This is a working overview of SR9009, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-01-16. Anything still debated is marked as such rather than presented as settled.
Regulatory and sporting contexts treat SR9009 as a prohibited substance in many elite competitions. Its presence on banned lists reflects concerns about performance enhancement and unknown long-term safety. Analytical chemists have developed methods to detect the parent compound and its metabolites in urine and blood. Literature discussions distinguish between in vitro potency, animal pharmacology, and anecdotal human reports. The latter are difficult to verify because products sold online may lack purity or contain different compounds.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. These receptors help regulate circadian rhythms, lipid metabolism, and inflammatory gene expression. In cell and animal experiments, SR9009 alters transcription of clock-controlled genes and metabolic pathways. The compound is not a hormone and does not resemble classical steroid structures. Its activity depends on binding to the ligand-binding domain of REV-ERB, where it can modify corepressor recruitment.
Research interest in SR9009 grew from studies of circadian biology and metabolic disease. Preclinical reports describe effects on exercise capacity, muscle metabolism, and blood lipid levels in rodents, but these findings come from controlled laboratory settings. The compound has low oral bioavailability in animals, which limits systemic exposure after swallowing. Investigators often use injected routes in experiments to achieve measurable plasma concentrations. Human clinical data are sparse, no approved therapeutic product exists, and whether animal effects translate to humans remains an open question.
In rodent studies, SR9009 has been reported to increase mitochondrial content in skeletal muscle and improve exercise endurance under some conditions. These findings led to popular descriptions such as an exercise mimetic, although that term oversimplifies the biology. Effects vary by dose, timing, tissue, and model. The compound's influence on circadian pathways means that time of administration can matter in experiments. Whether similar metabolic changes occur in humans remains largely unexplored in controlled published trials.
Pharmacokinetic data for SR9009 are limited in published literature. Some reports indicate low oral bioavailability and rapid clearance in animals, which complicates interpretation of exposure and effect. Researchers often use injected routes in preclinical work to achieve measurable systemic levels. Analytical studies rely on mass spectrometry to detect the parent compound and its metabolites. Questions about tissue distribution, active metabolites, and long-term consequences remain open. Species differences in metabolism can affect observed half-life and target engagement.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ in preclinical models |
| Molecular formula | C20H24ClN3O4S | Reported for the parent compound |
| CAS Registry Number | 1379686-30-2 | Common identifier in chemical databases |
| Appearance | Off-white to pale yellow solid | Typical research chemical solid |
| Solubility | Soluble in DMSO and ethanol; low in water | Class: small organic molecule |
Laboratory studies often administer SR9009 by injection because oral absorption appears poor in rodents. Reported pharmacokinetic properties include rapid metabolism and low systemic exposure after oral dosing. Human pharmacokinetic data are sparse, so absorption, distribution, metabolism, and excretion in people are not well defined. Some research explores related REV-ERB compounds with improved drug-like properties. Regulatory approval for any REV-ERB agonist as a human medicine has not been granted to date.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ, also called NR1D1 and NR1D2. These receptors help regulate circadian rhythms and metabolic gene programs. The compound was developed for laboratory research, not as an approved therapeutic. Its identity is distinct from steroid hormones and selective androgen receptor modulators. Scientific interest centers on how REV-ERB activation changes gene expression in cells and animal models.
SR9009 is frequently discussed in fitness and research-chemical contexts, yet it has no approved medical indication. Regulatory agencies have not authorized it for human use, and it is not a standard prescription drug. Some sports organizations list it as a prohibited substance because of its potential performance-enhancing properties. Published human data are sparse, so claims about its effects in people often rely on animal models or anecdotal reports. Quality and identity of online materials can vary widely.
SR9009 is a synthetic small molecule studied as a REV-ERB agonist. REV-ERBα and REV-ERBβ are nuclear receptors that help regulate circadian rhythms and metabolic gene expression. The compound was identified in academic screening efforts to find synthetic ligands for these receptors. In cell and animal studies, SR9009 alters transcription of genes involved in lipid and glucose metabolism, and it can shift circadian behavior. It is not an approved therapeutic agent.
