A Burris-lab Rev-erbα agonist tool compound from Scripps Florida (Solt 2012). Coherent mouse data, but two facts dominate: oral F% ~2.2% kills any oral protocol, and Dierickx 2019 showed substantial Rev-erb-independent activity in receptor-knockout cells.
SR9009 (Stenabolic) is a synthetic small-molecule Rev-erbα / Rev-erbβ dual agonist developed in the Burris lab at Scripps Florida. It's not a peptide and not a SARM — it's a synthetic small molecule, despite living in peptide-adjacent vendor catalogs. Founding paper: Solt et al. Nature 2012, "Regulation of circadian behaviour and metabolism by synthetic REV-ERB agonists" (PMID 22460951), which characterized SR9009 and companion compound SR9011 as Rev-erb agonists with circadian and metabolic effects.
Rev-erbα is a nuclear receptor that acts as a transcriptional repressor. It plays roles in circadian rhythm (repressing Bmal1, Npas2, Clock), skeletal-muscle oxidative metabolism (high expression in oxidative muscle), hepatic and adipose lipid metabolism, and macrophage inflammation regulation. SR9009 binds Rev-erbα/β as a synthetic agonist, enhancing the receptor's repressor activity.
Downstream effects from the Solt 2012 (PMID 22460951) and Woldt 2013 Nature Medicine (PMID 23852339) papers: mitochondrial biogenesis in oxidative muscle; increased running endurance via the Lkb1–AMPK–SIRT1–PGC-1α axis; reduced fat mass with improved dyslipidemia and hyperglycemia in DIO mice; reduced atherosclerotic plaque size in Ldlr−/− mice (Sitaula 2015, PMID 25800870); and selective killing of cancer cells and oncogene-induced senescent cells via autophagy and lipogenesis dysregulation (Sulli 2018, Nature, PMID 29320480).
The receptor-independence challenge. Dierickx et al. PNAS 2019 (PMID 31127047), from the Lazar lab at Penn, tested SR9009 in cells genetically deleted for both Rev-erbα and Rev-erbβ. SR9009 retained substantial effects on cell viability, metabolism, and gene transcription in the receptor-knockout cells. Translation: a meaningful fraction of SR9009's biology isn't mediated by its nominal target. Rev-erbα is still a legitimate target, but how much of SR9009-the-tool-compound's effect runs through Rev-erb is uncertain. Vendor framing of "SR9009 is a Rev-erbα agonist that does X" overstates the certainty.
Trump et al. J Med Chem 2013 (PMID 23656296), titled "Optimized Chemical Probes for REV-ERBα," is the Burris-lab follow-up that characterized SR9009 PK in rodents.
| Parameter | SR9009 |
|---|---|
| Terminal half-life | ~0.55 h (~33 min) |
| Oral bioavailability | ~2.2% |
| Clearance | High (rapid metabolic clearance) |
Practical implication: almost no oral capsule protocol in community use replicates the preclinical exposure that produced the published mouse effects. The Burris lab itself developed follow-up chemotypes precisely because the parent SR9009/SR9011 series had high clearance and low oral exposure — that's what the "Optimized Chemical Probes" title is signaling.
Vendor protocols of "20–40 mg oral 3× daily" produce blood levels far below those used in the Solt 2012 and Woldt 2013 mouse studies (which used IP-dosed 100 mg/kg). Whatever results community users see at oral doses aren't directly anchored to the published preclinical effect curves.
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Start Tracking Free| Claim | Evidence | Tier |
|---|---|---|
| Mitochondrial biogenesis in oxidative muscle | Solt 2012, Woldt 2013 | Mouse, IP-dosed |
| Improved running endurance (mice) | Woldt 2013 | Mouse, IP-dosed |
| Reduced fat mass / metabolic syndrome (mice) | Solt 2012 | Mouse, IP-dosed |
| Reduced atherosclerotic plaque (mice) | Sitaula 2015 | Mouse |
| Selective killing of cancer / senescent cells | Sulli 2018 | In vitro / mouse |
| "Cardarine without the cancer risk" | None | Unsupported |
| Human exercise / fat loss / body composition | None | No human trial |
Rule of thumb: almost every benefit claim for SR9009 should land at "preclinical, mouse, IP-dosed." Anything stronger is overreach. Any claim that implies the SR9009 effect is definitely mediated through Rev-erbα should also acknowledge the Dierickx 2019 receptor-independence finding.
The PK numbers mean any oral SR9009 protocol is unanchored to the published preclinical effect data. The community dosing below is what users actually do — not what the science supports.
| Parameter | Common Range |
|---|---|
| Dose | 20–40 mg oral 3× daily |
| Total daily | 60–120 mg |
| Cycle length | 4–12 weeks |
| Route | Oral (despite F% ~2.2%); some users inject SC for higher exposure |
Half-life ~33 minutes means even multi-daily oral dosing produces only brief plasma exposure. SC injection achieves higher exposure but isn't how the published mouse studies dosed (those were IP).
Pre-filled with a typical SR9009 (Stenabolic) setup. Edit any field — the draw updates live.
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No published human safety data. All concerns are mechanism- or animal-anchored.
Acute: sleep disruption and circadian desynchronization (SR9009 enhances Rev-erb repression of Bmal1 and other clock genes; community users report disrupted sleep with evening dosing); GI upset; mood and cognitive changes (community).
