The short version of REV-ERB agonist fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2026-04-17. Anything still debated is marked as such rather than presented as settled.
Preclinical reports have linked SR9009 to improved endurance and altered energy expenditure in rodents. Such findings have prompted interest in whether REV-ERB activation can influence skeletal muscle metabolism. However, the reported effects depend on dose, route, and experimental model, and replication across laboratories is limited. Human trials have not established comparable outcomes, so claims about exercise performance remain speculative. The absence of controlled human data is a central limitation in interpreting these observations.
The mechanism of action involves binding to REV-ERB receptors and recruiting corepressor complexes, which represses target gene transcription. This contrasts with many nuclear receptor agonists that activate transcription. Downstream effects may include changes in autophagy, mitochondrial biogenesis, and lipid handling, but the precise pathways remain an active area of study. Whether these molecular events translate into meaningful physiological effects in humans is unresolved. Most evidence comes from cultured cells and rodent models rather than human participants.
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.
Mechanistically, SR9009 binds the ligand-binding domain of REV-ERBα/β and enhances recruitment of corepressor complexes. This represses target genes rather than activating them. Because REV-ERB proteins normally compete with ROR proteins at shared response elements, the net effect depends on tissue and timing. Researchers use SR9009 to probe how nuclear receptor signaling links the clock to metabolism, inflammation, and muscle biology. Findings are largely preclinical, and the precise contribution of each receptor subtype remains under study.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small molecule; not a steroid or peptide. |
| Primary targets | NR1D1 and NR1D2 | Also known as REV-ERBα and REV-ERBβ. |
| Studied routes | Intraperitoneal in rodents | Oral bioavailability in humans is not established. |
| Human approval | No approved therapeutic indication | No recognized clinical use. |
| Key uncertainty | Human physiological effects | Preclinical findings may not translate. |
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.
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 and metabolic gene expression. In laboratory experiments, SR9009 binds these receptors and alters transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. It is not a naturally occurring compound and has no approved therapeutic use. Research interest stems from its ability to modify energy metabolism in cells and animal models.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not an approved medicine and has no established human therapeutic use. The compound appears in scientific literature as a tool for probing circadian and metabolic regulation. Online sellers often label it as a research chemical, sometimes using the nickname Stenabolic. Its chemical identity is distinct from selective androgen receptor modulators, stimulants, and peroxisome proliferator-activated receptor delta agonists. Researchers use it mainly in cell and animal experiments.
At the molecular level, SR9009 binds REV-ERBα and REV-ERBβ and alters their repressive activity on target genes. These nuclear receptors help regulate the circadian clock, lipid synthesis, glucose metabolism, and inflammatory pathways. By changing transcription, the compound can shift the timing or magnitude of downstream metabolic processes in model systems. It does not act through androgen receptors or adenosine receptors, which distinguishes it from several substances sold for athletic performance. Whether the same transcriptional changes occur in humans at tolerable exposures remains an open question because controlled human studies are lacking.
Preclinical reports describe effects on exercise endurance, mitochondrial content, and lipid profiles in rodents, but these findings come from specific experimental conditions. Many studies use high doses or delivery methods that may not translate directly to human use. SR9009 has been reported to have low oral bioavailability and a short half-life, which complicates interpretation of oral dosing studies. It is not established as safe or effective for any indication. Literature discussions often separate its pharmacological mechanism from unverified claims made in fitness and supplement markets.
== tRNA genes == Organisms vary in the number of tRNA genes in their genome. For example, the nematode worm C. elegans, a commonly used model organism in genetics studies, has 29,647 genes in its nuclear genome, of which 620 code for tRNA. The budding yeast Saccharomyces cerevisiae has 275 tRNA genes in its genome. The number of tRNA genes per genome can vary widely, with bacterial species from groups such as Fusobacteria and Tenericutes having around 30 genes per genome while complex eukaryotic genomes such as the zebrafish (Danio rerio) can bear more than 10 thousand tRNA genes. In the human genome, which, according to January 2013 estimates, has about 20,848 protein-coding genes in total, there are 497 nuclear genes encoding cytoplasmic tRNA molecules, and 324 tRNA-derived pseudogenes—tRNA genes thought to be no longer functional (although pseudo tRNAs have been shown to be involved in antibiotic resistance in bacteria). One study has shown that the copy number of tRNA genes varies among individuals. As with all eukaryotes, there are 22 mitochondrial tRNA genes in humans. Mutations in some of these genes have been associated with severe diseases like the MELAS syndrome. Regions in nuclear chromosomes, very similar in sequence to mitochondrial tRNA genes, have also been identified (tRNA-lookalikes). These tRNA-lookalikes are also considered part of the nuclear mitochondrial DNA (genes transferred from the mitochondria to the nucleus).
