SR9009 (Stenabolic)

1. Overview and Critical Context

SR9009, commonly sold under the trade name Stenabolic, is a synthetic small-molecule pyrrole derivative with a molecular weight of approximately 437.9 daltons and the chemical formula C20H24ClN3O4S. It is an agonist of the nuclear receptors REV-ERBα (gene symbol NR1D1) and REV-ERBβ (gene symbol NR1D2), which function as transcriptional repressors and are key components of the mammalian circadian clock and of energy-metabolism gene networks [1][16].

Before anything else, readers should understand three statements that define the honest science on SR9009:

1. SR9009 is NOT a peptide. It has no amino-acid backbone. It is a synthetic small molecule developed by a medicinal-chemistry program at The Scripps Research Institute (Florida) in the laboratory of Thomas P. Burris. It appears on peptide-vendor websites and in peptide-adjacent communities purely because it has been swept into the broader research-chemical market alongside SARMs and other non-peptide compounds. Peptide is a category label, not a pharmacological description, in those contexts.

2. SR9009 is NOT a SARM. It does not bind the androgen receptor. It operates through an entirely different nuclear-receptor family (the REV-ERBs) and has no anabolic androgenic activity. Marketing that implies muscle-building from androgen action is wrong about the mechanism.

3. Oral SR9009 has no evidence base. The Burris laboratory, which designed and characterized SR9009, has published that the molecule has extremely high metabolic clearance and functionally zero oral bioavailability in rodents. The very same lab, in its follow-up medicinal-chemistry paper (Trump et al., J Med Chem 2013), explicitly moved away from SR9009 as a chronic-dosing compound because of this problem, describing optimized successor compounds with oral bioavailability around 23 percent as the useful in-vivo probes [3]. Every rodent experiment that is cited in consumer marketing — endurance (Woldt 2013), atherosclerosis (Sitaula 2015), myocardial infarction (Stujanna 2017) — used intraperitoneal (IP) injection at 100 mg/kg. None of these experiments used oral dosing. A consumer swallowing SR9009 in a capsule is not reproducing the conditions under which any of the published biology was observed.

This page is written to present the science honestly, not to promote the compound. There are no human clinical trials of SR9009 of any phase. The substance was added to the World Anti-Doping Agency (WADA) Prohibited List in 2016 under class S4.5 (hormone and metabolic modulators) [12][14].

Compound Class

Synthetic pyrrole derivative (small molecule); NOT a peptide, NOT a SARM

Molecular Weight

~437.9 Da (C20H24ClN3O4S)

Molecular Target

REV-ERBα (NR1D1) and REV-ERBβ (NR1D2) nuclear receptors

Mechanism

Agonist of REV-ERB; promotes NCoR-HDAC3 corepressor recruitment and represses BMAL1 and metabolic target genes

Receptor Potency

REV-ERBα EC50 ~670 nM; REV-ERBβ EC50 ~800 nM (Solt et al., Nature 2012)

Origin

Designed and synthesized at The Scripps Research Institute (Florida) in the laboratory of Thomas P. Burris, reported 2012

Oral Bioavailability

Approximately 0 to 2 percent in rodents; published as functionally zero in the Burris lab's optimization paper (Trump et al., J Med Chem 2013)

Routes With Published Efficacy

Intravenous (IV) and intraperitoneal (IP) in mice only; no oral efficacy data support the product form sold to consumers

Clinical Trials

None; zero human clinical trials have been completed or registered for SR9009

Regulatory Status

Not approved for any use by FDA, EMA, or any regulatory authority; research chemical only

WADA Status

Prohibited (added to the WADA Prohibited List in 2016 as a metabolic modulator under class S4.5, hormone and metabolic modulators)

Typical Preclinical Dose

100 mg/kg/day IP in mice (Woldt 2013 endurance paper; Sitaula 2015 atherosclerosis paper; Stujanna 2017 cardiac paper)

Endogenous Ligand of Target

Heme (identified as the physiological ligand of REV-ERBα/β by Raghuram et al. 2007 and Yin et al. 2007)

2. REV-ERB Biology - Why the Target is Interesting

Nuclear receptors and the circadian clock

REV-ERBα and REV-ERBβ are nuclear hormone receptors. Like other members of the nuclear receptor superfamily, they have a DNA-binding domain that recognizes specific response elements in the genome and a ligand-binding domain that accepts small-molecule regulators. Unusually among nuclear receptors, REV-ERBs lack the classical AF-2 activation helix required to recruit coactivators; they function essentially as obligate transcriptional repressors that recruit the NCoR (nuclear receptor corepressor) complex together with histone deacetylase 3 (HDAC3) to target genes [16].

