A single unlabeled amber glass dropper bottle beside a small clear glass vial on a matte stainless steel laboratory bench under neutral clinical lighting, no text or logos.

Stenabolic (SR9009): The REV-ERB Agonist, Why the Oral Pills Probably Do Not Work, and Its WADA Status

Updated 2026-06-22T00:00:00.000Z25 min read · 6,592 words

Stenabolic, better known by its lab code SR9009, is a synthetic REV-ERB agonist that became a fitness-forum favorite on the back of a single striking mouse result: injected rodents ran farther. The honest problem is the part the capsule sellers skip. SR9009 has near-zero oral bioavailability, so the pills and liquids most people buy are very likely inactive as taken, and every effect ever attributed to it comes from animals, never a human trial. This page foregrounds that reality instead of burying it.

Most "Stenabolic guide" pages open with the endurance and fat-loss promises and tuck the absorption problem into a footnote, because many of them sell oral SR9009. We invert that on purpose. The decision-shaping facts are the route-of-administration problem, the total absence of human data, and the WADA ban, so they lead. For where SR9009 sits among aerobic compounds generally, see our hub on the best peptides and compounds for endurance. For the deeper science we add primary pharmacology and first-party community data that the affiliate pages do not have.

Key Takeaways

  • Stenabolic (SR9009) is a REV-ERB agonist, not a SARM, not a steroid, not a peptide. It acts on the REV-ERB nuclear receptors tied to the circadian clock and metabolism, and it does not touch the androgen receptor (Solt et al., Nature, 2012, retrieved 2026-06-22).
  • The oral product you bought is probably inactive. SR9009 has near-zero oral bioavailability (about 2% in rodents), and the studies that produced its effects used injection, so swallowed capsules likely deliver very little active compound (Trump et al., Journal of Medicinal Chemistry, 2013, retrieved 2026-06-22).
  • The famous endurance result is mouse data from injection. REV-ERB activation raised mitochondrial content and running time and distance in mice; this has never been shown in a person (Woldt et al., Nature Medicine, 2013, retrieved 2026-06-22).
  • There are zero human trials of any phase. All SR9009 data is preclinical (rodent or in vitro), and the short half-life (under 3 hours) made it "an unsatisfactory dosing regimen for humans," which is partly why the field moved to successor molecules (Wang et al., Theranostics, 2020, retrieved 2026-06-22).
  • It is banned in sport at all times. SR9009 is on the WADA Prohibited List under class S4.4.1 (REV-ERB-alpha agonists, named explicitly), and targeted lab methods can detect its metabolites (WADA, Prohibited List, retrieved 2026-06-22).
  • Some reported effects are not even due to REV-ERB. Several SR9009 phenotypes occur independently of the receptor it is supposed to target, which undermines attributing the rodent results to the intended mechanism (Dierickx et al., PNAS, 2019, retrieved 2026-06-22).

A single unlabeled amber glass dropper bottle beside a small clear glass vial on a matte stainless steel laboratory bench under neutral clinical lighting, no text or logos.

[!WARNING] Banned in sport. Not for human use. No human data. Likely inactive orally. SR9009 is sold as a "research chemical not for human consumption." It is on the WADA Prohibited List and can trigger an anti-doping violation. Every claimed benefit comes from injected rodents, and the oral consumer product is poorly absorbed. Nothing on this page is a green light to take it.

What is Stenabolic (SR9009)?

Stenabolic is a lab-made REV-ERB agonist developed as a research tool to study the body clock and metabolism, not as a medicine. It is a small synthetic molecule, not a peptide or a hormone, and it works by switching on the REV-ERB nuclear receptors. Those receptors sit at the crossroads of circadian rhythm, fat metabolism, and mitochondrial activity. SR9009 was never designed for sport or fat loss; the fitness use is entirely off-label adoption of a chemistry-lab probe.

