Stenabolic (SR9009)

What it is

SR9009 is a small synthetic molecule, not a peptide and not a hormone. It was developed in 2012 by a group at the Scripps Research Institute in Jupiter, Florida, together with the closely related SR9011. The name Stenabolic comes from the gray market, not from research.

The classification as a SARM that you read everywhere is wrong. A SARM acts at the androgen receptor, where testosterone also works. SR9009 instead binds two nuclear receptors of the internal clock. The confusion is persistent; it even appears in the title of a 2025 medical case report — and the World Anti-Doping Agency, too, lists SR9009 not among the anabolic agents but among the metabolic modulators.

How it is supposed to work

REV-ERBalpha and REV-ERBbeta are nuclear receptors that switch genes on and off in the rhythm of the day. Their natural ligand is heme, the same iron-containing molecule that binds oxygen in the blood. If a synthetic agonist sits in this binding pocket instead, the clock’s program shifts — and with it a range of metabolic genes in liver, muscle and fat tissue.

The part that interests athletes lies in muscle. REV-ERBalpha is particularly abundant in oxidative, that is, endurance-oriented muscle. If it is missing, mitochondrial content and oxidative capacity fall, autophagy ramps up and exercise capacity drops. Via the Lkb1-Ampk-Sirt1-Ppargc-1alpha signaling pathway, this is tied to the same switches that real endurance training also engages. Switching this on pharmacologically, the idea goes, yields training adaptation without training. SR9009 binds both receptors in the submicromolar range: 670 nM at REV-ERBalpha, 800 nM at REV-ERBbeta.

A footnote belongs here. In 2019, a group built mice in which both receptors can be switched off together. In cells without REV-ERBalpha and REV-ERBbeta, SR9009 still altered viability, metabolism and gene activity. Part of the effect therefore runs elsewhere; there are indications of additional activity at the liver X receptor.

What happened in animals

The 2012 metabolism paper gave mice 100 mg/kg twice daily into the abdominal cavity. Oxygen consumption rose by 5 percent, while movement activity was 15 percent lower. In the diet-induced obesity model (20-week-old animals, mean weight 41 g, previously 14 weeks of high-fat diet), weight loss after 12 days was 60 percent greater than in the control group; in the blood, total cholesterol fell by 47 percent, glucose by 19 percent and leptin by 80 percent.

The endurance paper followed in 2013. It first showed genetically that a lack of Rev-erb-alpha in muscle lowers performance, and then pharmacologically that SR9009 at 100 mg/kg over 30 days increases running performance: significantly longer and farther until exhaustion, with six animals per group. In muscle cell cultures, SR9009 and SR9011 at 5 µM increased mitochondrial content.

Around this lies further animal literature: more wakefulness and shorter REM and deep sleep in mice, and in 2018, in a Nature paper, a selectively lethal effect on cancer and senescent cells. Remarkable basic research — and all of it data from cells and rodents.

The capsule question

This is where the scene’s narrative and the data diverge. All efficacy findings come from experiments with injection into the abdominal cavity. The substance is used as a capsule.

Two research groups have measured this. After administration by gavage, plasma levels in mice remained below 0.3 µg/ml, while more than 10 µg/ml arrived in the gut; four weeks of daily oral administration reduced weight gain on a high-fat diet but left the fat-burning genes in muscle unchanged. The effect of orally administered SR9009 may be limited to the gut, the authors state. A second group arrived at the same picture in 2025: after seven days of gavage, concentrations in the hippocampus were below 5 ng/mg.

Then the residence time: half-life after oral administration about 0.5 hours, serum empty after around 4 hours. A 2020 review explicitly names poor bioavailability as the reason why none of the synthetic REV-ERB ligands has become a medicine.

What is known in humans

Nothing about its effects. A query of the ClinicalTrials.gov interface on September 27, 2026 returns no entry for SR9009 or Stenabolic: no phase 1 study, no pharmacokinetics in humans, no investigation of endurance or body composition.

What does exist are two harm reports. A 17-year-old developed acute liver failure with grade 3 hepatic encephalopathy after about eight weeks of oral intake of an SR9009 product bought online and needed an emergency liver transplant; viral, autoimmune, metabolic and obstructive causes had been ruled out. A 40-year-old developed hepatocellular liver injury after starting Stenabolic and recovered after stopping it. Two cases do not prove a cause. But they are all that exists in humans.

What is in the capsule is the third open question: of 44 internet products sold as SARMs, only 52 percent contained a SARM, and 39 percent contained another unapproved agent — including SR9009.

