SARMs

Stenabolic (SR9009)

Updated · 18 sources · Editorial policy

SR9009 is a synthetic research compound that activates REV-ERBα and REV-ERBβ, two nuclear receptors that help run the body’s internal 24-hour clock. Thomas Burris’s group at the Scripps Research Institute described it in 2012 as a tool for studying how the circadian clock controls metabolism (Solt et al., Nature 2012). Online it is often sold as “Stenabolic” and grouped with SARMs, but it does not act on the androgen receptor.

The single most important fact: SR9009 has never been tested in a human clinical trial. Every reported benefit, including fat loss and longer running time, comes from mice or cell culture, almost always with the drug injected into the abdomen rather than swallowed. The human record so far consists of liver-injury case reports, including one that ended in a liver transplant.

This page summarizes what the animal studies, anti-doping laboratories and published case reports show. It is for education only and is not medical advice.

Property Detail
Class Synthetic REV-ERBα/β agonist (circadian clock modulator); not a SARM
Origin Scripps Research Institute, first reported 2012
Approval None. Never approved anywhere; no registered human trials
Route in studies Mostly intraperitoneal injection in mice (typically 100 mg/kg twice daily)
Human dose None established; no human dosing data exist
Half-life Not determined in humans. In mice, effects of one injection were gone within 24 h
Potency (cell assay) IC50 670 nM at REV-ERBα and 800 nM at REV-ERBβ
WADA status Prohibited at all times (S4.4.1, “Rev-erbα agonists, e.g. SR9009, SR9011”)
US controlled substance Not listed in Schedule III

What it is

SR9009 is a small synthetic molecule, ethyl 3-[[(4-chlorophenyl)methyl-[(5-nitrothiophen-2-yl)methyl]amino]methyl]pyrrolidine-1-carboxylate. Its formula is C₂₀H₂₄ClN₃O₄S, and its molecular weight is 437.9 g/mol (PubChem). It is not a steroid and shares no structure with testosterone.

Its targets, REV-ERBα (gene NR1D1) and REV-ERBβ (NR1D2), are nuclear receptors that switch genes off. In the daily clock they repress BMAL1, a core clock gene. They also regulate genes for fat and glucose metabolism and for inflammation (Solt et al., Nature 2012).

The 2012 paper introduced SR9009 together with a close relative, SR9011. Both were built from an earlier REV-ERB ligand, GSK4112, which reached too little of the drug in the blood to be studied in animals. In cell assays the two compounds were similar:

Assay (Solt et al., 2012) SR9009 SR9011
REV-ERBα, IC50 670 nM 790 nM
REV-ERBβ, IC50 800 nM 560 nM
BMAL1-promoter reporter, IC50 710 nM 620 nM

The authors reported that neither compound was active at the other nuclear receptors they tested. SR9009 is therefore not a selective androgen receptor modulator, despite how it is often sold.

Does SR9009 only act through REV-ERB? Not entirely. A 2019 study deleted both REV-ERBα and REV-ERBβ in mouse liver cells and embryonic stem cells. SR9009 still reduced cell viability, changed cell metabolism and altered gene expression in cells with no REV-ERB at all. The authors concluded that SR9009’s effects “cannot be used solely as surrogate for REV-ERB activity” (Dierickx et al., PNAS 2019). Some effects credited to the circadian clock may come from off-target actions.

How it behaves in the body

No human pharmacokinetic study exists. Absorption, half-life and safe exposure in people are unknown. What is known comes from mice and from test-tube metabolism studies:

  • Route. The key animal studies gave SR9009 by intraperitoneal (abdominal) injection, usually 100 mg/kg twice daily (Solt et al., Nature 2012; Woldt et al., Nat Med 2013).
  • Short action. After a single injection, mouse behavior returned to normal the next day. The authors read this as clearance of the drug in less than 24 h.
  • Poor oral absorption. A 2025 mouse study gave SR9009 by mouth (50–100 mg/kg) specifically because it acted mainly in the gut with very little reaching the liver. The authors described its oral bioavailability as poor, and brain levels stayed under 5 ng/mg after 7 days of oral dosing (Chen et al., Adv Sci 2025). Products sold for people are usually oral capsules, so mouse results from injections may not carry over.
  • Metabolism. In human liver microsomes (liver enzymes in a test tube), SR9009 was broken down into 13 metabolites by CYP3A4, CYP3A5, CYP2C19 and CYP2D6. The most abundant were N-dealkylated products (Mazzarino et al., Drug Test Anal 2018). An earlier study found 8 metabolites (Geldof et al., Int J Mol Sci 2016).
  • Possible interactions. In the same test-tube work, ketoconazole, miconazole, fluoxetine, nefazodone and paroxetine significantly altered SR9009 metabolism. This has not been studied in people.