=== Act 2 === Lucinda, a runaway slave, rifles through the pockets of the dead chain gang prisoners. Inman regains consciousness and awakens, which startles her. Lucinda frees Inman, who resumes his journey. Back at Black Cove Farm, Stobrod and his traveling companion Pangle still rely upon Ruby and Ada for sustenance. Stobrod tries to convince Ruby that he is a changed man, but Ruby remains skeptical. Inman meets Sara, a war widow, who is trying to comfort her baby. Inman helps her, gains her trust, and is invited to spend the night. At Black Cove Farm, Teague appears, with a copy of the newspaper that lists the names of deserters, on which Ruby sees her father's name. The next morning, Inman and Sara react quickly when Union soldiers appear. At a campfire in the woods, Teague and his men confront Stobrod and Pangle, shoot them and leave them for dead. Ada finds the two men, and expresses compassion for Stobrod ("I feel sorry for you"). Ada later goes hunting in the woods. There, she and Inman reunite. The other characters whom Inman has encountered on his odyssey appear to Inman, and urge him to tell Ada about his adventures ("Tell her of the slave you met"; "Tell her how the boat went down"). The couple affirms their pledge to each other. Teague continues his pursuit. Ada and Inman consummate their love, on their final night together. Eventually, Teague and the Home Guard track down Inman. In the final battle, Inman is killed.
== Rice == From 2009 to 2019, Thailand's hom mali 105 (jasmine) rice has been declared the world's best rice five times. But in 2018, Cambodian Malys Angkor jasmine rice was the winner, and Vietnam's ST24 rice took top honours in 2019, causing panic among Thai rice producers as ST24 is half the price of Thai hom mali.
Sources: en.wikipedia.org
=== Obsessive–compulsive disorder === Sertraline is effective for the treatment of OCD in adults, adolescents and children. It was better tolerated and, based on intention-to-treat analysis, performed better than the gold standard of OCD treatment clomipramine. Continuing sertraline treatment helps prevent relapses of OCD with long-term data supporting its use for up to 24 months. The sertraline dosages necessary for the effective treatment of OCD are higher than the usual dosage for depression. The onset of action is also slower for OCD than for depression. The treatment recommendation is to start treatment with half of the maximal recommended dose for at least two months. After that, the dose can be raised to the maximal recommended in the cases of unsatisfactory response. Cognitive behavioral therapy alone is not more effective than sertraline in adolescents and children; however, a combination of these treatments is effective.
== Pharmacology == Cangrelor is a high-affinity, reversible inhibitor of P2Y12 receptors that causes almost complete inhibition of ADP-induced platelet aggregate. It is a modified ATP derivative stable to enzymatic degradation. It does not require metabolic conversion to an active metabolite. This allows cangrelor's immediate effect after infusion, and the therapeutic effects can be maintained with continuous infusion. The pharmacokinetics of cangrelor has allowed it to rapidly achieve steady-state concentrations with a clearance of 50 L/h and a half-life of 2.6 to 3.3 minutes. Cessation of its administration is associated with rapid removal, and normal platelet function is restored within 1 hour.
4-Hydroxyphenylpyruvic acid (4-HPPA) is an intermediate in the metabolism of the amino acid phenylalanine. The aromatic side chain of phenylalanine is hydroxylated by the enzyme phenylalanine hydroxylase to form tyrosine. The conversion from tyrosine to 4-HPPA is in turn catalyzed by tyrosine aminotransferase. Additionally, 4-HPPA can be converted to homogentisic acid which is one of the precursors to ochronotic pigment. It is an intermediary compound in the biosynthesis of scytonemin.