What the studies show

Solt et al., Nature 2012 — the metabolism paper

Chemical and animal-experimental work without a human component. SR9009 and SR9011 were characterized as REV-ERB agonists and given to mice at 100 mg/kg twice daily intraperitoneally. In the obesity model (20-week-old animals, 41 g, 14 weeks of high-fat diet, 12 days of treatment), weight loss was 60 percent greater than in the control, and cholesterol fell by 47 percent.

Woldt et al., Nature Medicine 2013 — the endurance paper

First genetically: Rev-erb-alpha deficiency in muscle lowers mitochondrial content and oxidative function, and running performance falls. Then pharmacologically: SR9009 at 100 mg/kg over 30 days, six animals per group, treadmill to exhaustion — the treated mice ran longer and farther.

Yu et al., Nature Communications 2021 — the oral question

The decisive measurement for the capsule. After gavage, plasma levels were below 0.3 µg/ml, in the gut above 10 µg/ml. Mice on a high-fat diet received SR9009 orally once daily for four weeks: lower weight gain with unchanged food intake, but unchanged fatty acid oxidation genes in muscle.

Dierickx et al., PNAS 2019 — the mechanism check

Mice with conditional deletion of REV-ERBalpha and REV-ERBbeta. In cells without both receptors, SR9009 still altered viability, metabolism and gene transcription — the effects are therefore not suitable as a surrogate for REV-ERB activity.

Where the data stop

There are no efficacy data in humans. No study, no registration, no pharmacokinetics — the ClinicalTrials.gov query on September 27, 2026 returns zero hits. Everything said about endurance and fat loss comes from mouse experiments with injection into the abdominal cavity, over 12 to 30 days, with surrogate markers as the endpoint. Long-term data do not exist in any species.

In addition, there are three documented limitations: taken orally, the substance barely reaches the systemic circulation, and its effect could be confined to the gut. Part of the effects also occur without the target receptors. And product quality on the market is demonstrably unreliable. Anyone assessing Stenabolic is working with an exciting hypothesis, not with a tested drug.

Status, approval and legal

SR9009 is not approved in Germany, the EU or the US, either as a medicine or as a dietary supplement; it is distributed as a research chemical or as an unapproved supplement. In sport the substance is banned at all times: the WADA 2026 prohibited list, in force since January 1, 2026, explicitly names Rev-erb-alpha agonists, with the examples SR9009 and SR9011, in section S4.4.1 of the metabolic modulators; class S4.4 is non-specified and prohibited in and out of competition. In Germany, SR9009, synonym Stenabolic, is listed by name in the annex to Section 2 (3) of the Anti-Doping Act; this prohibits acquiring, possessing and bringing it into the country in non-negligible quantities for the purpose of doping, as well as trading and supplying it for this purpose. The substance is detectable via N-dealkylated metabolites.

Safety

Nothing has been systematically studied in humans. Two case reports of liver injury after oral intake are known: acute liver failure in a 17-year-old that required an emergency liver transplant, and hepatocellular liver injury in a 40-year-old with improvement after stopping. Both demonstrate a temporal association, not a cause — but they are the entire human experience in the literature. A second signal comes from animal experiments: REV-ERB agonists shortened REM and deep sleep. Interactions have not been studied, and there is no upper limit from EFSA, BfR or NIH, because the substance is not a food ingredient. Then there is product quality: in 59 percent of the 44 internet products examined, the amount of active ingredient deviated from the label. For people with liver disease, during pregnancy and breastfeeding, and for adolescents, the substance is out of the question; for tested athletes, it means a ban.

Sources

• Solt et al., Nature 2012 — synthetic REV-ERB agonists, behavior and metabolism
• Woldt et al., Nature Medicine 2013 — Rev-erb-alpha, mitochondria and running performance
• Dierickx et al., PNAS 2019 — SR9009 also acts without REV-ERB
• Yu et al., Nature Communications 2021 — oral administration, plasma levels and gut effect
• Chen et al., Advanced Science 2025 — oral administration, exposure in the brain
• Wang et al., Theranostics 2020 — review of REV-ERBalpha as a drug target
• Shams Bin Shaheen et al., Case Reports in Hepatology 2026 — acute liver failure after SR9009
• Govil et al., Cureus 2025 — liver injury after Stenabolic
• Van Wagoner et al., JAMA 2017 — ingredients of 44 internet products sold as SARMs
• WADA — Prohibited List 2026, section S4.4.1 (Rev-erb-alpha agonists)