Stenabolic (SR9009)

Overview

Stenabolic (research code SR9009, also SR-9009) is a synthetic agonist of the Rev-ErbA nuclear receptors (REV-ERBα and REV-ERBβ) — the heme-binding circadian-clock proteins that repress transcription. It is NOT a SARM (it does not act on the androgen receptor) and it is NOT a peptide (it is a small lab-made chemical, not an amino-acid chain). It appears on this peptide reference because it is frequently discussed and stacked alongside SARMs and peptides in the "research chemical" community, not because it belongs to either class.

SR9009 was created in an academic laboratory — Thomas Burris and colleagues at The Scripps Research Institute — as a tool compound to probe circadian and metabolic biology, not as a physique or performance drug. Its reputation as "exercise in a bottle" traces to a single 2012 mouse study (Solt et al., Nature) in which injected SR9009 increased mitochondrial content and running capacity and improved metabolic parameters in obese mice.

Chemistry and structure

SR9009 is a small-molecule chemical, not an amino-acid chain.

Mechanism of action

• Rev-ErbA (REV-ERBα/β) agonism. SR9009 acts as a synthetic agonist of the nuclear receptors REV-ERBα and REV-ERBβ, the heme-binding transcriptional repressors of the circadian clock; reported in-vitro potency is EC50 ~670 nM (REV-ERBα) and ~800 nM (REV-ERBβ). [In vitro]
• Clock-controlled metabolism. REV-ERB activation represses BMAL1/CLOCK and reprograms clock-controlled genes governing lipid, glucose and energy metabolism, mitochondrial biogenesis and oxidative capacity in skeletal muscle, plus adipogenesis and inflammation. [Animal]
• "Exercise in a bottle" (origin). In diet-induced obese mice, injected SR9009 increased mitochondrial content and running/exercise capacity in skeletal muscle and improved metabolic parameters (reduced adiposity; altered lipid/glucose gene expression in liver, muscle and fat) — the origin of the framing (Solt 2012). [Animal]
• Anti-inflammatory signal. SR9009 suppresses NLRP3-inflammasome-driven IL-1β/IL-18 in macrophages in a BMAL1-dependent manner and shifts macrophage polarization toward anti-inflammatory M2, reducing atherosclerotic plaque in a mouse model at 100 mg/kg. [Animal]
• CRITICAL CONFOUND — off-target activity. SR9009 decreases cell viability, rewires metabolism and alters gene transcription in hepatocytes and embryonic stem cells lacking BOTH REV-ERBα and REV-ERBβ, so its effects are largely off-target; the authors conclude "the effects of SR9009 cannot be used as a proxy for REV-ERB activity" (Dierickx 2019). [In vitro]
• No meaningful oral delivery. SR9009 has essentially no oral bioavailability — reported ~2% oral absorption vs ~100% by injection in rodents, with extensive first-pass hepatic metabolism — so oral consumer capsules are unlikely to reproduce the injected-mouse biology; no human exposure/efficacy data exist. [Animal]

Research and evidence

All evidence for SR9009 is preclinical — animal and cell studies only. There is no trial phase because no human clinical trial has ever been conducted for any indication.

Human evidence in context. There is none. Every observation attributed to SR9009 comes from injected rodents or cell culture. The "exercise in a bottle" claim rests on a single mouse study using injections of a compound that is barely absorbed orally, and a later study showed a large share of SR9009's cellular effects occur even when its supposed targets are genetically removed. Human half-life, oral bioavailability, efficacy, and whether oral consumer doses produce any meaningful effect are all Not established / not found in sources.

Status and regulation

• Regulatory approval: None. SR9009 is not approved by the FDA, the EMA, or any other regulator for any indication. It has never reached any clinical phase — no IND, no registered human trial.
• Origin / development: Created as an academic tool compound by Thomas Burris and colleagues at The Scripps Research Institute. Its purpose was to interrogate circadian and metabolic biology, not to serve as a therapeutic or performance product.
• Anti-doping: Prohibited by WADA under S4.4 — Metabolic Modulators (Rev-Erbα agonists; SR9009 is named), in-competition and out-of-competition. This is a sport-eligibility fact, separate from legality.
• Market reality: Sold only as a "research chemical," frequently mislabeled and stacked with SARMs. Such products are of unknown identity, purity, and potency.

Safety

Safety signals, tagged by evidence type:

• No human safety data. SR9009 has never completed a human clinical trial; all data are from injected rodents and cell culture. [Hypothesis]
• Off-target / non-specific cellular effects. Reduces cell viability and rewires metabolism even in cells lacking both REV-ERB receptors — broad, poorly-characterized off-target activity of unknown safety consequence in humans. [In vitro]
• Heavy first-pass hepatic metabolism. Essentially no oral bioavailability; oral capsules place a large metabolic load on the liver, and hepatic exposure to parent compound and metabolites is unquantified in humans. [Animal]
• Class-wide FDA warning context. The FDA has warned that body-building products containing SARMs (the channel SR9009 is illicitly sold alongside) are linked to serious harms including liver injury and increased risk of heart attack/stroke. SR9009 itself is not a SARM but is sold in the same unregulated channel. [Human]
• WADA-prohibited. Banned in sport under S4.4 (Metabolic Modulators, Rev-Erbα agonists). A sport-eligibility axis — it does not imply safety or approval. [Human]

Contamination reality. In an analysis of 44 products sold online as SARMs (Van Wagoner et al., JAMA 2017;318(20):2004-2010, PMID 29183075), only 52% actually contained the labeled SARM, 39% contained a different unapproved drug (including SR9009 itself, ibutamoren/MK-677, and GW501516), 9% contained no active compound, and only 41% matched the labeled dose. A "SR9009" or "SARM" label is not a reliable statement of contents. [Human]

Legal status

How it compares

SR9009 is usually grouped with "exercise mimetic" and metabolic compounds sold in the research-chemical channel. The honest comparison:

• Cardarine (GW-501516) — a synthetic PPARδ agonist (also not a SARM, not a peptide), likewise popularized as an "exercise mimetic" from a mouse study. Both are unapproved research chemicals; Cardarine additionally carries a rodent multi-organ cancer signal, while SR9009's defining problem is off-target activity and near-zero oral bioavailability.
• SLU-PP-332 — a synthetic ERRα/β/γ pan-agonist studied as an "exercise mimetic" in mice. Same theme (nuclear-receptor endurance signaling, strictly preclinical), distinct target and molecule.

The decisive point: none of these is an approved, evidence-backed performance therapy. See the Weight management overview.

Common misconceptions

• "SR9009 is a SARM." No. SARMs act on the androgen receptor; SR9009 is a Rev-ErbA (REV-ERBα/β) agonist acting on circadian nuclear receptors. It is only sold alongside SARMs, which is the source of the confusion.
• "SR9009 is a peptide." No. It is a synthetic small molecule (C20H24ClN3O4S, 437.94 g/mol). It appears here only because it is discussed and stacked with peptides.
• "SARMs and 'research chemicals' are a mild, legal alternative to steroids." No. SR9009 is not approved for human use, is not a benchmarked safe therapy, and is WADA-prohibited. Being non-hormonal says nothing about safety — SR9009's evidence is confounded by off-target effects and it is barely absorbed orally.
• "The mouse study proves it works in humans as an oral capsule." No. The endurance and metabolic effects were seen with injections in mice; SR9009 has essentially no oral bioavailability, and there are no human data at all.

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This entry is educational and summarizes published research and public regulatory information. It is not medical or legal advice, a recommendation, or a guide to obtaining or using any substance.