The compound came out of the Burris laboratory and was first described in a 2012 paper showing that synthetic REV-ERB agonists altered circadian behavior, raised energy expenditure, and caused weight loss and lipid changes in mice dosed by injection at 100 mg/kg twice daily (Solt et al., Nature, 2012, retrieved 2026-06-22). That single animal finding, an injected research dose in mice, is the seed of every "Stenabolic burns fat and boosts endurance" claim you will read on a sales page. The leap from that mouse experiment to a human capsule is enormous, and it is the leap this guide is built to interrogate.

The most important framing fact is the gap between what SR9009 is and what it is sold as. It is an investigational REV-ERB probe with no human trials and a serious delivery problem. Everything below should be read through that lens. If you want the molecule next to its commonly-compared sibling, we keep that brief and link out rather than repeat a full head-to-head, because the comparison lives on its own page: our Cardarine versus SR9009 risk and anti-doping breakdown.

Is Stenabolic a SARM? Clearing up the biggest misconception

No, Stenabolic is not a SARM, not a steroid, and not a peptide; it is a REV-ERB agonist that acts on a circadian-clock receptor. This is the single most common error in SR9009 search results, and it matters because calling it a SARM imports the wrong risk model. SR9009 does not bind the androgen receptor at all, so the usual SARM worries about testosterone suppression and post-cycle therapy do not apply here.

A SARM (selective androgen receptor modulator) works on the androgen receptor, the same target as testosterone. SR9009 works on REV-ERB-alpha and REV-ERB-beta, nuclear receptors tied to the body clock and to mitochondrial biology, a completely different pathway (Solt et al., Nature, 2012, retrieved 2026-06-22). The misfiling is partly an artifact of search-engine placement: several large guides park SR9009 under their "/sarms/" sections because that is where the traffic is, which quietly teaches readers the wrong mechanism. The honest correction is simple. SR9009's real concerns are the lack of human testing and the oral-delivery problem, not androgen suppression.

We deliberately keep the sibling comparison to this clarifier. A full SR9009-versus-Cardarine head-to-head would cannibalize the dedicated page, so for the side-by-side risk, anti-doping, and community-usage breakdown, see the dedicated Cardarine and SR9009 comparison. For Cardarine on its own, see our standalone Cardarine guide.

Does oral Stenabolic actually work? The bioavailability problem most sellers skip

Largely no, as commonly sold: SR9009 has near-zero oral bioavailability, so the capsules and liquids most people buy are very likely delivering almost nothing. This is the signature, buried fact about Stenabolic, and it is the one the oral-capsule market has every reason not to lead with. The studies that produced SR9009's endurance and metabolic effects used injection, not swallowed pills, so the consumer oral product is a poor stand-in for the route that was actually studied.

In the Burris-lab medicinal-chemistry work, SR9009's oral bioavailability was reported as very poor, with plasma exposure after oral gavage in mice in the low single-digit percent range, commonly rounded to about 2% (Trump et al., Journal of Medicinal Chemistry, 2013, retrieved 2026-06-22). Put plainly: if roughly 98% of an oral dose never reaches the bloodstream intact, the pill is mostly a placebo with a banned-substance label. A buyer is then exposing themselves to an unapproved, untested, prohibited research chemical for an effect that may not even be reaching their system. The "Stenabolic is safer because it has no cancer signal" line that floats around forums leans partly on a compound that, taken orally, may not be doing much of anything.

A capsule and a syringe lying side by side on a clean white clinical surface in soft daylight, contrasting two routes of administration, no text or logos.

The half-life makes it worse. SR9009 is cleared rapidly, with a half-life under three hours, which is why the animal protocols injected it repeatedly through the day rather than once (Wang et al., Theranostics, 2020, retrieved 2026-06-22). A single daily capsule cannot reproduce that exposure pattern even if absorption were not a problem. The sublingual and "liposomal" formats marketed to dodge the absorption issue are not validated; there is no published human pharmacokinetic data showing they deliver a meaningful, sustained blood level, so they are best read as marketing rather than solved engineering. The net is an awkward bind: if the oral product is inactive, you took a banned chemical for nothing; if a workaround format somehow does deliver it, you are now getting an untested dose of an untested compound. Neither outcome is good, and a grey-market label cannot tell you which one you have.

