Everything below concerns SR9009. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-02-26. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic small molecule | Studied as a REV-ERB agonist |
| Molecular formula | C20H24ClN3O4S | Reported for the neutral compound |
| Appearance | Off-white to pale yellow solid | Typical research-grade material |
| Solubility | Sparingly soluble in water | Soluble in solvents such as DMSO |
| Common synonyms | SR9009; Stenabolic | Stenabolic is an informal alias |
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.
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.
The mechanism of action involves binding to REV-ERB receptors and recruiting corepressor complexes, which represses target gene transcription. This contrasts with many nuclear receptor agonists that activate transcription. Downstream effects may include changes in autophagy, mitochondrial biogenesis, and lipid handling, but the precise pathways remain an active area of study. Whether these molecular events translate into meaningful physiological effects in humans is unresolved. Most evidence comes from cultured cells and rodent models rather than human participants.
SR9009 is a synthetic small molecule developed as an agonist of the nuclear receptors REV-ERBα (NR1D1) and REV-ERBβ (NR1D2). These receptors help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, SR9009 alters transcription of genes involved in lipid metabolism, inflammation, and mitochondrial function. It is not an approved medicine, and its pharmacological profile in humans remains largely uncharacterized. The compound is frequently discussed in the context of circadian biology and metabolic research rather than clinical use.
Preclinical reports have linked SR9009 to improved endurance and altered energy expenditure in rodents. Such findings have prompted interest in whether REV-ERB activation can influence skeletal muscle metabolism. However, the reported effects depend on dose, route, and experimental model, and replication across laboratories is limited. Human trials have not established comparable outcomes, so claims about exercise performance remain speculative. The absence of controlled human data is a central limitation in interpreting these observations.
Medications for treatment of cases that do not improve include calcium channel blockers and iloprost. There is little evidence that alternative medicine reduce symptoms. Severe Raynaud's may in rare cases lead to complications, specifically skin sores or gangrene. About 4% of people have the condition. Onset of the primary form is typically between ages 15 and 30. The secondary form usually affects older people. Both forms are more common in cold climates.
Glycine amidinotransferase, mitochondrial is an enzyme that in humans is encoded by the GATM gene. This gene encodes a mitochondrial enzyme that belongs to the Amidinotransferase family. This enzyme is involved in creatine biosynthesis, whereby it catalyzes the transfer of a guanido group from L-arginine to glycine, resulting in guanidinoacetic acid, the immediate precursor of creatine. Mutations in this gene cause arginine:glycine amidinotransferase deficiency, an inborn error of creatine synthesis characterized by mental retardation, language impairment, and behavioral disorders.
Whilst the British considered this consistent with the Balfour Declaration's commitment to protect the rights of non-Jews, many Zionists saw it as a repudiation of the declaration. Although this policy lasted until the British surrendered the Mandate in 1948, it served only to highlight the fundamental difficulty for Britain in carrying out the Mandate obligations. Britain's involvement in this became one of the most controversial parts of its Empire's history and damaged its reputation in the Middle East for generations. According to historian Elizabeth Monroe: "measured by British interests alone, [the declaration was] one of the greatest mistakes in [its] imperial history" which greatly damaged Britain. However, others argue that this approach ignores the emergence of nationalism and the dismantling of major empires throughout the world, and the Britain would likely not have been able to maintain its presence in the Middle East in any case. The 2010 study by Jonathan Schneer, specialist in modern British history at Georgia Tech, concluded that because the build-up to the declaration was characterized by "contradictions, deceptions, misinterpretations, and wishful thinking", the declaration sowed dragon's teeth and "produced a murderous harvest, and we go on harvesting even today". The foundational stone for modern Israel had been laid, but the prediction that this would lay the groundwork for harmonious Arab-Jewish cooperation proved to be wishful thinking.
