REV-ERB agonist raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2026-02-27 and is reviewed periodically as new material appears.
At the molecular level, SR9009 binds REV-ERBα and REV-ERBβ and alters their repressive activity on target genes. These nuclear receptors help regulate the circadian clock, lipid synthesis, glucose metabolism, and inflammatory pathways. By changing transcription, the compound can shift the timing or magnitude of downstream metabolic processes in model systems. It does not act through androgen receptors or adenosine receptors, which distinguishes it from several substances sold for athletic performance. Whether the same transcriptional changes occur in humans at tolerable exposures remains an open question because controlled human studies are lacking.
Preclinical reports describe effects on exercise endurance, mitochondrial content, and lipid profiles in rodents, but these findings come from specific experimental conditions. Many studies use high doses or delivery methods that may not translate directly to human use. SR9009 has been reported to have low oral bioavailability and a short half-life, which complicates interpretation of oral dosing studies. It is not established as safe or effective for any indication. Literature discussions often separate its pharmacological mechanism from unverified claims made in fitness and supplement markets.
SR9009 is a synthetic small molecule studied as an agonist of REV-ERB nuclear receptors. REV-ERB alpha and REV-ERB beta help regulate circadian rhythms and metabolic gene expression. In laboratory research, SR9009 has been used to probe how these receptors affect skeletal muscle, liver, and adipose tissue. The compound was identified in academic drug-discovery work and is often described in scientific literature by its chemical name and research code. It is not an approved medicine, and human clinical data remain limited or absent.
SR9009 binds REV-ERB receptors and alters their repressive activity on target genes. This action can change transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. In rodent studies, treated animals have shown changes in muscle oxidative capacity and exercise performance, though effects vary by dose, duration, and model. The precise molecular steps connecting receptor binding to whole-body outcomes are still an active area of investigation. Findings in animals do not automatically translate to humans.
Because REV-ERB receptors are core clock components, SR9009 has been examined for effects on daily rhythms as well as metabolism. Research has explored whether the compound can shift or reinforce circadian gene expression in tissues such as liver and muscle. Some studies report improved metabolic markers in obese or diabetic mice, while others show context-dependent responses. Questions remain about which effects are direct, which are secondary to timing, and how they might differ across species.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C20H24ClN3O4S | Derived from published structure. |
| Molecular weight | 437.94 g/mol | Calculated value. |
| Appearance | White to off-white solid | Typical for purified research samples. |
| Solubility | DMSO, ethanol; low in water | Class: poorly water-soluble. |
| Typical storage | -20 °C, desiccated, protected from light | Limits degradation. |
Laboratory samples of SR9009 are typically supplied as a white to off-white powder. The compound dissolves readily in organic solvents such as dimethyl sulfoxide and ethanol, while its solubility in water is low. Because of this solubility profile, researchers often prepare concentrated stock solutions in an organic solvent before diluting them into aqueous assay buffers. Light exposure, moisture, and repeated freeze-thaw cycles can degrade many small molecules, so handling procedures usually aim to minimize these factors. Purity is commonly checked before use.
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.
Analytical methods for SR9009 typically rely on liquid chromatography coupled with tandem mass spectrometry. The technique can separate the parent compound from related substances and detect low concentrations in biological matrices. Urine and blood are common samples in anti-doping testing, while in vitro studies may use cell culture media. Rapid metabolism and low expected concentrations make method validation important for reliable identification. Exact metabolite patterns can vary by species and are not fully mapped.
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.
== Dosing considerations == The recommended intravenous dosage in adults is 500 mg every 6 hours or 1000 mg every 12 hours, with modification to achieve a therapeutic range as needed. The recommended oral dosage in the treatment of antibiotic-induced pseudomembranous enterocolitis is 125 to 500 mg every 6 hours for 7 to 10 days. Dose optimization and target attainment of vancomycin in children involves adjusting the dosage to maximize effectiveness while minimizing the risk of adverse effects, specifically acute kidney injury. Dose optimization is achieved by therapeutic drug monitoring (TDM), which allows measurement of vancomycin levels in the blood. TDM using area under the curve (AUC)-guided dosing, preferably with Bayesian forecasting, is recommended to ensure that the AUC0-24h/minimal inhibitory concentration (MIC) ratio is maintained above a certain threshold (400–600) associated with optimal efficacy.