SR9009 barely absorbs orally: about 2 percent versus injectionHow much SR9009 actually reaches the blood, by routeRodent bioavailability. The studied effects used injection; the consumer product is oral.Injection (studied route)~100% referenceOral (the pills you buy)~2% absorbedSource: Trump et al., J. Med. Chem., 2013 (rodent oral bioavailability about 2%). No human PK data exists.
The red sliver is the whole story: an oral SR9009 capsule delivers a tiny fraction of what injection does, which is the route every effect study used.

How is Stenabolic supposed to work? The REV-ERB mechanism

In theory, SR9009 works by activating the REV-ERB receptors, which dial up mitochondrial activity and fat metabolism and nudge the body clock, so the marketing pitch is "endurance and fat loss without exercise." That is the mechanism on paper. The catch is that the supporting evidence is rodent-only, and some of the observed effects do not even run through REV-ERB.

REV-ERB-alpha and REV-ERB-beta are nuclear receptors that repress target genes as part of the circadian clock. When a synthetic agonist like SR9009 activates them, the downstream effects in animals include shifts in lipid handling, raised energy expenditure, and changes in circadian behavior (Solt et al., Nature, 2012, retrieved 2026-06-22). The specific endurance story, the one fitness pages love, comes from a separate and often-miscited paper: REV-ERB-alpha modulates skeletal-muscle oxidative capacity through mitochondrial biogenesis and autophagy, and pharmacologic activation raised mitochondrial content and increased running time and distance in mice (Woldt et al., Nature Medicine, 2013, retrieved 2026-06-22). That is the real source of "exercise in a bottle," and it is a mouse running-wheel result, not a human outcome.

A clean clinical rendering of an abstract microscopy field suggesting a circadian-clock pattern interlaced with mitochondria, cool laboratory tones, no text or logos.

Here is the honest wrinkle that no affiliate guide includes, and it is important enough to get a full section below. Several reported SR9009 phenotypes occur independently of REV-ERB, through unidentified off-target pathways, which means you cannot cleanly attribute the rodent effects to the receptor the drug is named for (Dierickx et al., PNAS, 2019, retrieved 2026-06-22). A clean mechanism story is reassuring; SR9009's is not clean. We unpack what that does to both the marketing claim and the safety picture in the dedicated off-target section further down.

Do the endurance and fat-loss claims have human evidence?

No: there is no human evidence for any SR9009 benefit, because there are no human trials of any phase. Every endurance and fat-loss claim traces back to rodent experiments, mostly using injection. Treat any "Stenabolic boosts your endurance" or "burns fat" headline as a mouse finding wearing a human costume, not as a demonstrated human effect.

The endurance claim rests on the 2013 mouse work where REV-ERB activation raised mitochondrial content and increased treadmill running time and distance (Woldt et al., Nature Medicine, 2013, retrieved 2026-06-22). The fat-loss and metabolic claims rest on the 2012 mouse work showing raised energy expenditure and lipid changes (Solt et al., Nature, 2012, retrieved 2026-06-22). Both used injected compound in rodents. There is no completed human efficacy study, no phase 1, nothing; the entire human file is empty, and the short half-life and poor oral delivery are part of why it never advanced to people (Wang et al., Theranostics, 2020, retrieved 2026-06-22).

This is a recurring pattern in metabolism research: a compound shrinks or strengthens mice and then does nothing useful in humans, because rodent metabolism and dosing do not map cleanly onto people. SR9009 has not even been given the chance to fail in a human trial; it simply was never tested. So the most honest summary of the evidence is not "it works" or "it does not work" in people. It is "we have no idea, because no one has ever properly looked," combined with "the way you are taking it probably is not delivering the drug anyway." For how this compares with other aerobic-goal compounds that also lean on thin or animal evidence, see compounds targeting mitochondrial function and energy.

