REV-ERB agonist comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Last reviewed on 2025-12-18. Where a claim depends on a specific study, the study is described rather than over-claimed.
SR9009 is a synthetic small molecule that acts on the nuclear receptors REV-ERBα and REV-ERBβ. These receptors are part of the circadian clock machinery and normally repress transcription of certain target genes. In laboratory research, SR9009 is used as a chemical tool to study how REV-ERB activity influences metabolism, inflammation, and daily biological rhythms. The compound is not an approved medicine, and its effects in humans remain largely uncharacterized. It is often described as an investigational agent rather than a therapeutic product.
REV-ERB proteins typically suppress gene expression by recruiting corepressor complexes to DNA response elements. SR9009 binds these receptors and strengthens that repressive action in cell-based assays. Studies in rodents have reported changes in lipid handling, mitochondrial function, and exercise capacity after treatment. Such findings are often cited as evidence for metabolic effects, but species differences and limited pharmacokinetic data make direct translation to humans uncertain. Researchers continue to examine which effects are robust and which depend on specific experimental conditions.
SR9009 is frequently discussed alongside other REV-ERB ligands, including synthetic agonists and natural heme-related molecules. Its selectivity for REV-ERB over related nuclear receptors has been measured in binding and reporter assays, though off-target activity at higher concentrations is possible. The compound is prohibited in sport by the World Anti-Doping Agency, and it is not approved for any medical use in major jurisdictions. Products sold online may be labeled as research chemicals, and their identity and purity are not guaranteed by regulatory review.
At the molecular level, SR9009 binds the ligand-binding domain of REV-ERB and strengthens recruitment of corepressor proteins such as NCoR and HDAC3. This increases repression of target genes, including Bmal1 and other clock-controlled and metabolic genes. In rodent studies, such changes have been linked to altered lipid handling, glucose metabolism, and energy expenditure. The precise chain of events between receptor binding and whole-body effects remains an active area of research. Findings in animals do not automatically translate to humans.
Laboratory studies often administer SR9009 by injection because oral absorption appears poor in rodents. Reported pharmacokinetic properties include rapid metabolism and low systemic exposure after oral dosing. Human pharmacokinetic data are sparse, so absorption, distribution, metabolism, and excretion in people are not well defined. Some research explores related REV-ERB compounds with improved drug-like properties. Regulatory approval for any REV-ERB agonist as a human medicine has not been granted to date.
| Property | Value | Notes |
|---|---|---|
| Common name | SR9009 | Also marketed informally as Stenabolic |
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ |
| Molecular formula | C24H30ClN3O4S | Approximate molecular weight 492 g/mol |
| CAS Registry Number | 1379686-30-2 | Identifier for the parent compound |
| Regulatory status | Not approved for human use | Prohibited in sport by WADA |
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.
Most published work on SR9009 consists of preclinical studies. It is widely sold as a research chemical, a category that does not imply safety, efficacy, or pharmaceutical-grade quality. Sports anti-doping organizations have listed SR9009 as a prohibited substance, and its presence in an athlete sample can lead to sanctions. Legal status differs by country; in several jurisdictions it is not approved for human consumption and may be treated as an unapproved new drug.
Handling practices for SR9009 focus on minimizing degradation and contamination. The solid is generally stored desiccated at or below -20 °C, protected from light and moisture. Stock solutions are often prepared in dimethyl sulfoxide or ethanol, then aliquoted to avoid repeated freeze–thaw cycles. Aqueous solubility is low, so formulations for animal studies may require cosolvents or suspending agents. Personnel should follow institutional chemical safety procedures, because toxicological data for humans are incomplete.
Regulatory status varies by country and intended use. Major drug agencies have not granted marketing authorization for SR9009 as a medicine, and it is not listed as a controlled substance in many jurisdictions. It is often sold as a research chemical, a category that may fall outside pharmaceutical manufacturing rules. Buyers should verify local laws and supplier documentation, including certificates of analysis. The lack of standardized quality controls raises concerns about identity, purity, and actual content in products marketed online.