The extent to which the findings of a clinical trial can be reliably extrapolated from the subjects who participated in the trial to a broader patient population and a broader range of clinical settings. (ICH E9) Global assessment variable
=== Drug and weapons operations === Panama's and Noriega's involvement in drug-trafficking grew considerably over the early 1980s, peaking in 1984. Intensifying conflicts in Colombia, El Salvador, Guatemala, and Nicaragua had led to the creation of covert transportation networks that Noriega used to transport drugs to the U.S., particularly cocaine. During this period, Colombia's Medellín Cartel was also seeking allies. Noriega became intimately involved with their drug trafficking and money-laundering operations, and received considerable sums as protection money, bribes, or shares of profits. In June 1986, investigative journalist Seymour Hersh recorded a U.S. White House official as saying that reducing Noriega's activities could greatly reduce international drug trafficking. Hersh reported unnamed U.S. officials as saying that Noriega had amassed a personal fortune in European banks as a result of his illegal activities, as well as owning two homes in Panama and one in France. The wealth generated for the Panamanian military from drug-smuggling also helped stabilize the authoritarian government that it dominated. However, the military's control over wealth from illicit trade alienated the Panamanian business elite that had previously also benefited from such trade. Under Noriega, these profits were shared within the military less evenly than under Torrijos, eventually creating friction in the military leadership. Many of the operations Noriega benefited from were run by associates such as Floyd Carlton and Cesar Rodríguez.
== Enzyme mechanism == Cystathionase uses pyridoxal phosphate to facilitate the cleavage of the sulfur-gamma carbon bond of cystathionine, resulting in the release of cysteine. The lysine residue reforms the internal aldimine by kicking off α-iminobutyric acid. Afterwards the external ketimine is hydrolyzed, causing the formation of α-ketobutyrate. The amino group on cystathionine is deprotonated and undergoes a nucleophilic attack of the internal aldimine. An additional deprotonation by a general base results in the formation of the external aldimine and removal of the lysine residue. The basic lysine residue is then able to deprotonate the alpha carbon, pushing electron density into the nitrogen of the pyridine ring. Pyridoxal phosphate is necessary to stabilize this carbanionic intermediate; otherwise the proton's pKa would be too high. The beta carbon is then deprotonated, creating an alpha-beta unsaturation and pushing a lone pair onto the aldimine nitrogen. To reform the aldimine, this lone pair pushes back down, cleaving the sulfur-gamma carbon bond, resulting in the release of cysteine. A pyridoxamine derivative of vinyl glyoxylate remains after the gamma elimination. The lone pair from the pyridine nitrogen pushes electron density to the gamma carbon, which is protonated by lysine. Lysine then attacks the external aldimine, pushing electron density to the beta carbon, which is protonated by a general acid. The imine is then hydrolyzed to release α-ketobutyrate. Deprotonation of the lysine residue causes ammonia to leave, thus completing the catalytic cycle.
== Gameplay == Day of Defeat is a multiplayer first-person shooter that simulates squad-level infantry combat between the adversaries of World War II's European Theatre; the Allies and the Axis powers. Players can choose to join either the Allied or Axis armies, with the Allies including the United States or Great Britain and the Axis including Germany. A round begins with two opposing teams starting simultaneously in their respective spawn area of a map, both acting towards the goal of achieving their respective objectives whilst preventing the enemy team from accomplishing theirs. A round ends when one team accomplishes all of its objectives, with that team claiming victory. Eventually, the game ends with the expiration of a set time limit, and the team with the most objectives achieved is the winning team regardless of kills or casualties, except in the case of both teams having not achieved any objectives or having achieved the same number of objectives. Weaponry in the game attempts to realistically portray those that would be found in World War II, and the gameplay reflects this aesthetic choice. Recoil can be heavy and the game does not allow the player to fire while running or jumping. The game also features a stamina bar, preventing the player from sprinting for long periods of time and forcing them to actively conserve energy.
Sources: en.wikipedia.org
On 14 January 2026, Denmark started to send military reinforcements to Greenland to strengthen its military presence. Later that day, it became known that both Sweden and Norway sent military forces to support the Danish Defence in protecting Greenland. The Ministry of Defence on 14 January 2026 announced "an increased military presence in and around Greenland, comprising aircraft, vessels and soldiers, including from NATO allies". After consultations between a group of European countries, Germany announced it was sending a small contingent to Greenland on a reconnaissance mission with other European nations. On 15 January 2026, a French military contingent arrived in Greenland. On 16 January, Danish F-35 and French A330 MRTT jets conducted a training mission in southeast Greenland. On 17 January, Major General Søren Andersen stated that at least 100 units have arrived in Nuuk, and another 100 in Kangerlussuaq. By 18 January, the deployment involved Belgium, France, Germany, Sweden, Norway, Finland, the Netherlands, the United Kingdom, Estonia, Slovenia, and Iceland, with Estonia's deployment yet to be executed. French president Emmanuel Macron stated that the deployment would soon be reinforced with land, air, and sea assets as part of Operation Arctic Endurance. Denmark is planning a larger and more permanent NATO presence. On 18 January, Germany's reconnaissance team returned to Germany, with the Bundeswehr stating that the mission to plan for future engagements had been "completed, as planned".