Regulatory status

What the research shows

All data below come from animals or cells. No controlled human data exist for any outcome.

Fat mass and blood lipids in obese mice

The 2012 Nature paper treated diet-induced obese mice with SR9009 at 100 mg/kg by injection twice daily for 30 days (Solt et al., Nature 2012). The stress of twice-daily injections made the control mice lose weight too, so results are relative to those controls:

Outcome in obese mice SR9009 vs vehicle
Weight loss 60% greater than in controls
Fat mass Larger reduction
Food intake No significant difference
Plasma triglycerides −12%
Plasma total cholesterol −47%
Non-esterified fatty acids −23%
Plasma glucose −19%
Plasma insulin −35% (trend only)
Plasma leptin −80%
IL-6 (an inflammatory signal) −72%

With SR9011 in lean mice, the same paper measured a 5% rise in oxygen consumption, a sign of higher energy expenditure, even though the mice moved 15% less. Muscle showed higher activity of genes for fat and glucose burning, while fat tissue showed lower activity of fat-storage genes. In genetically obese ob/ob mice, 12 days of SR9009 reduced weight gain, without significant changes in glucose or insulin tolerance.

Endurance in mice

The finding behind SR9009’s reputation as an “exercise in a pill” comes from one experiment. Mice given SR9009 at 100 mg/kg by injection for 30 days ran significantly longer, in both time and distance, on a treadmill endurance test than vehicle-treated mice. There were 6 mice per group (Woldt et al., Nat Med 2013). In muscle cells, SR9009 increased mitochondrial number.

The paper showed that REV-ERBα supports mitochondrial content in muscle. It did not test SR9009 in people, by mouth, or in trained animals. It also did not measure muscle size or strength.

Sleep, anxiety and memory

  • Sleep. In mice, a single injection of SR9009 caused wakefulness and cut slow-wave and REM sleep for several hours, followed by a rebound. Sleep returned to normal about 12 h after the dose (Banerjee et al., Nat Commun 2014). The same work found less anxiety-like behavior with REV-ERB agonists.
  • Circadian behavior. Under constant darkness, one injection wiped out the mice’s next active period, and in normal light-dark conditions it delayed activity onset by 1–3 h (Solt et al., Nature 2012).
  • Memory. In a 2025 study, SR9009 by mouth suppressed the gut clock and led to memory deficits in male mice on object-recognition and maze tests (Chen et al., Adv Sci 2025).

Cancer cells

SR9009 and SR9011 killed several cancer cell lines and oncogene-driven senescent cells in culture, while sparing normal cells. In mice with transplanted human glioblastoma, SR9009 injected at 100–200 mg/kg twice daily slowed tumor growth and improved survival without overt toxicity (Sulli et al., Nature 2018). The later finding that SR9009 kills cells even without REV-ERB complicates how this result is read (Dierickx et al., PNAS 2019). None of this has been tested in patients.

Muscle growth

No study has shown that SR9009 builds muscle in animals or people. The mouse work concerns fat, lipids, mitochondria and endurance, not muscle mass or strength. The “Stenabolic” name and the SARM label suggest an anabolic effect that the published evidence does not support.

Side effects and risks

No human safety data

Because SR9009 has never been in a clinical trial, its side effects, safe dose and long-term effects in people are unknown. Statements in the mouse papers about “no overt toxicity” refer to short courses in mice, mostly by injection.

Liver injury

Two published case reports link SR9009 products to liver injury in previously healthy men:

Case Exposure Outcome
40-year-old man, US (Govil et al., Cureus 2025) Recently started “Stenabolic” alongside other supplements Jaundice and hepatocellular liver injury, total bilirubin 7.7 mg/dL at admission. Improved after stopping and supportive care
17-year-old male, Australia (Shams Bin Shaheen et al., Case Reports Hepatol 2026) About 8 weeks of oral SR9009 bought online; symptoms about 3 months later Acute liver failure with severe necrosis on biopsy and grade 3 encephalopathy. Needed emergency liver transplant

In both cases, viral, autoimmune and other causes were excluded. Neither report analyzed the product the patient took, so contamination or mislabeling cannot be ruled out. Case reports cannot show how often liver injury occurs.