In laboratory settings, SR9009 is commonly identified by its molecular structure and its interaction with REV-ERB receptors. Vendors may list it under synonyms such as Stenabolic or REV-ERB agonist, but those names do not define purity or identity. Analytical confirmation typically uses high-performance liquid chromatography with ultraviolet detection or liquid chromatography–mass spectrometry. A reference standard is needed to compare retention time and mass spectrum, because the compound can be confused with related research chemicals.
Handling recommendations for SR9009 in a laboratory setting include storing the solid at low temperature, protected from light and moisture. The compound is often dissolved in dimethyl sulfoxide or ethanol for experiments. Solutions should be prepared with appropriate personal protective equipment and disposed of according to local rules. Stability data for long-term storage are limited, so stock solutions are typically kept cold and used within defined periods. Records of preparation date and concentration support reproducibility.
SR9009 is not approved as a medicine by major regulatory agencies. It is commonly sold as a research chemical, a category that may fall outside customary drug approval and quality rules. In sports, the World Anti-Doping Agency lists SR9009 as a prohibited substance. Athletes who use it can face sanctions if it is detected in a sample. Legal status varies by country, and importation may be restricted. Enforcement practices differ across borders.
Detection of SR9009 in biological samples usually employs liquid chromatography coupled with tandem mass spectrometry. This method can identify the parent compound and sometimes metabolites in urine or blood. Because exposure can be low and clearance may be rapid, sample timing and limits of detection matter. Laboratories validate assays for sensitivity and specificity. Results are interpreted alongside chain-of-custody and quality-control records. Urine is the common matrix for anti-doping analysis, while blood may be used in research settings.
Mescaline given orally appears to be subject to first-pass metabolism of about 50%. Following the first pass, mescaline appears to be subject to relatively limited metabolism. The primary metabolic pathway of mescaline is oxidative deamination. The specific enzymes mediating the deamination of mescaline are controversial however. Monoamine oxidase (MAO), diamine oxidase (DAO; histamine oxidase), semicarbazide-sensitive amine oxidase (SSAO), and/or other enzymes may be responsible. Preclinical studies of mescaline given in combination with inhibitors of MAO and/or DAO, such as iproniazid, pargyline, and semicarbazide, have been conducted, but findings have been conflicting. Mescaline has been reported to be a poor or negligible substrate of highly purified human MAO in-vitro. Mescaline is converted via deamination into 3,4,5-trimethoxyphenylacetaldehyde (TMPA) as an intermediate and then into 3,4,5-trimethoxyphenylacetic acid (TMPAA) or 3,4,5-trimethoxyphenylethanol (TMPE). β-Hydroxymescaline may also be a minor metabolite of mescaline formed by dopamine β-hydroxylase (DBH), though this remains unclear. Mescaline appears not to be subject to metabolism by CYP2D6 based on in-vitro studies with human liver microsomes. Similarly, the in-vitro cytotoxicity of mescaline does not appear to be affected by cytochrome P450 (CYP450) enzyme inhibitors. Conversely, it was potentiated by the MAO-A inhibitor clorgiline but not by the MAO-B inhibitor rasagiline.
== Select research interests == Research in Cooks' laboratory (the Aston Laboratories) has contributed to a diverse assortment of areas within mass spectrometry, ranging from fundamental research to instrument and method development to applications. Cooks' research interests over the course of his career have included the study of gas-phase ion chemistry, tandem mass spectrometry, angle-resolved mass spectrometry and energy-resolved mass spectrometry (ERMS); dissociation processes, including collision-induced dissociation (CID), surface-induced dissociation (SID), and photodissociation (PD); and desorption processes, including secondary ion mass spectrometry (SIMS), laser desorption ionization (LDI) and desorption electrospray ionization (DESI). His research has ranged through areas from preparative mass spectrometry, ionization techniques and quadrupole ion traps (QITs) and related technologies to as far afield as abiogenisis (also known as "the origin of life") via homochirality.
