Everything below concerns SR9009. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-07-06. Where a claim depends on a specific study, the study is described rather than over-claimed.
SR9009 is a synthetic small molecule developed as an agonist of the nuclear receptors REV-ERBα (NR1D1) and REV-ERBβ (NR1D2). These receptors help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, SR9009 alters transcription of genes involved in lipid metabolism, inflammation, and mitochondrial function. It is not an approved medicine, and its pharmacological profile in humans remains largely uncharacterized. The compound is frequently discussed in the context of circadian biology and metabolic research rather than clinical use.
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 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.
| 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. |
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.
Analytical identification and purity assessment often use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Liquid chromatography–tandem mass spectrometry is used to detect and quantify SR9009 in biological matrices, including urine and blood, for anti-doping or pharmacokinetic studies. Nuclear magnetic resonance spectroscopy can confirm molecular structure. Stability depends on form and storage: the solid is generally more stable than solutions, and repeated freeze–thaw cycles may degrade samples. Purity is typically reported as a percentage from a certificate of analysis.
Regulatory treatment of SR9009 varies by country and context. It is not approved as a therapeutic drug by agencies such as the United States Food and Drug Administration or the European Medicines Agency. Sports authorities list it as a prohibited substance; the World Anti-Doping Agency classifies it among hormone and metabolic modulators. Legal status for personal possession or sale differs across jurisdictions, and some countries may restrict it under analog or research chemical laws. Buyers who seek verified material often rely on independent laboratory testing because online product labels may not match contents.
Scientific discussion of SR9009 often separates animal evidence from human anecdote. Rodent studies provide controlled data on endurance, metabolism, and gene expression, but they use specific strains, doses, and treatment durations. Human reports are mostly uncontrolled and cannot establish cause and effect. Open questions include oral bioavailability, tissue distribution, metabolic stability, and long-term effects. Review articles generally call for more rigorous pharmacokinetic and safety research before any clinical use could be considered.
Analytical methods for SR9009 typically rely on liquid chromatography coupled with tandem mass spectrometry. The technique can separate the parent compound from related substances and detect low concentrations in biological matrices. Urine and blood are common samples in anti-doping testing, while in vitro studies may use cell culture media. Rapid metabolism and low expected concentrations make method validation important for reliable identification. Exact metabolite patterns can vary by species and are not fully mapped.
Regulatory treatment of SR9009 reflects its investigational status. The compound has no approved human therapeutic indication, and sports authorities prohibit its use. It appears on anti-doping lists as a non-approved substance or metabolic modulator, depending on the list version. Products sold online as research chemicals are not quality-controlled medicines, so their identity and purity can differ from the label. Such products may also contain unlisted compounds, which complicates both testing and safety assessment.
== Select publications == Masur, S.K. (1969). "Fine structure of the autotransplanted pituitary of the red eft. Notophthalmus viridescens". Gen. Comp. Endocrin. 12: 12–32. Masur, S.K.; Holtzman, E.; Schwartz, I.L.; Walter, R. (1971). "Correlation between pinocytosis and hydroosmosis induced by neurohypophyseal hormone and mediated by adenosine 3', 5'-cyclic monophosphate". J. Cell Biol. 49: 582–589. Masur, S.K.; Dewal, H.S.; Dinh, T.T.; Erenburg, I.; Petridou, S. (1996). "Myofibroblasts differentiate from fibroblasts plated at low density". Proc. Natl. Acad. Sci. 93: 4219–4223. Maltseva, O; Folger, P; Zekaria, D; Petridou, S; Masur, SK (2001). "Fibroblast growth factor reversal of the corneal myofibroblast phenotype". Invest Ophthalmol Vis Sci. 42: 2490–5. PMID 11581188.. Masur, S.; Kane, C. M. (2001-12-21). "Tapping science's women for the podium". Science. 294 (5551): 2480. doi:10.1126/science.294.5551.2480a. ISSN 0036-8075. PMID 11770518.. Bernstein, AM; Twining, SS; Warejcka, DJ; Tall, E; Masur, SK (2007). "Urokinase receptor cleavage: a crucial step in fibroblast-to-myofibroblast differentiation". Mol Biol Cell. 18: 2716–27. doi:10.1091/mbc.e06-10-0912. PMC 1924808. PMID 17507651.. Masur, Sandra Kazahn (January 2013). "Women in cell biology: a seat at the table and a place at the podium". Molecular Biology of the Cell. 24 (2): 57–60. doi:10.1091/mbc.E12-07-0517. ISSN 1939-4586. PMC 3541963. PMID 23307103.. Masur, Sandra K. (2015-08-01). "Invisible woman?". Trends in Cell Biology. 25 (8): 437–439. doi:10.1016/j.tcb.2015.06.001. ISSN 0962-8924.
Like the CNO-III, this branch is also only significant in massive stars. The reactions are started when one of the reactions in CNO-III results in fluorine-19 and a photon instead of nitrogen-15 and an alpha particle, and continues
CORD provides a strong common voice to advocate for health policy and a healthcare system that works for those with rare disorders. NORD - National Organization for Rare Disorders (NORD) is an American national non-profit patient advocacy organization that is dedicated to individuals with rare diseases and the organizations that serve them. EURODIS - Rare Diseases Europe (EURODIS) is a unique, non-profit alliance of over 700 rare disease patient organizations across Europe that work together to improve the lives of the 30 million people living with a rare disease in Europe.
