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Sr9009 Identity And Mechanism — Evidence Review

By Editorial Desk · published 2026-02-18 · last reviewed 2026-03-29 · Topic

If you have been reading about research chemical 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 2026-03-29. Numbers and descriptions here follow the published literature rather than marketing material.

SR9009 Identity and Mechanism

SR9009 is frequently discussed alongside other REV-ERB ligands, including synthetic agonists and natural heme-related molecules. Its selectivity for REV-ERB over related nuclear receptors has been measured in binding and reporter assays, though off-target activity at higher concentrations is possible. The compound is prohibited in sport by the World Anti-Doping Agency, and it is not approved for any medical use in major jurisdictions. Products sold online may be labeled as research chemicals, and their identity and purity are not guaranteed by regulatory review.

SR9009 is a synthetic small molecule that acts on the nuclear receptors REV-ERBα and REV-ERBβ. These receptors are part of the circadian clock machinery and normally repress transcription of certain target genes. In laboratory research, SR9009 is used as a chemical tool to study how REV-ERB activity influences metabolism, inflammation, and daily biological rhythms. The compound is not an approved medicine, and its effects in humans remain largely uncharacterized. It is often described as an investigational agent rather than a therapeutic product.

REV-ERB proteins typically suppress gene expression by recruiting corepressor complexes to DNA response elements. SR9009 binds these receptors and strengthens that repressive action in cell-based assays. Studies in rodents have reported changes in lipid handling, mitochondrial function, and exercise capacity after treatment. Such findings are often cited as evidence for metabolic effects, but species differences and limited pharmacokinetic data make direct translation to humans uncertain. Researchers continue to examine which effects are robust and which depend on specific experimental conditions.

Background and Mechanism

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 at a glance

PropertyValueNotes
Common nameSR9009Also marketed informally as Stenabolic
Chemical classSynthetic REV-ERB agonistBinds REV-ERBα and REV-ERBβ
Molecular formulaC24H30ClN3O4SApproximate molecular weight 492 g/mol
CAS Registry Number1379686-30-2Identifier for the parent compound
Regulatory statusNot approved for human useProhibited in sport by WADA

Analytical Detection and Laboratory Handling

Detection in biological samples can be complicated by rapid metabolism and low circulating concentrations. Some studies report phase I and phase II metabolites, and analytical methods may need to target those species in addition to the parent compound. Immunoassays are not broadly available, so mass spectrometry remains the main confirmatory approach. For anti-doping testing, laboratories look for SR9009 and its metabolites using validated LC-MS methods. Open questions include how long metabolites remain detectable and how different routes of administration alter detection windows.

In laboratory settings, SR9009 is typically characterized by liquid chromatography–mass spectrometry (LC-MS) or high-performance liquid chromatography with ultraviolet detection (HPLC-UV). These methods can confirm identity and estimate purity, but they require reference standards for accurate quantification. Because SR9009 is not a licensed pharmaceutical, no harmonized pharmacopeial monograph exists. Laboratories often validate in-house methods for matrices such as plasma, urine, or cell culture media. Sample preparation may involve protein precipitation or liquid-liquid extraction before analysis.

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Supporting material

Progesterone is the most important progestogen in the body. As a potent agonist of the nuclear progesterone receptor (nPR) (with an affinity of KD = 1 nM), the resulting effects on ribosomal transcription play a major role in regulation of female reproduction. In addition, progesterone is an agonist of the more recently discovered membrane progesterone receptors (mPRs), of which the expression has regulation effects in reproduction function (oocyte maturation, labor, and sperm motility) and cancer, although the roles are not yet well defined. Progesterone is also a ligand of the PGRMC1 (progesterone receptor membrane component 1) which impacts tumor progression, metabolic regulation, and viability control of nerve cells. Moreover, progesterone is also known to be an antagonist of the sigma σ1 receptor, a negative allosteric modulator of nicotinic acetylcholine receptors, and a potent antagonist of the mineralocorticoid receptor (MR). Progesterone prevents MR activation by binding to this receptor with an affinity exceeding even those of aldosterone, and glucocorticoids such as cortisol and corticosterone, and it produces antimineralocorticoid effects, such as natriuresis, at physiological concentrations. Progesterone also binds to, and behaves as a partial agonist of, the glucocorticoid receptor (GR), albeit with very low potency (EC50 >100-fold less relative to cortisol). Through its neurosteroid active metabolites, such as 5α-dihydroprogesterone and allopregnanolone, progesterone acts indirectly as a positive allosteric modulator of the GABAA receptor.

