemical.
Its broad activity across melanocortin receptors makes it a tool for probing pigmentation, appetite and vascular signalling. Early trials recorded skin darkening and other effects that were not the original focus of the work. Those observations generated hypotheses that later studies have examined.
Regulatory treatment varies by country. In the United States, the European Union and Australia it is an unapproved drug and its sale is restricted, while some other jurisdictions list it as prescription-only or controlled. The applicable rules depend on the country of import.