A practical reference on REV-ERB agonist: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
Reviewed 2026-05-03. Anything still debated is marked as such rather than presented as settled.
Analytical identification and purity assessment often use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Liquid chromatography–tandem mass spectrometry is used to detect and quantify SR9009 in biological matrices, including urine and blood, for anti-doping or pharmacokinetic studies. Nuclear magnetic resonance spectroscopy can confirm molecular structure. Stability depends on form and storage: the solid is generally more stable than solutions, and repeated freeze–thaw cycles may degrade samples. Purity is typically reported as a percentage from a certificate of analysis.
Regulatory treatment of SR9009 varies by country and context. It is not approved as a therapeutic drug by agencies such as the United States Food and Drug Administration or the European Medicines Agency. Sports authorities list it as a prohibited substance; the World Anti-Doping Agency classifies it among hormone and metabolic modulators. Legal status for personal possession or sale differs across jurisdictions, and some countries may restrict it under analog or research chemical laws. Buyers who seek verified material often rely on independent laboratory testing because online product labels may not match contents.
Laboratory samples of SR9009 are typically handled as research chemicals rather than pharmaceuticals. Suppliers usually state that the material is for research use only and not for human or veterinary administration. Storage recommendations generally call for a freezer at approximately −20 °C, protection from light, and a desiccated environment. The solid is often described as a white to off-white powder. Solubility is commonly reported in organic solvents such as dimethyl sulfoxide and ethanol, with low solubility in water.
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.
In rodent studies, SR9009 has been reported to increase mitochondrial content in skeletal muscle and improve exercise endurance under some conditions. These findings led to popular descriptions such as an exercise mimetic, although that term oversimplifies the biology. Effects vary by dose, timing, tissue, and model. The compound's influence on circadian pathways means that time of administration can matter in experiments. Whether similar metabolic changes occur in humans remains largely unexplored in controlled published trials.
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.
| Property | Value | Notes |
|---|---|---|
| Appearance | White to off-white powder | Common supplier description |
| Solubility | Soluble in DMSO and ethanol | Low solubility in water |
| Typical storage | −20 °C, desiccated, dark | For research samples |
| Analytical method | LC-MS/MS | Used for detection and quantification |
| Regulatory status | Prohibited in sport | WADA metabolic modulator class |
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.
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.
Storage conditions for research-grade SR9009 generally involve a freezer at approximately minus twenty degrees Celsius, sometimes lower for long-term preservation. Containers should remain tightly closed and protected from light. Desiccants may be used to limit moisture uptake. Solutions are often stored in aliquots to avoid repeated warming and cooling. Stability data for the compound under various conditions are limited, so laboratories typically follow supplier recommendations and verify performance through periodic analytical checks rather than assuming indefinite stability.
Identity and purity testing for SR9009 commonly uses liquid chromatography coupled with tandem mass spectrometry. This method separates the compound from matrix components and detects it by mass-to-charge transitions, providing sensitive and specific confirmation. Nuclear magnetic resonance spectroscopy can support structural identification, while high-performance liquid chromatography with ultraviolet detection may estimate purity. Because online products labeled as SR9009 may contain other substances or no active compound at all, independent verification is important in research settings. Certificates of analysis are useful but not a substitute for in-house testing.
== Type IV leader peptidase == Another family of signal aspartic endopeptidases was found in bacteria. Bacteria produce a number of protein precursors that undergo post-translational methylation and proteolysis prior to secretion as active proteins. Type IV prepilin leader peptidases are enzymes that mediate this type of post-translational modification. Type IV pilin is a protein found on the surface of Pseudomonas aeruginosa, Neisseria gonorrhoeae and other Gram-negative pathogens. Pilin subunits attach the infecting organism to the surface of host epithelial cells. They are synthesised as prepilin subunits, which differ from mature pilin by virtue of containing a 6-8 residue leader peptide consisting of charged amino acids. Mature type IV pilins also contain a methylated N-terminal phenylalanine residue. The bifunctional enzyme prepilin peptidase (PilD) from Pseudomonas aeruginosa is a key determinant in both type-IV pilus biogenesis and extracellular protein secretion, in its roles as a leader peptidase and methyl transferase (MTase). It is responsible for endopeptidic cleavage of the unique leader peptides that characterise type-IV pilin precursors, as well as proteins with homologous leader sequences that are essential components of the general secretion pathway found in a variety of Gram-negative pathogens. Following removal of the leader peptides, the same enzyme is responsible for the second posttranslational modification that characterises the type-IV pilins and their homologues, namely N-methylation of the newly exposed N-terminal amino acid residue.
Acrodermatitis chronica atrophicans (Herxheimer disease, primary diffuse atrophy) Actinic elastosis (solar elastosis) Anetoderma (anetoderma maculosa, anetoderma maculosa cutis, atrophia maculosa cutis, macular atrophy) Blepharochalasis Cutis laxa (chalazoderma, dermatochalasia, dermatolysis, dermatomegaly, generalized elastolysis, generalized elastorrhexis, pachydermatocele) Cutis rhomboidalis nuchae Ehlers–Danlos syndrome (cutis hyperelastica, elastic skin, India rubber skin) Elastosis perforans serpiginosa Homocystinuria Jadassohn–Pellizzari anetoderma Linear focal elastosis (elastotic striae) Loeys–Dietz syndrome Marfan syndrome Occipital horn syndrome Osteogenesis imperfecta (Lobstein syndrome) Perforating calcific elastosis (localized acquired cutaneous pseudoxanthoma elasticum, perforating periumbilical calcific elastosis, periumbilical perforating pseudoxanthoma elasticum) Pseudoxanthoma elasticum (Grönblad–Strandberg syndrome) Reactive perforating collagenosis Schweninger–Buzzi anetoderma Sclerotic fibroma Striae atrophicans Striae distensae Ullrich disease Verrucous perforating collagenoma Wrinkly skin syndrome
Further complicating the diagnosis is the fact that many patients with Parkinson's disease will have major depressive disorder, which may be the underlying cause of catatonia. Parkinson's disease can be distinguished from catatonia by a positive response to levodopa. Catatonia, on the other hand, will show a positive response to benzodiazepines. Extrapyramidal side effects of antipsychotic medication, especially dystonia and akathisia, can be difficult to distinguish from catatonic symptoms, or may confound them in the psychiatric setting. Extrapyramidal motor disorders usually do not involve social symptoms like negativism, while individuals with catatonic excitement typically do not have the physically painful compulsion to move that is seen in akathisia. Certain stimming behaviors and stress responses in individuals with autism spectrum disorders can present similarly to catatonia. In autism spectrum disorders, chronic catatonia is distinguished by a lasting deterioration of adaptive skills from the background of pre-existing autistic symptomatology that cannot be easily explained. Acute catatonia is usually clearly distinguishable from autistic symptoms. The diagnostic entities of obsessional slowness and psychogenic parkinsonism show overlapping features with catatonia, such as motor slowness, gegenhalten (oppositional paratonia), mannerisms, and reduced or absent speech. However, psychogenic parkinsonism involves tremor which is unusual in catatonia.
Sources: en.wikipedia.org
The Rhodesian Land Tenure Act was introduced the same year, which ostensibly introduced parity by reducing the amount of land reserved for white ownership to the same 45 million acres as for blacks: in practice, the most fertile farmlands remained in white hands, and some farmers took advantage by shifting their boundaries into black-populated territories, often without notifying others, thereby necessating government evictions. In 1977, the party had a schism in which the more hardline wing broke off to form the Rhodesian Action Party (RAP), which opposed Smith's proposals to negotiate a settlement with black nationalist leaders. In the elections leading to the country's independence in 1980, as the Republic of Zimbabwe, the RF won all 20 parliamentary seats reserved for whites in the power-sharing agreement that it had forged. On 6 June 1981, the party changed its name to the Republican Front, and on 23 July 1984, that party became the Conservative Alliance of Zimbabwe (CAZ) and opened its membership to Zimbabweans of all colours and all ethnic groups. Eleven of its 20 parliamentarians defected over the following four years, but the party again won 15 of the 20 parliamentary seats reserved for whites in the 1985 election. In October 1987, the ruling government of Robert Mugabe officially abolished all reserved seats for whites. When these were abolished, many white MPs became independents or joined the ruling ZANU–PF party.
== Research directions == Current research and recommendations to manage severe acute malnutrition (SAM), such as kwashiorkor, in children, are largely based on expert opinions. Only one-third of the WHO guidelines for the management of SAM are based on epidemiological and clinical research. Further studies are needed to "improve treatment outcomes in the large number of children with SAM."
Pharmacokinetics is the study of the bodily absorption, distribution, metabolism, and excretion of drugs. When describing the pharmacokinetic properties of the chemical that is the active ingredient or active pharmaceutical ingredient, pharmacologists are often interested in L-ADME:
Sources: en.wikipedia.org
Legality depends on the country and the intended use. In many places it is sold as a research chemical, but sports and medicine regulations restrict it.
Detection commonly uses liquid chromatography–tandem mass spectrometry. This method can identify the compound in urine or blood at low concentrations.
Typical guidance is −20 °C, dry, and protected from light. Solutions should be aliquoted and limited freeze–thaw cycles should be used.
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.