SR-9009
Stenabolic
SR-9009 (Stenabolic) is a metabolic & fat loss research compound. REV-ERB agonist — shifts circadian/metabolic gene programs toward fat oxidation and mitochondrial output ('exercise-mimetic' class).
SR-9009 quick facts
| Reported research dose (Oral) | 10mg-40mg (split 3-4x) |
| Route | Oral |
| Frequency | 3-4x Daily |
| Half-life | Very short (poor oral bioavailability) |
| Forms | Oral, Injectable |
| Evidence level | Animal; poor human PK |
| Other forms available | Injectable — dosed differently |
Cool on paper, but oral bioavailability is terrible — most of what people feel is likely dosing frequency, not the compound. Manage expectations.
How SR-9009 works
REV-ERB agonist — shifts circadian/metabolic gene programs toward fat oxidation and mitochondrial output ('exercise-mimetic' class).
Proposed benefits
Researched for fat oxidation, appetite and energy regulation, insulin sensitivity and endurance capacity.
Where to get SR-9009
SR-9009 is sold in 2 forms. They are not interchangeable — the dose and the route differ, so pick the one this page describes unless you know why you want another.
Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for SR-9009
Graded by what exists behind each claim.
Human clinical evidence
- No human trials: development stopped at preclinical, so the ceiling on any claim here is a rodent model — and these transfer poorly.
📊 Correlative data
- Widely sold and heavily marketed on the 2012 mouse endurance paper. The most important practical fact is pharmacokinetic: oral bioavailability is very poor — reported in the low single-digit percent range — so a large share of what people take orally never reaches circulation.
- Banned by WADA. Reported experience is inconsistent, which is exactly what poor and variable absorption produces.
- Beyond that the record is self-reported: community dosing logs are real information about tolerability and almost none about efficacy.
🧪 How the mechanism reads
- A REV-ERB agonist — REV-ERB is a nuclear receptor forming part of the core circadian clock, and it represses genes controlling lipid and glucose metabolism and mitochondrial biogenesis.
- In mice it increased mitochondrial content and running endurance, which is the basis of the entire marketing claim.
- A later paper argued some of the reported in-vitro effects occurred independently of REV-ERB, which is a serious challenge to the stated mechanism and rarely mentioned by anyone selling it. Acting on a core clock gene also predicts sleep and circadian disruption as an intrinsic cost.
Why an empty tier is not a verdict → · What community dosing logs are worth →
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What SR-9009 actually does
REV-ERB is a real and unusual target, and the biology is the best part of this page. REV-ERB-alpha and REV-ERB-beta are nuclear receptors that act as transcriptional repressors rather than activators — they bind DNA and recruit the NCoR–HDAC3 corepressor complex, and their natural ligand is heme. They sit inside the core circadian loop, repressing Bmal1, and through it they set the daily phase of a large part of metabolic gene expression. Agonizing a repressor is a genuinely different pharmacological act from agonizing an activator: you are turning something off, harder, on a schedule.
What the target does in muscle, established by genetics rather than by drug. Woldt 2013 showed REV-ERB-alpha is highly expressed in oxidative skeletal muscle and that muscle-specific deficiency produced reduced mitochondrial content, impaired oxidative function, upregulated autophagy and compromised exercise capacity, with deactivation of the Lkb1–Ampk–Sirt1–Ppargc-1alpha pathway. Overexpression in vitro increased mitochondrial number and respiratory capacity; muscle overexpression or pharmacological activation in vivo increased exercise capacity. That is a well-built loss-of-function and gain-of-function pair, and it is the reason anyone cares about this receptor.
What the drug did in mice. Solt 2012 reported potent synthetic REV-ERB agonists with in vivo activity: they altered circadian behavior and the circadian pattern of core clock gene expression in mouse hypothalamus, altered metabolic gene expression in liver, skeletal muscle and adipose, increased energy expenditure, and in diet-induced obese mice decreased obesity by reducing fat mass and markedly improving dyslipidemia and hyperglycemia. Every one of those is a real result and every one of them is a mouse.
Now the finding that undermines all of it as evidence about the receptor. Dierickx 2019 built a mouse model for conditional genetic deletion of both REV-ERB-alpha and REV-ERB-beta and then applied SR9009 to cells that had neither. SR9009 still decreased cell viability, rewired cellular metabolism and altered gene transcription in hepatocytes and embryonic stem cells lacking both proteins. Their conclusion is unambiguous: “the effects of SR9009 cannot be used solely as surrogate for REV-ERB activity”. That is the control experiment the original papers could not do because the knockout did not exist yet, and it means an unknown fraction of everything attributed to this compound belongs to something else.
