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DPreclinical / mechanistic only
High riskNo human data

SR9009

Stenabolic

SR9009 (Stenabolic) is a synthetic agonist of the REV-ERB nuclear receptors (REV-ERBα/β), circadian-clock proteins that regulate lipid, glucose, and mitochondrial metabolism. It was created as a laboratory tool compound and is marketed in the fitness world as an "exercise mimetic" or "endurance/fat-loss" agent. The critical fact is that all supporting evidence comes from mice, cultured cells, and test-tube experiments — there are no human trials, no established human dose, and no human safety data of any kind. Two facts should dominate any risk assessment: (1) SR9009 has poor oral bioavailability, so orally taken "Stenabolic" products deliver very little intact drug systemically — meaning users are ingesting an uncharacterized research chemical with unknown purity for likely minimal predictable effect; and (2) SR9009 produces documented REV-ERB-independent (off-target) effects on cell metabolism and viability, so it is not a clean, target-specific agent and its true toxicology in humans is unknown. It is prohibited in sport by WADA. Because the evidence base is entirely preclinical, no organ-specific human safety profile can be given; the honest position is that the risks are unquantified rather than proven low.

Clinical readoutPED-adjacent · research-chemical
Hepatic strainNone
CardiovascularNone
HPTA suppressionNone
Half-life
Not characterized…
Route
In published research S…
Evidence
D
Active
Not established in huma…
1·t½2·t½3·t½4·t½5·t½
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Not characterized in humans. In rodent studies the plasma half-life is short (on the order of a few hours), which — together with poor oral bioavailability — is why preclinical work dosed by injection rather than by mouth.
Pharmacology

Mechanism of action

SR9009 is a small-molecule synthetic agonist of the nuclear receptors REV-ERBα and REV-ERBβ (encoded by NR1D1/NR1D2), which are heme-binding transcriptional repressors and core components of the circadian clock. By activating REV-ERB, SR9009 enhances repression of target genes, altering the circadian expression of metabolic gene networks in liver, skeletal muscle, and adipose tissue, increasing energy expenditure and suppressing lipid and cholesterol biosynthesis in mice. In skeletal muscle, REV-ERBα activation increases mitochondrial biogenesis and oxidative capacity via the LKB1–AMPK–SIRT1–PGC-1α pathway. SR9009 also has demonstrated REV-ERB-independent actions: it alters cellular metabolism, gene transcription, and reduces cell viability even in cells genetically lacking both REV-ERB proteins, so its biological effects cannot be attributed solely to on-target REV-ERB activity. All mechanistic data are preclinical.
Kinetics

Pharmacokinetics

Half-life

Not characterized in humans. In rodent studies the plasma half-life is short (on the order of a few hours), which — together with poor oral bioavailability — is why preclinical work dosed by injection rather than by mouth.

Active duration

Not established in humans; short in rodents, consistent with the frequent parenteral dosing schedules used in animal studies. Human duration of action is unknown.

Route

In published research SR9009 was administered parenterally (intraperitoneal injection) to mice because oral bioavailability is poor. It is sold to consumers as an oral product, but oral absorption of intact drug is low, so systemic exposure from oral use is expected to be limited and unpredictable. No human route/exposure data exist.

Metabolism & clearance

Hepatic. In human liver microsomes SR9009 is extensively metabolized by cytochrome P450 enzymes CYP3A4, CYP3A5, CYP2C19, and CYP2D6 into at least 13 metabolites (hydroxylation, de-alkylation, oxidation), which are then glucuronidated. CYP2D6/CYP2C19 genetic polymorphism and CYP-inhibitor drugs (e.g., ketoconazole, fluoxetine, paroxetine, nefazodone) significantly alter its metabolism, implying real potential for drug–drug interactions. These are in-vitro human data; in-vivo human clearance is uncharacterized.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • All effects below are from animal or cell studies only; none are demonstrated in humans.
  • In diet-induced obese mice: reduced fat mass, decreased plasma cholesterol and triglycerides, improved hyperglycemia, and increased energy expenditure (preclinical).
  • In mice: increased skeletal-muscle mitochondrial content and improved running/exercise capacity (basis of the 'endurance/exercise-mimetic' marketing claim) (preclinical).
  • Altered circadian behavior and shifted circadian clock-gene expression in mice (preclinical).
  • Suppression of hepatic cholesterol biosynthesis genes and lowered plasma cholesterol in mice (preclinical).
  • Cytotoxic/antiproliferative effects on cultured cancer cell lines (glioblastoma, hepatoma), reflecting off-target effects on cell metabolism and viability (in-vitro).
Safety