The physiological ligand of REV-ERBα and REV-ERBβ is heme. Raghuram and colleagues (2007) and Yin and colleagues (2007) independently showed that heme binds the REV-ERB ligand-binding domain with 1 to 1 stoichiometry and stabilizes the receptor [16]. Heme binding modulates corepressor recruitment, providing a link between cellular heme status (which varies with oxidative metabolism) and transcriptional output.

In the core circadian transcription-translation feedback loop, REV-ERBα represses the transcription of BMAL1 (ARNTL), the master positive-arm clock gene. Because BMAL1 drives expression of CLOCK-BMAL1 heterodimer targets, REV-ERBα functions as a critical rhythmic brake on the clock. Loss of REV-ERBα produces a shortened circadian period; gain of function (via agonists) dampens BMAL1 and perturbs downstream clock-controlled gene networks [1].

Metabolic outputs of REV-ERB activity

Beyond BMAL1 repression, REV-ERBα and REV-ERBβ directly repress hundreds of metabolic genes in liver, skeletal muscle, adipose tissue, and macrophages. Reported REV-ERB target gene categories include:

• Lipogenesis and cholesterol synthesis (SREBP target genes, HMGCR pathway)
• Bile-acid metabolism
• Glucose handling
• Mitochondrial biogenesis (paradoxically, REV-ERBα loss reduces mitochondrial oxidative capacity in muscle despite being a repressor — the net effect depends on which genes it represses)
• Autophagy (regulated indirectly through BMAL1 and other intermediates)
• Inflammation (macrophage NF-kB pathway; NLRP3 inflammasome) [2][6][9]

The net effect of pharmacological REV-ERB agonism in rodent studies has typically been to increase energy expenditure, reduce plasma lipids and glucose, reduce fat mass in diet-induced obesity, and dampen inflammatory responses [1][4][6][9]. Because these effects resemble some of the consequences of endurance training, the REV-ERB pharmacology program was quickly labelled by science media as exercise in a pill or cardio in a pill — a framing that became the consumer marketing pitch when SR9009 leaked into the research-chemical market.

Why REV-ERB is a genuinely attractive drug target

Setting SR9009 itself aside, REV-ERB is a plausible drug target. The overlap of circadian dysfunction with metabolic disease, cardiovascular disease, and inflammation is well established. REV-ERB agonists could, in principle, rebalance tissue rhythms in shift-work-like conditions, suppress pathologic inflammasome activation, and modulate cancer metabolism. Several academic and industrial programs have since pursued improved REV-ERB agonists with superior oral bioavailability and specificity [3][15]. SR9009 is best understood as an early tool compound from the Burris lab that opened up this field without being drug-like itself.

3. The Burris Scripps Discovery Program and the Solt 2012 Nature Paper

Origin at Scripps Florida

SR9009 was designed and synthesized at The Scripps Research Institute in Jupiter, Florida, in the laboratory of Thomas P. Burris, together with medicinal chemist Theodore M. Kamenecka. The lab's earlier probe, GSK4112, had poor pharmacokinetics and off-target activity at LXR. SR9009 and SR9011 were designed as pyrrole-series analogs with improved REV-ERB agonist potency (sub-micromolar EC50) [1][3].