Cantrell had the band's engineer, Paul Figueroa, come in to his house and record a lot of his vocals and solos there. The band finished recording the album at the Henson Recording Studios in Los Angeles. Cantrell also said he expected the album to be released "probably sometime this summer." At the press room of the Rock and Roll Hall of Fame Induction Ceremony on April 14, 2018, Cantrell revealed that Alice in Chains had just signed with BMG, and that they had finished mixing their new album. Alice in Chains did not perform live in 2017. The band performed their first concert since October 2016 at the House of Blues in Boston on April 28, 2018. In May 2018, Alice in Chains headlined the festivals Carolina Rebellion, Lunatic Luau, Pointfest, Northern Invasion, the WMMR BBQ festival in Philadelphia, and the Rock on the Range festival in Columbus, Ohio on May 18, 2018, in which they paid tribute to Chris Cornell on the first anniversary of his death covering two Soundgarden songs to close their set, "Hunted Down" and "Boot Camp", respectively. At the end of the show, the lights on stage spelled out "CC" for Chris Cornell and "SG" for Soundgarden as feedback rang out. The band started their European tour in June 2018, and headlined the Tons Of Rock Festival in Norway alongside Ozzy Osbourne and Helloween. Alice in Chains are also scheduled to headline KISW's Pain in the Grass festival in August 2018. The band released a new single, "The One You Know", via Spotify, Amazon and iTunes on May 3, 2018. A music video directed by Adam Mason was released on YouTube the same day.
==== Early 1990s ==== The Virgilio Barco Vargas (1986–1990) administration, in addition to continuing to handle the difficulties of the complex negotiations with the guerrillas, also inherited a particularly chaotic confrontation against the drug lords, who were engaged in a campaign of terrorism and murder in response to government moves in favor of their extradition overseas. In June 1987, the ceasefire between FARC and the Colombian government formally collapsed after the guerrillas attacked a military unit in the jungles of Caquetá. According to journalist Steven Dudley, FARC founder Jacobo Arenas considered the incident to be a "natural" part of the truce and reiterated the group's intention to continue the dialogue, but President Barco sent an ultimatum to the guerrillas and demanded that they immediately disarm or face military retaliation. Regional guerrilla and Army skirmishes created a situation where each violation of the ceasefire rendered it null in each location, until it became practically nonexistent. By 1990, at least 2,500 members of the FARC-founded Patriotic Union had been murdered, according to historian Daniel Pecáut, which led up to that year's assassination of presidential candidate Bernardo Jaramillo Ossa.
Sources: en.wikipedia.org
==== Synthesis in Yoctoreactor ==== The yoctoreactor method introduced by Hansen et al. is based on the geometry and stability of a three-dimensional DNA structure that creates a yoctoliter (10−24 L) size chemical reactor in which proximity of BBs brings about reactions among them. The DNA oligomers comprise the DNA-barcode for the attached BBs and form the structural elements of the reactor. One kind of yoctoreactor format is shown in the figure.
=== Cultural depictions === Jean-Michel Basquiat depicted two angel dust users in his 1982 painting Dustheads. Tsukasa Hojo's 1985 manga City Hunter features a drug, Angel Dust, presumably a reference to PCP's street name. The related 2023 animated film, City Hunter: Angel Dust, more directly moved the franchise's angel dust into the realm of fantasy, as it is portrayed as a science fiction nanomachine serum developed by a biotech company to create super-soldiers with a tendency to drive them berserk, side-stepping the real-life PCP.
Samidorphan (INNTooltip International Nonproprietary Name, USANTooltip United States Adopted Name) is an opioid antagonist that in the form of olanzapine/samidorphan (sold as Lybalvi) is used in the treatment of schizophrenia and bipolar disorder. Samidorphan reduces the weight gain associated with olanzapine. Samidorphan is taken by mouth. Samidorphan was under development as a standalone medication for various indications but has been discontinued. Buprenorphine/samidorphan for the treatment of major depressive disorder was rejected by the US Food and Drug Administration (FDA) due to insufficient evidence of effectiveness, but remains in preregistration as of September 2021. Development of baclofen/samidorphan has also been discontinued.