SR9009 evidence ladder: rodent yes, every human stage zeroWhere the evidence actually isEach rung is a stage of evidence. Only the bottom rung is filled.YesRodent /in vitro0Phase 10Phase 20Phase 30ApprovedNo human trials of any phase exist.Source: Wang et al., Theranostics, 2020.
The whole evidence base sits on one rung. Every human stage, from first-in-human to approval, is empty.

What about cholesterol, blood sugar, and cardiovascular markers?

In animals, REV-ERB activation shifted how the body handled fats and burned energy, so cholesterol and blood-sugar changes are plausible on paper; but these are mouse surrogate markers, not human outcomes, and the oral-inactivity problem means most users may move nothing at all. There is no human metabolic data, and we will not invent any numbers.

The animal basis is the 2012 work. Synthetic REV-ERB agonists, SR9009 included, altered lipid handling, raised energy expenditure, and changed body weight in mice dosed by injection (Solt et al., Nature, 2012, retrieved 2026-06-22). On a sales page that becomes "improves your cholesterol and metabolic health." The honest translation is narrower. Those were biochemical readouts in injected rodents, not clinical endpoints in people, and a mouse lipid panel does not forecast a human one.

Two filters should sit between that rodent signal and any human expectation. First, these are surrogate markers, changes in a measured value, not proven changes in cardiovascular risk or long-term outcomes; even in approved drugs a moved surrogate does not always translate into benefit. Second, and more bluntly, the route problem swallows the rest: with near-zero oral bioavailability, a swallowed capsule likely never reaches the exposure that produced any of these animal effects (Trump et al., Journal of Medicinal Chemistry, 2013, retrieved 2026-06-22). So the realistic expectation for an oral user is not a dramatic lipid or glucose shift; it is, quite possibly, no measurable change at all, because the drug barely arrives.

There is a further wrinkle that should temper any "it cleans up your blood work" claim. Some SR9009 metabolic effects in cells do not run through REV-ERB at all, so even the animal metabolic story is not cleanly attributable to the intended target (Dierickx et al., PNAS, 2019, retrieved 2026-06-22). If you care about cholesterol, blood sugar, or cardiovascular risk, the defensible move is a clinician-ordered panel and an intervention with actual human evidence, not an untested probe you may not even be absorbing. For tracking the markers themselves rather than chasing an unproven compound, see our guide to baseline and follow-up lab panels.

Does Stenabolic affect sleep or circadian rhythm?

Mechanistically, yes, it could: REV-ERB is a core component of the body clock, so circadian and sleep effects are plausible in principle. But there is no human data, the timing claims people pass around are extrapolation, and, as with everything else here, an oral capsule that barely absorbs may not do anything at all. Treat sleep or "take it in the morning" advice as theory, not evidence.

The biology is real enough to take seriously. REV-ERB-alpha and REV-ERB-beta are part of the molecular circadian clock, and in the original mouse work synthetic REV-ERB agonists altered circadian behavior directly, not just metabolism (Solt et al., Nature, 2012, retrieved 2026-06-22). Because the clock and the sleep-wake cycle are linked, it is reasonable to expect that a compound which shifts clock activity could nudge sleep timing or quality. That is a mechanistic hypothesis, and it is the strongest honest statement available.

What does not follow is any specific human claim. There is no study measuring SR9009's effect on human sleep, sleep latency, or circadian phase, so popular guidance like "dose it early so it does not disrupt your sleep" is pure extrapolation from mouse clock biology (Wang et al., Theranostics, 2020, retrieved 2026-06-22). It might be sensible, it might be irrelevant, and with near-zero oral bioavailability the question may be moot for most users. We flag the plausible mechanism because it is genuinely on-intent, and we stop there, because inventing a sleep protocol from rodent data is exactly the kind of overreach this guide exists to avoid.

Why might the same compound act differently than the receptor predicts? The off-target problem

A clean "REV-ERB agonist therefore endurance" story is what sells SR9009, but the evidence is not clean: several reported SR9009 effects happen even when REV-ERB is removed, through pathways no one has fully mapped, which means the rodent results cannot be confidently pinned on the intended target. This is the single most important caveat the affiliate guides omit, so it gets its own treatment here.