What the Solt 2012 Nature paper actually showed

Solt et al., Nature, 29 March 2012 (volume 485, pages 62 to 68) is the foundational paper [1]. Its core experiments were:

• Cell-based cofactor recruitment and reporter gene assays confirming SR9009 and SR9011 as REV-ERB agonists with EC50 values of approximately 670 nM (REV-ERBα) and 800 nM (REV-ERBβ) and selectivity over LXR.
• In vivo mouse dosing at 100 mg/kg intraperitoneally (IP), twice daily, to test circadian-gene and metabolic-gene effects in hypothalamus, liver, skeletal muscle, and white adipose tissue. Core clock gene expression (BMAL1, CLOCK, CRY, PER, and downstream targets) was altered as predicted.
• Diet-induced obese (DIO) mouse metabolic experiments showing reduced fat mass, improved plasma lipid profile, reduced plasma glucose, and increased oxygen consumption after repeated IP dosing.

What the paper did NOT show and did NOT claim:

• It did NOT demonstrate efficacy by oral administration.
• It did NOT report the compound as a drug candidate.
• It did NOT perform human studies.
• It did NOT establish pharmacokinetics compatible with chronic dosing in humans.

The paper was a proof of concept that synthetic REV-ERB agonism could produce measurable metabolic effects in mice. It was received as a landmark paper in circadian pharmacology — not as a clinical readout.

The medicinal-chemistry follow-up (Trump 2013) that consumer marketing ignores

Within 14 months of the Nature paper, a medicinal-chemistry team — including collaborators closely linked to the original Scripps program — published Optimized chemical probes for REV-ERBα in the Journal of Medicinal Chemistry (Trump et al., 2013) [3]. The paper explicitly states, in its own introduction and results, that:

• The parent pyrrole series (including SR9009 and SR9011) has high metabolic clearance.
• Oral bioavailability of the parent compounds is very poor, making meaningful oral exposure difficult even at high doses.
• The series as originally disclosed is not suitable for long-term in-vivo dosing studies through the oral route.

Optimized analogs (e.g., their compound 4, GSK2945) were reported with oral bioavailability of approximately 23 percent and a half-life around 2 hours, a profile the authors describe as finally suitable for chronic oral dosing at 20 to 30 mg/kg. The unambiguous message of Trump 2013 is that SR9009 itself is a poor oral drug and was superseded within the medicinal-chemistry program. Consumer products nevertheless continue to sell SR9009 in oral capsule and sublingual liquid form.

4. The Oral Bioavailability Gap in Detail

The pharmacokinetic facts

Published PK data for SR9009 in rodents indicate:

• IV administration produces measurable plasma exposure consistent with the compound reaching systemic circulation, but with short half-life and high clearance [3].
• Oral gavage at 1 mg/kg in mice has been reported to yield plasma exposure on the order of 2 percent (and in some experiments effectively undetectable at later time points) relative to IV dosing at the same dose [3].
• Parent-compound metabolism in human liver microsomes generates at least eight Phase I metabolites; the molecule is a substrate for rapid oxidative metabolism [5][13].
• In human doping-control urine samples (n=1,511) surveyed by Geldof et al. (2016), neither parent SR9009 nor its metabolites were detected under routine screening conditions, consistent with either low oral bioavailability after consumer use, low detection windows, or both [5].

Why this matters for consumers

Every rodent efficacy study cited to justify SR9009 as a performance, endurance, cardiovascular, or anti-inflammatory compound used parenteral dosing (IP injection) at doses of 100 mg/kg per day. The systemic exposures achieved in those experiments are not reproducible by swallowing an oral capsule of SR9009. The mouse IP dose of 100 mg/kg is already very high on a per-kilogram basis; translated by human-equivalent scaling it would correspond to very large absolute doses that consumers are not taking, and even if consumers did take such doses orally, the published oral bioavailability data predict that plasma exposure would still be a small fraction of the IP equivalent.

In plain language: the biology that made SR9009 interesting was produced by injecting mice with large doses. The product sold to humans is an oral capsule or sublingual drop of a compound with approximately zero oral bioavailability in the species in which the biology was demonstrated. The evidence that oral SR9009 at consumer doses produces any meaningful biological effect in humans is not weak; it is nonexistent.

Note also that sublingual and transdermal formulations marketed as solutions to the bioavailability problem have no controlled human pharmacokinetic data to support those claims. Absorption across oral mucosa and skin for a molecule of this size and logP is not a given, and vendor assertions about sublingual bioavailability are not published evidence.

