If you have been reading about NR1D1 and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Last reviewed on 2026-08-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
SR9009 is not approved as a medicine by major regulatory agencies. It is commonly sold as a research chemical, a category that may fall outside customary drug approval and quality rules. In sports, the World Anti-Doping Agency lists SR9009 as a prohibited substance. Athletes who use it can face sanctions if it is detected in a sample. Legal status varies by country, and importation may be restricted. Enforcement practices differ across borders.
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.
| 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 |
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not an approved medicine and has no established human therapeutic use. The compound appears in scientific literature as a tool for probing circadian and metabolic regulation. Online sellers often label it as a research chemical, sometimes using the nickname Stenabolic. Its chemical identity is distinct from selective androgen receptor modulators, stimulants, and peroxisome proliferator-activated receptor delta agonists. Researchers use it mainly in cell and animal experiments.
At the molecular level, SR9009 binds REV-ERBα and REV-ERBβ and alters their repressive activity on target genes. These nuclear receptors help regulate the circadian clock, lipid synthesis, glucose metabolism, and inflammatory pathways. By changing transcription, the compound can shift the timing or magnitude of downstream metabolic processes in model systems. It does not act through androgen receptors or adenosine receptors, which distinguishes it from several substances sold for athletic performance. Whether the same transcriptional changes occur in humans at tolerable exposures remains an open question because controlled human studies are lacking.
Preclinical reports describe effects on exercise endurance, mitochondrial content, and lipid profiles in rodents, but these findings come from specific experimental conditions. Many studies use high doses or delivery methods that may not translate directly to human use. SR9009 has been reported to have low oral bioavailability and a short half-life, which complicates interpretation of oral dosing studies. It is not established as safe or effective for any indication. Literature discussions often separate its pharmacological mechanism from unverified claims made in fitness and supplement markets.
Laboratory identification of SR9009 typically relies on chromatographic separation coupled to mass spectrometry, often with ultraviolet detection as a secondary check. Nuclear magnetic resonance spectroscopy can confirm molecular structure when a reference standard is available. Because many suppliers sell the compound as a research chemical, independent identity testing is important for experimental reproducibility. A single retention time is not sufficient proof of identity, especially when related compounds may be present. Purity assessments usually report a percentage based on area normalization.
SR9009 is generally described as poorly soluble in water and more soluble in organic solvents such as dimethyl sulfoxide and ethanol. Stock solutions are commonly prepared in an organic solvent before dilution into an aqueous buffer or vehicle. Precipitation can occur if the organic fraction is reduced too quickly or if the final concentration exceeds the compound's solubility limit. Sonication or gentle warming may aid dissolution in some protocols, but excessive heat can promote degradation. Container material and pH can also influence observed solubility.
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.
The Hammer Editor, the engine's official level editor, uses rendering and compiling tools included in the SDK to create maps using the binary space partitioning (BSP) method. Level geometry is created with 3D polygons called brushes; each face can be assigned a texture which also defines the properties of the surface such as the sounds used for footsteps. Faces can also be converted into a displacement allowing for more natural shapes such as hills to be created. Scenery objects or complex geometry can be imported as separate 3D models from the game directory. These models can also be used as physics objects or interactive props. The editor also features an in-depth logic I/O system that can be used to create complex interactive elements. Signals to trigger different responses or change the state of an entity can be sent between entities such as buttons, NPCs, intangible trigger brushes, and map props.