The finding is specific and well sourced. A 2019 study showed that SR9009 still changed cell proliferation and metabolism in cells that lacked REV-ERB entirely, demonstrating REV-ERB-independent, off-target activity (Dierickx et al., PNAS, 2019, retrieved 2026-06-22). In plain terms: if the drug does things with its supposed target deleted, then some of what it does in a normal animal is being driven by something else, and that something else is unidentified. The neat mechanism on the sales page is, at best, only part of the story.

Why this undermines the marketing mechanism

This cuts straight through the core selling point. The pitch is that SR9009 activates REV-ERB and REV-ERB drives endurance, so the compound is "exercise in a pill." If a meaningful share of SR9009's biology does not go through REV-ERB, that tidy causal chain loosens, and you can no longer assume the rodent endurance and metabolic effects are the predictable result of hitting one well-understood receptor. The mechanism story becomes "it does several things, some through REV-ERB and some not, and we have not mapped the rest."

Why it matters for safety, not just marketing

Unmapped off-target activity is also a safety problem, not only a marketing one. A compound with no human trials is already an unknown; a compound with no human trials and documented activity on pathways no one has characterized is a deeper unknown (Dierickx et al., PNAS, 2019, retrieved 2026-06-22). You cannot reason about the long-term effects of actions you have not identified. That is the practical cost of the off-target finding: it removes the comfort of a fully understood mechanism precisely where, with zero human data, that comfort would matter most.

Why did the field move on from SR9009?

The lab that built SR9009 largely moved on because its drug-like properties were poor: it is cleared too fast and barely absorbed orally, so chemists designed better successor molecules. In other words, SR9009 was a useful first-generation research probe, not a finished drug, and the people who know it best treated it that way. The fitness market adopted the abandoned prototype while the science moved to its replacements.

The core problem is pharmacokinetics. SR9009 and its close relative SR9011 have short half-lives (under three hours) and poor oral bioavailability, which a 2020 review described as "an unsatisfactory dosing regimen for humans" (Wang et al., Theranostics, 2020, retrieved 2026-06-22). That review traces how poor DMPK drove the design of optimized REV-ERB scaffolds, including SR12418, the THIQ series, and GSK2945, the last of which reached a half-life around 2.0 hours and oral bioavailability around 23%, far better than SR9009's roughly 2% (Wang et al., Theranostics, 2020, retrieved 2026-06-22). The direction of travel tells you something: when researchers wanted a REV-ERB agonist that might actually work in a body, they did not reach for SR9009.

This is the quiet rebuttal to the entire SR9009 supplement category. If the original molecule were a viable oral REV-ERB drug, the chemists would not have spent years engineering around its absorption and clearance. The grey market is selling the prototype the inventors deliberately improved upon. That is not a conspiracy; it is just what the published medicinal chemistry shows, and it is the kind of context an affiliate page selling capsules has no reason to surface.

Why the field moved on: successors absorb far better than SR9009Oral bioavailability: SR9009 versus its engineered successorsHigher is better. The optimized scaffold GSK2945 absorbs roughly ten times as well.0%15%30%SR9009~2%, t1/2 under 3 hSR9011~2%, short half-lifeGSK2945~23%, t1/2 ~2.0 hSource: Wang et al., Theranostics, 2020. The grey market sells SR9009, the prototype the chemists improved upon.
When researchers wanted a REV-ERB agonist that might work in a body, they engineered successors. SR9009 is the one they moved past.

Is Stenabolic banned by WADA, and will it fail a drug test?

Yes: SR9009 is banned by WADA at all times, in and out of competition, and it is detectable by targeted laboratory methods. It sits in the metabolic-modulator family of the Prohibited List, named explicitly, so any athlete subject to testing risks an anti-doping rule violation by using it. The "it is too obscure to be tested" assumption is outdated.