5. The Woldt 2013 Endurance Paper (the source of the cardio-in-a-pill claim)

Woldt and colleagues (2013, Nature Medicine) is the single most cited study in SR9009 marketing [2]. The key features and the parts that are often omitted:

What the paper showed

• REV-ERBα modulates mitochondrial biogenesis and autophagy in mouse skeletal muscle.
• Rev-erbα knockout mice had reduced exercise capacity; conversely, pharmacological activation with SR9009 in wild-type mice increased running capacity.
• SR9009-treated mice showed roughly a 50 percent increase in running time and distance on a standardized treadmill test.

What is often omitted in marketing

• Route of administration was intraperitoneal injection, not oral.
• The dose was 100 mg/kg twice daily, for up to 30 days.
• Endurance was measured in mice, not humans. No human study has replicated this finding.
• Even some in-vivo endpoints later attributed to SR9009 have been shown by genetic-knockout studies to occur in the absence of REV-ERB, calling into question whether SR9009 is actually operating through its nominal target in all of the phenotypes attributed to it [8][11].

The leap from mouse IP 100 mg/kg endurance to a human oral capsule marketed as cardio in a pill is not supported by the published science.

6. REV-ERB-Independent Effects - The Dierickx 2019 Problem

A pivotal and often-ignored paper is Dierickx et al., PNAS, 2019 [8]. The authors used mouse embryonic stem cells and hepatocytes in which both REV-ERBα and REV-ERBβ had been genetically deleted (double-knockout) as a clean genetic background to ask whether SR9009's cellular effects actually require REV-ERB. The answer was: often not.

Key findings:

• SR9009 reduced cell viability in double-knockout cells to a similar extent as in control cells.
• SR9009 altered gene transcription and cellular metabolism in cells that have no REV-ERBα or REV-ERBβ.
• The authors explicitly conclude that the effects of SR9009 cannot be exclusively attributed to REV-ERB and caution that investigators using SR9009 as a pharmacological probe for REV-ERB biology must account for this.

A subsequent 2022 cardiac study confirmed the same pattern in vivo: SR9009 improved heart function after pressure overload even in mice lacking cardiomyocyte REV-ERBα/β [11].

The practical implication is that many of the effects seen in prior SR9009 papers — including anti-cancer, anti-inflammatory, and metabolic phenotypes — may be off-target effects of the molecule rather than genuine REV-ERB biology. The REV-ERB target validation story is therefore partially decoupled from the SR9009 pharmacology story. SR9009 marketing conflates them as if they are the same thing, which they are not.

7. Preclinical Pharmacology - What Was Actually Tested (and How)

Circadian and metabolic phenotypes (Solt 2012, IP dosing)

100 mg/kg IP SR9009 twice daily shifted clock-controlled gene expression, reduced serum triglycerides and cholesterol, improved glucose homeostasis, and decreased fat mass in diet-induced obese mice [1].

Endurance and mitochondrial biogenesis (Woldt 2013, IP dosing)

100 mg/kg IP twice daily increased mitochondrial biogenesis markers in skeletal muscle, increased oxidative capacity, and raised treadmill running time by roughly 50 percent in mice [2].

Atherosclerosis (Sitaula 2015, IP dosing)

100 mg/kg/day IP for 7 weeks reduced plaque size in LDL-receptor-null mice on Western diet and shifted macrophage polarization from M1 toward M2 [4].

Myocardial infarction and ischemia-reperfusion (Stujanna 2017; Reitz 2019; IP dosing)

100 mg/kg/day IP after experimental MI improved survival and LV function [6]. Even a single day of SR9009 dosing after I/R injury suppressed the NLRP3 inflammasome and prevented progression to heart failure in mice [9].

Cancer selectivity (Sulli et al., Nature 2018; IP dosing)

IP SR9009 and SR9011 were selectively cytotoxic to cancer cells and oncogene-induced senescent cells in cell culture and in glioblastoma PDX mice, sparing normal tissue; proposed mechanism was simultaneous inhibition of autophagy and de novo lipogenesis [7]. However, subsequent work (Dierickx 2019, and prostate-cancer studies) has shown that at least some of the antitumor effect is REV-ERB-independent [8].

