SR9009

Dosing from the Literature

Published for fat loss: mouse doses only: 100 mg/kg injected twice a day for 30 days (one lab, 2012) and 10 mg/kg once a day for eight weeks (another lab, 2025). Not published: any human dose; no trial exists, and neither human case report gives one.

No study has given SR9009 to people. The table records, as published, the doses in the mouse studies behind this page’s fat-loss and endurance findings, the one product label a published analysis reports, and the one human course a case report describes. They are study doses, a label claim and a case history, not recommendations. The mice received it by injection into the abdominal cavity (intraperitoneal, i.p.); the products documented for people are capsules taken by mouth.

What It Is

SR9009 is a synthetic small molecule, not a peptide: formula C20H24ClN3O4S, molecular weight 437.9 (PubChem). Its chemical name, ethyl 3-[[(4-chlorophenyl)methyl-[(5-nitrothiophen-2-yl)methyl]amino]methyl]pyrrolidine-1-carboxylate, includes a nitrothiophene group (PubChem). The lab of Thomas Burris at the Scripps Research Institute in Jupiter, Florida, described it in 2012 together with a sister compound, SR9011, as synthetic agonists of the nuclear receptors REV-ERBα and REV-ERBβ (Solt et al., 2012). Both were built on an earlier probe, GSK4112, with changes that raised their exposure in the body (Kojetin & Burris, 2014).

REV-ERBα and REV-ERBβ are part of the body’s circadian clock: they regulate core clock genes that drive daily rhythms in activity and metabolism, and their natural ligand is heme; the 2012 paper proposed REV-ERB ligands for sleep disorders and metabolic diseases (Solt et al., 2012). Since then SR9009 has been widely used as a laboratory tool (Wang et al., 2020): PubMed lists 149 records that name it in the title or abstract, from obesity and exercise to sleep, heart, liver and cancer models, and none is indexed as a clinical trial (PubMed search, September 29, 2026).

Outside the lab it is sold as a supplement. A JAMA analysis of products sold online as SARMs (selective androgen receptor modulators) lists SR9009, “also known as Stenabolic,” among the compounds named on their labels (Van Wagoner et al., 2017), and the authors of a 2026 case report describe it as “widely marketed online as a performance‐enhancing supplement” (Shams Bin Shaheen et al., 2026). It is often grouped with SARMs; it is not one. A 2025 case report that called Stenabolic “a newer SARM” also wrote: “While Stenabolic is commonly categorized as a SARM, it technically functions as a Rev-ErbA ligand” (Govil et al., 2025). Anti-doping chemists found internet discussion forums calling SR9009 and SR9011 “the ultimate ‘exercise in a pill’ compounds” (Geldof et al., 2016).

What has not been published: any human trial and any human pharmacokinetic data. The 2026 case-report authors wrote that SR9009 “has never undergone clinical evaluation in humans and there are currently no published data regarding its pharmacokinetics, long‐term safety or hepatotoxic potential” (Shams Bin Shaheen et al., 2026). In 2014 its developers wrote that “no dedicated toxicological studies have been performed for any of the REV-ERB ligands” (Kojetin & Burris, 2014).

Mechanism of Action

What the papers show about how SR9009 acts, all of it in cells and mice. None of it has been measured in people.

