SR9009 and SR9011 are both synthetic REV-ERB agonists that emerged from the same discovery program at Scripps Research, but they are not the same molecule and do not behave identically in experimental protocols. This page separates what is actually documented for each compound from what gets assumed because they share a receptor target.
- SR9009 and SR9011 both activate REV-ERBα and REV-ERBβ but have distinct chemical scaffolds and binding affinities.
- SR9011 is generally reported as the more potent ligand at the REV-ERB binding domain across published assays.
- A 2019 EMBO Molecular Medicine analysis found SR9009 produces REV-ERB-independent effects on cell metabolism at commonly used concentrations.
- Neither compound has published human trial data as of 2026 — both remain preclinical tool compounds.
- SR9009 vs SR9011 mechanism differences matter most for in vitro dose selection and data interpretation.
Why this matters
REV-ERBα and REV-ERBβ (encoded by NR1D1 and NR1D2) are core repressive components of the circadian transcriptional-translational feedback loop. They compete for binding sites with the CLOCK/BMAL1 activator complex and recruit NCoR/HDAC3 corepressor machinery to shut down target gene transcription, including BMAL1 itself. Because SR9009 and SR9011 both act on this shared mechanism, researchers frequently treat them as interchangeable in citations and protocol design. The published pharmacology says otherwise, and conflating the two compounds is a common source of misattributed findings in secondary literature.
4-Amino-Labs supplies both compounds for laboratory research, and documentation practices differ enough between vendors that batch-specific analytical data matters more here than with simpler reagents.
How do SR9009 and SR9011 differ in REV-ERB research?
Both molecules were characterized in the original 2012 Nature Medicine paper by Solt et al. that first described synthetic REV-ERB agonists altering circadian behavior and metabolic gene expression in mice. From that point forward, the two compounds diverge in structure, relative potency, and how cleanly their effects map back to REV-ERB activation alone.
| Feature | SR9009 | SR9011 |
|---|---|---|
| Receptor target | REV-ERBα / REV-ERBβ agonist | REV-ERBα / REV-ERBβ agonist |
| Chemical scaffold | Distinct core structure from SR9011 | Structurally related but not identical to SR9009 |
| Relative potency | Reported as the less potent of the pair in most assays | Generally reported as more potent at the ligand-binding domain |
| Pharmacokinetics in rodent studies | Poor oral bioavailability, short systemic half-life, required repeated intraperitoneal dosing | Similarly poor oral bioavailability and rapid clearance |
| Documented off-target activity | REV-ERB-independent effects on cell metabolism reported in 2019 (EMBO Mol Med) | Less extensively characterized for off-target effects in published literature |
| Evidence base as of 2026 | Preclinical, rodent and in vitro only | Preclinical, rodent and in vitro only |
The shared pathway — REV-ERB activation, corepressor recruitment, BMAL1 repression, downstream shift in clock and metabolic gene transcription — is identical for both compounds. What differs is how selectively each one produces that effect at working concentrations, and how well each has held up to independent scrutiny.
SR9009: structure and receptor activity
SR9009 was one of two lead compounds from the original synthetic REV-ERB agonist screen. In the 2012 characterization, it altered expression of clock and metabolic genes in mouse liver and skeletal muscle following repeated systemic dosing. Its pharmacokinetic profile is a limiting factor for any protocol design: poor oral bioavailability and rapid clearance meant the original studies relied on multiple daily intraperitoneal injections rather than a single dose.
The more consequential finding came later. A 2019 analysis published in EMBO Molecular Medicine reported that SR9009 alters cellular respiration and proliferation independent of REV-ERB expression, at concentrations commonly used in published in vitro protocols. That means some effects attributed to REV-ERB activation in SR9009 studies may reflect off-target activity instead, and it is the single most important caveat for anyone designing a new SR9009 protocol in 2026.
SR9011: structure and receptor activity
SR9011 shares the discovery paper and general chemical lineage with SR9009 but is a structurally distinct molecule, not a formulation variant of the same compound. Across the assays reported in the founding literature, SR9011 is generally described as the more potent REV-ERB ligand of the pair, meaning less compound is needed to achieve comparable receptor occupancy in vitro.
SR9011's pharmacokinetic limitations mirror SR9009's: short half-life and low oral bioavailability in the original rodent work, again requiring repeated systemic dosing to sustain circadian gene effects. The off-target characterization work that flagged REV-ERB-independent activity for SR9009 has not been replicated to the same extent for SR9011, which is a gap in the evidence base rather than evidence of a cleaner mechanism — it simply has not been tested as thoroughly.
