NR1D1 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 2025-10-13. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
Several misconceptions surround SR9009. It is often described as a SARM, a steroid, or an exercise pill, but its known target is the REV-ERB receptor family. Rodent studies have examined exercise capacity and metabolic markers, yet human outcomes remain unproven. Oral bioavailability appears low in animals, and human pharmacokinetics are not well characterized. Online products may contain impurities or different compounds, so identity and purity testing are important for research use.
| 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 studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.
Fully annexed localities (Auteuil, Batignolles-Monceau, Belleville, Bercy, Charonne, Grenelle, La Chapelle, La Villette, Montmartre, Passy, and Vaugirard): Everything disappeared along with the registers of the Parisian arrondissements—both originals and duplicates. Partially annexed localities (Aubervilliers, Bagnolet, Clichy, Gentilly, Ivry, Montrouge, Neuilly, Pantin, Le Pré-Saint-Gervais, Saint-Mandé, Saint-Ouen, and Vanves) or non-annexed areas (the rest of what is today known as the Petite Couronne): The originals, having been preserved locally, are still accessible in municipal archives unless transferred to the Departmental Archives of Hauts-de-Seine, Seine-Saint-Denis, or Val-de-Marne. The duplicates, however, were destroyed, except for the decennial tables covering 1793–1859.
Various bacteria Fungi Phylogenetically distant plants Nematodes like C. elegans Insects Fish Birds Various rodents Lagomorphs like rabbits Mammals (including humans) Distribution within (higher) organisms also appears to be ubiquitous as it has been found in the:
Hypnotica was a class of somniferous drugs and substances tested in medicine of the 1890s and later. These include urethan, acetal, methylal, sulfonal, paraldehyde, amylenhydrate, hypnon, chloralurethan, ohloralamid, or chloralimid. Research about using medications to treat insomnia evolved throughout the last half of the 20th century. Treatment for insomnia in psychiatry dates back to 1869, when chloral hydrate was first used as a soporific. Barbiturates emerged as the first class of drugs in the early 1900s, after which chemical substitution allowed derivative compounds. Although they were the best drug family at the time (with less toxicity and fewer side effects), they were dangerous in overdose and tended to cause physical and psychological dependence. During the 1970s, quinazolinones and benzodiazepines were introduced as safer alternatives to replace barbiturates; by the late 1970s, benzodiazepines emerged as the safer drug. Benzodiazepines are not without their drawbacks; substance dependence is possible, and deaths from overdoses sometimes occur, especially in combination with alcohol or other depressants. Questions have been raised as to whether they disturb sleep architecture. Nonbenzodiazepines or Z-drugs like zolpidem were introduced in the 1980s and 1990s. Although it is clear that they are less toxic than barbiturates, their predecessors, comparative efficacy over benzodiazepines has not been established. Such efficacy is hard to determine without longitudinal studies.
Sources: en.wikipedia.org
==== Mycosporine-like amino acids ==== Mycosporine-like amino acids are small secondary metabolites produced by organisms that live in environments with high volumes of sunlight, usually marine environments.
=== Pharmacological === The medications available differ between substances. For opioid use disorder, opioid agonist maintenance treatment with methadone or buprenorphine is common. It retains people in treatment and suppresses illicit opioid use more effectively than placebo. A systematic review and meta-analysis of 15 trials and 36 cohort studies found that time spent receiving opioid agonist treatment was associated with lower all-cause and overdose mortality, with the risk of death around six times higher in the four weeks after treatment stopped. A Cochrane review also found that opioid substitution therapy reduces the risk of acquiring hepatitis C among people who inject drugs, with a larger reduction when combined with high-coverage needle and syringe programmes. For alcohol use disorder, oral naltrexone and acamprosate are recommended as first-line medications alongside psychosocial support, whereas trial evidence that disulfiram reduces drinking is weaker. For tobacco (nicotine) dependence, varenicline, cytisine and nicotine e-cigarettes are among the most effective aids for quitting long-term, followed closely by using two forms of nicotine replacement therapy at once (for example a patch together with gum or a lozenge). Bupropion is also used. No medication has been approved for cocaine or amphetamine (stimulant) use disorder, for which psychosocial treatment remains the principal care.
=== Genetically modified crops === The first transgenic crop, which incorporated an insecticidal PIP, contained a gene for the CRY toxin from Bacillus thuringiensis (B.t.) and was introduced in 1997. For the next ca 25 years the only insecticidal agents used in GMOs were the CRY and VIP toxins from various strains of B.t, which control a wide number of insect types. These are widely used with > 100 million hectares planted with B.t. modified crops in 2019. Since 2020 several novel agents have been engineered into plants and approved. ipd072Aa from Pseudomonas chlororaphis, ipd079Ea from Ophioglossum pendulum, and mpp75Aa1.1 from Brevibacillus laterosporus code for protein toxins. The trait dvsnf7 is an RNAi agent consisting of a double-stranded RNA transcript containing a 240 bp fragment of the WCR Snf7 gene of the western corn rootworm (Diabrotica virgifera virgifera).
Sources: en.wikipedia.org
== Practice == In the practice of chemistry, pure chemistry is the study of the fundamental principles of chemistry, while applied chemistry applies that knowledge to develop technology and solve real-world problems.
== Applications == In biochemistry, the process of breaking down large molecules by splitting their internal bonds is catabolism. Enzymes which catalyse bond cleavage are known as lyases, unless they operate by hydrolysis or oxidoreduction, in which case they are known as hydrolases and oxidoreductases respectively. In proteomics, cleaving agents are used in proteome analysis, where proteins are cleaved into smaller peptide fragments. Examples of cleaving agents used are cyanogen bromide, pepsin, and trypsin.
==== Auxiliary channel ==== The DisplayPort AUX channel is a half-duplex data channel used for miscellaneous additional data beyond video and audio, such as EDID (I2C) or CEC commands. This bidirectional data channel is required, since the video lane signals are unidirectional (simplex) from source to display. AUX signals are transmitted across a dedicated set of twisted-pair wires. DisplayPort 1.0 specified Manchester encoding with a 2 MBd signal rate (1 Mbit/s data rate). Version 1.2 of the DisplayPort standard introduced a second transmission mode called FAUX (Fast AUX), which operated at 720 Mbit/s with 8b/10b encoding (576 Mbit/s data rate), but it was deprecated in version 1.3.
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.
Legality depends on the country and the intended use. In many places it is not approved as a medicine and may be sold only as a research chemical. Importation or possession can be restricted, and sports organizations prohibit it.