A practical reference on SR9009: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2026-01-17 and is reviewed periodically as new material appears.
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.
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 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 |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small-molecule ligand; not a hormone or peptide |
| Molecular formula | C20H24ClN3O4S | Reported for the free base |
| CAS Registry Number | 1379686-30-2 | Unique chemical identifier |
| Common synonyms | SR9009; stenabolic | Stenabolic is informal and not an official name |
| Reported targets | REV-ERBα and REV-ERBβ | Nuclear receptors linked to circadian and metabolic regulation |
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.
Regulatory agencies have not approved SR9009 for human therapeutic use. It is typically sold as a research chemical with labels stating that it is not for human consumption. The World Anti-Doping Agency prohibits the substance in sport, generally under the category of non-approved substances. Customs and national laws may restrict importation, sale, or possession. Product quality and legal status can vary by country and vendor, and therapeutic claims are not permitted in regulated advertising because the compound lacks approval.
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 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.
Fentanyl is a highly potent synthetic opioid of the piperidine family, used primarily as pain medication. It is 50 to 100 times more potent than morphine. Its primary clinical use is in pain management for cancer patients and those recovering from surgery. Fentanyl is also used as a sedative for intubated patients. Fentanyl has a short duration of action. Fentanyl works by activating μ-opioid receptors. Brand names include Actiq, Duragesic, and Sublimaze, among others. Fentanyl was first synthesized by Paul Janssen in 1960 and was approved for medical use in the United States in 1968. In 2015, 1,600 kilograms (3,500 pounds) were used in healthcare globally. As of 2017, fentanyl was the most widely used synthetic opioid in medicine; in 2019, it was the 278th most commonly prescribed medication in the United States, with more than a million prescriptions. It is on the World Health Organization's List of Essential Medicines. The effects of fentanyl are similar to those of other opioids, causing sedation and analgesia at clinical doses. The most common adverse effects are respiratory depression, emesis, and asthenia. Bradycardia and apnea are uncommon side effects but are serious and can lead to death outside of clinical settings. Fentanyl exerts its actions as an agonist of the μ-opioid receptor and κ-opioid receptor. The μ-receptor agonism is responsible for the respiratory depression and generalized analgesia whilst the κ-receptor agonism is responsible for sedation and spinal analgesia. Fentanyl is a potent μ-receptor agonist but has less affinity for the κ-receptor.
Umetaro Suzuki (鈴木 梅太郎, Suzuki Umetarō; April 7, 1874 – September 20, 1943) was a Japanese scientist, born in what is now part of Makinohara, Shizuoka, Japan. He was a member of the Imperial Academy, and a recipient of the Grand Cordon of the Order of the Sacred Treasure and the Order of Culture. His research was among the earliest of modern vitamin research.
Pregabalin is a member of the gabapentinoid class, also known as α2δ ligands. Despite being a structural analog of γ-aminobutyric acid (GABA), pregabalin is inactive at GABA receptors and does not mimic GABA. Instead, its action involves binding to a specific site on the α2δ-1 protein and reducing the release of excitatory neurotransmitters in synapses. Pregabalin does not directly block calcium channels (it is not a calcium channel blocker), as it does not bind to the ion conducting channel protein, called α1. However, in vitro studies show that pregabalin can reduce the normal traffic of calcium channels from intracellular sites (where they do not function) to membrane sites where they are functional. While the mechanism of action of pregabalin is not definitively characterized, its action in animal models of pain, seizures and anxiety requires binding to the α2δ-1 protein. It has been found that this binding inhibits several actions of α2δ-1 and also inhibits the release of excitatory neurotransmitters. These excitatory neurotransmitters include glutamate, norepinephrine (noradrenaline), serotonin, dopamine, substance P, and calcitonin gene-related peptide. By inhibiting the release of these neurotransmitters, pregabalin reduces excess activity of neuron networks, which helps alleviate symptoms and provides relief for patients experiencing pain, seizures, or other related symptoms.
D-amino acid oxidase (DAAO; also OXDA or DAMOX) is an enzyme with the function on a molecular level to oxidize D-amino acids to the corresponding α-keto acids, producing ammonia and hydrogen peroxide. This results in a number of physiological effects in various systems, most notably the brain. The enzyme is most active toward neutral D-amino acids, and not active toward acidic D-amino acids. One of its most important targets in mammals is D-serine in the central nervous system. By targeting this and other D-amino acids in vertebrates, DAAO is important in detoxification. The role in microorganisms is slightly different, breaking down D-amino acids to generate energy. DAAO is expressed in a wide range of species from yeasts to human. It is not present in plants or in bacteria which instead use D-amino acid dehydrogenase. DAAO in humans is a candidate susceptibility gene and together with G72 may play a role in the glutamatergic mechanisms of schizophrenia. DAAO also plays a role in both biotechnological and medical advancements. Risperidone and sodium benzoate are inhibitors of DAAO. D-amino acid oxidase is different from diamine oxidase that are both sometimes referred to as DAO.