Why SR9009 and SR9011 produce different research outcomes
- Scaffold difference: the two compounds are not positional isomers or salt forms of one molecule — they are separately synthesized agonists with different core chemistry.
- Potency gap: SR9011 is consistently reported as more potent at the REV-ERB ligand-binding domain than SR9009 across the published assays.
- Off-target confound: SR9009's REV-ERB-independent metabolic effects (Dierickx et al., EMBO Mol Med, 2019) are documented; an equivalent off-target profile for SR9011 has not been established either way.
- Pharmacokinetics: both compounds show poor oral bioavailability and rapid clearance in rodent models, which shapes dosing frequency in any in vivo design regardless of which compound is used.
- Evidence maturity: SR9009 has a larger published body of follow-up characterization (including the off-target work); SR9011 has comparatively less independent scrutiny.
- Vendor labeling inconsistency: both compounds are sometimes marketed alongside unrelated receptor classes (androgen receptor modulators, for example), which has no basis in their actual pharmacology.
“SR9009 and SR9011 share a target receptor, not a chemical identity — treating the potency, off-target, and pharmacokinetic data as interchangeable is the most common error in secondary citations of this compound pair.”
Is SR9009 a SARM?
No. SR9009 (sold under the informal name Stenabolic) does not bind the androgen receptor and is not a selective androgen receptor modulator despite frequent mislabeling in vendor catalogs and forum discussion. Its documented mechanism is REV-ERBα/β agonism, an entirely separate nuclear receptor pathway from the androgen receptor targets that define the actual SARM class.
Does GW501516 work through the same pathway as SR9009 and SR9011?
No — GW501516 is a PPARδ agonist, a different nuclear receptor family from REV-ERB, though both pathways intersect on overlapping lipid and glucose metabolism gene networks studied in rodent models. Researchers sometimes group all three compounds together in review discussion because of that overlapping downstream biology, but the upstream receptor targets and binding chemistry are unrelated.
Has SR9009 or SR9011 been studied in humans?
No published human trial data exists for either SR9009 or SR9011 as of 2026. Both compounds remain preclinical tool compounds characterized in rodent and in vitro systems, and the compliance framing on any supplier catalog listing should reflect that research-only status.
FAQ
What receptor do SR9009 and SR9011 both target?
Both compounds are synthetic agonists of REV-ERBα and REV-ERBβ, nuclear receptors encoded by NR1D1 and NR1D2 that repress BMAL1 transcription as part of the core circadian feedback loop.
Which is more potent, SR9009 or SR9011?
SR9011 is generally reported as the more potent REV-ERB ligand of the two across the published characterization assays from the original 2012 discovery paper and subsequent literature.
Does SR9009 have off-target effects?
Yes. A 2019 EMBO Molecular Medicine analysis found SR9009 alters cellular respiration and proliferation independent of REV-ERB expression at concentrations used in many published in vitro protocols.
Are SR9009 and SR9011 the same molecule with different names?
No. They are structurally distinct compounds discovered in the same research program, not a single molecule sold under two names.
Is SR9009 classified as a SARM?
No, SR9009 does not bind the androgen receptor. It is a REV-ERBα/β agonist, a mechanism unrelated to the androgen receptor modulator class it is sometimes incorrectly grouped with.
What pathway do REV-ERB agonists act through?
REV-ERB agonists bind the receptor’s ligand-binding domain, recruit NCoR/HDAC3 corepressor complexes, and repress BMAL1 and other clock-controlled genes, which is the same downstream pathway for both SR9009 and SR9011.
Has SR9011 been tested for the same off-target effects as SR9009?
Not to the same extent. The REV-ERB-independent effects documented for SR9009 in 2019 have not been equivalently characterized for SR9011, which reflects a gap in published data rather than a confirmed absence of off-target activity.
Why do pharmacokinetics matter for SR9009 and SR9011 study design?
Both compounds showed poor oral bioavailability and short systemic half-lives in the original rodent studies, requiring repeated intraperitoneal dosing to sustain measurable circadian gene effects.
One last thing
The detail most secondary sources drop is the 2019 off-target finding on SR9009 — it means a portion of the metabolic effects attributed to REV-ERB activation in older SR9009 papers may not be REV-ERB-mediated at all, which is exactly the kind of distinction that matters when citing this compound pair in new research design for 2026 and beyond. Purity documentation and batch-specific certificates of analysis matter more here than with simpler reagents, since concentration accuracy directly affects whether observed effects stay in the on-target range.
Research Use Only. Not for human consumption. This content is not medical advice and is not intended to diagnose, treat, cure, or prevent any disease.
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