And the off-target list is not empty. The field's own review notes these compounds show certain LXR activity and that SR9009 and SR9011 displace a radioligand from the LXR-alpha binding site Wang 2020. LXR-alpha drives hepatic lipogenesis and SREBP-1c. A compound sold for fat loss that also touches the receptor which switches on hepatic fat synthesis is not a compound whose net effect can be predicted from its headline target.
The potency, for scale. The same review reports SR9009 suppressing Bmal1-luciferase reporter activity with an IC50 of 710 nM, against 68 nM for the later probe SR12418 Wang 2020. Seven hundred nanomolar is a working concentration for a chemical tool in a dish. Holding it at a receptor in a living human being is a different problem entirely, and it is the problem this page turns on.
Cell, rodent, human — and where it stops
Step one, cells and mice. Solt 2012: synthetic REV-ERB agonists, circadian behavior altered, energy expenditure up, fat mass down in diet-induced obese mice. Woldt 2013: REV-ERB-alpha modulates skeletal muscle oxidative capacity, with pharmacological activation in vivo increasing exercise capacity. Two high-profile papers, 2012 and 2013, both in mice.
Step two, the medicinal chemists went back to the drawing board, and their stated reason is the whole story. Trump 2013 reports “the optimization of a series of REV-ERB-alpha agonists based on GSK4112 for potency, selectivity, and bioavailability”. You do not run an optimization campaign for bioavailability on a compound that has enough of it. The paper's own success criterion is instructive: “Amine 4 demonstrated in vivo bioavailability after either iv or oral dosing” — a different molecule, singled out for being orally bioavailable, in a paper about improving this chemical series. SR9009 is not that compound.
Step three, and this is the sentence that should end the argument: there is no published human pharmacokinetic study of SR9009. None. In fourteen years. No oral bioavailability figure. No half-life. No Cmax. No AUC. No clearance. Not in a healthy volunteer, not in a patient, not in a case report. The number every retail page quotes for this compound's oral bioavailability has no primary source in the indexed literature that could be located for this page, and a number without a source is not a number.
Step four, what the in vivo record does say about route, which is more useful than the missing percentage. The one published study that gave SR9009 to a live large mammal and measured it in plasma is a doping-control method paper: Kwak 2022 developed and validated an LC-MS/MS assay in equine plasma and “was successfully applied to plasma samples of thoroughbreds injected intramuscularly with SR9009”. An anti-doping laboratory, trying to generate real in vivo plasma concentrations in a horse, injected it. That choice is a pharmacokinetic statement in itself.
Step five, the population-scale measurement nobody quotes. Geldof 2016 identified eight metabolites of SR9009 in human liver microsomes by high-resolution mass spectrometry, confirmed the presence of SR9009 in a black-market product purchased over the internet, and then applied retrospective data analysis to 1,511 doping control samples previously run through a full-scan LC-HRMS screen. The result: neither the parent compound nor any of its metabolites could be detected in any routine urine sample. The authors state the honest limitation themselves — misuse “could however not be demonstrated in our study”, and these were not samples from known users. But it is the only population-scale exposure measurement that exists for this molecule, and in a sport population where the compound was openly for sale, 1,511 urines produced zero detections of a parent or any of eight metabolites.
The obstacle, stated exactly. The compound has real pharmacology in a dish and real effects in a mouse. It has zero published human pharmacokinetic data, zero published oral bioavailability measurements in any species, zero published in vivo studies using the oral route, and zero detections in 1,511 real doping-control urines. Meanwhile an entire retail category sells it as oral capsules at 10–40 mg split three to four times daily — a schedule whose very existence is an admission that whatever is being absorbed does not stay. The dosing pattern is the market's own evidence against itself.
SR-9009 pharmacokinetics — how much of it actually gets in
This site's card says ‘Very short (poor oral bioavailability)’. That is correct, and here is precisely what sits behind it — and what does not.
What does not sit behind it: a measurement. There is no published oral bioavailability figure for SR9009 in humans or in any animal species that could be located for this page, and no published human pharmacokinetic study of any kind. The commonly repeated low-single-digit percentage circulating on vendor and forum pages is not traceable to a primary source. This page will not repeat an unsourced number to make a point it can make with sourced ones.
What does sit behind it, item by item. (1) The medicinal chemistry program built on this scaffold set out explicitly to improve bioavailability, and the compound it celebrated for working after oral dosing was a different amine Trump 2013. (2) The only published in vivo administration in a large mammal was intramuscular Kwak 2022. (3) 1,511 doping-control urines, screened for the parent and eight metabolites, produced zero detections Geldof 2016. (4) The retail schedule is three to four divided doses a day, which is what a formulator does when exposure collapses between doses.