Amane Waseda reported δD of oil samples in northeast Japan to increase from around −130‰ to around −110‰ with higher maturity. At low thermal maturity, dos Santos Neto and Hayes reported δD of saturate fraction of oil in Portiguar Basin derived from a lacustrine environment is -90‰, and from a marine-evaporitic environment is -120‰ to −135‰. Bulk analysis of oil, which yields a complex mixture of organic compounds, obscures much of the valuable information. Switching to compound-specific study greatly expanded our understanding of hydrogen isotopes of oil. Analyzing HIC at the compound level avoids problems from differences in exchange rates, simplifies sources and products relationships, and draws a much more detailed picture. δDs of n-alkanes are generally thought to be representative of oil as they are the major components. Schimmelmann et al. confirmed that alkane fractions have almost the same DHRs as whole oils. Depending on source material type and maturity, δD of n-alkanes can vary from −100‰ to −180‰. A common phenomenon of various oil and matured rock derived n-alkanes is a trend of increasing δD with chain length. For example, Li et al. analyzed oils from the Western Canada Sedimentary Basin and found δD increased between 20‰ and 40‰ from C13 to C27. This "isotope slope" is an artifact of kinetic fractionation associated with thermal cracking of carbon chains. This trend has been experimentally reproduced and theoretically modeled by Tang et al. N-alkanes are also known to preserve detailed information of source material. Li et al.
Calvo Sotelo did not manage to stop the internal crisis of UCD ─ the "critical sector" led by Miguel Herrero y Rodríguez de Miñón and Oscar Alzaga approached Alianza Popular and the "social democratic sector" led by Francisco Fernández Ordóñez approached PSOE ─ which was aggravated by the defeat in the Galician elections of October 1981, in which the centrists were overtaken by Alianza Popular. Calvo Sotelo then tried to recompose the unity of the party by personally assuming the presidency of the party and reshuffling his government, in which the "strong man" became the vice-president Rodolfo Martín Villa, but at the beginning of 1982, the "flight" of deputies to Alianza Popular began. In May, UCD suffered a new setback in the Andalusian autonomic elections, in which the PSOE obtained the absolute majority and Alianza Popular again surpassed UCD in votes. Then Landelino Lavilla took over the presidency of the party but also failed to stop the "bleeding of splits". The Christian Democrats founded a new party, the Partido Demócrata Popular, and even Suárez left UCD to form his own, the Centro Democrático y Social. Faced with this situation, a broken and disbanded party, Calvo Sotelo dissolved the Cortes in August 1982 and called general elections.
Sources: en.wikipedia.org
Ethanol is only one of several types of chemical alcohols, and has a variety of analogues. Most other alcohols are considered poisonous. In general, higher alcohols are less toxic. Alcoholic beverages are sometimes laced with toxic alcohols. The toxicity of isopropyl alcohol is about twice that of ethanol; a mild, brief exposure to isopropyl alcohol is unlikely to cause any serious harm, although ingesting significant quantities can lead to vomiting, abdominal pain, and internal bleeding. Methanol is the most toxic alcohol. Ingestion of as little as 3.16 grams of methanol can cause irreversible optic nerve damage, and the oral LD50 for humans is estimated to be 56.2 grams. Many methanol poisoning incidents have occurred through history. n-Butanol is reported to produce similar effects to those of ethanol and relatively low toxicity (one-sixth of that of ethanol in one rat study). However, its vapors can produce eye irritation, and inhalation can cause pulmonary edema. Acetone (propanone) is a ketone rather than an alcohol, and is reported to produce similar toxic effects; it can be extremely damaging to the cornea. Although ethanol is the most prevalent alcohol in alcoholic beverages, alcoholic beverages contain several types of psychoactive alcohols, that are categorized as primary, secondary, or tertiary. Primary and secondary alcohols, are oxidized to aldehydes, and ketones, respectively, while tertiary alcohols are generally resistant to oxidation. The Lucas test differentiates between primary, secondary, and tertiary alcohols.
== Problems faced in drug delivery == Other problems persist besides just simply getting through the blood–brain barrier. The first of these is that a lot of times, even if a compound transverses the barrier, it does not do it in a way that the drug is in a therapeutically relevant concentration. This can have many causes, the most simple being that the way the drug was produced only allows a small amount to pass through the barrier. Another cause of this would be the binding to other proteins in the body rendering the drug ineffective to either be therapeutically active or able to pass through the barrier with the adhered protein. Another problem that must be accounted for is the presence of enzymes in the brain tissue that could render the drug inactive. The drug may be able to pass through the membrane fine, but will be deconstructed once it is inside the brain tissue rendering it useless. All of these are problems that must be addressed and accounted for in trying to deliver effective drug solutions to the brain tissue.
