SR9011

Overview

SR9011 (also SR-9011, Rev-ErbA agonist SR9011) is a synthetic agonist of the Rev-ErbA nuclear receptors (REV-ERBα and REV-ERBβ) — the circadian-clock proteins that repress transcription and coordinate metabolic gene networks. It is NOT a SARM (it has no androgen-receptor activity) and it is NOT a peptide (it is a small lab-made chemical, not an amino-acid chain). It appears in this peptide reference because it is discussed and stacked alongside SARMs and peptides in the "research chemical" community, not because it belongs to either class.

SR9011 is the N-pentyl-carboxamide sister compound of SR9009 (stenabolic), described in the same academic discovery program — Thomas Burris and colleagues at The Scripps Research Institute (Solt, Wang, Banerjee et al.) — and reported together in Solt et al., Nature 2012 (PMID 22460951). Its reputation as a "fat-loss / endurance" compound traces to that study, where in diet-induced obese mice SR9011 altered circadian and metabolic gene expression in liver, muscle and fat, increased energy expenditure, reduced fat mass, and improved dyslipidaemia and hyperglycaemia. All of that evidence is preclinical (rodent and cell).

Chemistry and structure

SR9011 is a small-molecule chemical, not an amino-acid chain.

SR9011 is the N-pentyl analogue of SR9009, sharing the same core chemotype (including a nitrothiophene moiety) from the same discovery program.

Mechanism of action

• Rev-ErbA (REV-ERBα/β) agonism. SR9011 binds and activates the nuclear receptors REV-ERBα (NR1D1) and REV-ERBβ (NR1D2), enhancing recruitment of the NCoR–HDAC3 corepressor complex to repress target genes including the core clock activator BMAL1 (Arntl). Reported in-vitro potency is EC50 ~790 nM (REV-ERBα) and ~560 nM (REV-ERBβ) (Solt 2012). [In vitro]
• Circadian clock gene expression. In mice, SR9011 alters the circadian pattern of core clock gene expression in the hypothalamus and modifies circadian locomotor behaviour (Solt 2012). [Animal]
• Metabolic gene networks. SR9011 rewires expression of lipid/glucose metabolism genes in liver, skeletal muscle and adipose tissue, increasing energy expenditure; in diet-induced obese mice it reduced fat mass and improved dyslipidaemia and hyperglycaemia. This rodent metabolic phenotype is the origin of the "fat-loss / metabolic" reputation — it has never been reproduced in a human trial. [Animal]
• Autophagy and de novo lipogenesis (oncology context). In cancer and oncogene-induced-senescent cells, pharmacological REV-ERB activation (SR9009/SR9011) inhibits autophagosome formation and suppresses lipogenic enzymes (FAS, SCD1), triggering apoptosis selectively in those cells (Sulli et al., Nature 2018). This is an oncology research context, not a performance or safety rationale. [In vitro]
• CRITICAL CONFOUND — REV-ERB-independent off-target activity. The SR900x chemotype produces effects on proliferation, metabolism and transcription even in cells with REV-ERBα/β deleted, and carries a known toxicophore (nitrothiophene) (Dierickx 2019). SR9011's biological effects therefore cannot be attributed cleanly to REV-ERB agonism, and the safety implications are not characterized. [In vitro]

Research and evidence

All evidence for SR9011 is preclinical — animal, cell, and in-vitro studies only. There is no trial phase because no human clinical trial has ever been conducted for any indication (ClinicalTrials.gov search, 2026).

Human evidence in context. There is none. Every observation attributed to SR9011 comes from rodents or cell culture. The "fat-loss / endurance" claim rests on the 2012 mouse study, and a later study on the chemotype showed a large share of its cellular effects occur even when the REV-ERB receptors are genetically removed. Human half-life, pharmacokinetics, oral bioavailability, efficacy, and toxicity are all Not established / not found in sources.

Status and regulation

• Regulatory approval: None. SR9011 is not approved by the FDA, the EMA, or any other regulator for any indication. Its highest development phase is preclinical (animal/in-vitro only) — no IND, no registered human trial.
• Origin / development: Described in an academic discovery program by Thomas Burris / Scripps Research (Solt, Wang, Banerjee et al.) as the N-pentyl sister of SR9009 — a tool compound to probe circadian and metabolic biology, not a therapeutic or performance product. No current program advancing SR9011 toward clinical development has been identified.
• Anti-doping: Prohibited by WADA under S4.4 — Metabolic Modulators (Rev-ErbA agonists; SR9011 is named as an example, alongside SR9009), in-competition and out-of-competition. It can be detected in doping control via characteristic metabolites. 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:

• Essentially no human safety data. SR9011 has never completed a human clinical trial; no established human dose, no human PK, no human toxicity profile. Any human use is uncontrolled self-experimentation. [Human]
• Poor drug-like properties and extensive hepatic metabolism. Poor bioavailability; 14 phase-I metabolites in human liver microsomes, with metabolite identities and toxicities uncharacterized for human safety. [In vitro]
• REV-ERB-independent off-target activity + toxicophore. Effects persist in REV-ERB-null cells and the molecule carries a nitrothiophene toxicophore, so its actions cannot be assumed clean or predictable; off-target toxicity is unstudied in humans. [In vitro]
• Pro-apoptotic / autophagy-blocking activity in cells. The same mechanism that kills cancer cells (autophagy inhibition, apoptosis) acts on normal cellular housekeeping pathways; the net effect of chronic exposure on healthy human tissue is unknown. [Hypothesis]
• WADA-prohibited. Banned in sport under S4.4 (Metabolic Modulators, Rev-ErbA agonists). Detected via characteristic metabolites. A sport-eligibility axis — it does not imply safety or approval, and is separate from legality. [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 compound, 39% contained a different unapproved drug, and 9% contained no active drug. A "SR9011" or "SARM" label is not a reliable statement of contents. [Human]

Legal status

How it compares

SR9011 is usually grouped with "exercise mimetic" and metabolic compounds sold in the research-chemical channel. The honest comparison:

• Stenabolic (SR9009) — SR9011's direct sister compound (SR9011 is the N-pentyl analogue of SR9009) from the same 2012 Solt et al. program. Same Rev-ErbA target and the same core problems: strictly preclinical evidence, near-zero oral bioavailability / poor drug-like properties, and documented REV-ERB-independent off-target activity. SR9011 additionally shows a more complex metabolite profile (14 vs 8 metabolites in human liver microsomes).
• Cardarine (GW-501516) — a synthetic PPARδ agonist (also not a SARM, not a peptide), likewise popularized as an "exercise mimetic" from a mouse study. Different target; both are unapproved research chemicals with a preclinical-only evidence base.

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

Common misconceptions

• "SR9011 is a SARM." No. SARMs act on the androgen receptor; SR9011 is a Rev-ErbA (REV-ERBα/β) agonist with no androgen-receptor activity. It is only sold alongside SARMs, which is the source of the confusion.
• "SR9011 is a peptide." No. It is a synthetic small molecule (C23H31ClN4O3S, 479.0 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. SR9011 is not approved for human use, is not a benchmarked safe therapy, and is WADA-prohibited. Being non-hormonal says nothing about safety — SR9011's evidence is confounded by off-target effects, it carries a toxicophore, and there are no human data.
• "The mouse study proves it burns fat in humans." No. The fat-loss and metabolic effects were seen in diet-induced obese mice with injections; SR9011 has poor drug-like properties 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.