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 2025-09-24. 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.
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.
Most published work on SR9009 consists of preclinical studies. It is widely sold as a research chemical, a category that does not imply safety, efficacy, or pharmaceutical-grade quality. Sports anti-doping organizations have listed SR9009 as a prohibited substance, and its presence in an athlete sample can lead to sanctions. Legal status differs by country; in several jurisdictions it is not approved for human consumption and may be treated as an unapproved new drug.
| 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. |
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.
A study by Aphekom comparing ten large French cities showed that Le Havre is the least polluted urban commune of France. Le Havre is also the third best city in France with more than 100,000 inhabitants for air quality. A Carbon accounting showed in 2009 that the municipality ejected some 32,500 tonnes of CO2 per year. In 2011 the average annual emissions of sulfur dioxide by industry was between three micrograms per cubic metre in the centre of Le Havre to twelve micrograms per cubic metre in the district of Caucriauville. The municipality has set a target to reduce emissions of CO2 by 3% per year. To achieve this solar panels have been installed on several municipal buildings (city hall, hanging gardens). Since 2008, Le Havre has been part of the network of Energy Cities and, in this context, it applies the steps of Agenda 21 and an Environmental Approach to Urban Planning. The city has received many awards of eco-labels several times (Energy of the Future label in 2009–2011, sustainable Earth label in 2009). Since 1998, Le Havre's beach has received the Blue Flag yearly thanks to its range of facilities, which extend over 30,000 m2. Le Havre has kept extensive green areas (750 hectares or 41 m2 per inhabitant), the two largest areas are the Montgeon Forest and Rouelles Park which are both located in the upper town. The gardens of the Priory of Graville and the hanging gardens offer views of the lower city. In the city centre, Saint-Roch Square and the City Hall Gardens provide the people with urban recreation areas.
=== Glycolysis === When more R5P is needed than NADPH, R5P can be formed through glycolytic intermediates. Glucose 6-phosphate is converted to fructose 6-phosphate (F6P) and glyceraldehyde 3-phosphate (G3P) during glycolysis. Transketolase and transaldolase convert two molecules of F6P and one molecule of G3P to three molecules of R5P. During rapid cell growth, higher quantities of R5P and NADPH are needed for nucleotide and fatty acid synthesis, respectively. Glycolytic intermediates can be diverted toward the non-oxidative phase of PPP by the expression of the gene for pyruvate kinase isozyme, PKM. PKM creates a bottleneck in the glycolytic pathway, allowing intermediates to be utilized by the PPP to synthesize NADPH and R5P. This process is further enabled by triosephosphate isomerase inhibition by phosphoenolpyruvate, the PKM substrate.
=== Enzyme activity === Enzyme activity is a measure of the quantity of active enzyme present and is thus dependent on various physical conditions, which should be specified. It is calculated using the following formula:
Sources: en.wikipedia.org
where ρf is the density of the fluid, Vdisp is the volume of the displaced body of liquid, and g is the gravitational acceleration at the location in question. If this volume of liquid is replaced by a solid body of exactly the same shape, the force the liquid exerts on it must be exactly the same as above. In other words, the "buoyancy force" on a submerged body is directed in the opposite direction to gravity and is equal in magnitude to
=== Launch === At 8:04:13 a.m. EST, May 15, 1963, Faith 7 was launched from Launch Complex 14. At T+60 seconds, the Atlas started its pitch program. Shortly afterward, MA-9 passed through max Q. At T+2 minutes 14 seconds Cooper felt BECO (Booster Engine Cutoff) and staging. The two Atlas booster engines had been left behind. The Launch Escape Tower was then jettisoned. At T+3 minutes the cabin pressure sealed at 5.5 psi (38 kPa). Cooper reported, "Faith 7 is all go."
Stomach (when combined with gimeracil and oteracil) Breast (with uracil) Gallbladder Lung (specifically adenocarcinoma, typically with uracil) Colorectal (usually when combined with gimeracil and oteracil) Head and neck Liver (with uracil) Pancreatic It is often given in combination with drugs that alter its bioavailability and toxicity such as gimeracil, oteracil or uracil. These agents achieve this by inhibiting the enzyme dihydropyrimidine dehydrogenase (uracil/gimeracil) or orotate phosphoribosyltransferase (oteracil).
=== As an invasive species === Although listed as an invasive species in several countries, one source reports that M. oleifera has "not been observed invading intact habitats or displacing native flora", so "should be regarded at present as a widely cultivated species with low invasive potential."
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.
It is a synthetic compound studied as an agonist of REV-ERB nuclear receptors. It is not an approved medicine and has mainly been examined in laboratory and animal research.