SR9009 is listed under WADA class S4 (Hormone and Metabolic Modulators), within S4.4 Metabolic Modulators, at S4.4.1, which names "REV-ERB-alpha agonists, e.g. SR9009 and SR9011." It was added to the Prohibited List in 2016 and has been clarified and relocated under S4.4.1 in recent annual lists (WADA, Prohibited List, retrieved 2026-06-22). The naming is explicit, not a catch-all category, which removes any "it was not specifically banned" defense.

On detection: a 2016 study used high-resolution mass spectrometry on human liver microsomes and identified eight SR9009 metabolites (and fourteen for SR9011) as candidate markers for anti-doping screening; at the time these were not caught by routine urine panels but were detectable by targeted methods (Geldof et al., PMC5085709, 2016, retrieved 2026-06-22). The practical reading is that detection science exists and has only matured since. Anyone who competes in tested sport should treat SR9009 as a substance that can end a career, not a clever loophole. For the broader legal picture beyond sport, see our overview of research-chemical legal status.

Is Stenabolic safe? What the risks really are

There is no human safety data for SR9009, so its true risk profile is unknown, and the honest answer is "untested," not "safe." It was never run through human trials, the consumer oral product is poorly characterized, and the molecule has documented off-target activity that no one has fully mapped. "No reported cancer signal" reflects a near-total absence of testing, not a clean bill of health.

The safety picture has three distinct gaps. First, the complete lack of human trials means there is no monitored dataset on side effects, organ effects, or long-term outcomes in people (Wang et al., Theranostics, 2020, retrieved 2026-06-22). Second, the REV-ERB-independent off-target effects mean SR9009 acts on pathways outside its intended target, so even the animal safety inferences are shakier than they look (Dierickx et al., PNAS, 2019, retrieved 2026-06-22). Third, because it is sold as an unregulated research chemical, the vial in hand may be mislabeled, underdosed, or contaminated, a quality problem that is independent of the molecule itself.

On storage and spotting a likely-inactive product, the honest framing is the same as everywhere else: there is no published human stability or shelf-life data for consumer SR9009, so any "store cool and dark, lasts X months" claim is a general research-chemical convention, not a validated figure, and we will not invent one. The bigger quality tell is upstream of storage. Because the studied effects required injection and oral SR9009 absorbs at roughly 2%, the formats most aggressively marketed as fixes, plain oral capsules, flavored oral liquids, and "liposomal" or sublingual products sold without any pharmacokinetic data, are the ones most likely to be inactive as taken (Trump et al., Journal of Medicinal Chemistry, 2013, retrieved 2026-06-22). A bottle with no certificate of analysis, no batch number, and a "delivers full bioavailability orally" claim it cannot support is a likely-inactive product wearing confident packaging. For how to read a COA and pressure-test those claims, see our guide to vetting research-compound quality and reading a COA.

A useful way to hold all this: SR9009 stacks two kinds of uncertainty. There is biological uncertainty, since we do not know what it does in a human body over time, and there is product uncertainty, since grey-market sourcing means you may not even know what is in the bottle. The compound that "looks safer because nothing bad has been reported" is mostly a compound that has barely been studied in the place it would matter. If your goal is performance or metabolic health, the defensible path is a clinician-guided plan and options that are actually legal and tested, not an unapproved probe.

What does the ProtocolPlus community actually do with Stenabolic?

Among users who log SR9009, the community treats it primarily as an endurance and fat-loss experiment, but we present this strictly as a usage signal, not evidence that it works. Everything below describes self-reported behavior, not trial incidence and not an efficacy verdict. The value here is transparency about what people actually do with a compound the evidence base cannot support, not a recommendation to join them.

The honest gaps matter as much as the numbers. Self-reported goals tell you why people say they are tracking SR9009, not whether it delivered anything; with near-zero oral bioavailability, a large share of these users may be logging a compound that is barely reaching their bloodstream. We do not show structured tolerability or outcome data for SR9009, because a research chemical with no validated dose and no human pharmacology does not produce a trustworthy outcome signal, and we will not fabricate one. The adoption and goal split are the parts we can stand behind; the implication that those goals were met is not something the data supports.