Sources: en.wikipedia.org
Full clients verify transactions directly by downloading a full copy of the blockchain. They do not require trust in any external parties. Full clients check the validity of mined blocks, preventing them from transacting on a chain that breaks or alters network rules. Because of its size and complexity, downloading and verifying the entire blockchain is not suitable for all computing devices. Lightweight clients consult full nodes to send and receive transactions without requiring a local copy of the entire blockchain (see simplified payment verification – SPV). This makes lightweight clients much faster to set up and allows them to be used on low-power, low-bandwidth devices such as smartphones. When using a lightweight wallet, however, the user must trust full nodes, as it can report faulty values back to the user. Lightweight clients follow the longest blockchain and do not ensure it is valid, requiring trust in full nodes. Third-party internet services called online wallets or webwallets offer similar functionality but may be easier to use. In this case, credentials to access funds are stored with the online wallet provider rather than on the user's hardware. As a result, the user must have complete trust in the online wallet provider. A malicious provider or a breach in server security may cause entrusted crypto to be stolen. An example of such a security breach occurred with Mt. Gox in 2011.
Biotech and pharmaceutical companies in the New York metropolitan area Companies of the United States with untaxed profits Fire in the Blood (2013 film) List of pharmaceutical companies Pfizer Building, its former New York City headquarters Pfizergate
== History == Tuscaloosa succeeded Cahaba as Alabama's state capitol. The Childress Hill site fronting Broad Street and adjacent to the river was selected for the new capitol building, designed by English architect William Nichols. In 1829, Alabama Governor Gabriel Holmes addressed the legislature in the new building. The capitol building became Alabama Central Female College. It burned down in 1923.
Sources: en.wikipedia.org
=== Batten disease === Milasen is a novel individualized therapeutic agent that was designed and approved by the FDA for the treatment of Batten disease. This therapy serves as an example of personalized medicine. In 2019, a report was published detailing the development of milasen, an antisense oligonucleotide drug for Batten disease, under an expanded-access investigational clinical protocol authorized by the Food and Drug Administration (FDA). Milasen "itself remains an investigational drug, and it is not suited for the treatment of other patients with Batten's disease" because it was customized for a single patient's specific mutation. However it is an example of individualized genomic medicine therapeutical intervention.
== Tolerance and overdoses == Fatal opioid overdose typically occurs due to bradypnea, hypoxemia, and decreased cardiac output (hypotension occurs due to vasodilation, and bradycardia further contributes to decreased cardiac output). A potentiation effect occurs when opioids are combined with ethanol, benzodiazepines, barbiturates, or other central depressants which can result in rapid loss of consciousness and an increased risk of fatal overdose. Substantial tolerance to respiratory depression develops quickly, and tolerant individuals can withstand larger doses. However, tolerance to respiratory depression is quickly lost during withdrawal and may be completely reversed within a week. Many overdoses occur in people who return to their previous dose after having lost their tolerance following cessation of opioids. This puts addicts who receive medical treatment for opioid addiction at great risk of overdose when they are released, as they may be particularly vulnerable to relapse. Less commonly, massive overdoses have been known to cause circulatory collapse from vasodilation and bradycardia. Opioid overdoses can be rapidly reversed through the use of opioid antagonists, naloxone being the most widely used example. Opioid antagonists work by binding competitively to μ-opioid receptors and displacing opioid agonists. Additional doses of naloxone may be necessary and supportive care should be given to prevent hypoxic brain injury by monitoring vital signs.
== Structure == ATP consists of three parts: a sugar, an amine base, and a phosphate group. More specifically, ATP consists of an adenine attached by the #9-nitrogen atom to the 1′ carbon atom of a sugar (ribose), which in turn is attached at the 5' carbon atom of the sugar to a triphosphate group. In its many reactions related to metabolism, the adenine and sugar groups remain unchanged, but the triphosphate is converted to di- and monophosphate, giving respectively the derivatives ADP and AMP. The three phosphoryl groups are labeled as alpha (α), beta (β), and, for the terminal phosphate, gamma (γ). In neutral solution, ionized ATP exists mostly as ATP4−, with a small proportion of ATP3−.
which is 50 times bigger than the force on the left piston. The difference between force and pressure is important: the additional pressure is exerted against the entire area of the larger piston. Since there is 50 times the area, 50 times as much force is exerted on the larger piston. Thus, the larger piston will support a 50 N load – fifty times the load on the smaller piston. Forces can be multiplied using such a device. One newton input produces 50 newtons output. By further increasing the area of the larger piston (or reducing the area of the smaller piston), forces can be multiplied, in principle, by any amount. Pascal's principle underlies the operation of the hydraulic press. The hydraulic press does not violate energy conservation, because a decrease in distance moved compensates for the increase in force. When the small piston is moved downward 100 centimeters, the large piston will be raised only one-fiftieth of this, or 2 centimeters. The input force multiplied by the distance moved by the smaller piston is equal to the output force multiplied by the distance moved by the larger piston; this is one more example of a simple machine operating on the same principle as a mechanical lever. A typical application of Pascal's principle for gases and liquids is the automobile lift seen in many service stations (the hydraulic jack). Increased air pressure produced by an air compressor is transmitted through the air to the surface of oil in an underground reservoir. The oil, in turn, transmits the pressure to a piston, which lifts the automobile.
Sources: en.wikipedia.org
SR9009 is a synthetic compound investigated as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is used in preclinical research on circadian rhythm and metabolism. It is not an approved drug.
No. It has no approved medical indication, and human safety and efficacy data are limited. It appears in research chemical markets and is banned by some sports authorities.
Natural ligands include heme and certain metabolites; SR9009 is a synthetic small molecule with higher potency and selectivity in some assays. Its effects depend on cell type and timing. It is not a naturally occurring compound.
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.