The employees were young men: handsome jocks in form-fitting red-and-white striped soccer shirts; when a patron was celebrating a birthday, the entire restaurant crew came around with a cake and sang TGI Fridays' traditional birthday song. Footage of interviews with patrons from this TGI Fridays was featured in Robert Downey Sr.'s film No More Excuses (1968). The first location closed in 1994 and became a British-style pub called "Baker Street". Although Malachy McCourt's nearby Malachy's singles bar preceded TGI Fridays and Stillman credited the media for creating the term, he had unintentionally created one of the first singles bars. It benefited from the near-simultaneous availability of the birth-control pill and Betty Friedan's book The Feminine Mystique:
=== Ocular myxoma === Myxoma is a rare, benign stromal tumor of mesenchymal origin often confused with other conjunctival stromal tumors. Conjunctival myxomas are thought to originate in Tenon's capsule and can masquerade as conjunctival lymphoma, lymphangioma, ocular surface squamous neoplasia (OSSN), or amelanotic melanoma.
Vasoactive intestinal peptide (VIP) is a 28-residue amino acid peptide first characterized in 1970 that was initially isolated from porcine duodenum. A member of the secretin/glucagon hormone superfamily, VIP was initially discovered owing to its potent vasodilatory effects (as its name implies). VIP is widely distributed in the central and peripheral nervous system as well as in the digestive, respiratory, reproductive, and cardiovascular systems as a neurotransmitter and neuroendocrine releasing factor. These effects contribute to an extensive range of physiological and pathological processes related to development, growth, and the control of neuronal, epithelial, and endocrine cell function. VIP acts on two receptors - VPAC1 and VPAC2, which are class B of G-protein-coupled receptors (GPCRs).VPAC1 is mainly present in the lung and T-lymphocytes, whereas VPAC2 is mainly seen in the smooth muscle, mast cells and the basal parts of the lung mucosa.
The NDUFB4 gene, located on the q arm of chromosome 3 in position 13.33, is 6,130 base pairs long. The NDUFB4 protein weighs 15 kDa and is composed of 129 amino acids. NDUFB4 is a subunit of the enzyme NADH dehydrogenase (ubiquinone), the largest of the respiratory complexes. The structure is L-shaped with a long, hydrophobic transmembrane domain and a hydrophilic domain for the peripheral arm that includes all the known redox centers and the NADH binding site. NDUFB4 is one of about 31 hydrophobic subunits that form the transmembrane region of Complex I and is of the non-catalytic subunits of the complex. It has been noted that the N-terminal hydrophobic domain has the potential to be folded into an alpha helix spanning the inner mitochondrial membrane with a C-terminal hydrophilic domain interacting with globular subunits of Complex I. The highly conserved two-domain structure suggests that this feature is critical for the protein function and that the hydrophobic domain acts as an anchor for the NADH dehydrogenase (ubiquinone) complex at the inner mitochondrial membrane.
Sources: en.wikipedia.org
== Bibliography == Greenwood, Norman N.; Earnshaw, Alan (1997). Chemistry of the Elements (2nd ed.). Butterworth-Heinemann. doi:10.1016/C2009-0-30414-6. ISBN 978-0-08-037941-8. Penneman, R. A. and Keenan T. K. The radiochemistry of americium and curium, University of California, Los Alamos, California, 1960 Wiberg, Nils (2007). Lehrbuch Der Anorganischen Chemie. De Gruyter. ISBN 978-3-11-017770-1.