In the following years, it became the basis for the prosecutions of the opposition and the officers during the imposition of the totalitarian regime in the country. Between 23 and 31 January, Kimon Georgiev visited Moscow, where he met Joseph Stalin and Georgi Dimitrov for the first time. The main purpose of the visit was the conclusion, with Soviet mediation, of an alliance treaty between Bulgaria and Yugoslavia. Secret letters to the treaty envisaged the future creation of a federation, without specifying whether on an equal basis between the two countries, which Bulgaria insisted on, or by incorporating Bulgaria into Yugoslavia as a sixth republic, which was the Yugoslav position. The treaty was never concluded because of the opposition of the United Kingdom and the United States, who believed that Bulgaria could not act independently until a peace treaty was concluded. On 9 February 1945, Kimon Georgiev gave a report on the government's work to the First Congress of the Fatherland Front. Days after the first executions under the decision of the so-called People's Court, he deplored the "cases of self-destruction, arbitrariness and violence" that had been allowed to take place, claimed that they had been curbed quickly, and expressed satisfaction at their being channeled through the People's Court. He states that the constitution and "the rights and liberties of the Bulgarian people" have been restored, although the Council of Ministers rules by ordinance-laws and political organizations outside the Fatherland Front have not been legalized.
Sources: en.wikipedia.org
Korsmeyer Award, ASCI (2008) Distinguished Leader in Insulin Resistance Award (2008) Elected Fellow, American Association for the Advancement of Science (2009) Outstanding Clinical Investigator Award, Endocrine Society (2012) Sir Philip Randle Award, Biochemical Society (2013) Elected to Master, American Association of Clinical Endocrinology (2015) Solomon Berson Award, American Physiological Society (2016) Harrington Scholar-Innovator (2016) Inaugural Fellow, American Physiological Society (2016) Distinguished Alumni Award, Wayne State University (2016) Banting Medal for Lifetime Scientific Achievement, American Diabetes Association (2018) Elected to the American Academy of Arts and Sciences (2018) Arthur Riggs Award, City of Hope (2019) Stanley Mirsky Award, Icahn School of Medicine at Mount Sinai (2019) Samuel Eichold II Memorial Award, American College of Physicians (2020) Manpei Suzuki International Prize for Diabetes Research (2021) Elected to Master, American College of Physicians (2021) Fellow of the Royal College of Physicians (2021) EASD-Lilly Centennial Anniversary Prize for Landmark Discoveries in Diabetes, European Association for the Study of Diabetes (2023) Bodil Schmidt-Nielsen Distinguished Mentor and Scientist Award, American Physiological Society (2024) EASD-Novo Nordisk Foundation Diabetes Prize for Excellence (2025)
=== Coagulation factor disorders === The best-known coagulation factor disorders are the hemophilias. The three main forms are hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency or "Christmas disease") and hemophilia C (factor XI deficiency, mild bleeding tendency). Von Willebrand disease (which behaves more like a platelet disorder except in severe cases), is the most common hereditary bleeding disorder and is characterized as being inherited autosomal recessive or dominant. In this disease, there is a defect in von Willebrand factor (vWF), which mediates the binding of glycoprotein Ib (GPIb) to collagen. This binding helps mediate the activation of platelets and formation of primary hemostasis. In acute or chronic liver failure, there is insufficient production of coagulation factors, possibly increasing risk of bleeding during surgery. Thrombosis is the pathological development of blood clots. These clots may break free and become mobile, forming an embolus or grow to such a size that occludes the vessel in which it developed. An embolism is said to occur when the thrombus (blood clot) becomes a mobile embolus and migrates to another part of the body, interfering with blood circulation and hence impairing organ function downstream of the occlusion. This causes ischemia and often leads to ischemic necrosis of tissue. Most cases of venous thrombosis are due to acquired states (older age, surgery, cancer, immobility).
=== Other causes === Cranial CSF leaks result from intracranial hypertension in the vast majority of cases. The increased pressure causes a rupture of the cranial dura mater, leading to a CSF leak and intracranial hypotension. Patients with a nude nerve root, where the root sleeve is absent, are at increased risk for developing recurrent CSF leaks. Lumbar disc herniation has been reported to cause CSF leaks in at least one case. Degenerative spinal disc diseases cause a disc to pierce the dura mater, leading to a CSF leak. CSF leaks can result from a lumbar puncture procedure.
Sources: en.wikipedia.org
It is a synthetic compound that acts as an agonist at REV-ERBα and REV-ERBβ. It is used mainly as a research chemical to study circadian and metabolic pathways. It is not approved for human therapeutic use.
REV-ERB receptors generally repress transcription when bound by natural heme. SR9009 is described as an agonist that enhances this repressive activity. The result is altered expression of clock and metabolic genes.
Published controlled human trials are lacking. Some sources cite limited or unofficial reports, but these do not establish safety or efficacy. Claims about human performance effects remain unverified.
SR9009 is a synthetic compound investigated as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is used in preclinical research on circadian rhythm and metabolism. It is not an approved drug.