This is problematic long-term and can lead to ACTH-receptor pathway-related side effects including: Cushing's syndrome, fluid retention, glaucoma, and cardiovascular disorders. Mutations in this receptor cause familial glucocorticoid deficiency (FGD) type 1, in which patients have high levels of serum ACTH and low levels of cortisol. Mutation of the receptor gene causes 25% of FGD, and mutation on the MRAP gene causes 20% of FGD. Mutations of ACTH can also contribute to this pathology: mutation of the "message sequence" inhibits cAMP production when bound to the ACTH receptor, and mutation of the "address sequence" inhibits binding to the receptor altogether.

== Pulsatile insulin and the liver == Normally, insulin is secreted from the pancreas in pulses into the portal vein which brings blood into the liver in variable amounts, closely related to ingestion of meals. For induction and maintenance of insulin-dependent enzymes essential for glucose metabolism in the liver (e.g. hepatic glucokinase, phosphofructokinase, and pyruvate kinase), the hepatocytes require a defined insulin level (200-500 μU/ml in the portal vein) concomitant with high glucose levels (which acts as a bimolecular signal). In non-diabetic subjects, portal insulin concentrations are twofold to threefold greater than those in the peripheral circulation. During the first pass through the liver, 50% of the insulin is removed, strongly insinuating that the liver is the principal metabolic target organ of the gastrointestinal tract and the pancreas. The insulin retained by the hepatocytes may itself be essential for the long-term effects of insulin on hepatic glucose metabolism as well as growth and de novo enzyme synthesis. Following oral glucose intake, the liver accounts for an equal or greater portion of total net glucose uptake compared to the periphery. Insulin exerts pivotal control of glucose levels through its ability to regulate hepatic glucose production directly or indirectly. The traditional subcutaneous (S.C.) insulin administration regimens used by diabetic patients fails to capture the pulsatile nature of natural insulin secretion and does not reach high enough insulin concentrations at the hepatocyte level (e.g., 10 U regular insulin injected S.C.

Male sex Plus three of the following in the first two years of disease: Erythrocyte sedimentation rate (ESR) >30 mm/h Unresponsive to NSAIDs Limitation of lumbar spine range of motion Sausage-like fingers or toes Oligoarthritis Onset <16 years old

Sources: en.wikipedia.org

Notes from published material

A total of 21 patients who died triggered an adverse event finding. The investigation into the deaths of the elderly military veterans began in June 2018 and lasted over two years. Mays remained free; she was questioned three times during the course of the investigation. Each time, she denied any involvement in the deaths. Mays's second interview was conducted by a special agent from the FBI Academy in Quantico, Virginia, and lasted five hours. By then, investigators had built up a strong circumstantial case against Mays, including her internet search history of female serial killers; her Netflix viewing of the series Nurses Who Kill, one episode of which focused on insulin killings; and phone calls made by Mays to her husband, Gordon, who was serving time in jail for child pornography charges in which she bemoaned having to sit with a patient that she wanted to "freaking strangle." Investigators stated that call had been made the morning after one of the blood sugar episodes.

25298Cf + 115B → 263103Lr* → 258103Lr + 5 10n The first work at Dubna on element 103 came in 1965, when they reported to have made 256Lr in 1965 by bombarding 243Am with 18O, identifying it indirectly from its granddaughter fermium-252. The half-life they reported was somewhat too high, possibly due to background events. Later 1967 work on the same reaction identified two decay energies in the ranges 8.35–8.50 MeV and 8.50–8.60 MeV: these were assigned to 256Lr and 257Lr. Despite repeat attempts, they were unable to confirm assignment of an alpha emitter with a half-life of 8 seconds to 257Lr. The Russians proposed the name "rutherfordium" for the new element in 1967; this name was later proposed by Berkeley for element 104.

== Side effects == A press release by GlaxoSmithKline in February 2007 noted that there is a greater incidence of fractures of the upper arms, hands and feet in female diabetics given rosiglitazone compared with those given metformin or glyburide. The information was based on data from the ADOPT trial. Following release of this statement, Takeda Pharmaceutical Company, the developer of pioglitazone (sold as Actos in many markets) admitted that it has similar implications for female patients. The risk of hypoglycemia is low in the absence of other drugs that lower blood glucose. Pioglitazone can cause fluid retention and peripheral edema. As a result, it may precipitate congestive heart failure (which worsens with fluid overload in those at risk). It may cause anemia. Mild weight gain is common due to increase in subcutaneous adipose tissue. In studies, patients on pioglitazone had an increased proportion of upper respiratory tract infection, sinusitis, headache, myalgia and tooth problems. Chronic administration of the drug has led to occasional instances of cholestatic hepatitis, reversible upon drug discontinuation. On 30 July 2007, an Advisory Committee of the Food and Drug Administration concluded that the use of rosiglitazone for the treatment of type 2 diabetes was associated with a greater risk of "myocardial ischemic events" when compared to placebo, but when compared to other diabetes drugs, there was no increased risk. Pioglitazone is currently being reviewed.

Bolivian officials also asserted that more than 1,660 antidrug operations during 1988 had resulted in the destruction of from 1,000 to 1,400 clandestine cocaine factories and laboratories (80 percent of them in Cochabamba and Santa Cruz departments), the confiscation of about 10,000 kilograms of cocaine, and the arrest of some 700 individuals. The minister of planning and coordination stated in December that 2,900 hectares of coca crops had been eradicated under the financial compensation program. Bolivia's anti-narcotics units apprehended several prominent traffickers in 1988. At the same time that the 1988 Antinarcotics Law was promulgated, the Umopar arrested Suárez at his hacienda in Beni Department. According to one theory, Suárez allowed himself to be arrested in a bid to avoid extradition to the United States. In October 1988, the Special Antinarcotics Forces captured an alleged drug "godfather," Mario Araoz Morales ("El Chichin"), by chance during a training exercise in a jungle area. In November antidrug police in the Chapare also arrested Rosa Flores de Cabrera, alias Rosa Romero de Humérez ("La Chola Rosa"), described as one of the most-wanted women in the Bolivian drugtrafficking network, with connections to the Medellín Cartel. In 1991, under pressure from the United States, Bolivia involved its military forces in anti-drugs actions, despite local opposition. Under the government of Jaime Paz Zamora (1989-1993), antidrug institutions were restructured, but Conalid remained the regulatory body.

==== History ==== The Cincinnati College of Pharmacy was chartered by the Ohio Legislature in 1850 and it was the first pharmacy school west of the Allegheny Mountains. It operated as a private college until July 1954 when it became an integral part of the University of Cincinnati. The college is named based on Jim Winkle's pledge of $10 million from his estate or trust. A Hamilton, Ohio, resident who graduated from the college in 1958. The college occupies newly remodeled research space in the Medical Sciences Building and was renovated in 2017. That space includes new classrooms, teaching labs, student club meeting space, faculty and staff offices, conference rooms and an IT help desk.

Sources: en.wikipedia.org

Further detail

It was once generally believed that life and its materials had some essential property or substance (often referred to as the "vital principle") distinct from any found in non-living matter, and it was thought that only living beings could produce the molecules of life. In 1828, Friedrich Wöhler published a paper on his serendipitous urea synthesis from potassium cyanate and ammonium sulfate; some regarded that as a direct overthrow of vitalism and the establishment of organic chemistry. However, the Wöhler synthesis has sparked controversy as some reject the death of vitalism at his hands. Since then, biochemistry has advanced, especially since the mid-20th century, with the development of new techniques such as chromatography, X-ray diffraction, dual polarisation interferometry, NMR spectroscopy, radioisotopic labeling, electron microscopy and molecular dynamics simulations. These techniques allowed for the discovery and detailed analysis of many molecules and metabolic pathways of the cell, such as glycolysis and the Krebs cycle (citric acid cycle), and led to an understanding of biochemistry on a molecular level. Another significant historic event in biochemistry is the discovery of the gene, and its role in the transfer of information in the cell. In the 1950s, James D. Watson, Francis Crick, Rosalind Franklin and Maurice Wilkins were instrumental in solving DNA structure and suggesting its relationship with the genetic transfer of information. In 1958, George Beadle and Edward Tatum received the Nobel Prize for work in fungi showing that one gene produces one enzyme.