What dose of Stenabolic was studied, and what do people report?

The only real, studied dose is an animal injection dose; there is no validated human dose, and the oral convention people pass around forums is pharmacologically unsound. We will not invent a number. The single dose with any experimental basis is the rodent injection used in the original studies, and it does not translate to a human protocol.

In the foundational mouse work, SR9009 was given by intraperitoneal injection at 100 mg/kg twice daily over roughly 10 to 30 days (Solt et al., Nature, 2012, retrieved 2026-06-22). That is a research dose, by injection, in mice; it is not a human dose, and body-weight scaling from rodents to people is not a valid way to derive one. There is no human pharmacokinetic study to anchor any oral figure, which is why we do not publish one.

The community convention, which we describe only to explain what people do and why it is flawed, is to take oral SR9009 split into several small doses across the day, precisely because the half-life is so short (Wang et al., Theranostics, 2020, retrieved 2026-06-22). The logic is internally honest, frequent dosing does match the short half-life, but it runs straight into the wall of near-zero oral bioavailability (Trump et al., Journal of Medicinal Chemistry, 2013, retrieved 2026-06-22). Splitting an oral dose more often does not fix a route that barely absorbs in the first place. So the convention is unvalidated, has no human-trial basis, and uses the route the science suggests is mostly inactive. Present it as a description of behavior, never as guidance.

A microplate and a single pipette on a neutral laboratory bench under even clinical lighting, no animals, no text or logos.

In most places SR9009 occupies a legal grey area: it is not an approved medicine and is sold as a research chemical "not for human consumption," so buying and using it for yourself sits outside the legitimate drug system. It was never approved by any regulator for any human use. The "you can buy it online easily" fact says nothing about whether it is legal to consume or safe to take.

SR9009 has no marketing authorization anywhere; it exists as a laboratory reagent and a grey-market supplement, not as a prescribable drug (Wang et al., Theranostics, 2020, retrieved 2026-06-22). On top of the regulatory status, it is prohibited in sport at all times under WADA S4.4.1, so for any tested athlete the legality question is moot, since use is a sanctionable violation regardless (WADA, Prohibited List, retrieved 2026-06-22). Exact rules vary by country, and "research chemical" labeling is a way for sellers to route around consumer-product laws, not a guarantee that personal use is permitted.

The practical takeaway is consistent with everything else on this page. Easy to buy is not the same as legal, effective, or safe, and the "not for human consumption" label on the bottle is doing real legal work for the seller, not for you. For the fuller cross-compound picture, see our breakdown of how research-compound legality actually works.

The honest verdict

Stenabolic (SR9009) is a textbook case of a research-lab prototype that escaped into the supplement market and outran its evidence. The science behind it is genuinely interesting: REV-ERB agonism raised endurance and shifted metabolism in mice. But the chain from that mouse result to a human capsule breaks at almost every link. There are no human trials, the oral product is barely absorbed, the half-life is too short for sensible dosing, some effects are not even due to REV-ERB, and the inventors moved on to better-behaved successor molecules.

To make the takeaway concrete:

  • If your goal is endurance or fat loss: the evidence is mouse-only and from injection; nothing here has been shown in a person, and the oral product you would buy is probably inactive.
  • If you compete in tested sport: SR9009 is WADA-prohibited at all times under S4.4.1 and is detectable by targeted methods; using it risks a sanction.
  • If you are weighing safety: there is no human safety data, plus documented off-target activity and grey-market quality risk; "no bad reports" means "barely studied," not "safe."
  • If you are set on the science: know that the field engineered successors precisely because SR9009's drug-like properties were poor.

For where SR9009 sits among other aerobic-goal compounds, see the endurance compounds hub. For the side-by-side with its most-compared sibling, see the Cardarine and SR9009 head-to-head.