== Pharmacology == Pramlintide is an analogue of amylin, a small peptide hormone that is released into the bloodstream by the β cells of the pancreas along with insulin after a meal. Like insulin, amylin is completely absent in individuals with Type I diabetes. In synergy with endogenous amylin, pramlintide aids in the regulation of blood glucose by slowing gastric emptying, promoting satiety via hypothalamic receptors (different receptors than for GLP-1), and inhibiting inappropriate secretion of glucagon, a catabolic hormone that opposes the effects of insulin and amylin. Pramlintide also has effects in raising the acute first-phase insulin response threshold following a meal. Both a reduction in glycated hemoglobin and weight loss have been shown in insulin-treated patients with type 2 diabetes taking pramlintide as an adjunctive therapy.
The aldehyde groups of the triose sugars are oxidised, and inorganic phosphate is added to them, forming 1,3-bisphosphoglycerate. The hydrogen is used to reduce two molecules of NAD+, a hydrogen carrier, to give NADH + H+ for each triose. Hydrogen atom and ion balance and charge balance are both maintained because the phosphate (Pi) group actually exists in the form of a hydrogen phosphate anion (HPO2−4), which dissociates to contribute the extra H+ ion and gives a net charge of −3 on both sides. Here, arsenate ([AsO4]3−), an anion akin to inorganic phosphate may replace phosphate as a substrate to form 1-arseno-3-phosphoglycerate. This, however, is unstable and readily hydrolyzes to form 3-phosphoglycerate, the intermediate in the next step of the pathway. As a consequence of bypassing this step, the molecule of ATP generated from 1–3 bisphosphoglycerate in the next reaction will not be made, even though the reaction proceeds. As a result, arsenate is an uncoupler of glycolysis.
New Zealand has a long history of sporting contact with South Africa, especially through rugby union. Until the 1970s this resulted in discrimination against Māori players, since the apartheid political system in South Africa for most of the twentieth century did not allow people of different races to play sport together, and therefore South African officials requested that Māori players not be included in sides which toured their country. Despite some of New Zealand's best players being Māori, this was agreed to, and Māori were excluded from tours of South Africa. Some Māori always objected to this, but it did not become a major issue until 1960, when there were several public protests at Māori exclusion from that year's tour. The protest group Halt All Racist Tours was formed in 1969. Although this was an issue in which Māori were central, and Māori were involved in the protests, the anti-tour movement was dominated by Pākehā (white New Zealanders). In 1973 a proposed Springbok (South African rugby team) tour of New Zealand was cancelled. In 1976 the South African government relented and allowed a mixed-race All Black team to tour South Africa. However, by this time international opinion had turned against any sporting contact with South Africa, and New Zealand faced significant international pressure to cut ties. Despite this, in 1981 the Springboks toured New Zealand, sparking mass protests and civil disobedience.
The third season of the American satirical superhero television series The Boys, the first series in the franchise based on the comic book series of the same name written by Garth Ennis and Darick Robertson, was developed for television by American writer and television producer Eric Kripke. The season is produced by Sony Pictures Television Studios and Amazon Studios in association with Point Grey Pictures, Original Film, Kripke Enterprises, Kickstart Entertainment and KFL Nightsky Productions. The show's third season stars Karl Urban, Jack Quaid, Antony Starr, Erin Moriarty, Dominique McElligott, Jessie T. Usher, Laz Alonso, Chace Crawford, Tomer Capone, Karen Fukuhara, Nathan Mitchell, Colby Minifie, and Claudia Doumit returning from prior seasons, with Jensen Ackles joining the cast. Taking place a year after the events of the previous season, the season follows the titular Boys now working for Victoria Neuman's Bureau of Superhero Affairs to apprehend problematic Supes, having been at peace with the Seven. However, the conflict is resurrected once Butcher, Hughie & the rest of the Boys reunite to investigate the truth about the apparent death of Soldier Boy, one of Vought's first American superheroes, with the hopes of killing Homelander for good. Concurrently, Homelander's mental stability begins to deteriorate as Vought attempts to restrict his power while other Seven members, such as Annie January/Starlight and Queen Maeve, assist the Boys in their plots against him.
Sources: en.wikipedia.org
SR9009 is a synthetic small molecule studied as an agonist of the REV-ERB nuclear receptors. It is not an approved medicine, and its effects in humans are not well characterized.
No. It is a synthetic ligand that binds nuclear receptors, not a steroid or peptide hormone. Its activity depends on receptor binding rather than endocrine secretion.
Clinical evidence is limited. Most published data come from cell and animal experiments. Human safety and efficacy remain uncertain.
It is a synthetic research compound that activates REV-ERB nuclear receptors. It is not an approved drug or dietary supplement. Most information comes from cell and animal studies.