Effects on sleep and the body clock

SR9009 was designed to disrupt the body clock. In mice it suppressed sleep, shifted daily activity and, given by mouth, impaired memory tests (see above). Whether similar effects occur in people is unknown.

Product quality

Products sold online as research chemicals are often not what the label says. A 2017 JAMA analysis bought 44 products sold as SARMs. Only 52% contained a SARM, and 39% contained a different unapproved drug, including SR9009. Only 41% had the labeled amount of active compound (Van Wagoner et al., JAMA 2017). Anti-doping chemists have also confirmed SR9009 in black-market products (Geldof et al., Int J Mol Sci 2016).

Athletes

Tested athletes face an anti-doping violation for any SR9009 use, in or out of competition. Anti-doping chemists flagged REV-ERB agonists as likely doping agents in 2016 and have since developed methods to detect SR9009 and its metabolites (Thevis and Schänzer, Rapid Commun Mass Spectrom 2016; Cutler et al., Drug Test Anal 2022).

Key takeaways

  • A circadian clock drug, not a SARM. SR9009 activates the REV-ERB nuclear receptors and has no reported activity at the androgen receptor.
  • No human trials. Fat loss, lipid, endurance and anticancer findings all come from mice or cells, mostly with injected doses of 100 mg/kg or more.
  • Oral use is poorly supported. Mouse data suggest little SR9009 reaches the body beyond the gut when it is swallowed, and no human pharmacokinetic data exist.
  • Not all effects are via REV-ERB. SR9009 changed cell viability and metabolism even in cells lacking both REV-ERBs.
  • Real liver risk signals. Two case reports describe liver injury, one requiring a transplant in a 17-year-old.
  • Banned in sport. WADA prohibits SR9009 at all times, and labs can detect its metabolites.

Sources

  1. Solt LA, Wang Y, Banerjee S, et al. Regulation of circadian behaviour and metabolism by synthetic REV-ERB agonists. Nature. 2012;485(7396):62–68. PubMed.
  2. 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. PubMed.
  3. Dierickx P, Emmett MJ, Jiang C, et al. SR9009 has REV-ERB-independent effects on cell proliferation and metabolism. Proc Natl Acad Sci U S A. 2019;116(25):12147–12152. PubMed.
  4. 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. PubMed.
  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. PubMed.
  6. Chen M, Zhang F, Xiao Y, et al. Intestinal clock promotes cognitive memory through adenosine signaling. Adv Sci (Weinh). 2025;12(34):e04526. PubMed.
  7. Mazzarino M, Rizzato N, Stacchini C, et al. A further insight into the metabolic profile of the nuclear receptor Rev-erb agonist, SR9009. Drug Test Anal. 2018;10(11-12):1670–1681. PubMed.
  8. Geldof L, Deventer K, Roels K, et al. In vitro metabolic studies of REV-ERB agonists SR9009 and SR9011. Int J Mol Sci. 2016;17(10):1676. PubMed.
  9. 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. PubMed.
  10. Davies SR, Chan BKH, Moawad M, et al. Production of certified reference materials for the sports doping control of the REV-ERB agonist SR9009. Drug Test Anal. 2019;11(2):257–266. PubMed.
  11. 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. PubMed.
  12. Van Wagoner RM, Eichner A, Bhasin S, et al. Chemical composition and labeling of substances marketed as selective androgen receptor modulators and sold via the internet. JAMA. 2017;318(20):2004–2010. PubMed.
  13. Govil D, Afram R, Alkhafaji A, et al. When gains go wrong: a case of selective androgen receptor modulator-related liver injury. Cureus. 2025;17(7):e87376. PubMed.
  14. 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 Reports Hepatol. 2026;2026:9926772. PubMed.
  15. National Center for Biotechnology Information. PubChem Compound Summary for CID 57394020, SR9009. PubChem.
  16. World Anti-Doping Agency. The 2026 Prohibited List: International Standard. In effect January 1, 2026. WADA 2026 Prohibited List.
  17. Code of Federal Regulations. 21 CFR 1308.13, Schedule III. 21 CFR 1308.13.
  18. ClinicalTrials.gov. Search results for “SR9009” (no registered studies, searched October 2026). ClinicalTrials.gov.