Sources: en.wikipedia.org
== Supply chain == As of 2021, almost 90% of raw lithium extraction originated from three countries: Australia (53%), Chile (24%), and China (10%), with almost all production coming from China (56%), Chile (32%) and Argentina (11%).
=== Files === Copying files: Making copies of files is the simplest and most common way to perform a backup. A means to perform this basic function is included in all backup software and all operating systems. Partial file copying: A backup may include only the blocks or bytes within a file that have changed in a given period of time. This can substantially reduce needed storage space, but requires higher sophistication to reconstruct files in a restore situation. Some implementations require integration with the source file system. Deleted files: To prevent the unintentional restoration of files that have been intentionally deleted, a record of the deletion must be kept. Versioning of files: Most backup applications, other than those that do only full only/System imaging, also back up files that have been modified since the last backup. "That way, you can retrieve many different versions of a given file, and if you delete it on your hard disk, you can still find it in your [information repository] archive."
Many important chemical compounds are derived from benzene by replacing one or more of its hydrogen atoms with another functional group. Examples of simple benzene derivatives are phenol, toluene, and aniline, abbreviated PhOH, PhMe, and PhNH2, respectively. Linking benzene rings gives biphenyl, C6H5–C6H5. Further loss of hydrogen gives "fused" aromatic hydrocarbons, such as naphthalene, anthracene, phenanthrene, and pyrene. The limit of the fusion process is the hydrogen-free allotrope of carbon, graphite. In heterocycles, carbon atoms in the benzene ring are replaced with other elements. The most important variations contain nitrogen. Replacing one CH with N gives the compound pyridine, C5H5N. Although benzene and pyridine are structurally related, benzene cannot be converted into pyridine. Replacement of a second CH bond with N gives, depending on the location of the second N, pyridazine, pyrimidine, or pyrazine.
Sources: en.wikipedia.org
== Interactions == The substance is metabolised by the liver enzyme CYP3A4. In a study, the strong CYP3A4 inhibitor ketoconazole increased the maximal blood plasma concentrations of lercanidipine by a factor of eight, and the area under the curve by a factor of 15. In another study, ciclosporin increased lercanidipine plasma levels threefold when given at the same time. Other inhibitors of this enzyme, such as itraconazole, erythromycin, and grapefruit juice, are also expected to increase plasma concentrations and thus amplify the antihypertensive effect. Conversely, CYP3A4 inductors such as carbamazepine, rifampicin, and St John's wort probably lower plasma levels and effectiveness of lercanidipine. By comparison, amlodipine has a lower potential for CYP3A4 mediated interactions. Lercanidipine increases plasma levels of ciclosporin and digoxin.
== History == The toxin was first described in detail in 1969 by two Brazilian researchers from University of Campinas, Júlia Prado-Franceschi and Oswaldo Vital-Brazil. The snake C-type lectin convulxin was reported to activate platelets in a similar way to collagen in the late 1970s, but this was only announced after the discovery of the association with the FcR γ-chain and after it was recognized to mediate activation through GPVI. Now this toxin is widely used to study mammalian platelet receptors.
=== As the OAM (1991–1998) === Joseph J. Jacobs was appointed the first director of the OAM in 1992. Jacobs' support for rigorous scientific methodology caused friction with Democrat U.S. Senator Tom Harkin and other OAM patrons. Harkin believed his allergies had been cured by bee pollen pills and expressed frustration with the "unbendable rules" of randomized clinical trials, saying, "it is not necessary for the scientific community to understand the process before the American public can benefit from these therapies." Harkin's office reportedly pressured the OAM to fund studies of favored theories, including the use of bee pollen and antineoplastons as treatments. OAM board member Barrie Cassileth publicly criticized the office as a purveyor of nonsense and described it as a "place where opinions are counted as equal to data". After Harkin appeared on television in 1994 with cancer patients who blamed Jacobs for blocking their access to antineoplastons, Jacobs resigned from the OAM in frustration. In an interview with Science, Jacobs criticized Harkin and other politicians for pressuring his office, promoting certain therapies, and, he says, attempting an end-run around objective science." Harkin drew support from Iowa Democrat Representative Berkley Bedell, who believed that cow colostrum had cured his Lyme disease. The OAM's budget grew in the 1990s. The office drew increasing criticism for its perceived lack of rigorous scientific study of alternative approaches favoring uncritical boosterism.
Molecular biomarkers have been defined as biomarkers that can be discovered using basic and acceptable platforms such as genomics and proteomics. Many genomic and proteomics techniques are available for biomarker discovery and a few techniques that are recently being used can be found on that page. Apart from genomics and proteomics platforms biomarker assay techniques, metabolomics, lipidomics, glycomics, and secretomics are the most commonly used as techniques in identification of biomarkers. Biomarkers can be classified on their clinical applications as molecular biomarkers, cellular biomarkers or imaging biomarkers. Four of the main types of molecular biomarkers are genomic biomarkers, transcriptomic biomarkers, proteomic biomarkers and metabolic biomarkers.
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 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.