=== Infection === Cirrhosis can cause immune system dysfunction, leading to infection. Signs and symptoms of infection may be nonspecific and are more difficult to recognize (for example, worsening encephalopathy but no fever). Moreover, infections in cirrhosis are major triggers for other complications (ascites, variceal bleeding, hepatic encephalopathy, organ failures, death). Those with cirrhosis are at increased risk of infections as well as increased mortality from infections. This is due to a combination of factors, including cirrhosis-associated immune dysfunction, reduced gut barrier function, reduced bile flow, and changes in the gut microbiota, with an increase in pathobionts (native bacteria that, under certain conditions, may cause infection). Cirrhosis associated immune dysfunction is caused by reduced complement component synthesis in the liver including C3, C4 and reduced total complement activity (CH50). The complement system is a part of the innate immune system and assists immune cells and antibodies in destroying pathogens. The liver produces complement factors, but this may be reduced in cirrhosis, raising the risk of infections. Acute phase proteins (which help mount an immune response) and soluble pattern recognition receptors (which help immune cells to identify pathogens) are also reduced in those with cirrhosis, leading to further immune dysfunction. Cirrhosis is also associated with reduced Kupfer cell function, further increasing the risk for infections. Kupfer cells are resident macrophages in the liver, which help to destroy pathogens.
Sources: en.wikipedia.org
== Mechanism of action == Ipglycermides bind at the interface of the iPGM phosphotransferase and phosphatase domains as revealed in several co-crystal structures obtained with C. elegans (5KGN, 7KNF, 7KNG, 7TL7) and Staphylococcus aureus (7TL8) iPGMs and a variety of ipglycermides. Lariate ipglycermides containing either a terminal cysteine or hydroxamic acid have sub-nanomolar affinity for C. elegans iPGM, while truncated analogs, such as ipglycermide Ce-2d bind potently in the low nanomolar range.
=== Medication === Opioid replacement therapy (ORT), also known as opioid substitution therapy (OST), Medication for Addiction Treatment (MAT), or Medications for Opioid Use Disorder (MOUD), involves replacing an opioid, such as heroin. Commonly used drugs for ORT are methadone and buprenorphine/naloxone (Suboxone), which are taken under medical supervision. Buprenorphine/naloxone is usually preferred over methadone because of its safety profile, which is considered significantly better, primarily regarding its risk of overdose and effects on the heart (QTc prolongation). Buprenorphine/naloxone, methadone, and naltrexone are approved by the U.S. Food and Drug Administration (FDA) for medication-assisted treatment (MAT). In the U.S., the Substance Abuse and Mental Health Services Administration (SAMHSA) certifies opioid treatment programs (OTPs), where methadone can be dispensed at methadone clinics. As of 2023, the Waiver Elimination (MAT Act), also known as the "Omnibus Bill", removed the federal requirement for medical providers to obtain a waiver to prescribe buprenorphine, in an attempt to increase access to OUD treatment. The driving principle behind ORT is the patient's reclamation of a self-directed life. ORT facilitates this process by reducing symptoms of drug withdrawal and drug cravings. In some countries (not the U.S. or Australia), regulations enforce a limited time for people on ORT programs that conclude when a stable economic and psychosocial situation is achieved.
== Pharmacokinetics == The molecular weight, bioavailability, protein binding, elimination half-life, the time to achieve maximum plasma concentration and binding affinity are present in the table below.
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.
Its legal status depends on the country and intended use. It is not an approved medicine in major jurisdictions. In sport, it is prohibited by anti-doping rules.