This is a working overview of REV-ERB agonist, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-04-21. Anything still debated is marked as such rather than presented as settled.
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.
At the molecular level, SR9009 binds the ligand-binding domain of REV-ERB and strengthens recruitment of corepressor proteins such as NCoR and HDAC3. This increases repression of target genes, including Bmal1 and other clock-controlled and metabolic genes. In rodent studies, such changes have been linked to altered lipid handling, glucose metabolism, and energy expenditure. The precise chain of events between receptor binding and whole-body effects remains an active area of research. Findings in animals do not automatically translate to humans.
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.
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 small molecule | Studied as a REV-ERB agonist |
| Molecular formula | C20H24ClN3O4S | Reported for the neutral compound |
| Appearance | Off-white to pale yellow solid | Typical research-grade material |
| Solubility | Sparingly soluble in water | Soluble in solvents such as DMSO |
| Common synonyms | SR9009; Stenabolic | Stenabolic is an informal alias |
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.
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.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.
SR9009 is a synthetic small molecule studied as an agonist of REV-ERB nuclear receptors. REV-ERB alpha and REV-ERB beta help regulate circadian rhythms and metabolic gene expression. In laboratory research, SR9009 has been used to probe how these receptors affect skeletal muscle, liver, and adipose tissue. The compound was identified in academic drug-discovery work and is often described in scientific literature by its chemical name and research code. It is not an approved medicine, and human clinical data remain limited or absent.
SR9009 binds REV-ERB receptors and alters their repressive activity on target genes. This action can change transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. In rodent studies, treated animals have shown changes in muscle oxidative capacity and exercise performance, though effects vary by dose, duration, and model. The precise molecular steps connecting receptor binding to whole-body outcomes are still an active area of investigation. Findings in animals do not automatically translate to humans.
== History == In 1943, diphenhydramine was discovered by chemist George Rieveschl and one of his students, Fred Huber, while they were conducting research into muscle relaxants at the University of Cincinnati. Huber first synthesized diphenhydramine. Rieveschl then worked with Parke-Davis to test the compound, and the company licensed the patent from him. In 1946, it became the first prescription antihistamine in the United States approved by the FDA. In the 1960s, diphenhydramine was found to weakly inhibit reuptake of the neurotransmitter serotonin. This discovery led to a search for viable antidepressants with similar structures and fewer side effects, culminating in the invention of fluoxetine (Prozac), a selective serotonin reuptake inhibitor (SSRI). A similar search had previously led to the synthesis of the first SSRI, zimelidine, from brompheniramine, also an antihistamine. In 1975, diphenhydramine was still available only by prescription in the US and required medical supervision.
17-26 August The 196th Light Infantry Brigade, 23rd Infantry Division (Americal) and ARVN 5th Regiment, 2nd Division killed more than 650 PAVN/VC from the 1st Regiment and 3rd Regiment, 2nd Division, in an operation in the Quế Sơn Valley for the loss of 60 U.S. killed. The 7th Marines conducted supporting operations in the Hiệp Đức District.
PMID 30938236.{{cite journal}}: CS1 maint: multiple names: authors list (link) Acharya, B; Wang, K; Kim, IS; Kang, W; Moon, C; Lee, BH (2013). "In vivo imaging of myocardial cell death using a peptide probe and assessment of long-term heart function". Journal of Controlled Release. 172 (1): 367–73. doi:10.1016/j.jconrel.2013.08.294. PMID 24021357. Acharya, B; Chun, SY; Kim, SY; Moon, C; Shin, HI; Park, EK (2012). "Surface immobilization of MEPE peptide onto HA/β-TCP ceramic particles enhances bone regeneration and remodeling". Journal of Biomedical Materials Research Part B: Applied Biomaterials. 100 (3): 841–9. doi:10.1002/jbm.b.32648. PMID 22278974. Choi, YA; Lim, J; Kim, KM; Acharya, B; Cho, JY; Bae, YC; Shin, HI; Kim, SY; Park, EK (2010). "Secretome analysis of human BMSCs and identification of SMOC1 as an important ECM protein in osteoblast differentiation". Journal of Proteome Research. 9 (6): 2946–56. doi:10.1021/pr901110q. PMID 20359165. He, X; Bonaparte, N; Kim, S; Acharya, B; Lee, JY; Chi, L; Lee, HJ; Paik, YK; Moon, PG; Baek, MC; Lee, EK; KIM, JH; KIM, IS; Lee, BH (2012). "Enhanced delivery of T cells to tumor after chemotherapy using membrane-anchored, apoptosis-targeted peptide". Journal of Controlled Release. 162 (6): 521–8. doi:10.1016/j.jconrel.2012.07.023. PMID 22824781. Venkatesha, S. H.; Dudics, S; Acharya, B; Moudgil, K. D. (2014). "Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy". International Journal of Molecular Sciences. 16 (1): 887–906. doi:10.3390/ijms16010887. PMC 4307281. PMID 25561237.