Sources: en.wikipedia.org
=== Disease mechanism === Exactly how disturbances of production and aggregation of the Aβ peptide give rise to the pathology of Alzheimer's disease is not known. The amyloid hypothesis (also known as the 'amyloid cascade hypothesis') posits that the accumulation of abnormally shaped Aβ peptides is the central event triggering the sequence of changes that eventually lead to neurodegeneration and dementia. Misfolded Aβ accumulates in the brain because it causes normal Aβ molecules to similarly misfold by a prion-like 'seeding' mechanism. The aggregated Aβ takes the form of small oligomers (which are particularly toxic to neurons) and amyloid fibrils, the long polymers that are the main components of Aβ plaques. Some researchers have argued that the amyloid fibrils bind up smaller oligomers and thus protect brain cells from the injurious effects of the oligomers. However, the plaques are not benign inasmuch as they are associated with abnormal neuronal processes and local inflammation. Whatever the relative influence of Aβ oligomers and fibrils, the presence of aggregated Aβ is associated with the disruption of neuronal metabolism and various other changes such as inflammation. Aβ also selectively builds up in mitochondria in the cells of Alzheimer's-affected brains, and it inhibits certain enzyme functions and the utilisation of glucose by neurons. Evidence supports Aβ as playing a central role in the pathogenesis of Alzheimer's disease.
The diagnosis of polyneuropathy begins with a history (anamnesis) and physical examination to ascertain the pattern of the disease process (such as arms, legs, distal, proximal), if they fluctuate, and what deficits and pain are involved. If pain is a factor, determining where and how long it has been present is important; one also needs to know what disorders are present within the family and what diseases the person may have. Although diseases often are suggested by the physical examination and history alone, tests that may be employed include electrodiagnostic testing, serum protein electrophoresis, nerve conduction studies, urinalysis, serum creatine kinase (CK) and antibody testing; nerve biopsy is done sometimes. Other tests may be used, especially tests for specific disorders associated with polyneuropathies; quality measures have been developed to diagnose patients with distal symmetrical polyneuropathy (DSP).
== Optical properties == The organic ligands of the interfacial layer can influence the photoluminescence (PL) of a nanoparticle via various mechanisms, two of which are surface passivation and carrier trapping. Surface passivation: At the surface of an uncovered nanoparticle (without an interfacial layer) dangling atoms are found. These bonds form energy levels between the HOMO–LUMO gap, thereby leading to non-radiative relaxation. Due to the binding of ligand molecules with the dangling orbitals, the energy of these states is shifted away from the HOMO-LUMO gap. This prevents nonradiative relaxation, and thus results in more PL. The strength of this effect strongly depends on the type of ligands. In general, small, linear ligands, do better than bulky ligands, because they lead to a higher surface coverage density, therefore allowing more dangling orbitals to be passivated. Another surface effect is carrier trapping. Here the ligands can scavenge the electron(holes) in the nanoparticle, thereby precluding radiative recombination and thus leading towards a reduction in PL. A well-known example of such ligands are thiols. The light conversion efficiency can also be improved using an interfacial layer that exists of compounds that absorb in a wider energy range and emit at the absorption energy of the nanoparticle. According to C. S. Inagaki et al the absorption band of a metallic nanoparticle was shown to drastically increase in width, caused by the overlap of transitions in the interfacial layer and the plasmon resonance band of the nanoparticle.
Bragg was influential in the effort to beat a leading American chemist, Linus Pauling, to the discovery of DNA's structure (after having been pipped at the post by Pauling's success in determining the alpha helix structure of proteins). At the same time Bragg's Cavendish Laboratory was also effectively competing with King's College London, whose Biophysics department was under the direction of Randall (Randall had refused Crick's application to work at King's College). Francis Crick and Maurice Wilkins of King's College were personal friends, which influenced subsequent scientific events as much as the close friendship between Crick and James Watson. Crick and Wilkins first met at King's College and not, as erroneously recorded by two authors, at the Admiralty during World War II. In 1995 Francis Crick signed the Ashley Montagu Resolution petitioning the International Court of Justice (previously the World Court) to help end genital mutation of children, including female genital mutilation, circumcision, and penile subincision.
Sources: en.wikipedia.org
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.
No. SR9009 is frequently mislabeled as a SARM in online discussions, but it does not target androgen receptors. Its known mechanism involves REV-ERB nuclear receptors and circadian-metabolic gene regulation.
Human clinical data are very limited. There is no approved human use, and safety and efficacy in people are not established. Most evidence comes from preclinical models, so effects observed in animals may not apply to humans.
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.