Everything below concerns REV-ERB agonist. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-04-03. Numbers and descriptions here follow the published literature rather than marketing material.
Research interest in SR9009 grew from studies showing improved running endurance in mice after short treatment periods. Those experiments linked the compound to increased mitochondrial content and fatty acid oxidation in muscle, but the findings come from animal models and specific dosing schedules. Independent replication has been limited, and the pathways connecting REV-ERB activation to exercise performance are still being mapped. Whether similar responses occur in humans is an open question.
SR9009 is often grouped with compounds studied for circadian and metabolic regulation rather than with classical anabolic steroids. Its interactions with nuclear receptors differ from those of androgen receptor ligands, and its proposed mechanisms involve transcriptional control rather than direct hormone signaling. Some sources classify it as a metabolic modulator because of observed effects on energy utilization. The distinction matters for regulation and for interpreting research results across different compound classes.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C20H24ClN3O4S | Reported for the free base |
| Molecular weight | 437.9 g/mol | Calculated from the formula |
| Primary target | REV-ERBα and REV-ERBβ | Nuclear receptors involved in circadian regulation |
| Solubility | Soluble in DMSO and ethanol | Poorly soluble in water |
| Typical storage | -20 °C, desiccated | Protect from light and moisture |
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.
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.
=== ColdFusion 4 === Released in Nov 1998, version 4 is when the name was changed from "Cold Fusion" to "ColdFusion" - possibly to distinguish it from Cold fusion theory. The release also added the initial implementation of cfscript, support for locking (cflock), transactions (cftransaction), hierarchical exception handling (cftry/cfcatch), sandbox security, as well as many new tags and functions, including cfstoredproc, cfcache, cfswitch, and more.
When NBOMes are administered sublingually, numbness of the tongue and mouth followed by a metallic chemical taste was observed, and researchers describe this physical side effect as one of the main discriminants between NBOMe compounds and LSD.
== Nomenclature == This enzyme belongs to the family of oxidoreductases, specifically those acting on NADH or NADPH with a quinone or similar compound as acceptor. The systematic name of this enzyme class is 2-hydroxy-1,4-benzoquinone:NADH oxidoreductase. Other names in common use include hydroxybenzoquinone reductase, 1,2,4-trihydroxybenzene:NAD oxidoreductase, and NADH:2-hydroxy-1,4-benzoquinone oxidoreductase.
=== List of side effects === Cardiovascular: Myocardial infarction; stroke; heart block; arrhythmias; hypotension, particularly orthostatic hypotension; hypertension; tachycardia; palpitation. Psychiatric: Confusional states (especially in the elderly) with hallucinations, disorientation, delusions, anxiety, restlessness, agitation; hypomania; exacerbation of psychosis; insomnia, panic, and nightmares. Neurological: Seizures; incoordination; ataxia; tremors; peripheral neuropathy; numbness, tingling, and paresthesias of extremities; extrapyramidal symptoms; drowsiness; dizziness; weakness and fatigue; headache; syndrome of inappropriate ADH (antidiuretic hormone) secretion; tinnitus; alteration in EEG patterns. Anticholinergic: Paralytic ileus; hyperpyrexia; urinary retention, delayed micturition, dilatation of the urinary tract; constipation; blurred vision, disturbance of accommodation, increased intraocular pressure, mydriasis; dry mouth and rarely associated sublingual adentitis. Allergic: Drug fever; petechiae, skin rash, urticaria, itching, photosensitization (avoid excessive exposure to sunlight); edema (general, or of face and tongue). Hematologic: Agranulocytosis; bone marrow depression; leukopenia;thrombocytopenia; purpura; eosinophilia. Gastrointestinal: Nausea and vomiting; anorexia; epigastric distress; diarrhea; peculiar taste; stomatitis; abdominal cramps; black tongue.
