If you have been reading about anti-doping and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Last reviewed on 2025-12-09. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
SR9009 is not approved as a medicine by major regulatory agencies. It is commonly sold as a research chemical, a category that may fall outside customary drug approval and quality rules. In sports, the World Anti-Doping Agency lists SR9009 as a prohibited substance. Athletes who use it can face sanctions if it is detected in a sample. Legal status varies by country, and importation may be restricted. Enforcement practices differ across borders.
Detection of SR9009 in biological samples usually employs liquid chromatography coupled with tandem mass spectrometry. This method can identify the parent compound and sometimes metabolites in urine or blood. Because exposure can be low and clearance may be rapid, sample timing and limits of detection matter. Laboratories validate assays for sensitivity and specificity. Results are interpreted alongside chain-of-custody and quality-control records. Urine is the common matrix for anti-doping analysis, while blood may be used in research settings.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C20H24ClN3O4S | Derived from published structure. |
| Molecular weight | 437.94 g/mol | Calculated value. |
| Appearance | White to off-white solid | Typical for purified research samples. |
| Solubility | DMSO, ethanol; low in water | Class: poorly water-soluble. |
| Typical storage | -20 °C, desiccated, protected from light | Limits degradation. |
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.
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.
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.
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 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.
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.
Laboratory samples of SR9009 are typically handled as research chemicals rather than pharmaceuticals. Suppliers usually state that the material is for research use only and not for human or veterinary administration. Storage recommendations generally call for a freezer at approximately −20 °C, protection from light, and a desiccated environment. The solid is often described as a white to off-white powder. Solubility is commonly reported in organic solvents such as dimethyl sulfoxide and ethanol, with low solubility in water.
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.
== Function == As their names suggests, the Prolyl 3-hydroxylase 2 and its relatives Prolyl 3-hydroxylase 1 and 3 function as collagen prolyl 3-hydroxylases. This means they act on the amino acid, proline, located in collagen precursor proteins, and attach a hydroxyl at the 3-position, converting the proline into 3-hydroxyproline. This seems to function to help the corresponding collagen fibrils bind together and align properly. P3H2 differs from P3H1 in a number of important ways. It is primarily expressed in basement membrane-rich tissues (P3H1 is primarily in fibrillar collagens rich tissues). It is also able to act on type IV collagen (especially COL4A1), unlike P3H1. Both enzymes are able to act on Type I collagen (and COL1A1), but they tend to modify the prolines at different positions. P3H2 also appears to function on its own, while P3H1 forms a complex with two other proteins (CRTAP and CypB).
=== Plant glutamate cysteine ligase === The plant glutamate cysteine ligase is a redox-sensitive homodimeric enzyme, conserved in the plant kingdom. In an oxidizing environment, intermolecular disulfide bridges are formed and the enzyme switches to the dimeric active state. The midpoint potential of the critical cysteine pair is -318 mV. In addition to the redox-dependent control, the plant GCL enzyme is feedback inhibited by glutathione. GCL is exclusively located in plastids, and glutathione synthetase (GS) is dual-targeted to plastids and cytosol, thus GSH and gamma-glutamylcysteine are exported from the plastids. Studies also shown that restricting GCL activity to the cytosol or glutathione biosynthesis to the plastids is sufficient for normal plant development and stress tolerance. Both glutathione biosynthesis enzymes are essential in plants; knock-outs of GCL and GS are lethal to embryo and seedling, respectively. As of late 2007, six structures have been solved for this class of enzymes, with PDB accession codes PDB: 1V4G, PDB: 1VA6, PDB: 2D32, PDB: 2D33, PDB: 2GWC, and PDB: 2GWD.
