NR1D2 comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Last reviewed on 2026-08-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
In laboratory settings, SR9009 is commonly identified by its molecular structure and its interaction with REV-ERB receptors. Vendors may list it under synonyms such as Stenabolic or REV-ERB agonist, but those names do not define purity or identity. Analytical confirmation typically uses high-performance liquid chromatography with ultraviolet detection or liquid chromatography–mass spectrometry. A reference standard is needed to compare retention time and mass spectrum, because the compound can be confused with related research chemicals.
Handling practices for SR9009 focus on minimizing degradation and contamination. The solid is generally stored desiccated at or below -20 °C, protected from light and moisture. Stock solutions are often prepared in dimethyl sulfoxide or ethanol, then aliquoted to avoid repeated freeze–thaw cycles. Aqueous solubility is low, so formulations for animal studies may require cosolvents or suspending agents. Personnel should follow institutional chemical safety procedures, because toxicological data for humans are incomplete.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small molecule; not a steroid or peptide. |
| Primary targets | NR1D1 and NR1D2 | Also known as REV-ERBα and REV-ERBβ. |
| Studied routes | Intraperitoneal in rodents | Oral bioavailability in humans is not established. |
| Human approval | No approved therapeutic indication | No recognized clinical use. |
| Key uncertainty | Human physiological effects | Preclinical findings may not translate. |
SR9009 is a synthetic small molecule developed as a REV-ERB agonist. It binds to REV-ERBα and REV-ERBβ, nuclear receptors that help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, the compound alters lipid and glucose handling and influences skeletal muscle oxidative capacity. Its exact effects in humans remain largely uncharacterized because controlled clinical trials have not been reported. The molecule is frequently described in preclinical literature as a metabolic modulator.
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.
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.
Scientific discussion of SR9009 often separates animal evidence from human anecdote. Rodent studies provide controlled data on endurance, metabolism, and gene expression, but they use specific strains, doses, and treatment durations. Human reports are mostly uncontrolled and cannot establish cause and effect. Open questions include oral bioavailability, tissue distribution, metabolic stability, and long-term effects. Review articles generally call for more rigorous pharmacokinetic and safety research before any clinical use could be considered.
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.
== Properties == The finest turquoise reaches a maximum Mohs hardness of just under 6, or slightly more than window glass. Characteristically a cryptocrystalline mineral, turquoise almost never forms single crystals, and all of its properties are highly variable. X-ray diffraction testing shows its crystal system to be triclinic. With lower hardness comes greater porosity. The lustre of turquoise is typically waxy to subvitreous, and its transparency is usually opaque, but may be semitranslucent in thin sections. Colour is as variable as the mineral's other properties, ranging from white to a powder blue to a sky blue and from a blue-green to a yellowish green. The blue is attributed to idiochromatic copper while the green may be the result of iron impurities (replacing copper.) The refractive index of turquoise varies from 1.61 to 1.65 on the three crystal axes, with birefringence 0.040, biaxial positive, as measured from rare single crystals. Crushed turquoise is soluble in hot hydrochloric acid. Its streak is white to greenish to blue, and its fracture is smooth to conchoidal. Despite its low hardness relative to other gems, turquoise takes a good polish. Turquoise may also be peppered with flecks of pyrite or interspersed with dark, spidery limonite veining. Turquoise is nearly always cryptocrystalline and massive and assumes no definite external shape. Crystals, even at the microscopic scale, are rare. Typically the form is a vein or fracture filling, nodular, or botryoidal in habit. Stalactite forms have been reported.
Complete blood count and reticulocyte count; in active G6PD deficiency, Heinz bodies can be seen in red blood cells on a blood film; Liver enzymes (to exclude other causes of jaundice); Lactate dehydrogenase (elevated in hemolysis and a marker of hemolytic severity) Haptoglobin (decreased in hemolysis); A "direct antiglobulin test" (Coombs' test) – this should be negative, as hemolysis in G6PD is not immune-mediated; When there are sufficient grounds to suspect G6PD, a direct test for G6PD is the "Beutler fluorescent spot test", which has largely replaced an older test (the Motulsky dye-decolouration test). Other possibilities are direct DNA testing and/or sequencing of the G6PD gene. The Beutler fluorescent spot test is a rapid and inexpensive test that visually identifies NADPH produced by G6PD under ultraviolet light. When the blood spot does not fluoresce, the test is positive; it can be falsely negative in patients who are actively hemolysing. It can therefore only be done 2–3 weeks after a hemolytic episode. When a macrophage in the spleen identifies an RBC with a Heinz body, it removes the precipitate and a small piece of the membrane, leading to characteristic "bite cells". However, if a large number of Heinz bodies are produced, as occurs in G6PD deficiency, some Heinz bodies will be visible when viewing RBCs stained with crystal violet. This easy and inexpensive test can lead to an initial presumption of G6PD deficiency, which can be confirmed with the other tests.