Frequently Asked Questions

No. SR9009 is not a SARM, not a steroid, and not a peptide. It is a REV-ERB agonist, a compound that acts on the REV-ERB nuclear receptors tied to the circadian clock and metabolism, not on the androgen receptor that SARMs target. It is frequently misfiled under SARM sections by sellers because of search placement, but it works through a completely different pathway, so the usual SARM concerns about testosterone suppression do not apply.

Sources

  • Solt LA, Wang Y, Banerjee S, et al. "Regulation of Circadian Behaviour and Metabolism by Synthetic REV-ERB Agonists." Nature, 2012;485(7396):62-68. SR9009 circadian behaviour, energy expenditure, weight, and lipid changes in mice; injection dose 100 mg/kg twice daily. Basis for the cardiovascular/lipid surrogate-marker and circadian/sleep sections (animal surrogate markers, not human outcomes). Retrieved 2026-06-22. https://pubmed.ncbi.nlm.nih.gov/22460951/
  • Woldt E, Sebti Y, Solt LA, et al. "Rev-erb-alpha modulates skeletal muscle oxidative capacity by regulating mitochondrial biogenesis and autophagy." Nature Medicine, 2013;19(8):1039-1046. Pharmacologic REV-ERB activation raised mitochondrial content and running time and distance in mice. Retrieved 2026-06-22. https://pubmed.ncbi.nlm.nih.gov/23852339/
  • Trump RP, Bresciani S, Cooper AWJ, et al. "Optimized chemical probes for REV-ERB-alpha." Journal of Medicinal Chemistry, 2013;56(11):4729-4737. Reports SR9009's poor oral bioavailability (about 2% in rodents); efficacy studies used injection. Retrieved 2026-06-22. https://pubmed.ncbi.nlm.nih.gov/23656296/
  • Wang S, Li F, Lin Y, Wu B. "Targeting REV-ERB-alpha for therapeutic purposes: great opportunities and challenges." Theranostics, 2020;10(9):4168-4182. Short half-life under 3 hours, poor oral bioavailability, "unsatisfactory dosing regimen for humans," and successor scaffolds (SR12418, THIQ series, GSK2945 t1/2 ~2.0 h, oral BA ~23%); no human trials. Retrieved 2026-06-22. https://pmc.ncbi.nlm.nih.gov/articles/PMC7086371/
  • Dierickx P, Emmett MJ, Jiang C, et al. "SR9009 has REV-ERB-independent effects on cell proliferation and metabolism." PNAS, 2019;116(25):12147-12152. SR9009 changed cell proliferation and metabolism in cells lacking REV-ERB, demonstrating REV-ERB-independent off-target activity; basis for the dedicated off-target section and the cardiovascular caveat (rodent/cell effects not cleanly attributable to the intended target). Retrieved 2026-06-22. https://www.pnas.org/doi/abs/10.1073/pnas.1904226116
  • Geldof L, Deventer K, Roels K, et al. "In Vitro Metabolic Studies of REV-ERB Agonists SR9009 and SR9011." International Journal of Molecular Sciences (PMC5085709), 2016. LC-HRMS of human liver microsomes identified 8 SR9009 metabolites (14 for SR9011) as anti-doping markers; detectable by targeted methods. Retrieved 2026-06-22. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5085709/
  • World Anti-Doping Agency. "The Prohibited List": SR9009 and SR9011 named under S4.4.1 (REV-ERB-alpha agonists), Metabolic Modulators; prohibited at all times; added 2016. Retrieved 2026-06-22. https://www.wada-ama.org/en/prohibited-list
  • SR9009. Wikipedia (citing Solt et al. and follow-up pharmacology): REV-ERB agonist, near-zero oral bioavailability, short half-life, WADA-prohibited research chemical. Retrieved 2026-06-22. https://en.wikipedia.org/wiki/SR9009
  • ProtocolPlus. "Community tracking data: Stenabolic (SR9009)." First-party app data, 2026. Tracking overview and self-reported goal distribution. A usage signal only, self-reported and not trial incidence; not a clinical efficacy or safety verdict.