We use essential cookies (authentication, your saved goals/stack) by default. With your permission we'll also enable privacy-respecting analytics (Vercel Web Analytics, anonymous load-time metrics) and error-replay diagnostics (Sentry — DOM snapshots only when an error fires) so we can fix bugs faster. Learn more about cookies
Sr93.0
SR9009 (Stenabolic) Research
Mostly mechanism / observationalLimited safety
5 peer-reviewed studies
What the evidence says
Mostly mechanism / observational
Most SR9009 (Stenabolic) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 2012–2024.
Based on 5 studies
Confidence
Low
By outcome
Metabolism & fat loss (preclinical)
Mostly mechanism / observational4 studies
Exercise capacity (preclinical)
Too few graded studies2 studies
Weight management
Too few graded studies2 studies
Safety profile
Too few graded studies2 studies
Active research area
2 studies in the last 5 years
201220182024
1Animal2012
Treatment of diet-induced obese mice with a REV-ERB agonist decreased obesity by reducing fat mass and markedly improving dyslipidaemia and hyperglycaemia.
Solt LA, Wang Y, Banerjee S, Hughes T, Kojetin DJ, Lundasen T, et al. · Nature (2012)
Foundational paper introducing potent synthetic REV-ERB agonists (the SR9009/SR9011 series) with in-vivo activity in mice
REV-ERB agonism altered circadian behaviour and clock-gene expression in the hypothalamus and shifted rhythmic metabolic-gene expression in liver, muscle and adipose tissue, increasing energy expenditure
In diet-induced-obese mice, treatment reduced fat mass and improved dyslipidaemia and hyperglycaemia
Muscle overexpression or pharmacological activation of Rev-erb-α in vivo increased exercise capacity.
Woldt E, Sebti Y, Solt LA, Duhem C, Lancel S, Eeckhoute J, et al. · Nature medicine (2013)
REV-ERB-α is highly expressed in oxidative skeletal muscle and controls mitochondrial content and oxidative function via the LKB1–AMPK–SIRT1–PGC-1α pathway
REV-ERB-α deficiency reduced mitochondrial content, increased autophagy, and compromised exercise capacity in mice
Pharmacological REV-ERB activation in vivo increased exercise capacity — the origin of the 'exercise mimetic' framing
SR9009 can decrease cell viability, rewire cellular metabolism, and alter gene transcription in hepatocytes and embryonic stem cells lacking both REV-ERBα and -β ... Thus, the effects of SR9009 cannot be used solely as surrogate for REV-ERB activity.
Dierickx P, Emmett MJ, Jiang C, Uehara K, Liu M, Adlanmerini M, et al. · Proceedings of the National Academy of Sciences of the United States of America (2019)
The key counter-evidence: the authors generated mice with conditional deletion of BOTH REV-ERB-α and -β
SR9009 still decreased cell viability, rewired metabolism, and altered transcription in hepatocytes and embryonic stem cells with no REV-ERB present
Demonstrates that a meaningful share of SR9009's effects are REV-ERB-independent (off-target), not the advertised mechanism
The results of multiple studies in preclinical models demonstrate that Rev-Erb is an attractive target for positively influencing dysregulated metabolism, inflammation, and fibrosis, but more specific tools and studies would be needed.
Raza GS, Sodum N, Kaya Y, Herzig KH. · International journal of molecular sciences (2022)
Review framing REV-ERB as a master regulator of metabolism, mitochondrial biogenesis, inflammation and fibrosis across liver, heart, lung, muscle and adipose tissue
Summarizes that REV-ERB activation alleviated cardiac hypertrophy and increased exercise capacity, reduced pulmonary fibrosis, and reduced fat mass in adipose tissue
Explicitly notes the evidence is from preclinical models and that more specific tools and studies are needed before therapeutic potential is established
It failed to receive the United States Food and Drug Administration (USFDA) approval and its illegal distribution has raised concerns. As a result, it has been classified as a prohibited substance by the World Anti-Doping Agency.
Kwak YB, Yoon J, Yoo HH · Journal of pharmaceutical and biomedical analysis (2024)
In-vitro liver-microsome study mapping SR9009 phase-I metabolites for anti-doping forensic detection
States plainly that SR9009 failed to receive FDA approval, that its illegal distribution is a concern, and that it is prohibited by the World Anti-Doping Agency and horse-racing authorities
Anchors the regulatory/grey-market reality and the rapid hepatic metabolism that underlies SR9009's poor bioavailability