Summary of the preclinical package

Every headline result comes from mouse IP or IV dosing. No preclinical model was built on oral dosing with SR9009 in its original form. No human data exist.

8. Why SR9009 is on the WADA Prohibited List (2016)

The World Anti-Doping Agency added SR9009 to its Prohibited List in 2016 under class S4 (hormone and metabolic modulators), specifically S4.5 (other metabolic modulators) [12][14]. The rationale was not that SR9009 is a proven ergogenic aid in humans — no such human data exist — but rather:

• Its mechanism (REV-ERB agonism, mitochondrial biogenesis enhancement in preclinical models) would plausibly confer an endurance advantage if effective in humans.
• It is already available on the research-chemical market and being used by athletes and bodybuilders.
• The Woldt 2013 mouse endurance paper (IP dosing) received widespread attention and explicit media framing as an exercise mimetic.

WADA's position does not imply that SR9009 works in humans; it implies that the anti-doping system chose a precautionary listing. Certified reference materials have been developed for doping-control laboratories [12], and SR9009 metabolites have been identified for targeted urine screening [13][14].

Athletes in any WADA-code sport, including NCAA-aligned competitions and most Olympic federations, can test positive for SR9009 or its metabolites, and this is a sanctionable offense independent of whether the dose they took did anything biologically.

9. Safety and Toxicology - What We Do and Do Not Know

What we have

• Short-term rodent studies at 100 mg/kg IP (from weeks to a few months) generally did not report gross toxicity in the published papers [1][2][4][6].
• No organ-specific chronic toxicology package of the kind required for IND enablement has been disclosed publicly for SR9009.
• No genotoxicity, carcinogenicity, reproductive, or developmental toxicity data have been published in peer-reviewed form.

What we do not have

• Zero human safety data. There are no Phase 1 trials. There is no NOAEL or maximum tolerated dose in humans.
• No pharmacokinetic data in humans by any route.
• No drug-interaction data. Because SR9009 undergoes extensive Phase I metabolism [5][13], cytochrome-P450 interactions and inhibitor/inducer status are plausible but unstudied.
• No data on effects of chronic REV-ERB agonism in humans, including possible disruption of sleep-wake rhythm, mood, glucose homeostasis, and cardiovascular rhythms in ambulatory adults.

Theoretical concerns

• REV-ERB agonism strongly affects the circadian clock. Disruption of normal clock output can, in principle, produce sleep-wake disturbance, metabolic dysregulation, and impaired long-term entrainment. The wake-promoting effect in mice [10] raises questions about the effect on human sleep architecture.
• Many of SR9009's phenotypes are REV-ERB-independent [8][11]. The molecular mechanism of these off-target effects has not been identified, and the safety implications of a compound that is biologically active through unknown pathways are inherently uncertain.
• Because the oral route is so poorly absorbed [3], some consumers escalate doses or attempt parenteral routes. Injection of research-chemical-grade material from unregulated vendors carries additional sterility and impurity risks that have nothing to do with the pharmacology of SR9009 itself.

10. How to Read SR9009 Marketing Claims

Common marketing claims about SR9009 and how they map onto the actual science:

• Cardio in a pill. Source: media coverage of Woldt 2013. Actual study: mice, IP dosing, 100 mg/kg, twice daily. Not an oral pill. Not in humans.

• Burns fat without exercise. Source: Solt 2012 energy-expenditure and DIO-mouse data. Actual study: mice, IP dosing. Oral bioavailability in the same species is functionally zero [3].

• Improves endurance by 50 percent. Source: Woldt 2013. Actual study: mouse treadmill, IP injection.

• Activates REV-ERB specifically. Partially correct pharmacologically (REV-ERB agonism has been demonstrated in cell-based assays) but incomplete - a significant fraction of in-vivo effects have been shown to be REV-ERB-independent [8][11].

• Safe because it is non-hormonal. Absence of androgenic action does not equal safety. No human safety data exist for SR9009 by any route. Non-hormonal is a true statement; safe is not a supported one.

