This is a working overview of REV-ERB, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-07-06. Anything still debated is marked as such rather than presented as settled.
Pharmacokinetic data for SR9009 are limited in published literature. Some reports indicate low oral bioavailability and rapid clearance in animals, which complicates interpretation of exposure and effect. Researchers often use injected routes in preclinical work to achieve measurable systemic levels. Analytical studies rely on mass spectrometry to detect the parent compound and its metabolites. Questions about tissue distribution, active metabolites, and long-term consequences remain open. Species differences in metabolism can affect observed half-life and target engagement.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. These receptors help regulate circadian rhythms and metabolic gene expression. In laboratory experiments, SR9009 binds these receptors and alters transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. It is not a naturally occurring compound and has no approved therapeutic use. Research interest stems from its ability to modify energy metabolism in cells and animal models.
Several misconceptions surround SR9009. It is often described as a SARM, a steroid, or an exercise pill, but its known target is the REV-ERB receptor family. Rodent studies have examined exercise capacity and metabolic markers, yet human outcomes remain unproven. Oral bioavailability appears low in animals, and human pharmacokinetics are not well characterized. Online products may contain impurities or different compounds, so identity and purity testing are important for research use.
Analytical chemists detect SR9009 with liquid chromatography-tandem mass spectrometry, commonly abbreviated LC-MS/MS. Sample preparation may involve protein precipitation, liquid-liquid extraction, or solid-phase extraction before analysis. Laboratories can target the parent compound or its metabolites, depending on the matrix and the purpose of testing. Anti-doping methods require sensitive and specific assays because concentrations in biological samples can be low. Reference standards and validated methods are essential for reliable identification and quantification.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic small-molecule REV-ERB agonist | Not a hormone or natural product |
| Primary targets | REV-ERBα and REV-ERBβ | Nuclear receptors involved in circadian and metabolic regulation |
| Appearance | White to off-white solid | Typical for purified research samples |
| Solubility | Soluble in DMSO and ethanol; low water solubility | Laboratory solubility depends on solvent and purity |
| Common synonyms | SR9009; Stenabolic | Stenabolic is a colloquial name, not a formal chemical name |
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.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ, also called NR1D1 and NR1D2. These receptors help regulate circadian rhythms and metabolic gene programs. The compound was developed for laboratory research, not as an approved therapeutic. Its identity is distinct from steroid hormones and selective androgen receptor modulators. Scientific interest centers on how REV-ERB activation changes gene expression in cells and animal models.
In laboratory settings, SR9009 is typically characterized by liquid chromatography–mass spectrometry (LC-MS) or high-performance liquid chromatography with ultraviolet detection (HPLC-UV). These methods can confirm identity and estimate purity, but they require reference standards for accurate quantification. Because SR9009 is not a licensed pharmaceutical, no harmonized pharmacopeial monograph exists. Laboratories often validate in-house methods for matrices such as plasma, urine, or cell culture media. Sample preparation may involve protein precipitation or liquid-liquid extraction before analysis.
Physicochemical behavior influences handling. SR9009 is described as a solid with limited aqueous solubility, so organic solvents such as dimethyl sulfoxide or ethanol are common in research stock solutions. Aqueous dilution can produce precipitates if the organic content is too low. Light, heat, and repeated freeze-thaw cycles may affect stability. Storage recommendations usually specify a desiccated freezer environment protected from light, but exact stability data depend on the formulation and matrix.
SR9009 is a synthetic small molecule studied as a REV-ERB agonist. REV-ERBα and REV-ERBβ are nuclear receptors that help regulate circadian rhythms and metabolic gene expression. The compound was identified in academic screening efforts to find synthetic ligands for these receptors. In cell and animal studies, SR9009 alters transcription of genes involved in lipid and glucose metabolism, and it can shift circadian behavior. It is not an approved therapeutic agent.
Mechanistically, SR9009 binds the ligand-binding domain of REV-ERBα/β and enhances recruitment of corepressor complexes. This represses target genes rather than activating them. Because REV-ERB proteins normally compete with ROR proteins at shared response elements, the net effect depends on tissue and timing. Researchers use SR9009 to probe how nuclear receptor signaling links the clock to metabolism, inflammation, and muscle biology. Findings are largely preclinical, and the precise contribution of each receptor subtype remains under study.
SR9009 is frequently discussed in fitness and research-chemical contexts, yet it has no approved medical indication. Regulatory agencies have not authorized it for human use, and it is not a standard prescription drug. Some sports organizations list it as a prohibited substance because of its potential performance-enhancing properties. Published human data are sparse, so claims about its effects in people often rely on animal models or anecdotal reports. Quality and identity of online materials can vary widely.
Regulatory treatment of SR9009 reflects its investigational status. The compound has no approved human therapeutic indication, and sports authorities prohibit its use. It appears on anti-doping lists as a non-approved substance or metabolic modulator, depending on the list version. Products sold online as research chemicals are not quality-controlled medicines, so their identity and purity can differ from the label. Such products may also contain unlisted compounds, which complicates both testing and safety assessment.