=== Surgery === On 12 June 1831, Dupuytren performed a surgical procedure on a person with contracture of the fourth and fifth digits who had been previously told by other surgeons that the only remedy was cutting the flexor tendons. He described the condition and the operation in The Lancet in 1834 after presenting it in 1833, and posthumously in 1836 in a French publication by Hôtel-Dieu de Paris. The procedure he described was a minimally invasive needle procedure. Because of high recurrence rates, new surgical techniques were introduced, such as fasciectomy and then dermofasciectomy. Most of the diseased tissue is removed with these procedures.Recurrence rates are low. For some individuals, the partial insertion of "K-wires" into either the DIP or PIP joint of the affected digit for a period of a least 21 days to fuse the joint is the only way to halt the disease's progress. After removal of the wires, the joint is fixed into flexion, which is considered preferable to fusion at extension. Research using large datasets in the UK has shown surgery to be safe and effective. When surgery needs to be repeated, however, the research suggests there are higher risks of serious complications such as finger amputation. Amputation of fingers may be needed for severe or recurrent cases or after surgical complications.

However, it is also in contrast to higher doses of doxepin (50 to 300 mg/day), which have been found to significantly reduce latency to sleep onset. A positive dose–response relationship on sleep measures was observed for doses of doxepin between 1 and 6 mg in clinical studies, whereas the incidence of adverse effects remained constant across this dose range in both young and older adults. However, the incidence of adverse effects appeared to increase with longer treatment duration. A dose of doxepin as low as 1 mg/day was found to significantly improve most of the assessed sleep measures, but unlike the 3 and 6 mg/day doses, was not able to improve wake time during sleep. This, along with greater effect sizes with the higher doses, was likely the basis for the approval of the 3 and 6 mg doses of doxepin for insomnia and not the 1 mg dose. At very low doses, doxepin has not shown discontinuation or withdrawal effects nor rebound insomnia. Sustained effectiveness without apparent tolerance was demonstrated in clinical studies of up to 12 weeks duration. This appears to be in contrast to over-the-counter antihistamines like diphenhydramine and doxylamine and all other first-generation antihistamines, which are associated with rapid development of tolerance and dependence (by day 3 or 4 of continuous dosing) and loss of hypnotic effectiveness. It is for this reason that, unlike doxepin, they are not recommended for the chronic management of insomnia and are advised for only short-term treatment (i.e., 1 week).

== History == Efficacy was evaluated in TROPION-Breast01 (NCT05104866), a multicenter, open-label, randomized trial. Participants must have experienced disease progression, been deemed unsuitable for further endocrine therapy, and have received one or two lines of prior chemotherapy for unresectable or metastatic disease. Participants were excluded for a history of ILD/pneumonitis requiring steroids, ongoing ILD/pneumonitis, clinically active brain metastases, or clinically significant corneal disease. Participants also were excluded for ECOG performance status >1. Randomization was stratified by previous lines of chemotherapy, prior CDK4/6 inhibitor treatment, and geographical region. A total of 732 participants were randomized (1:1) to datopotamab deruxtecan (n=365) or investigator's choice of chemotherapy (n=367); eribulin (60%), capecitabine (21%), vinorelbine (10%), or gemcitabine (9%). Efficacy was evaluated in a pooled subgroup of 114 participants with locally advanced or metastatic epidermal growth factor receptor-mutated non-small cell lung cancer who had received prior treatment with an epidermal growth factor receptor-directed therapy and platinum-based chemotherapy and received datopotamab deruxtecan at the recommended dose across two clinical trials: TROPION-Lung05 and TROPION-Lung01. TROPION-Lung05 (NCT04484142) was a multi-center, single-arm trial, while TROPION-Lung01 (NCT04656652) was a multi-center, open-label, randomized controlled trial.

In the healthcare industry, open-source AI has been used in diagnostics, patient care, and personalized treatment options. Open-source libraries have been used for medical imaging for tasks such as tumor detection, improving the speed and accuracy of diagnostic processes. Additionally, OpenChem, an open-source library specifically geared toward chemistry and biology applications, enables the development of predictive models for drug discovery, helping researchers identify potential compounds for treatment.

Sources: en.wikipedia.org

Frequently asked questions

What is SR9009?

SR9009 is a synthetic research compound that binds and modulates the nuclear receptors REV-ERBα and REV-ERBβ. It is used in laboratory studies of circadian biology and metabolism, not as an approved medicine. It is also known by the informal name Stenabolic.

Is SR9009 approved for human use?

No. SR9009 has not been approved as a therapeutic drug in the United States, European Union, or other major markets. Human safety and efficacy data are very limited. Its presence in consumer products does not imply regulatory approval.

Why is SR9009 banned in sport?

The World Anti-Doping Agency lists SR9009 as a prohibited substance because it can alter gene expression and metabolic pathways relevant to performance. The ban applies at all times, not only during competition. Detection relies on laboratory methods such as mass spectrometry.

What is SR9009?

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.

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