11. Comparison with Related Research Chemicals

SR9009 is often grouped with GW501516 (Cardarine, a PPARδ agonist) and with SARMs (ostarine, LGD-4033, RAD140), although pharmacologically they are entirely different classes.

• GW501516 (PPARδ agonist) similarly has preclinical endurance data and similarly lacks human efficacy or safety data; it was additionally flagged for carcinogenicity signals in rodent 2-year studies that led GlaxoSmithKline to discontinue development. SR9009 has no comparable carcinogenicity study on record.

• Ostarine, LGD-4033, and RAD140 are SARMs acting on the androgen receptor. SR9009 has no androgenic activity and no androgen-receptor binding. Cross-labelling SR9009 as a SARM is a category error found in some vendor product descriptions.

• The common thread across this cluster of compounds is not mechanism; it is market presence. They are all sold through the same channels, often in similar formats, to the same customer base, and they share the feature of lacking any completed human clinical-trial program.

12. Dosing in Published Research

13. Pharmacokinetics

Intravenous (mice)

• Short plasma half-life (on the order of tens of minutes) [3]
• High total clearance (the Burris lab explicitly calls SR9009 a high-clearance compound)
• Distribution not fully characterized in peer-reviewed human data

Intraperitoneal (mice; typical preclinical route)

• 100 mg/kg twice daily is the dose used in nearly all landmark papers [1][2][4][6]
• Produces measurable tissue exposure sufficient to modulate REV-ERB target genes in multiple organs
• Not a route available to consumers

Oral (mice)

• Approximately 2 percent oral bioavailability relative to IV in mouse PK studies cited by the Burris lab [3]
• Not sufficient to reproduce the plasma concentrations associated with IP efficacy at any plausible oral dose
• The medicinal-chemistry successor compounds (Trump 2013, compound 4 / GSK2945, approximately 23 percent oral F, about 2 hour half-life) were explicitly developed because SR9009 itself was not usable by this route [3]

Oral and sublingual (humans)

• No published human PK data exist for any route
• Vendor claims about sublingual bioavailability are not supported by peer-reviewed human pharmacokinetic studies
• Detection of SR9009 or its metabolites in human urine at the population level (Geldof 2016, n=1,511 routine doping samples) was negative under the screening conditions used, consistent with either low exposure or low detection windows [5]

Metabolism

• Extensive Phase I oxidative metabolism; at least eight identified metabolites in human liver microsomes [5][13]
• Both parent and metabolite detection methods have been developed for doping control in human and equine samples [12][13][14]

14. Regulatory Status

• FDA: Not approved for any indication. Not an Investigational New Drug (no active IND filing has been publicly disclosed). Not a dietary supplement ingredient under DSHEA.
• EMA: No authorization; not under centralized review.
• WADA (2016 onward): Prohibited in all sport, all times, as a metabolic modulator under class S4.5 [12][14].
• Sold as: a research chemical, typically labelled not for human consumption, through unregulated online vendors. This labelling does not make the compound safe and does not protect users from consumer-protection and anti-doping consequences.

15. Bottom Line for the Reader

• SR9009 is a real and scientifically interesting REV-ERB agonist tool compound from the Burris lab at Scripps Florida.
• The preclinical biology is real but is based entirely on IP and IV dosing in mice.
• The compound has essentially no oral bioavailability in the rodent species in which the biology was shown, and the Burris lab itself abandoned SR9009 as a chronic-dosing vehicle and moved on to optimized successors.
• Many published SR9009 phenotypes are now known to be REV-ERB-independent, meaning the molecule operates through at least some unidentified off-target pathways.
• There are no human clinical trials, no human pharmacokinetic data, and no human safety data.
• It is on the WADA Prohibited List and can trigger sanctions for athletes in regulated sport.
• The oral capsule sold to consumers as Stenabolic is not a recreation of the laboratory experiments that made SR9009 famous. The scientifically defensible statement about oral SR9009 at consumer doses is: there is no evidence it produces any biological effect.