Sources: en.wikipedia.org
=== Topoisomerase-mediated ligation === Topoisomerase can be used instead of ligase for ligation, and the cloning may be done more rapidly without the need for restriction digest of the vector or insert. In this TOPO cloning method a linearized vector is activated by attaching topoisomerase I to its ends, and this "TOPO-activated" vector may then accept a PCR product by ligating to both of the 5' ends of the PCR product, the topoisomerase is released and a circular vector is formed in the process.
== Characteristics == Limosilactobacillus fermentum belongs to the genus Limosilactobacillus. Species in this genus are heterofermentative and adapted to the intestinal tract of vertebrates but also used for a wide variety of applications including food and feed fermentation. L. fermentum differs from most or all other species in the genus as it has a nomadic lifestyle and is not a stable member of human or animal intestinal microbiota. It has been found that some strains for L. fermentum have natural resistances to certain antibiotics and chemotherapeutics. They are considered potential vectors of antibiotic resistance genes from the environment to humans or animals to humans. Some strains of L. fermentum have been associated with cholesterol metabolism.
. The UV lamp is directly above the sample and it releases photons to interact with the desorbed molecules that are formed. The conventional method generally uses a higher heating power and gas flow rate for the nebulizer gas, while also increasing the amount of dopant used during the technique. These increases can cause higher background noise, analyte interference, substrate impurities, and more ion reactions from excess dopant ions.
Sources: en.wikipedia.org
Dried spirulina is 5% water, 24% carbohydrates, 8% fat, and 57% protein (table). In a reference amount of 100 g (3.5 oz), dried spirulina powder supplies 290 kilocalories (1,200 kJ) and is a rich source (20% or more of the Daily Value, DV) of numerous essential nutrients, particularly B vitamins (thiamin, riboflavin, and niacin), and dietary minerals, such as iron and manganese (table). The lipid content of spirulina is about 8% by weight. The polyunsaturated fatty acids include gamma-linolenic acid and linoleic acid. In contrast to the "high" content reported in a 2003 study, two other analyses found low levels of omega-3 fatty acids in spirulina.
CooA is a heme-containing transcription factor that responds to the presence of carbon monoxide. This protein forms homodimers and is a homolog of cAMP receptor protein. The most well-studied CooA homolog comes from Rhodospirillum rubrum (RrCooA), but the homolog from Carboxydothermus hydrogenoformans (ChCooA) has also been characterized. The main structural difference between these homologs lies in ferric heme coordination. In RrCooA, the ferric heme iron is ligated by a cysteine and the amine of the N-terminal proline; in the ferrous state, a ligand switch occurs in which a histidine replaces the thiolate. In contrast, ChCooA features histidine and the N-terminal amine as ligands in both ferric and ferrous states.
Ataxia Severe hypoventilation Acute narrow-angle glaucoma Severe hepatic deficiencies (hepatitis and liver cirrhosis decrease elimination by a factor of two) Severe renal deficiencies (for example, patients on dialysis) Liver disorders Severe sleep apnea Severe depression, particularly when accompanied by suicidal tendencies Psychosis Pregnancy or breastfeeding Caution required in elderly or debilitated patients Coma or shock Abrupt discontinuation of therapy Acute intoxication with alcohol, narcotics, or other psychoactive substances (with the exception of hallucinogens or some stimulants, where it is occasionally used as a treatment for overdose) History of alcohol or drug dependence Myasthenia gravis, an autoimmune disorder causing marked fatiguability Hypersensitivity or allergy to any drug in the benzodiazepine class
Sources: en.wikipedia.org
SR9009 is a synthetic research compound that activates the REV-ERBα and REV-ERBβ nuclear receptors. It is not an approved drug and has no established human therapeutic use. Most published biological data come from cell and rodent studies.
No. SR9009 is frequently mislabeled as a SARM in online discussions, but it does not target androgen receptors. Its known mechanism involves REV-ERB nuclear receptors and circadian-metabolic gene regulation.
Human clinical data are very limited. There is no approved human use, and safety and efficacy in people are not established. Most evidence comes from preclinical models, so effects observed in animals may not apply to humans.
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.