ANUBL1; BAG1; BAT3/BAG6; C1orf131; DDI1; DDI2; FAU; HERPUD1; HERPUD2; HOPS; IKBKB; ISG15; LOC391257; MIDN; NEDD8; OASL; PARK2; RAD23A; RAD23B; RPS27A; SACS; 8U SF3A1; SUMO1; SUMO2; SUMO3; SUMO4; TMUB1; TMUB2; UBA52; UBB; UBC; UBD; UBFD1; UBL4A; UBL4B; UBL7; UBLCP1; UBQLN1; UBQLN2; UBQLN3; UBQLN4; UBQLNL; UBTD1; UBTD2; UHRF1; UHRF2;
Sources: en.wikipedia.org
== Function == The encoded protein, commonly abbreviated IRR, is an orphan receptor and one of three receptor tyrosine kinases in the insulin receptor family, alongside the insulin receptor and insulin-like growth factor 1 receptor. No endogenous peptide or protein ligand is known for IRR. In experimental systems, extracellular pH above approximately 7.9 activates the receptor and triggers autophosphorylation. The Human Protein Atlas classifies INSRR RNA expression as cell type enhanced in renal collecting-duct intercalated cells. In rodents, IRR has been localized to non-A intercalated cells; a rat study reported basolateral localization in type B intercalated cells of the cortical collecting duct. In mice, inactivation of Insrr impairs urinary bicarbonate excretion following alkali loading, supporting a role for the receptor in renal acid–base homeostasis. A 2023 cryo-electron microscopy study of the human IRR ectodomain, combined with mutagenesis and cell-based assays, supported a model in which alkaline pH produces electrostatic repulsion involving pH-sensitive motifs at an interprotomer interface, disrupting the autoinhibited state and promoting a scissor-like rotation into a T-shaped active conformation.
=== Assisted children === The Paris Archives hold registers for the admission of foundlings, abandoned children, orphans, and rescued minors, referred to as “assisted children.” These records span from 1742 to 1924, with a gap between 1748 and 1754. Available online, they provide registration numbers that allow access to the admission files on-site.
Among other contributions, his research introduced oncocin, a novel antimicrobial peptide optimized for treating Gram-negative bacteria, showing effective activity and improved stability in mouse serum without causing lysis or toxicity. Later, he showed that LL-37 acts through pore formation in membranes made of unsaturated lipids whereas it yields membrane modulation in saturated lipids, suggesting new design strategies for antimicrobial peptide drugs.
Sources: en.wikipedia.org
=== Sweat drug screen === Sweat patches are attached to the skin to collect sweat over a long period of time (up to 14 days). These are used by child protective services, parole departments, and other government institutions concerned with drug use over long periods, when urine testing is not practical. There are also surface drug tests that test for the metabolite of parent drug groups in the residue of drugs left in sweat. An example of a rapid, non-invasive, sweat-based drug test is fingerprint drug screening. This 10 minute fingerprint test is in use by a variety of organisations in the UK and beyond, including within workplaces, drug treatment and family safeguarding services at airport border control (to detect drug mules) and in mortuaries to assist in investigations into cause of death.
== History == The impact factor was devised by Eugene Garfield, the founder of the Institute for Scientific Information (ISI) in Philadelphia. Impact factors began to be calculated yearly starting from 1975 for journals listed in the Journal Citation Reports (JCR). ISI was acquired by Thomson Scientific & Healthcare in 1992, and became known as Thomson ISI. In 2018, Thomson-Reuters spun off and sold ISI to Onex Corporation and Baring Private Equity Asia. They founded a new corporation, Clarivate, which continued publishing the JCR.
=== EU ban === The EU banned estradiol, progesterone, testosterone, zeranol, melengestrol acetate and trenbolone acetate. The first three are synthetic versions of endogenous hormones that are naturally produced in humans and animals, and in a wide range of foods, whereas the last two are synthetic, designed to mimic the behaviour of endogenous hormones. Zeranol (alpha-zearalanol) is produced semi-synthetically, but occurs naturally in some foods. It is one of several derivatives of zearalenone produced by certain Fusarium. Although its occurrence in animal products can be partly due to ingestion of such feeds, alpha-zearalanol can be produced endogenously in ruminants that have ingested zearalenone and some zearalenone derivatives. The EU did not impose an absolute ban. Under veterinary supervision, cattle farmers were permitted to administer the synthetic versions of natural hormones for cost-reduction and possibly therapeutic purposes, such as synchronising oestrus cycles. All six hormones were licensed for use in the US and in Canada. Under the Agreement on the Application of Sanitary and Phytosanitary Measures, signatories have the right to impose restrictions on health and safety grounds subject to scientific analysis. The heart of the dispute was the fact that risk analysis is statistical, and thus unable to determine with absolute certainty the absence of health risks. While US and Canada beef producers claimed that beef produced with the use of hormones was safe, the EU asserted that it was not safe.
=== Emil: The Beefy Barbarian Bully === First aired: 15 October 2009 Emil is a self-proclaimed Assyrian bully who was brought to the show by his victims, Anthony and Mo. Mo's girlfriend is friends with the bully and she feels bad because he has made their lives miserable with his bullying. Emil was pitted against emerging MMA fighter Nick Gaston, who forced him to tap out five times in one minute, thirty six seconds. He withdrew from the second round, the only contestant having done so to this point. Anthony and Mo won $10,000 and an apology from Emil.
Sources: en.wikipedia.org
It is a synthetic compound that acts as an agonist at REV-ERBα and REV-ERBβ. It is used mainly as a research chemical to study circadian and metabolic pathways. It is not approved for human therapeutic use.
REV-ERB receptors generally repress transcription when bound by natural heme. SR9009 is described as an agonist that enhances this repressive activity. The result is altered expression of clock and metabolic genes.
Published controlled human trials are lacking. Some sources cite limited or unofficial reports, but these do not establish safety or efficacy. Claims about human performance effects remain unverified.
Liquid chromatography–mass spectrometry is common for identity and purity checks. High-performance liquid chromatography with ultraviolet detection can also be used. Both methods require a suitable reference standard.