Adverse effects by system

Cardiovascular

No human data. No cardiovascular adverse effects have been characterized in humans; conversely, no cardiovascular safety has been demonstrated. Preclinical work focused on beneficial lipid/metabolic changes in mice and does not establish human cardiovascular safety.

Hepatic

No human data. SR9009 is heavily metabolized in the liver via multiple CYP450 enzymes (in-vitro human microsomes), and it reduces hepatocyte and hepatoma-cell viability in vitro, raising a theoretical hepatic-exposure/off-target concern; human hepatotoxicity is unstudied.

Endocrine / HPTA

No human data. SR9009 is not a hormone or a SERM and has no described direct action on the hypothalamic–pituitary–gonadal axis; effects on human sex hormones, cortisol, or thyroid have not been studied. REV-ERB is broadly involved in circadian/metabolic endocrinology, so systemic endocrine effects cannot be excluded, but none are documented in humans.

Reproductive

No human data. No reproductive or fertility studies in humans; effects during pregnancy or on fertility are unknown and it should be assumed unsafe in these settings.

Neuropsychiatric

No human data. SR9009 alters circadian rhythm and clock-gene expression in animals; because circadian disruption is linked to mood and sleep in general, neuropsychiatric effects are biologically plausible but entirely uncharacterized in humans.

Renal

No human data. No renal effects have been studied or reported in humans; renal safety is unknown.

Hematologic

No human data. No hematologic effects reported or studied in humans.

Dermatologic

No human data. No dermatologic effects reported or studied.

Recovery

HPTA suppression & recovery

Suppression: No known direct HPTA suppression; not studied in humans

SR9009 is not an anabolic-androgenic steroid or SERM and has no described mechanism of direct hypothalamic–pituitary–gonadal axis suppression, so classic post-cycle 'recovery' concepts do not clearly apply. However, human endocrine effects are entirely uncharacterized. Any concern about hormonal disruption or recovery should be evaluated with bloodwork and directed by an endocrinologist rather than self-managed; if a SERM is ever considered for a co-used compound, only a single-SERM approach under medical supervision is within scope here.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Comprehensive metabolic panel including liver function tests (AST, ALT, bilirubin) given extensive hepatic metabolism and in-vitro hepatocyte toxicityFasting lipid panelFasting glucose / HbA1cComplete blood count as general safety monitoring

Cadence: There is no evidence-based monitoring schedule because no human studies exist. If someone uses it despite the unknowns, baseline bloodwork before use and repeat testing (e.g., within a few weeks and if any symptoms arise) under a clinician's supervision is the conservative approach — but the primary recommendation is not to use an unstudied research chemical.

Warning signs — seek care
  • Right-upper-quadrant abdominal pain, nausea, dark urine, pale stools, or jaundice (possible liver injury) — stop and seek care
  • Unexplained fatigue, malaise, or loss of appetite
  • Palpitations, chest pain, shortness of breath, or fainting
  • New or worsening mood disturbance, severe insomnia, or circadian/sleep disruption
  • Any allergic-type reaction (rash, swelling, difficulty breathing)
Do not use if