Mammals serve a major role in science as experimental animals, both in fundamental biological research, such as in genetics, and in the development of new medicines, which must be tested exhaustively to demonstrate their safety. Millions of mammals, especially mice and rats, are used in experiments each year. A knockout mouse is a genetically modified mouse with an inactivated gene, replaced or disrupted with an artificial piece of DNA. They enable the study of sequenced genes whose functions are unknown. A small percentage of the mammals are non-human primates, used in research for their similarity to humans. Despite the benefits domesticated mammals had for human development, humans have an increasingly detrimental effect on wild mammals across the world. It has been estimated that the mass of all wild mammals has declined to only 4% of all mammals, with 96% of mammals being humans and their livestock now (see figure). In fact, terrestrial wild mammals make up only 2% of all mammals.
== Medical uses == Escitalopram is approved by the US Food and Drug Administration (FDA) for the treatment of major depressive disorder in adolescents and adults, and generalized anxiety disorder (GAD) in adults, in dosage from 5 to 20 mg. In European countries including the United Kingdom, it is approved for depression and anxiety disorders; these include: generalized anxiety disorder, social anxiety disorder (SAD), obsessive–compulsive disorder (OCD), and panic disorder with or without agoraphobia. In Australia it is approved for major depressive disorder.
Sources: en.wikipedia.org
== Death == Kimon Georgiev died suddenly of a stroke at around 1 pm on 28 September 1969 at the rest station of the Council of Ministers in Varna, shortly after visiting the Varna Thermal Power Plant, which had opened a month earlier. He was buried on 30 September in the Central Sofia Cemetery with state honours, with Prime Minister Todor Zhivkov attending the ceremony.
=== GPI-anchor === Bioinformatic analysis predicts the addition of a GPI-anchor on many AGPs. The early synthesis of the GPI moiety occurs on the ER cytoplasmic surface and subsequent assembly take place in the lumen of the ER. These include the assembly of tri-mannose (Man), galactose, non-N-acetylated glucosamine (GlcN) and ethanolamine phosphate to form the mature GPI moiety. AGPs undergo GPI-anchor addition while co-translationally migrating into the ER and these two processes finally converge. Subsequently, a transamidase complex simultaneously cleaves the core protein at the C-terminus when it recognizes the ω cleavage site and transfers the fully assembled GPI-anchor onto the amino acid residue at the C-terminus of the protein. These events occur prior to prolyl hydroxylation and glycosylation. The core glycan structure of GPI anchors is Man-α-1,2-Man-α-1,6-Man-α-1,4-GlcN-inositol (Man: mannose, GlcN: glucosaminyl), which is conserved in many eukaryotes. The only plant GPI anchor structure characterized to date is the GPI-anchored AGP from Pyrus communis suspension-cultured cells. This showed a partially modified glycan moiety compared to previously characterized GPI anchors as it contained β-1,4-Gal. The GPI anchor synthesis and protein assembly pathway is proposed to be conserved in mammals and plants. The integration of a GPI-anchor enables the attachment of the protein to the membrane of the ER transiting to the GA leading to secretion to the outer leaflet of the plasma membrane facing the wall.
PFAS are used in Class B firefighting foams due to their hydrophobic and lipophobic properties, as well as the stability of the chemicals when exposed to high heat. Though studies have been frequently limited by underpowered study designs, research indicates firefighters have higher blood levels of PFOS and PFHxS than the general population. PFAS exposure is prevalent among firefighters not only due to its use in emergencies but also because it is used in personal protective equipment. In support of these findings, states like Washington and Colorado have moved to restrict and penalize the use of Class B firefighting foam for firefighter training and testing. The September 11 attacks and resulting fires caused the release of toxic chemicals used in materials such as stain-resistant coatings. First responders to this incident were exposed to PFOA, PFNA, and PFHxS through inhalation of dust and smoke released during and after the collapse of the World Trade Center. First responders who were working at or near ground zero were assessed for respiratory and other health effects from exposure to emissions at the World Trade Center. Early clinical testing showed a high prevalence of respiratory health effects. Early symptoms of exposure often presented with persistent coughing and wheezing. PFOA and PFHxS levels were present in both smoke and dust exposure, but first responders exposed to smoke had higher concentrations of PFOA and PFHxS than those exposed to dust.
Sources: en.wikipedia.org
SR9009 is a synthetic REV-ERB agonist used in laboratory research. It is not an approved drug, and its effects in humans are not well characterized. It is often sold as a research chemical under the name Stenabolic.
No. SR9009 targets the nuclear receptors REV-ERBα and REV-ERBβ, not the androgen receptor. This mechanism differs from selective androgen receptor modulators and from exercise mimetics that act on PPARδ.
Published evidence is mainly preclinical, using cell cultures and animal models. Controlled human trials are not well documented in the public literature. Claims about human performance or health effects therefore remain unsupported by robust clinical data.
SR9009 is a synthetic research compound that acts on REV-ERB nuclear receptors. It is not approved for human use and is sold only as a research chemical. Its effects have been studied mainly in cells and rodents.