What degrades it, measured properly. Geldof 2016 incubated SR9009 with human liver microsomal preparations and identified eight metabolites, characterizing each by product-ion scanning in positive and negative ionization mode. Human liver microsomes are the cytochrome-P450 and flavin-monooxygenase fraction, so the metabolism is oxidative and hepatic. Eight metabolites from one small molecule in a microsomal incubation is a lot; it describes a scaffold with many soft spots, which is exactly the profile of a compound with heavy first-pass loss. The paper does not assign specific CYP isoforms, and this page will not guess them.
What the doping laboratories monitor, and why it matters. The validated equine assay tracks the transition 438.2 → 124.9 for SR9009 against a testosterone-d3 internal standard Kwak 2022. That is a measurement of the intact parent molecule. Set it beside Geldof 2016: a scaffold that yields eight distinct metabolites in a single human liver microsomal incubation has many points of enzymatic attack, which is the signature of heavy first-pass loss — and it is the intact parent, plus all eight of those metabolites, that 1,511 urines failed to contain.
What that means for the person swallowing a capsule. The honest bound is this: a compound with an in vitro working concentration around 710 nM Wang 2020, no demonstrated oral systemic exposure in any species, extensive hepatic oxidative metabolism Geldof 2016 and an ester bond exposed to plasma esterases is not a compound anyone can currently argue reaches its receptor after a capsule. That is the page. Everything above it about circadian biology is true, interesting, and describes an experiment that the oral route may never have performed.
What would have to be true, and how you would know it was not
Four predictions with a marker, a direction and a window. The first is a genuine test of whether the compound is present at all, and the third is the one that cuts hardest against it.
1. Sleep timing should shift, and that is the most sensitive read-out this compound has. REV-ERB sits in the core clock loop and Solt 2012 reported altered circadian behavior and altered hypothalamic clock gene expression in mice. Track actigraphy — or a wearable's sleep-onset and wake times — for two weeks before and four weeks during. A drug that engages this receptor systemically should move the timing of sleep, not just its quality, and it should do so before any body-composition change is measurable. No shift in sleep phase over four weeks is meaningful evidence that the compound is not reaching the hypothalamus.
2. Resting heart rate and morning body temperature should show a changed daily rhythm. Both are clock-driven outputs with clear diurnal profiles, both are measurable at home, and both are downstream of the same circadian machinery. Log resting heart rate on waking and again mid-evening; the interesting quantity is the difference between them, not either number alone.
3. The prediction that cuts against it: body composition should not change, and the lipid panel is the place to look for the off-target. In mice this compound reduced fat mass and improved dyslipidemia Solt 2012. In a person taking oral capsules there is no evidence any of it reaches the receptor. Weigh fasted weekly and draw a Lipid Panel with ApoB at baseline and 12 weeks with diet held constant. And note the direction is not guaranteed to be favorable even if the drug does arrive: these compounds displace a radioligand from the LXR-alpha binding site Wang 2020, and LXR-alpha agonism drives hepatic lipogenesis and raises triglycerides. A rising triglyceride level on SR9009 would be the off-target showing up rather than the target failing.
4. Liver enzymes deserve a look, because the compound's own control experiment found it kills hepatocytes. Dierickx 2019 reported SR9009 decreasing cell viability in hepatocytes lacking both REV-ERBs — a REV-ERB-independent cytotoxic effect in liver cells. Draw ALT and AST at baseline and at 8 weeks. This is extrapolation from a cell result to a person and it is labeled as such, but it is the only cytotoxicity signal in the compound's literature and it is in the organ that would be metabolizing it.
What nobody has tested yet
Nobody has measured the oral bioavailability of SR9009 in any species. This is the single most consequential missing number in the entire research-compound market, because it determines whether an entire product category is pharmacology or theater. The study is trivial by the standards of the assays that already exist: dose rats orally and intravenously, sample plasma using the validated LC-MS/MS transitions Kwak 2022, compare the AUCs. It costs a few thousand dollars. It has never been published, and the compound has been sold for over a decade.
Nobody has screened urines from known users. Geldof 2016 screened 1,511 routine doping samples and found nothing, but those were not samples from people who had definitely taken it. Twenty volunteers who are already using retail SR9009, one urine each, run against the eight known metabolites, would answer whether oral SR9009 produces any detectable systemic exposure at all. That is a study a well-organized forum could fund.