• REV-ERBα and REV-ERBβ (NR1D1, NR1D2): repressors in the clock — REV-ERBα and REV-ERBβ, also known as NR1D1 and NR1D2, are essential components of the circadian clock (Sulli et al., 2018). The core clock genes Bmal1 and Clock are direct REV-ERB target genes, and heme is the receptors’ physiological ligand (Solt et al., 2012). SR9009 increased REV-ERB-dependent repression in cells with IC50 values of 670 nM for REV-ERBα and 800 nM for REV-ERBβ, bound REV-ERBα directly (Kd 800 nM) and increased recruitment of a fragment of the co-repressor NCoR (Solt et al., 2012). In its developers’ assays it showed no significant activity at the 46 other members of the human nuclear receptor superfamily (Kojetin & Burris, 2014).
• The clock in the brain (mice) — One injection given to mice kept in constant darkness abolished their wheel running during the next active period, and normal activity returned the following cycle; under a normal light–dark cycle it delayed the start of activity by 1 to 3 hours (Solt et al., 2012). SR9009 and SR9011 suppressed Cry2, enhanced Per2, shifted Bmal1 and abolished the daily rhythm of Npas2 in the mouse hypothalamus (Kojetin & Burris, 2014).
• Fat, liver and muscle gene programs (obese mice) — In obese mice given SR9009 for 30 days, liver genes for fat and cholesterol synthesis (Fasn, Scd1, Hmgcr, Srebf2) fell, white-fat genes for triglyceride synthesis fell, and muscle genes for burning fat and glucose (Cpt1b, Ucp3, Ppargc1b, Pkm2, Hk1) rose (Solt et al., 2012).
• Energy use: measured on the sister compound — The 2012 paper’s energy measurements, a 5% rise in oxygen consumption over 10 days of twice-daily dosing with 15% less movement, were made with SR9011, not SR9009. For SR9009 the paper reports weight loss from lower fat mass in normal mice and, in obese mice, no significant difference in food intake (Solt et al., 2012).
• Muscle mitochondria: the Lkb1–Ampk–Sirt1–Ppargc-1α pathway — In mice, loss of REV-ERBα lowered muscle mitochondrial content, raised autophagy and cut exercise capacity, with this pathway switched off; in muscle cells, SR9009 (5 μM) increased the number of total and active mitochondria (Woldt et al., 2013). SR9009 did not change the distribution of muscle fiber types (Handschin, 2016).
• Sleep, wakefulness and orexin (mice) — SR9009 injected in the middle of the mice’s sleep period increased wakefulness and suppressed slow-wave and REM sleep (Banerjee et al., 2014). The wake effect was absent in mice lacking REV-ERBβ (Amador et al., 2018), and long-term dosing suppressed orexin gene expression (Amador et al., March 2016).
• Effects without REV-ERB — In liver cells and embryonic stem cells lacking both REV-ERBα and REV-ERBβ, SR9009 still lowered cell viability, rewired metabolism and changed gene transcription; the authors concluded that its effects “cannot be used solely as surrogate for REV-ERB activity” (Dierickx et al., 2019). Its protection of the mouse heart after pressure overload persisted without cardiac REV-ERBs (Li et al., 2022), and in prostate cancer cells it acted through another receptor, LXRα (Xu et al., 2022). GlaxoSmithKline researchers found that SR9009 and its relatives bind LXRα at about 10 μM (Trump et al., 2013); the Burris lab reported no LXR activation in its own assays (Kojetin & Burris, 2014). Other SR9009 effects, in mouse colitis and heart ischemia models, disappeared in mice lacking REV-ERBα, a 2020 review notes (Wang et al., 2020).

What the Research Shows

All of the research below is in cells or animals.