Sources: en.wikipedia.org
== Further reading == Altschul, SF (1991). "Amino acid substitution matrices from an information theoretic perspective". Journal of Molecular Biology. 219 (3): 555–65. doi:10.1016/0022-2836(91)90193-A. PMC 7130686. PMID 2051488. Dayhoff, M. O.; Schwartz, R. M.; Orcutt, B. C. (1978). "A model of evolutionary change in proteins". Atlas of Protein Sequence and Structure. 5 (3): 345–352. Eddy, SR (2004). "Where did the BLOSUM62 alignment score matrix come from?". Nature Biotechnology. 22 (8): 1035–6. doi:10.1038/nbt0804-1035. PMID 15286655. S2CID 205269887. Henikoff, S; Henikoff, JG (1992). "Amino acid substitution matrices from protein blocks". Proceedings of the National Academy of Sciences of the United States of America. 89 (22): 10915–9. Bibcode:1992PNAS...8910915H. doi:10.1073/pnas.89.22.10915. PMC 50453. PMID 1438297.
"The discovery of radium". Lateral Science. UK. 8 July 2012. Archived from the original on 9 March 2016. Retrieved 13 May 2017. Radium water bath in Oklahoma. markwshead.com (photographic images). "Radium, radioactive". NLM Hazardous Substances Databank. U.S. National Institutes of Health. Archived from the original on 1 July 2018. "Annotated bibliography for radium". Alsos Digital Library for Nuclear Issues. Lexington, VA: Washington and Lee University. Archived from the original on 25 June 2019. "Radium". The Periodic Table of Videos. University of Nottingham.
== Pharmacology == The therapeutic pharmacological properties of zopiclone include hypnotic, anxiolytic, anticonvulsant, and myorelaxant properties. Zopiclone and benzodiazepines bind to the same sites on GABAA receptors, causing an enhancement of the actions of GABA to produce the therapeutic and adverse effects of zopiclone. The metabolite of zopiclone desmethylzopiclone is also pharmacologically active, although it has predominately anxiolytic properties. One study found some slight selectivity for zopiclone on α1 and α5 subunits, although it is regarded as being unselective in its binding to GABAA receptors containing α1, α2, α3, and α5 subunits. Desmethylzopiclone has been found to have partial agonist properties, unlike the parent drug zopiclone, which is a full agonist. The mechanism of action of zopiclone is similar to benzodiazepines, with similar effects on locomotor activity and on dopamine and serotonin turnover. Zopiclone is in the cyclopyrrolone family of drugs. Other cyclopyrrolone drugs include suriclone. Zopiclone, although molecularly different from benzodiazepines, shares an almost identical pharmacological profile as benzodiazepines, including anxiolytic properties. Its mechanism of action is by binding to the benzodiazepine site and acting as a full agonist, which in turn positively modulates benzodiazepine-sensitive GABAA receptors and enhances GABA binding at the GABAA receptors to produce zopiclone's pharmacological properties. In addition to zopiclone's benzodiazepine pharmacological properties, it also has some barbiturate-like properties.
Smoking cessation may decrease the metabolism of acetaminophen, beta-blockers, caffeine, oxazepam, pentazocine, propoxyphene, theophylline, and tricyclic antidepressants, leading to higher plasma concentrations of these drugs. Possible alteration of nicotine absorption through the skin from the transdermal nicotine patch by drugs that cause vasodilation or vasoconstriction. Possible alteration of nicotine absorption through the nasal cavity from the nicotine nasal spray by nasal vasoconstrictors (e.g., xylometazoline). Possible alteration of nicotine absorption through oral mucosa from nicotine gum and lozenges by food and drink that modify salivary pH.
Sources: en.wikipedia.org
SR9009 is a synthetic research compound that binds and modulates the nuclear receptors REV-ERBα and REV-ERBβ. It is used in laboratory studies of circadian biology and metabolism, not as an approved medicine. It is also known by the informal name Stenabolic.
No. SR9009 has not been approved as a therapeutic drug in the United States, European Union, or other major markets. Human safety and efficacy data are very limited. Its presence in consumer products does not imply regulatory approval.
The World Anti-Doping Agency lists SR9009 as a prohibited substance because it can alter gene expression and metabolic pathways relevant to performance. The ban applies at all times, not only during competition. Detection relies on laboratory methods such as mass spectrometry.
SR9009 is a synthetic research compound that activates the REV-ERBα and REV-ERBβ nuclear receptors. It is not an approved drug and has no established human therapeutic use. Most published biological data come from cell and rodent studies.