Nobody has separated the REV-ERB effects from the REV-ERB-independent ones in a whole animal. Dierickx 2019 did it in cells with a double knockout. Repeating it in a muscle-specific double-knockout mouse, treated and run on a treadmill, would say how much of the famous endurance result belongs to the receptor at all. Seven years after the control experiment was published in cells, it has not been done in an animal.
Nobody has tested an injectable formulation in a human. The only route with published in vivo plasma data is intramuscular, in horses Kwak 2022. If the biology is right and the oral route is the problem, then a parenteral human study is the experiment that would settle whether REV-ERB agonism does anything in a person — and it would also make the compound far more serious, and far more regulated, than a capsule.
SR-9009 — its own safety story, not its class's
Start with the honest structure of the risk, because it is not the usual one. If the compound is not systemically absorbed after an oral dose — which is what the whole of the section above argues — then the dominant risk of a retail SR9009 capsule is not toxicity. It is money, time, and attributing to the capsule whatever the training block would have done anyway. That is worth saying first because it is probably the true answer, and because a safety section that opens with dramatic warnings about a molecule that may not be arriving is theater of a different kind.
The cytotoxicity finding, which is real and is in the right organ. Dierickx 2019 found SR9009 decreased cell viability and rewired metabolism in hepatocytes and embryonic stem cells that had no REV-ERB-alpha and no REV-ERB-beta at all. Whatever is producing that is a mechanism nobody has identified, it operates in liver cells, and it cannot be reasoned about from the circadian pharmacology because it is independent of it. There is no human toxicology to put a rate on this and no reason to assume it is irrelevant.
The off-target receptor, named. SR9009 and SR9011 displace a radioligand from the LXR-alpha binding site and show “certain LXR activity” Wang 2020. LXR-alpha agonism raises hepatic lipogenesis and plasma triglycerides — the classic reason LXR agonists failed as drugs. For a compound taken to improve metabolic health, an off-target that does the opposite is a risk that belongs on the page rather than in a footnote.
What there is no safety data for, listed so nobody imagines there is. No human trial of any kind. No repeated-dose toxicology in the public literature. No reproductive toxicology. No drug interaction data. No long-term rodent carcinogenicity study. The only human-tissue work is an in vitro metabolism study run to catch dopers Geldof 2016.
And the product itself is a documented problem. Geldof 2016 bought a black-market product over the internet and confirmed SR9009 was in it — which is the good outcome. The authors' framing is worth repeating exactly: they built the assay because “illicit use of SR9009 and SR9011 for doping purposes can be anticipated, especially since SR9009 is marketed in illicit products”. It is on the World Anti-Doping Agency's radar, it is detectable in principle by the eight-metabolite panel that paper defined, and any tested athlete should treat it as a positive waiting to happen the moment a laboratory adds it to a routine screen.
Sources read for this page
- Solt LA, Wang Y, Banerjee S, Hughes T, Kojetin DJ, Lundasen T, Shin Y, Liu J, Cameron MD, Noel R, Yoo SH, Takahashi JS, Butler AA, Kamenecka TM, Burris TP. Regulation of circadian behaviour and metabolism by synthetic REV-ERB agonists.. Nature 2012 · PMID 22460951
- Woldt E, Sebti Y, Solt LA, Duhem C, Lancel S, Eeckhoute J, Hesselink MK, Paquet C, Delhaye S, Shin Y, Kamenecka TM, Schaart G, Lefebvre P, Neviere R, Burris TP, Schrauwen P, Staels B, Duez H. Rev-erb-alpha modulates skeletal muscle oxidative capacity by regulating mitochondrial biogenesis and autophagy.. Nat Med 2013 · PMID 23852339
- Dierickx P, Emmett MJ, Jiang C, Uehara K, Liu M, Adlanmerini M, Lazar MA. SR9009 has REV-ERB-independent effects on cell proliferation and metabolism.. Proc Natl Acad Sci U S A 2019 · PMID 31127047
- Trump RP, Bresciani S, Cooper AW, Tellam JP, Wojno J, Blaikley J, Orband-Miller LA, Kashatus JA, Boudjelal M, Dawson HC, Loudon A, Ray D, Grant D, Farrow SN, Willson TM, Tomkinson NC. Optimized chemical probes for REV-ERBalpha.. J Med Chem 2013 · PMID 23656296
- Geldof L, Deventer K, Roels K, Tudela E, Van Eenoo P. In Vitro Metabolic Studies of REV-ERB Agonists SR9009 and SR9011.. Int J Mol Sci 2016 · PMID 27706103
- Kwak YB, Yu J, Yoo HH. A quantitative method for the simultaneous detection of SR9009 and SR9011 in equine plasma using liquid chromatography-electrospray ionization-tandem mass spectrometry.. Drug Test Anal 2022 · PMID 35396832
- Wang S, Li F, Lin Y, Wu B. Targeting REV-ERBalpha for therapeutic purposes: promises and challenges.. Theranostics 2020 · PMID 32226546
SR-9009 — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These act on mitochondrial function, NAD+ availability, sirtuin signaling or cellular clearance. The honest prediction is that acute harm is unlikely and the interesting risks are theoretical and long-range — which is a different shape of risk, not an absence of one.