• Fat loss in obese mice (Solt et al., 2012) — Twenty-week-old mice fed a high-fat diet for 14 weeks (average 41 g) got 100 mg/kg twice a day by injection for 30 days, 6 to 10 mice per group. Weight loss was 60% greater than in vehicle-injected mice, which also lost weight from the stress of handling and injections; adiposity fell more; food intake did not differ significantly. Plasma triglycerides fell 12%, total cholesterol 47%, free fatty acids 23%, glucose 19%, leptin 80% and IL-6 72%. In leptin-deficient ob/ob mice, 12 days of dosing reduced weight gain, with no significant change in glucose or insulin tolerance.
• Weight gain under constant light (Yang et al., 2025) — A second lab gave 10 mg/kg a day by injection for eight weeks to mice kept in constant light, which raises body weight, white fat and insulin resistance. Treated mice showed less weight gain, less white fat and less insulin resistance, with “no significant impact on overall energy homeostasis.” In fat-precursor cells, SR9009 inhibited the formation of fat cells.
• Endurance (Woldt et al., 2013; Li et al., 2024) — Mice given 100 mg/kg for 30 days ran longer, in both time and distance, than vehicle-treated mice, 6 per group; the paper’s text gives no percentage (Woldt et al., 2013). A 2024 study found that SR9009 and two new analogues improved exercise tolerance in normal mice (Li et al., 2024).
• Sleep and anxiety (Banerjee et al., 2014; Amador et al., September 2016) — At 100 mg/kg, SR9009 increased wakefulness and reduced slow-wave and REM sleep, and reduced anxiety-like behaviour in three tests (Banerjee et al., 2014). Its suppression of REM sleep was maintained over three days of daily dosing (Amador et al., September 2016).
• Arteries and liver (Sitaula et al., 2015; Griffett et al., 2020) — In mice lacking the LDL receptor, 100 mg/kg for seven weeks reduced atherosclerotic plaque size, 10 mice per group (Sitaula et al., 2015). In a mouse model of NASH, SR9009 suppressed liver fibrosis and inflammation (Griffett et al., 2020).
• Cancer cells (Sulli et al., 2018; Xu et al., 2022) — SR9009 and SR9011 killed cancer cells and oncogene-induced senescent cells, including mole cells, with no effect on the viability of normal cells; SR9009 improved survival in two mouse models of glioblastoma (Sulli et al., 2018). In prostate cancer cells the effect ran through LXRα rather than REV-ERB (Xu et al., 2022).
• Where it did not help (Slomnicki et al., 2026) — After spinal cord contusion in mice, a week of SR9009 (100 mg/kg a day by injection) reduced bleeding and injury-related gene activity at day 3, but hindlimb recovery over six weeks and white-matter sparing did not change.

Human Data

No controlled human study of SR9009 exists. ClinicalTrials.gov has no record of it, PubMed indexes no clinical trial of it (both searched September 29, 2026), and the 2017 JAMA analysis noted: “Preclinical studies have occurred for SR9009, but no human trials” (Van Wagoner et al., 2017).

How the body handles it is unpublished for people. Anti-doping chemists study its breakdown in human liver microsomes because “ethical objections and safety aspects limit the use of human volunteers” (Geldof et al., 2016). Those assays found eight metabolites (Geldof et al., 2016), and thirteen made by the liver enzymes CYP3A4, CYP3A5, CYP2C19 and CYP2D6 (Mazzarino et al., 2018). In mice, the 2012 paper reported “reasonable plasma exposure,” and after a single injection a return to normal behaviour the next day, “consistent with clearance of the drugs in less than 24h” (Solt et al., 2012). GlaxoSmithKline researchers wrote that SR9009 and its relatives have “high metabolic clearance rates that necessitate high dosing.” Their mouse pharmacokinetic table gives an oral bioavailability of 2.2% for the compound their text calls SR9009, but their structure table gives that compound the structure of SR9011, so this page does not assign the figure to either (Trump et al., 2013; Solt et al., 2012).

Two case reports describe liver injury after use.

• Acute liver failure and a liver transplant (Australia, 2026) — A previously healthy 17-year-old had finished an eight-week course of SR9009 taken by mouth, “purchased online for bodybuilding purposes,” about three months before he came to hospital with a week of jaundice, dark urine, lethargy and upper-right abdominal pain. He denied alcohol misuse, paracetamol overdose and other recreational drugs or supplements. Tests excluded viral, autoimmune, Wilson and obstructive causes, and a liver biopsy showed confluent and multiacinar necrosis “consistent with severe DILI” (drug-induced liver injury). Despite intravenous N-acetylcysteine he developed worsening coagulopathy, ascites and grade 3 hepatic encephalopathy, and had an emergency liver transplant; he recovered and went home on immunosuppressive therapy. The authors call the failure “temporally associated” with SR9009 and, to their knowledge, the first published report of its kind. The report describes no analysis of the product, and its text and its laboratory table give different values (Shams Bin Shaheen et al., 2026).
• Liver injury after “Stenabolic” (United States, 2025) — A 40-year-old man taking several over-the-counter supplements had recently started a product sold as Stenabolic. He came to hospital with jaundice, dark urine and upper-right abdominal pain; at admission his total bilirubin was 7.7 mg/dL (reference 0.1–1.2) and his ALT 108 U/L (reference 10–40), with a normal alkaline phosphatase. Viral and autoimmune causes were excluded, a causality score (RUCAM) came out “probable,” and he improved after stopping. The authors wrote that “it is difficult to determine whether the extent of injury was caused by Stenabolic or other contaminant SARMs”; the report describes no testing of the product (Govil et al., 2025).

Anti-doping findings show that it is being used; they are not studies of what it does.

• An athlete’s test (USADA, 2024) — A US track and field athlete’s out-of-competition test on September 20, 2023 found ostarine, RAD-140 and metabolites of LGD-4033 and SR9009; an arbitrator imposed an eight-year sanction, his second violation.
• Routine samples (Geldof et al., 2016) — Reprocessing 1,511 routine doping-control samples from June to September 2015 found neither SR9009 nor SR9011 nor their metabolites.
• Racing animals — In equine doping control, an N-dealkylated metabolite of SR9009 was found in a horse’s plasma and urine, to its authors’ knowledge the first adverse analytical finding for SR9009 in a horse (Cutler et al., 2022). A 2026 study mapped 17 of its metabolites in camel liver for camel-racing doping control (Palathinkal et al., 2026).

None of these is a study of what SR9009 does in people. The evidence meter on the SR9009 card reads “Animal only” because its fat-loss data come from mice.

Reconstitution & Storage

Nothing to reconstitute. SR9009 is sold to people as capsules taken by mouth: the one SR9009-labeled product in the JAMA analysis was 40 capsules labeled 20 mg each (Van Wagoner et al., 2017), and the 2026 case describes “orally administered SR9009” (Shams Bin Shaheen et al., 2026).

• Form in the studies — For injection, several mouse studies dissolved SR9009 in 15% Cremophor, which Yang et al. describe as “an oil-based vehicle” (Amador et al., September 2016; Yang et al., 2025). Cell studies dissolved it in DMSO (Sulli et al., 2018).
• What is in the capsule — Two published analyses of products sold as SR9009 found different things. A black-market product bought online contained SR9009, with no major impurities (Geldof et al., 2016). The product labeled 20 mg of SR9009 per capsule in the JAMA analysis contained none; it held 1–5 mg per capsule of androstatrienedione (Van Wagoner et al., 2017), which WADA lists among aromatase inhibitors under S4.1 (Prohibited List 2026).
• Storage — None of the documents read for this page gives storage conditions for products sold as SR9009.

Side Effects & Risks

No study has recorded side effects of SR9009 in people. What is documented:

• Liver — The two case reports above. In the 2026 case, ALT and AST rose into the thousands and the INR climbed as he got sicker; the authors note that liver enzymes “may decline despite worsening hepatic failure” (Shams Bin Shaheen et al., 2026). In the 2025 case, ALT was 108 U/L with a normal INR, and he improved after stopping (Govil et al., 2025).
• What is in the product — One product labeled SR9009 contained none of it and held an unlisted substance that WADA prohibits; another contained SR9009 (Van Wagoner et al., 2017; Geldof et al., 2016). Across the JAMA analysis, 11 of 44 products contained substances not on the label and 4 contained no active compound (Van Wagoner et al., 2017).
• Sleep and the body clock — In mice, SR9009 increased wakefulness and suppressed REM and slow-wave sleep (Banerjee et al., 2014), and one injection abolished the next active period’s wheel running in constant darkness (Solt et al., 2012). A review of exercise mimetics: “the consequences of using SR9009 as an exercise ‘mimetic’ in terms of circadian rhythms in humans will have to be carefully evaluated” (Handschin, 2016).
• The nitrothiophene group — SR9009, SR9011 and their parent probe contain a nitrothiophene group, “which carries a potential toxicological liability,” and as of 2014 “no dedicated toxicological studies have been performed for any of the REV-ERB ligands” (Kojetin & Burris, 2014).
• Effects beyond its target — Several labs have found SR9009 acting without REV-ERB, including through LXRα (Dierickx et al., 2019; Xu et al., 2022). What those effects mean for a person taking it has not been studied.
• Drug interactions (lab only) — In human liver microsomes, ketoconazole, miconazole, fluoxetine, nefazodone and paroxetine significantly altered SR9009’s breakdown, as did variants of CYP2D6 and CYP2C19 (Mazzarino et al., 2018). No interaction has been studied in people.
• WADA prohibited — WADA prohibits SR9009 at all times under S4.4.1 (“Rev-erbɑ agonists, e.g. SR9009, SR9011”), as a non-Specified substance (Prohibited List 2026). A positive test has ended in an eight-year sanction, for a second violation (USADA, 2024).

Bloodwork & Monitoring

No monitoring guidance for SR9009 has been published. The documents point to these:

• Liver tests — Both published human cases were identified through liver blood tests: bilirubin, ALT, AST and INR (Govil et al., 2025; Shams Bin Shaheen et al., 2026). The 2026 authors write that the course of acute liver failure is judged by the overall clinical picture, including the liver’s synthetic function and encephalopathy, because enzymes “may decline despite worsening hepatic failure.”
• The history — The same authors write that because these products are “often perceived to be safe, patients may not volunteer their use unless specifically asked” (Shams Bin Shaheen et al., 2026).
• Drug tests — Anti-doping laboratories detect SR9009 and its metabolites (Geldof et al., 2016; USADA, 2024), and certified reference materials of two human metabolites exist for that testing (Davies et al., 2019).
• Which tests fit a given person — A question for a licensed healthcare provider. This page can’t answer it.

Commonly Stacked With

No study has tested SR9009 with anything. One document shows it taken with other drugs, recorded here as documented. It is also sold in the same online market as SARMs (Van Wagoner et al., 2017).

Legal Status

Related Compounds

People researching SR9009 often also look at these:

Next Steps

References

1. Solt LA, Wang Y, Banerjee S, Hughes T, Kojetin DJ, Lundasen T, Shin Y, Liu J, Cameron MD, Noel R, Yoo SH, Takahashi JS, Butler AA, Kamenecka TM, Burris TP. Regulation of circadian behaviour and metabolism by synthetic REV-ERB agonists. Nature. 2012;485(7396):62-68. PMID: 22460951.
2. Trump RP, Bresciani S, Cooper AW, et al. Optimized chemical probes for REV-ERBα. J Med Chem. 2013;56(11):4729-4737. PMID: 23656296. (LXRα binding; “high metabolic clearance rates”; the pharmacokinetic and structure tables discussed under Human Data.)
3. Woldt E, Sebti Y, Solt LA, et al. Rev-erb-α modulates skeletal muscle oxidative capacity by regulating mitochondrial biogenesis and autophagy. Nat Med. 2013;19(8):1039-1046. PMID: 23852339.
4. Kojetin DJ, Burris TP. REV-ERB and ROR nuclear receptors as drug targets. Nat Rev Drug Discov. 2014;13(3):197-216. PMID: 24577401.
5. Banerjee S, Wang Y, Solt LA, et al. Pharmacological targeting of the mammalian clock regulates sleep architecture and emotional behaviour. Nat Commun. 2014;5:5759. PMID: 25536025.
6. Sitaula S, Billon C, Kamenecka TM, Solt LA, Burris TP. Suppression of atherosclerosis by synthetic REV-ERB agonist. Biochem Biophys Res Commun. 2015;460(3):566-571. PMID: 25800870.
7. Handschin C. Caloric restriction and exercise “mimetics”: ready for prime time? Pharmacol Res. 2016;103:158-166. PMID: 26658171.
8. Thevis M, Schänzer W. Emerging drugs affecting skeletal muscle function and mitochondrial biogenesis — potential implications for sports drug testing programs. Rapid Commun Mass Spectrom. 2016;30(5):635-651. PMID: 26842585.
9. Amador A, Wang Y, Banerjee S, Kamenecka TM, Solt LA, Burris TP. Pharmacological and genetic modulation of REV-ERB activity and expression affects orexigenic gene expression. PLoS One. 2016 Mar;11(3):e0151014. PMID: 26963516.
10. Amador A, Huitron-Resendiz S, Roberts AJ, Kamenecka TM, Solt LA, Burris TP. Pharmacological targeting the REV-ERBs in sleep/wake regulation. PLoS One. 2016 Sep;11(9):e0162452. PMID: 27603791.
11. Geldof L, Deventer K, Roels K, Tudela E, Van Eenoo P. In vitro metabolic studies of REV-ERB agonists SR9009 and SR9011. Int J Mol Sci. 2016;17(10):1676. PMID: 27706103.
12. Van Wagoner RM, Eichner A, Bhasin S, Deuster PA, Eichner D. Chemical composition and labeling of substances marketed as selective androgen receptor modulators and sold via the internet. JAMA. 2017;318(20):2004-2010. PMID: 29183075. (Full text read, including its product table.)
13. Sulli G, Rommel A, Wang X, et al. Pharmacological activation of REV-ERBs is lethal in cancer and oncogene-induced senescence. Nature. 2018;553(7688):351-355. PMID: 29320480.
14. Amador A, Kamenecka TM, Solt LA, Burris TP. REV-ERBβ is required to maintain normal wakefulness and the wake-inducing effect of dual REV-ERB agonist SR9009. Biochem Pharmacol. 2018;150:1-8. PMID: 29355503.
15. Mazzarino M, Rizzato N, Stacchini C, de la Torre X, Botrè F. A further insight into the metabolic profile of the nuclear receptor Rev-erb agonist, SR9009. Drug Test Anal. 2018;10(11-12):1670-1681. PMID: 30395700.
16. Davies SR, Chan BKH, Moawad M, Garrett TR, Brooker L, Chakrabarty R. Production of certified reference materials for the sports doping control of the REV-ERB agonist SR9009. Drug Test Anal. 2019;11(2):257-266. PMID: 30129998.
17. Dierickx P, Emmett MJ, Jiang C, Uehara K, Liu M, Adlanmerini M, Lazar MA. SR9009 has REV-ERB-independent effects on cell proliferation and metabolism. Proc Natl Acad Sci USA. 2019;116(25):12147-12152. PMID: 31127047.
18. Wang S, Li F, Lin Y, Wu B. Targeting REV-ERBα for therapeutic purposes: promises and challenges. Theranostics. 2020;10(9):4168-4182. PMID: 32226546.
19. Griffett K, Bedia-Diaz G, Elgendy B, Burris TP. REV-ERB agonism improves liver pathology in a mouse model of NASH. PLoS One. 2020;15(10):e0236000. PMID: 33002003.