=== Relapsing-remitting MS === Medications are modestly effective at decreasing the number of attacks in relapsing-remitting multiple sclerosis and in reducing the accumulation of brain lesions, which is measured using gadolinium-enhanced magnetic resonance imaging (MRI). Interferons reduce relapses by approximately 30% and their safe profile make them the first-line treatments. Nevertheless, not all the patients are responsive to these therapies. It is known that 30% of MS patients are non-responsive to Beta interferon. They can be classified in genetic, pharmacological and pathogenetic non-responders. One of the factors related to non-respondance is the presence of high levels of interferon beta neutralizing antibodies. Interferon therapy, and specially interferon beta 1b, induces the production of neutralizing antibodies, usually in the second 6 months of treatment, in 5 to 30% of treated patients. Moreover, a subset of RRMS patients with specially active MS, sometimes called "rapidly worsening MS" are normally non-responders to interferon beta 1a. While more studies of the long-term effects of the drugs are needed, existing data on the effects of interferons indicate that early-initiated long-term therapy is safe and it is related to better outcomes.
Sources: en.wikipedia.org
See the Bombers fly up, up! To win the premiership flag. Our boys who play this grand old game, Are always striving for glory and fame! See the Bombers fly up, up, The other teams they don't fear; They all try their best, But they can't get near, As the Bombers fly up! Songwriter Mike Brady, of "Up There Cazaly" fame, penned an updated version of the song in 1999 complete with a new verse arrangement, but it was not well received. However, this version is occasionally played at club functions. In 2018, Andrews revealed that there was an error in the lyrics, in which in the line "The other teams they don't fear", the word "they" was supposed to be "we".
Of the people studied, 66% were cocaine users. After experiencing long-term in-patient treatment, only 22% returned to the use of cocaine. During the 1990s, the Clinton administration commissioned a major cocaine policy study by the RAND Drug Policy Research Center. The report recommended that $3 billion be switched from federal and local law enforcement to treatment, concluding that treatment is the cheapest way to cut drug use, and twenty-three times more effective than the supply-side war on drugs.
== Natural occurrence of piperidine and derivatives == Piperidine itself has been obtained from black pepper, from Psilocaulon absimile (Aizoaceae), and in Petrosimonia monandra. The piperidine structural motif is present in numerous natural alkaloids. These include piperine, which gives black pepper its spicy taste. This gave the compound its name. Other examples are the fire ant toxin solenopsin, the nicotine analog anabasine of tree tobacco (Nicotiana glauca), lobeline of Indian tobacco, and the toxic alkaloid coniine from poison hemlock, which was used to put Socrates to death.
Initial letters are used where there is no ambiguity: C cysteine, H histidine, I isoleucine, M methionine, S serine, V valine. No other amino acids in this set begin with each of those letters. Where arbitrary assignment is needed, the structurally simpler amino acids are given precedence: A alanine, G glycine, L leucine, P proline, T threonine. For example, alanine is simpler than arginine or asparagine, the other amino acids starting with "a". F PHenylalanine and R aRginine are assigned by being phonetically suggestive, W tryptophan is assigned based on the double ring being visually suggestive to the bulky letter W, K lysine and Y tyrosine are assigned as alphabetically nearest to their initials L and T (note that U was avoided for its similarity with V, while X was reserved for undetermined or atypical amino acids); for tyrosine the mnemonic tYrosine was also proposed, D aspartate was assigned arbitrarily, with the proposed mnemonic asparDic acid; E glutamate was assigned in alphabetical sequence being larger by merely one methylene –CH2– group, N asparagine was assigned arbitrarily, with the proposed mnemonic asparagiNe; Q glutamine was assigned in alphabetical sequence of those still available (note again that O was avoided due to similarity with D), with the proposed mnemonic Qlutamine.
Sources: en.wikipedia.org
Pyroglutamic acid (also known as PCA, 5-oxoproline, pidolic acid) is a ubiquitous but understudied natural amino acid derivative in which the free amino group of glutamic acid or glutamine cyclizes to form a lactam. The names of pyroglutamic acid conjugate base, anion, salts, and esters are pyroglutamate, 5-oxoprolinate, or pidolate.
== Clinical pharmacology == Although the drugs omeprazole, lansoprazole, pantoprazole, and rabeprazole share common structure and mode of action, each differs somewhat in its clinical pharmacology. Differing pyridine and benzimidazole substituents result in small, but potentially significant different physical and chemical properties. Direct comparison of pantoprazole sodium with other anti-secretory drugs showed that it was significantly more effective than H2-receptor antagonists and either equivalent or better than other clinically used PPIs. Another study states rabeprazole undergoes activation over a greater pH range than omeprazole, lansoprazole, and pantoprazole, and converts to the sulphenamide form more rapidly than any of these three drugs. Most oral PPI preparations are enteric-coated, due to the rapid degradation of the drugs in the acidic conditions of the stomach. For example omeprazole is unstable in acid with a half-life of 2 min at pH 1–3, but is significantly more stable at pH 7 (half-life ca. 20 h). The acid protective coating prevents conversion to the active principle in the lumen of the stomach, which then will react with any available sulfhydryl group in food and will not penetrate to the lumen of the secretory canaliculus The oral bioavailability of PPIs is high; 77% for pantoprazole, 80–90% for lansoprazole and 89% for esomeprazole. All the PPIs except tenatoprazole are rapidly metabolized in the liver by CYP enzymes, mostly by CYP2C19 and CYP3A4. PPIs are sensitive to CYP enzymes and have different pharmacokinetic profiles.
=== Appeals === Since the amendment of the Criminal Procedure Code in 1992, all capital cases have been heard by a single judge in the High Court instead of two judges. After conviction and sentencing, the offender has the option of making an appeal to the Court of Appeal. If the appeal fails, the final recourse rests with the President of Singapore, who has the power to grant clemency on the advice of the Cabinet. In exceptional cases since 2012, the Court of Appeal would be asked to review its previous decisions in concluded criminal appeals where it was necessary to correct a miscarriage of justice, most of which involved drug cases attracting the death penalty. The exact number of successful appeals is unknown. In November 1995, one Poh Kay Keong had his conviction overturned after the court found that his statement to a Central Narcotics Bureau officer had been made under duress. Another was the case of Nadasan Chandra Secharan, who was initially found guilty of murder and condemned to death by the High Court in June 1996, but later acquitted of murder by the Court of Appeal in January 1997 after they found the evidence against him was insufficient to show that he had murdered his lover Ramapiram Kannickaisparry.
==== Analysis ==== Analysis of FISH specimens is done by fluorescence microscopy by a clinical laboratory specialist in cytogenetics. For oncology, generally, a large number of interphase cells are scored in order to rule out low-level residual disease, generally between 200 and 1,000 cells are counted and scored. For congenital problems usually 20 metaphase cells are scored.
=== N05AB Phenothiazines with piperazine structure === N05AB01 Dixyrazine N05AB02 Fluphenazine N05AB03 Perphenazine N05AB04 Prochlorperazine N05AB05 Thiopropazate N05AB06 Trifluoperazine N05AB07 Acetophenazine N05AB08 Thioproperazine N05AB09 Butaperazine N05AB10 Perazine N05AB13 Metofenazate
Sources: en.wikipedia.org
SR9009 is a synthetic REV-ERB agonist used in laboratory research. It is not an approved drug, and its effects in humans are not well characterized. It is often sold as a research chemical under the name Stenabolic.
No. SR9009 targets the nuclear receptors REV-ERBα and REV-ERBβ, not the androgen receptor. This mechanism differs from selective androgen receptor modulators and from exercise mimetics that act on PPARδ.
Published evidence is mainly preclinical, using cell cultures and animal models. Controlled human trials are not well documented in the public literature. Claims about human performance or health effects therefore remain unsupported by robust clinical data.
Its legal status depends on the country and intended use. It is not an approved medicine in major jurisdictions. In sport, it is prohibited by anti-doping rules.