Gs exerts its effects via two pathways. Firstly, it directly opens L-type calcium channels (LTCC) in the plasma membrane. Secondly, it renders adenylate cyclase activated, resulting in an increase of cAMP, activating protein kinase A (PKA) which in turn phosphorylates several targets, such as phospholamban, LTCC, Troponin I (TnI), and potassium channels. The phosphorylation of phospholamban deactivates its own function which normally inhibits SERCA on the sarcoplasmic reticulum (SR) in cardiac myocytes. Due to this, more calcium enters the SR and is therefore available for the next contraction. LTCC phosphorylation increases its open probability and therefore allows more calcium to enter the myocyte upon cell depolarisation. Both of these mechanisms increase the available calcium for contraction and therefore increase inotropy. Conversely, TnI phosphorylation results in its facilitated dissociation of calcium from troponin C (TnC) which speeds the muscle relaxation (positive lusitropy). Potassium channel phosphorylation increases its open probability which results in shorter refractory period (because the cell repolarises faster), also increasing lusitropy. Furthermore, in nodal cells such as in the SA node, cAMP directly binds to and opens the HCN channels, increasing their open probability, which increases chronotropy.
Sources: en.wikipedia.org
Messenger RNA (mRNA) carries information about a protein sequence to the ribosomes, the protein synthesis factories in the cell. It is coded so that every three nucleotides (a codon) corresponds to one amino acid. In eukaryotic cells, once precursor mRNA (pre-mRNA) has been transcribed from DNA, it is processed to mature mRNA. This removes its introns—non-coding sections of the pre-mRNA. The mRNA is then exported from the nucleus to the cytoplasm, where it is bound to ribosomes and translated into its corresponding protein form with the help of tRNA. In prokaryotic cells, which do not have nucleus and cytoplasm compartments, mRNA can bind to ribosomes while it is being transcribed from DNA. After a certain amount of time, the message degrades into its component nucleotides with the assistance of ribonucleases. Transfer RNA (tRNA) is a small RNA chain of about 80 nucleotides that transfers a specific amino acid to a growing polypeptide chain at the ribosomal site of protein synthesis during translation. It has sites for amino acid attachment and an anticodon region for codon recognition that binds to a specific sequence on the messenger RNA chain through hydrogen bonding.
The Prausnitz–Küstner test (PK test, Prausnitz-Küstner reaction) is an immunologic test formerly used by physicians to determine if a patient has an allergic reaction to a specific antigen. The test has been replaced by the safer skin prick test. The PK test involves transferring serum from the test subject to another healthy person, essentially using the second person as a mixing vessel for antibodies and antigen. This is a pathway for transmission of blood-borne ailments like variant Creutzfeldt–Jakob disease, AIDS, and others, which is why the test is no longer recommended. Or in simple words, a test for the presence of immediate hypersensitivity in humans; test serum from an atopic individual is injected intradermally into a normal subject; the normal subject is challenged 24–48 hours later with the antigen suspected of causing the immediate hypersensitivity reaction in the atopic individual.
CAVE systems included multiple flat screen displays, typically at least three walls to surround the human player, and incorporated some type of tracking sensor system to match the images on the walls to what direction the player was looking. Early applications of CAVE system were game-based demonstrations, but the cost remained prohibitive for commercial deployment even through the 2010s. Around this same time in the 1990s, major innovations in real-time 3D graphics had been made across computer, console, and arcade video games, and with further improvements in affordable consumer technologies, arcade games began to decline as they could not compete with these innovations. Arcade game manufacturers instead focused on offering games that could not easily be replicated at home, which included the introduction of VR-based arcade games. For example, the Virtuality Group produced its Virtuality line of arcade games starting in the early 1990s that typically included a VR headset with head-tracking and other features. However, the cost and upkeep of these machines made it difficult to continue support for them. There remained strong interest from academics to explore what VR, along with augmented reality and other mixed reality systems, could bring to video games, through the 2000s, but these games were mostly prepared for research proof-of-concepts to demonstrate the interaction of VR hardware, software, and human motion rather than for commercial release, since hardware costs were still high.
== History == BMS-986122 was first described in 2013, and along with BMS-986121, was the first selective MOR PAM to be discovered. They were identified via high-throughput screening (HTS). Their characterization led to the discovery of a putative conserved allosteric site across the MOR and other opioid receptors.
Sources: en.wikipedia.org
It is a synthetic REV-ERB agonist used mainly in preclinical research. It is not an approved medicine for human use.
It binds to REV-ERBα and REV-ERBβ, nuclear receptors involved in circadian and metabolic gene regulation. This can alter transcription of genes related to lipid and glucose metabolism in experimental models.
No controlled human trials have established that effect. Endurance findings come primarily from rodent studies, and human responses remain unknown.
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.