20. Cutler C, White DL, Viljanto M. In vitro metabolism of the REV-ERB agonist SR-9009 and subsequent detection of metabolites in associated routine equine plasma and urine doping control samples. Drug Test Anal. 2022;14(1):169-174. PMID: 34224639.
21. Li H, Song S, Tien CL, et al. SR9009 improves heart function after pressure overload independent of cardiac REV-ERB. Front Cardiovasc Med. 2022;9:952114. PMID: 35911512.
22. Xu H, Zhang J, Zheng X, et al. SR9009 inhibits lethal prostate cancer subtype 1 by regulating the LXRα/FOXM1 pathway independently of REV-ERBs. Cell Death Dis. 2022;13(11):949. PMID: 36357378.
23. Billon C, Schoepke E, Avdagic A, Chatterjee A, Butler AA, Elgendy B, Walker JK, Burris TP. A synthetic ERR agonist alleviates metabolic syndrome. J Pharmacol Exp Ther. 2024;388(2):232-240. PMID: 37739806. (SLU-PP-332.)
24. Li L, Yang C, Qiao X, et al. Regulation of exercise ability and glycolipid metabolism by synthetic SR9009 analogues as new REV-ERB-α agonists. Bioorg Med Chem. 2024;111:117845. PMID: 39059249.
25. Yang MY, Lin HY, Chen YM, Hu ML, Chen IY, Yang CH. Chronic low-dose REV-ERBs agonist SR9009 mitigates constant light-induced weight gain and insulin resistance via adipogenesis modulation. Biomed J. 2025;48(3):100830. PMID: 39800061.
26. Govil D, Afram R, Alkhafaji A, Woods E, Affas S. When gains go wrong: a case of selective androgen receptor modulator-related liver injury. Cureus. 2025;17(7):e87376. PMID: 40765588.
27. Slomnicki LP, Hodges E, Armstrong C, et al. Limited effects of the REV-ERB agonist SR9009 after mouse spinal cord contusion: reduced acute pathology with unaffected functional recovery and chronic white matter loss. Neurosci Lett. 2026;870:138443. PMID: 41232745.
28. Palathinkal AB, Farook Basha S, Laya S, et al. LC-HRMS-based metabolic profiling of the REV-ERB agonist SR9009 in camel liver homogenate and Cunninghamella elegans for anti-doping analysis. Rapid Commun Mass Spectrom. 2026;40(20):e70149. PMID: 42530886.
29. Shams Bin Shaheen S, Liu WJP, Cooper C, Wu MY. Acute liver failure in an adolescent following use of the synthetic REV-ERB agonist SR9009. Case Rep Hepatol. 2026;2026:9926772. PMID: 42750938. (Full text read.)
30. U.S. Anti-Doping Agency. Independent Arbitrator Imposes Eight-Year Sanction on Track & Field Athlete Gil Roberts for Second Anti-Doping Rule Violation. June 21, 2024. usada.org/sanction/gil-roberts-receives-sanction-second-violation/. Read September 29, 2026.
31. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S4.4.1, Metabolic modulators (Rev-erbɑ agonists); S4.1, Aromatase inhibitors. wada-ama.org.
32. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the Federal Food, Drug, and Cosmetic Act (categories 1–3). Updated May 14, 2026. fda.gov/media/94155/download.
33. Code of Federal Regulations. 21 CFR 216.23, Bulk drug substances that can be used to compound drug products in accordance with section 503A of the Federal Food, Drug, and Cosmetic Act. ecfr.gov. Read September 29, 2026.
34. openFDA. Drugs@FDA, NDC directory and drug-label searches for “SR9009,” “SR-9009” and “Stenabolic”: no matches. api.fda.gov. Searched September 29, 2026.
35. ClinicalTrials.gov. Searches for “SR9009,” “SR-9009,” “SR 9009,” “Stenabolic” and “REV-ERB agonist”: no records. Searched September 29, 2026.
36. PubChem. SR9009, compound CID 57394020: formula, molecular weight, IUPAC name, CAS number 1379686-30-2, synonyms including “Stenabolic (SR9009).” pubchem.ncbi.nlm.nih.gov. Read September 29, 2026.
37. PubMed. Search for SR9009, SR-9009 or Stenabolic in title or abstract: 149 records; limited to clinical trial, randomized controlled trial or case report publication types: 1 record (the 2025 case report). Searched September 29, 2026.

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