Contraindications

  • No human safety testing exists — it should be regarded as contraindicated outside a research setting for anyone unwilling to accept fully unknown risk.
  • Pregnancy, breastfeeding, and anyone trying to conceive (no reproductive safety data).
  • Concurrent use of CYP3A4/CYP2D6/CYP2C19 inhibitors or substrates (e.g., certain antifungals, SSRIs such as fluoxetine/paroxetine, nefazodone) due to demonstrated in-vitro metabolic drug–drug interactions.
  • Existing liver disease (extensive hepatic metabolism; in-vitro hepatocyte toxicity; no human liver-safety data).
  • Competitive athletes subject to anti-doping testing — SR9009 and its metabolites are WADA-prohibited and detectable.
  • Any pre-existing condition where an uncharacterized off-target metabolic/antiproliferative agent could be harmful.
Harm reduction

Reducing harm & when to stop

  • There is no human data. Every claimed benefit comes from mice or cells, and no human dose or safety margin exists. The conservative, evidence-based recommendation is not to use it.
  • Oral 'Stenabolic' delivers little intact drug because oral bioavailability is poor — meaning users take on the risks of an unregulated research chemical (unknown purity, contaminants, actual content) for a likely minimal and unpredictable effect.
  • SR9009 is not a clean REV-ERB drug: documented off-target effects on cell metabolism and viability mean its real human toxicology is unknown, not reassuringly low.
  • Do not combine with medications metabolized by or inhibiting CYP3A4/2D6/2C19 (including common antidepressants and antifungals) without a pharmacist/physician review, given demonstrated in-vitro interactions.
  • If used at all, get baseline and follow-up bloodwork (liver function, lipids, glucose, CBC) with a clinician, and stop immediately and seek medical care for any signs of liver injury (jaundice, dark urine, right-upper-quadrant pain), chest symptoms, or severe sleep/mood disturbance.
  • Avoid entirely in pregnancy, breastfeeding, when trying to conceive, and if you have liver disease.
  • Athletes: SR9009 and its metabolites are WADA-prohibited and detectable; this is a factual doping-control note, not guidance on use.
  • This is educational information only, not medical advice, and does not create a doctor–patient relationship; these substances carry serious risks — consult a qualified physician. 21+ only.
Evidence

Citations (7)

Every clinical claim above is tied to a primary source. Overall evidence grade D — this compound lacks adequate human data; claims rest on preclinical or mechanistic evidence.

  1. 01

    SR9009 is a synthetic REV-ERB agonist that alters circadian behavior/clock-gene expression and, in diet-induced obese mice, reduced fat mass, improved dyslipidemia and hyperglycemia, and increased energy expenditure.

    PreclinicalPMID 22460951 ↗

  2. 02

    Pharmacological REV-ERBα activation (including with SR9009) increases skeletal-muscle mitochondrial biogenesis/oxidative capacity and improves exercise (running) capacity in mice — the basis of the endurance/'exercise-mimetic' claim.

    PreclinicalPMID 23852339 ↗

  3. 03

    SR9009 has REV-ERB-independent (off-target) effects: it decreases cell viability, rewires cellular metabolism, and alters transcription even in cells genetically lacking both REV-ERBα and REV-ERBβ, so its effects are not cleanly target-specific.

    PreclinicalPMID 31127047 ↗

  4. 04

    SR9009 reduced plasma cholesterol and suppressed hepatic cholesterol-biosynthesis gene expression in mice.

    PreclinicalPMID 28213272 ↗

  5. 05

    SR9009 exerts cytotoxic/antiproliferative effects and reduces viability of cultured cancer cell lines (glioblastoma T98G, hepatoma HepG2), consistent with off-target effects on cell metabolism.

    PreclinicalPMID 31825658 ↗

  6. 06

    SR9009 is extensively metabolized in human liver microsomes by CYP3A4, CYP3A5, CYP2C19 and CYP2D6 into at least 13 metabolites followed by glucuronidation, with metabolism significantly altered by CYP genetic polymorphism and by CYP-inhibitor drugs (e.g., ketoconazole, fluoxetine, paroxetine, nefazodone), indicating drug-interaction potential.

    PreclinicalDOI 10.1002/dta.2538 ↗

  7. 07

    Poor oral bioavailability and short duration of action in rodents necessitated parenteral (intraperitoneal) dosing in preclinical studies.

    PreclinicalPMID 22460951 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice