D tier · weak
There are no human trials at all, and a 2019 PNAS study using REV-ERB double-knockout cells showed SR9009 retains its effects without its supposed target, undermining the mechanistic premise on which the entire rodent literature was interpreted.
sr9009
SR9009 is a synthetic REV-ERB agonist whose reputation rests on a single influential 2012 Nature study in mice reporting increased energy expenditure and reduced fat mass. No human trial has been published, and subsequent knockout work demonstrated that its cellular effects occur independently of REV-ERB, meaning the mechanism attributed to it does not explain what it actually does.
// we supply this one
available as a research reagent
≥ 98% HPLC · research solution · batch certificate published. Grade D above is our own and is not adjusted because we stock it.
the explanation
SR9009's reputation comes from one mouse study about exercise-like metabolic effects, and no human study has ever been published. A later experiment showed it still works in cells that have had its supposed target removed entirely, which means nobody actually knows how it works or what else it is doing.
regulatory status
Not approved by FDA or any regulator; never entered clinical development; WADA-prohibited; not a lawful dietary supplement ingredient
SR9009 has never been approved for any indication and has never entered published clinical development; it remains a laboratory tool compound. FDA treats such compounds sold in bodybuilding and 'research chemical' products as unapproved drugs, and its public safety notification on these products names liver injury and acute liver failure, heart attack and stroke among the risks. SR9009 and the related SR9011 were added to the WADA Prohibited List under Hormone and Metabolic Modulators following reported abuse in the bodybuilding community. It is discussed in the NIH LiverTox SARMs chapter alongside related non-androgenic performance compounds. The SARMs Control Act (S.2742, 2018; S.2895, 2019) proposed Schedule III placement for SARMs but was never enacted; SR9009 is not an androgen receptor ligand and would not have fallen under that definition in any case.
how it works · proposed mechanism
SR9009 was designed as a synthetic agonist of the REV-ERB nuclear receptors that link the circadian clock to metabolic gene expression.
REV-ERB agonism
SR9009 binds REV-ERBα and REV-ERBβ with reported IC50 values of 670 nM and 800 nM, nuclear receptors that repress transcription of core clock genes including BMAL1. Agonism was intended to shift circadian metabolic programmes toward increased energy expenditure.
Circadian metabolic reprogramming
In mice, REV-ERB agonists altered the circadian expression pattern of metabolic genes in liver, skeletal muscle and adipose tissue, with increased energy expenditure. This is the finding behind the 'exercise in a pill' framing that circulates in consumer material.
Target-independent activity
Knockout experiments showed SR9009 decreases cell viability, rewires cellular metabolism and alters gene expression in cells lacking both REV-ERBα and REV-ERBβ. Whatever SR9009 does, it does not require the receptor it was designed to hit.
what’s reported
evidence shape
6 sourcesThe composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.
⚠ the catch
SR9009 is the clearest case in this index of a compound whose entire consumer reputation rests on a single rodent paper that was later shown to have been interpreted through the wrong mechanism. A compound that decreases cell viability through unidentified pathways, with zero human exposure data, is not a characterised agent — it is an open question being sold as an answer.
key published findings
- Rodent (Solt et al., Nature, 2012): synthetic REV-ERB agonists altered circadian behaviour and the circadian pattern of core clock gene expression in mouse hypothalamus, and altered circadian metabolic gene expression in liver, skeletal muscle and adipose tissue, resulting in increased energy expenditure.
- Rodent (Solt et al., Nature, 2012): treatment of diet-induced obese mice with a REV-ERB agonist decreased obesity by reducing fat mass and markedly improved dyslipidaemia and hyperglycaemia.
- In vitro / rodent knockout (Dierickx et al., PNAS, 2019): in mice with conditional deletion of both REV-ERBα and REV-ERBβ, SR9009 still decreased cell viability, rewired cellular metabolism and altered gene expression, leading the authors to conclude that the effects of SR9009 cannot be used as a surrogate for REV-ERB activity.
- In vitro (pharmacology): SR9009 is characterised as a REV-ERB agonist with reported IC50 values of 670 nM at REV-ERBα and 800 nM at REV-ERBβ.
- Human: no clinical trial of SR9009 has been published at any phase, and there is no human pharmacokinetic, efficacy or safety dataset; the compound was added to the WADA Prohibited List on the basis of reported abuse rather than clinical evidence.
limitations of the evidence
- There is no human data of any kind — no pharmacokinetics, no efficacy endpoint and no safety monitoring — so nothing about behaviour in people can be evidence-based.
- The mechanistic premise underlying the rodent literature has been directly falsified by knockout work, meaning even the positive animal findings cannot be attributed to the intended target.
- Reports of poor oral bioavailability circulate widely in secondary and vendor literature but were not verifiable against a primary peer-reviewed human or comparative pharmacokinetic source during this review, so no bioavailability figure is asserted here.
documented safety signals
- SR9009 decreased cell viability in cells lacking both REV-ERB receptors (Dierickx, PNAS 2019), an off-target cytotoxic effect through unidentified pathways — a finding rarely mentioned in material promoting the compound.
- Because the operative molecular target is unknown, there is no basis for predicting organ toxicity, drug interactions or which laboratory parameters would detect harm early.
- Complete absence of human pharmacokinetic data means exposure duration, accumulation and washout are unpredictable, and there is no evidence base for recognising or managing an adverse reaction.
- SR9009 is discussed in the NIH LiverTox SARMs chapter among related performance-enhancing compounds, in a class assigned a likelihood score of B for clinically apparent liver injury; SR9009-specific hepatic data are absent.
- FDA public safety notification on bodybuilding products names heart attack, stroke, psychosis and hallucinations, sleep disturbance, sexual dysfunction, liver injury and acute liver failure among risks from unapproved drugs sold in this category.
- As a research chemical outside any regulated supply chain, product identity, purity and content are unverified, and analytical surveys of this market routinely find misidentified and adulterated products.
- Manipulating core circadian clock machinery has broad and poorly characterised systemic consequences, and no study has assessed long-term effects of chronic REV-ERB-targeting exposure in any species.
identity
| full name | SR9009 (stenabolic) |
| category | Anabolic & Receptor |
| modality | small molecule |
| formula | C20H24ClN3O4S |
| molar mass | 437.9 g/mol |
| cas | 1379686-30-2 |
laboratory handling
| storage | Reference material: store as a solid, desiccated and protected from light, at -20 °C for long-term stability; stock solutions typically stored at -80 °C with freeze-thaw cycles minimised. |
| solubility | Lipophilic small molecule; soluble in DMSO and ethanol, poorly soluble in aqueous buffer. Lot-specific solubility should be taken from the certificate of analysis. |
| co-studied with | Evidence caveat only: SR9009 is frequently presented alongside GW-501516 as an 'endurance' pairing, but neither compound has human efficacy data and GW-501516 carries a multi-organ rodent carcinogenicity finding, so the pairing has no supporting evidence base. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
5 citedU.S. Food and Drug Administration · 2025 · official
Nature · 2012 · preclinical
Proceedings of the National Academy of Sciences of the United States of America (PNAS) · 2019 · preclinical
International Journal of Molecular Sciences (via PMC) · 2023 · reviews
Wikipedia (secondary compilation of primary sources) · 2025 · reviews
others in Anabolic & Receptor