Chronic and theoretical: off-target effects (per Dierickx 2019, SR9009 has substantial Rev-erb-independent activity — by definition we don't know what those off-target hits do over months of human dosing); cancer-axis ambiguity (Sulli 2018 reported selective killing of cancer cells via autophagy disruption, but autophagy is essential in normal tissues too — chronic autophagy inhibition has cardiac, neuronal, and immune liabilities); cardiac (Rev-erbα has documented cardiac roles, chronic agonism uncharacterized); immune (Rev-erbα regulates macrophage inflammation, chronic agonism could shift inflammatory balance).
Cardarine (GW501516) — PPARδ agonist, completely different receptor target. Cardarine has documented multi-organ rodent carcinogenicity that GSK pulled the program over. Vendor framing of "SR9009 = safer Cardarine" is unsupported — no long-term tox study has been done for SR9009.
SR9011 — companion compound from Solt 2012, similar pharmacology, similar PK problems.
AICAR — AMPK activator. Different mechanism, also "exercise-mimetic" framing.
5-Amino-1MQ — NNMT inhibitor. Different mechanism.
SLU-PP-332 — ERRβ/γ agonist, different receptor. Another exercise-mimetic candidate.
MOTS-c — mitochondrial-derived peptide. Different family entirely but adjacent "exercise mimetic" framing.
SR9009 (Stenabolic) is a research peptide not approved by the FDA for human use. It is sold only as a research chemical, and StackTrax does not endorse or facilitate personal use.
Quality varies enormously among research-chemical suppliers. At minimum, look for:
StackTrax’s preferred partner NextGen Peptides does not currently carry SR9009 (Stenabolic)in their catalog, which is why you don’t see a direct purchase link here. Other major research-chemical suppliers carry it; we don’t specifically recommend one for this compound.
Build your protocol, log every dose, monitor your body's response, and get reminders so you never miss a dose.
Start Tracking FreeNo. SR9009 (Stenabolic) was developed in the Burris lab at Scripps Florida as a tool compound for studying Rev-erb biology — not as a drug candidate. It is not approved by the FDA for any indication and is sold gray-market as a research chemical. WADA prohibits it at all times under S4 (Hormone and Metabolic Modulators), and certified reference materials exist for doping-control detection.
No. SR9009 is a synthetic small-molecule Rev-erbalpha / Rev-erbbeta dual agonist, not a SARM. It is not a peptide either, despite living in peptide-adjacent vendor catalogs. The mechanism is nuclear-receptor agonism at Rev-erb, which acts as a transcriptional repressor — completely unrelated to androgen receptor modulation.
Community ranges are 20 to 40 mg oral, three times daily (60 to 120 mg total per day), in 4 to 12 week cycles. These numbers are not anchored in the published preclinical effect data. The terminal half-life is roughly 33 minutes and oral bioavailability is about 2.2%, so even multi-daily oral dosing produces only brief plasma exposure. Some users inject SC for higher exposure, but the published mouse studies dosed IP, not SC.
The pharmacokinetics make oral SR9009 protocols unanchored to the published preclinical effects. Trump 2013 (PMID 23656296) characterized SR9009 as having terminal half-life of about 33 minutes, oral bioavailability of about 2.2%, and high clearance. The Burris lab itself developed follow-up chemotypes precisely because the parent SR9009 / SR9011 series had high clearance and low oral exposure — that is what the "Optimized Chemical Probes" title is signaling. Vendor protocols produce blood levels far below those used in the published Solt 2012 and Woldt 2013 mouse studies (which dosed 100 mg/kg IP).
SR9009 binds Rev-erbalpha and Rev-erbbeta as a synthetic agonist, enhancing the receptor's transcriptional repressor activity. Downstream effects in mice (Solt 2012, Woldt 2013): mitochondrial biogenesis in oxidative muscle, increased running endurance via the Lkb1-AMPK-SIRT1-PGC-1alpha axis, reduced fat mass with improved dyslipidemia, and reduced atherosclerotic plaque in Ldlr-knockout mice. Important caveat: Dierickx 2019 (PMID 31127047) showed SR9009 retained substantial effects in cells genetically deleted for both Rev-erbalpha and Rev-erbbeta — a meaningful fraction of its biology is not mediated by its nominal target.
The vendor framing of "SR9009 = safer Cardarine" is unsupported. No long-term toxicology study has been done for SR9009, and Dierickx 2019 showed substantial Rev-erb-independent activity — by definition, we don't know what those off-target hits do over months of human dosing. Cardarine (a PPARdelta agonist) has documented multi-organ rodent carcinogenicity, but the absence of equivalent data for SR9009 reflects the absence of long-term studies, not evidence of safety.
No published human safety data exists. Community reports include sleep disruption and circadian desynchronization (SR9009 enhances Rev-erb repression of Bmal1 by design), GI upset, and mood or cognitive changes. Theoretical concerns include off-target effects (per Dierickx 2019), a cancer-axis ambiguity from chronic autophagy disruption (Sulli 2018), cardiac effects (Rev-erbalpha has documented cardiac roles), and shifts in macrophage inflammatory balance.
Disclaimer: This guide is for educational and informational purposes only and is not intended as medical advice, diagnosis, or treatment. The compounds discussed are not FDA approved for human use. Always consult a qualified healthcare provider before starting any new supplement or peptide protocol. StackTrax does not sell peptides or supplements directly — purchase links go to third-party vendors. StackTrax is not responsible for the products, quality, or business practices of any third-party vendor. This page contains affiliate links — StackTrax may earn a commission on purchases at no extra cost to you.
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StackTrax guides cover peptides and compounds that are not FDA-approved for the uses discussed. The dosing, reconstitution, and safety information is compiled from published research and community protocols for educational purposes only.
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