16. Related Compounds

See also: GW501516 (Cardarine; PPARδ agonist), Ostarine (MK-2866; SARM), LGD-4033 (Ligandrol; SARM)

17. References

1. [1] 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. (2012). Regulation of circadian behaviour and metabolism by synthetic REV-ERB agonists. Nature. DOI PubMed
2. [2] 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, Nevière R, Burris TP, Schrauwen P, Staels B, Duez H. (2013). Rev-erb-α modulates skeletal muscle oxidative capacity by regulating mitochondrial biogenesis and autophagy. Nature Medicine. DOI PubMed
3. [3] 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. (2013). Optimized chemical probes for REV-ERBα. Journal of Medicinal Chemistry. DOI PubMed
4. [4] Sitaula S, Billon C, Kamenecka TM, Solt LA, Burris TP. (2015). Suppression of atherosclerosis by synthetic REV-ERB agonist. Biochemical and Biophysical Research Communications. DOI PubMed
5. [5] Geldof L, Deventer K, Roels K, Tudela E, Van Eeno P, Van Eenoo P. (2016). In vitro metabolic studies of REV-ERB agonists SR9009 and SR9011. International Journal of Molecular Sciences. DOI PubMed
6. [6] Stujanna EN, Murakoshi N, Tajiri K, Xu D, Kimura T, Qin R, Feng D, Yonebayashi S, Ogura Y, Yamagami F, Sato A, Nogami A, Aonuma K. (2017). Rev-erb agonist improves adverse cardiac remodeling and survival in myocardial infarction through an anti-inflammatory mechanism. PLoS One. DOI PubMed
7. [7] Sulli G, Rommel A, Wang X, Kolar MJ, Puca F, Saghatelian A, Plikus MV, Verma IM, Panda S. (2018). Pharmacological activation of REV-ERBs is lethal in cancer and oncogene-induced senescence. Nature. DOI PubMed
8. [8] Dierickx P, Emmett MJ, Jiang C, Uehara K, Liu M, Adlanmerini M, Lazar MA. (2019). SR9009 has REV-ERB-independent effects on cell proliferation and metabolism. Proceedings of the National Academy of Sciences. DOI PubMed
9. [9] Reitz CJ, Alibhai FJ, Khatua TN, Rasouli M, Bridle BW, Burris TP, Martino TA. (2019). SR9009 administered for one day after myocardial ischemia-reperfusion prevents heart failure in mice by targeting the cardiac inflammasome. Communications Biology. DOI PubMed
10. [10] Amador A, Huitron-Resendiz S, Roberts AJ, Kamenecka TM, Solt LA, Burris TP. (2018). Pharmacological targeting of REV-ERBβ is required to maintain wakefulness. Journal of Biological Rhythms. DOI PubMed
11. [11] Zhang T, Zhao M, Lu D, Wang S, Yu F, Guo L, Wen S, Wu B. (2022). SR9009 improves heart function after pressure overload independent of cardiac REV-ERB. Frontiers in Cardiovascular Medicine. DOI PubMed
12. [12] Thevis M, Thomas A, Schänzer W. (2018). Production of certified reference materials for the sports doping control of the REV-ERB agonist SR9009. Drug Testing and Analysis. DOI PubMed
13. [13] Geldof L, Deventer K, Van Eenoo P. (2019). A further insight into the metabolic profile of the nuclear receptor Rev-erb agonist, SR9009. Drug Testing and Analysis. DOI PubMed
14. [14] Wong JKY, Chan GHM, Leung DKK, Tang FPW, Wan TSM. (2021). In vitro metabolism of the REV-ERB agonist SR-9009 and subsequent detection of metabolites in associated routine equine plasma and urine doping control samples. Drug Testing and Analysis. DOI PubMed
15. [15] Duez H, Pourcet B. (2023). Nuclear receptor REV-ERB - Regulating the clock and beyond (review). GEN Biotechnology / related review series. PubMed
16. [16] Raghuram S, Stayrook KR, Huang P, Rogers PM, Nosie AK, McClure DB, Burris LL, Khorasanizadeh S, Burris TP, Rastinejad F. (2007). Identification of heme as the ligand for the orphan nuclear receptors REV-ERBα and REV-ERBβ. Nature Structural and Molecular Biology. PubMed