- Growth and clearance signals cut both ways. Anything that improves the efficiency of cell survival is also improving it for cells you would rather not keep. Anything that pushes clearance hard is doing so indiscriminately.
- The near-term, practical ones: NAD+ precursors and infusions commonly cause flushing and a strong sensation if pushed fast, and several compounds in this class are stimulating enough to disrupt sleep.
What has actually been reported
- Generally well tolerated at studied doses. NAD+ infusion discomfort is rate-dependent and resolves by slowing down.
- The human evidence is mostly short trials with surrogate endpoints — a marker moved, not a life changed. That is worth knowing before you build a decade-long habit on it.
How to reduce the risk
Same mechanism as the prediction.
- Slow the infusion rate. Almost all NAD+ discomfort is rate, not dose. There is no prize for finishing quickly.
- Dose earlier in the day. Several of these are subtly stimulating, and sleep is where most of the repair you are paying for happens.
- Pick an endpoint you can actually measure, and take the baseline before you start. This is the class most prone to spending years on something with no way of knowing whether it did anything.
- Fix the basics first. Sleep, training and bloodwork move the same markers further than anything on this list, and they are free. A longevity compound stacked on four hours of sleep is a rounding error.
What it does to your bloodwork
A fact about the assay.
- There is no NAD+ assay worth ordering clinically. Judge this class on downstream markers — inflammatory markers, lipids, fasting glucose, and whatever your baseline panel showed as out of range.
Don't run this if
- Active malignancy, for the survival-signaling reasoning above.
- Pregnancy — uncharacterized.
The honest unknown
- Whether any of it extends healthspan in humans. Every honest person in this field is running on mechanism and animal data, and this catalog should say so rather than imply otherwise.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
SR-9009 — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What SR-9009 moves on your bloodwork
Expected direction, not a measured one.
- hs-CRP (High-Sensitivity C-Reactive Protein) — ↓ expected to fall
Where these work, systemic inflammation is the plausible readout.
What to do: hs-CRP is cheap and moves. Baseline and 12 weeks. - HbA1c (Hemoglobin A1c) — ↓ expected to fall
Improved mitochondrial and metabolic function should show here if the effect is real at all.
What to do: The honest use of these markers is as a falsification test: if nothing moves in 12 weeks, the compound is not doing much for you. - Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Liver and kidney function — the standard baseline for anything run long term.
What to do: Twice a year is enough on a stable protocol.
This class is where honest expectation-setting matters most: the markers above are how you find out whether anything happened, and for most of these compounds that question is genuinely open.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- How the forms differ in dose
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — SR-9009 in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside SR-9009
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| Comprehensive Metabolic Panel (CMP) | Baseline. Oral bioavailability is close to zero — most of this is theater |
| Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) | The claimed metabolic effect, measured |
| HbA1c (Hemoglobin A1c) | Whether anything actually happened |
The Metabolic Health & Prediabetes panel covers these in one order — 8 markers, $81.45 with the discount applied.
Check results you already have → · All 103 markers A–Z
SR-9009 — frequently asked questions
What is SR-9009?
SR-9009 (Stenabolic) is a metabolic & fat loss research compound. REV-ERB agonist — shifts circadian/metabolic gene programs toward fat oxidation and mitochondrial output ('exercise-mimetic' class).
Is the full SR-9009 protocol on this page?
The reported research dose is on this page, along with how SR-9009 works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of SR-9009?
SR-9009 has an approximate half-life of Very short (poor oral bioavailability), which is part of what determines how often it's dosed.
What forms does SR-9009 come in?
SR-9009 is available as: Oral, Injectable.
What's the evidence behind SR-9009?
Current evidence level: Animal; poor human PK. SR-9009 is offered for research purposes only and is not an approved medicine.
What SR-9009 is used for
SR-9009 appears under 2 goals in the goal router.
Related Metabolic & Fat Loss compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.