If you have been reading about anti-doping testing 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.
Updated 2026-05-01. Numbers and descriptions here follow the published literature rather than marketing material.
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.
Laboratory identification of SR9009 typically relies on chromatographic separation coupled to mass spectrometry, often with ultraviolet detection as a secondary check. Nuclear magnetic resonance spectroscopy can confirm molecular structure when a reference standard is available. Because many suppliers sell the compound as a research chemical, independent identity testing is important for experimental reproducibility. A single retention time is not sufficient proof of identity, especially when related compounds may be present. Purity assessments usually report a percentage based on area normalization.
SR9009 is generally described as poorly soluble in water and more soluble in organic solvents such as dimethyl sulfoxide and ethanol. Stock solutions are commonly prepared in an organic solvent before dilution into an aqueous buffer or vehicle. Precipitation can occur if the organic fraction is reduced too quickly or if the final concentration exceeds the compound's solubility limit. Sonication or gentle warming may aid dissolution in some protocols, but excessive heat can promote degradation. Container material and pH can also influence observed solubility.
| 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 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.
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.
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.
== Early life and education == Valerie Horsley was raised by a single mother, who was working toward her doctorate in industrial engineering throughout her early childhood. Horsley was often placed in the care of graduate students, who served as her babysitters. She initially considered a career in medicine working as a physician, but opted to pursue a career in research instead. In 1998, Horsley achieved a Bachelor of Science in biology at Furman University, and later her doctorate from Emory University in 2003.
demonstrated DE sorting and isolation on-chip followed by FACS that allows for high sorting throughput of encapsulated mammalian cells, from which genetic material can later be extracted. While fluorogenic labeling is a powerful tool for tracking and sorting, it is not always compatible with droplet-based microfluidic systems and experimental design. New label-free and non-fluorescence-based detection techniques have recently been reported. In 2016, Gielen et al. published an absorbance-activated droplet sorting (AADS) microfluidic device and demonstrated its functionality by directing the evolution of a phenylalanine dehydrogenase. In 2016, Sun et al. demonstrated the use of SE droplets and high-throughput MS to screen enzyme activators and inhibitors by screening a transaminase library. In 2019, Pan et al. showed sorting of droplets by interfacial tensions, which are affected by droplet content. In 2020, Haidas et al. presented a microfluidic approach that uses both matrix-assisted laser desorption ionization mass spectrometry (MALDI-MS) and fluorescence microscopy, which the authors used to measure the concentration and activity of phytase, respectively, in yeast cells. In 2020, Holland-Moritz et al. published their mass activated droplet sorting (MADS) method, which integrates MS analysis with fluorescence-activated droplet sorting (FADS). Using this method, droplets are split and analyzed separately by both MS and FADS. The power of this method was demonstrated by screening the activity of a transaminase library expressed in vitro.
=== Liver === As a meal containing carbohydrates or protein is eaten and digested, blood glucose levels rise, and the pancreas secretes insulin. Blood glucose from the portal vein enters liver cells (hepatocytes). Insulin acts on the hepatocytes to stimulate the action of several enzymes, including glycogen synthase. Glucose molecules are added to the chains of glycogen as long as both insulin and glucose remain plentiful. In this postprandial or "fed" state, the liver takes in more glucose from the blood than it releases. After a meal has been digested and glucose levels begin to fall, insulin secretion is reduced, and glycogen synthesis stops. When it is needed for energy, glycogen is broken down and converted again to glucose. Glycogen phosphorylase is the primary enzyme of glycogen breakdown. For the next 8–12 hours, glucose derived from liver glycogen is the primary source of blood glucose used by the rest of the body for fuel. Glucagon, another hormone produced by the pancreas, in many respects serves as a countersignal to insulin. In response to insulin levels being below normal (when blood levels of glucose begin to fall below the normal range), glucagon is secreted in increasing amounts and stimulates both glycogenolysis (the breakdown of glycogen) and gluconeogenesis (the production of glucose from other sources).
Sources: en.wikipedia.org
== History == Efficacy was evaluated in ARROS-1 (NCT05118789), a multi-center, single-arm, open-label, multi-cohort trial in participants with previously treated locally advanced or metastatic ROS1-positive NSCLC. The efficacy population included 117 participants; 59 who received one prior ROS1 tyrosine kinase inhibitor and 58 who received two or more prior ROS1 tyrosine kinase inhibitors, including lorlatinib, repotrectinib, and/or taletrectinib.
Though he claimed to have had a delusional episode triggered by PTSD and believed his children were in danger, Monk was sentenced to 13 years in prison, and was incarcerated at the Pasquotank Correctional Institution.
== Clinical significance == Tyrosine hydroxylase deficiency leads to impaired synthesis of dopamine as well as epinephrine and norepinephrine. It is represented by a progressive encephalopathy and poor prognosis. Clinical features include dystonia that is minimally or nonresponsive to levodopa, extrapyramidal symptoms, ptosis, miosis, and postural hypotension. This is a progressive and often lethal disorder, which can be improved but not cured by levodopa. Due to the low number of patients and overlapping symptoms with other disorders, early diagnosis and treatment remain challenging. Response to treatment is variable and the long-term and functional outcome is unknown. To provide a basis for improving the understanding of the epidemiology, genotype/phenotype correlation and outcome of these diseases, their impact on the quality of life of patients, and for evaluating diagnostic and therapeutic strategies, a patient registry was established by the noncommercial International Working Group on Neurotransmitter Related Disorders (iNTD). Furthermore, alterations in the tyrosine hydroxylase enzyme activity may be involved in disorders such as Segawa's dystonia, Parkinson's disease and schizophrenia. Tyrosine hydroxylase is activated by phosphorylation dependent binding to 14-3-3 proteins. Since the 14-3-3 proteins also are likely to be associated with neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease and Huntington's disease, it makes an indirect link between tyrosine hydroxylase and these diseases.
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.
Liquid chromatography with mass spectrometry is a common approach. Ultraviolet detection and nuclear magnetic resonance can support identification when suitable standards are available.