Scientific discussion of SR9009 often separates animal evidence from human anecdote. Rodent studies provide controlled data on endurance, metabolism, and gene expression, but they use specific strains, doses, and treatment durations. Human reports are mostly uncontrolled and cannot establish cause and effect. Open questions include oral bioavailability, tissue distribution, metabolic stability, and long-term effects. Review articles generally call for more rigorous pharmacokinetic and safety research before any clinical use could be considered.
== Prognosis == The long-term outlook (prognosis) for people with cold agglutinin disease varies based on many factors including the severity of the condition, the signs and symptoms present in each person and the underlying cause. For example, people with cold agglutinin disease caused by bacterial or viral infections tend to have an excellent prognosis; in these cases, the symptoms typically disappear within 6 months after the infection has resolved. Mild to moderate primary (unknown cause) cold agglutinin disease can also be associated with a good prognosis if excessive exposure to the cold is avoided. Those with cold agglutinin disease caused by HIV infection or certain types of cancer generally have a poor prognosis due to the nature of the underlying condition.
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The two substrates of this enzyme are dihydrobunolol and oxidised nicotinamide adenine dinucleotide phosphate (NADP+). Its products are bunolol, reduced NADPH, and a proton. This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-OH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is (+/−)-5-[(tert-butylamino)-2'-hydroxypropoxy]-1,2,3,4-tetrahydro-1-naphthol:NADP+ oxidoreductase. This enzyme is also termed bunolol reductase.
Protein splicing is an intramolecular reaction of a particular protein in which an internal protein segment (called an intein) is removed from a precursor protein with a ligation of C-terminal and N-terminal external proteins (called exteins) on both sides. The splicing junction of the precursor protein is mainly a cysteine or a serine, which are amino acids containing a nucleophilic side chain. The protein splicing reactions which are known now do not require exogenous cofactors or energy sources such as adenosine triphosphate (ATP) or guanosine triphosphate (GTP). Normally, splicing is associated only with pre-mRNA splicing. This precursor protein contains three segments—an N-extein followed by the intein followed by a C-extein. After splicing has taken place, the resulting protein contains the N-extein linked to the C-extein; this splicing product is also termed an extein.
Sources: en.wikipedia.org
Based on in vitro studies, it has been estimated that MAO-A is responsible for about 81% of psilocin's phase I hepatic metabolism. Psilocin and its metabolites are also glucuronidated by UDP-glucuronyltransferases (UGTs). UGT1A10 and UGT1A9 appear to be the most involved. Psilocybin's glucuronidated metabolites include psilocin-O-glucuronide and 4-HIAA-O-glucuronide. Approximately 80% of psilocin in blood plasma is in conjugated form, and conjugated psilocin levels are about fourfold higher than levels of free psilocin. Plasma 4-HIAA levels are also much higher than those of free psilocin. Norpsilocin (4-HO-NMT), formed from psilocin via demethylation mediated by the cytochrome P450 enzyme CYP2D6, is known to occur in mice in vivo and with human recombinant CYP2D6 in vitro but was not detected in humans in vivo. An oxidized psilocin metabolite of unknown chemical structure is also formed by hydroxyindole oxidase activity of CYP2D6. Oxidized psilocin is possibly a quinone-type structure like psilocin iminoquinone (4-hydroxy-5-oxo-N,N-DMT) or psilocin hydroquinone (4,5-dihydroxy-N,N-DMT). Additional metabolites formed by CYP2D6 may also be present. Besides CYP2D6, CYP3A4 showed minor activity in metabolizing psilocin, though the produced metabolite is unknown. Other cytochrome P450 enzymes besides CYP2D6 and CYP3A4 appear unlikely to be involved in psilocin metabolism.
==== Signalling ==== In innate immunity TLRs play an important role. These TLRs (mainly TLR7 and TLR9) can be proteolytically activated by AEP. The reduction of proinflammatory cytokines by stimulating TLR9 was found in myeloid cells and plasmacytoid dendritic cells which lacked AEP. Enzyme is also important in processing of influenza virus and immune response using TLR7. AEP plays a critical role in TLR processing. and AEP can initiate removal of invariant chain in MHC-II complex, which can critically influence peptide generation and activity of MHCII.
However, this difference is usually neglected most of the time (that is whenever we are not dealing with processes such as sound absorption and attenuation of shock waves, where second viscosity coefficient becomes important) by explicitly assuming
=== Horses === Horses are branded with both the hot-iron and cryogenic techniques. Their brands most often denote ownership. Owners will generally create a unique brand to identify the horses that belong to a given ranch. Freeze brands can also be used to denote a breed in general or to identify an animal with a specific breed registry. The brand is typically placed on a horse's haunches or its neck, near the crest.
Sources: en.wikipedia.org
It is a synthetic research compound that activates REV-ERB nuclear receptors. It is not an approved drug or dietary supplement. Most information comes from cell and animal studies.
It binds REV-ERBα and REV-ERBβ and changes transcription of metabolic genes. This can affect circadian rhythm, lipid use, and mitochondrial function. The full downstream effects are still under study.
No. Some rodent studies show increased endurance, but controlled human trials are lacking. Claims about human performance are not established by published evidence.
Legality depends on the country and the intended use. In many places it is not approved as a medicine and may be sold only as a research chemical. Importation or possession can be restricted, and sports organizations prohibit it.