If you have been reading about research chemical 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.
Updated 2026-02-05. Numbers and descriptions here follow the published literature rather than marketing material.
SR9009 is a synthetic small molecule studied as an agonist of REV-ERB nuclear receptors. REV-ERB alpha and REV-ERB beta help regulate circadian rhythms and metabolic gene expression. In laboratory research, SR9009 has been used to probe how these receptors affect skeletal muscle, liver, and adipose tissue. The compound was identified in academic drug-discovery work and is often described in scientific literature by its chemical name and research code. It is not an approved medicine, and human clinical data remain limited or absent.
SR9009 binds REV-ERB receptors and alters their repressive activity on target genes. This action can change transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. In rodent studies, treated animals have shown changes in muscle oxidative capacity and exercise performance, though effects vary by dose, duration, and model. The precise molecular steps connecting receptor binding to whole-body outcomes are still an active area of investigation. Findings in animals do not automatically translate to humans.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small-molecule nuclear receptor ligand |
| Appearance | Off-white to pale yellow solid | Typical for research-grade powder |
| Solubility class | Soluble in DMSO; low water solubility | Common stock solutions use organic solvent |
| Typical stock solvent | Dimethyl sulfoxide | Used for laboratory assays |
| Common analytical method | HPLC with UV or mass detection | Used for identity and purity checks |
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.
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.
Research interest in SR9009 grew from studies of circadian biology and metabolic disease. Preclinical reports describe effects on exercise capacity, muscle metabolism, and blood lipid levels in rodents, but these findings come from controlled laboratory settings. The compound has low oral bioavailability in animals, which limits systemic exposure after swallowing. Investigators often use injected routes in experiments to achieve measurable plasma concentrations. Human clinical data are sparse, no approved therapeutic product exists, and whether animal effects translate to humans remains an open question.
Regulatory and sporting contexts treat SR9009 as a prohibited substance in many elite competitions. Its presence on banned lists reflects concerns about performance enhancement and unknown long-term safety. Analytical chemists have developed methods to detect the parent compound and its metabolites in urine and blood. Literature discussions distinguish between in vitro potency, animal pharmacology, and anecdotal human reports. The latter are difficult to verify because products sold online may lack purity or contain different compounds.
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.
In rodent studies, SR9009 has been reported to increase mitochondrial content in skeletal muscle and improve exercise endurance under some conditions. These findings led to popular descriptions such as an exercise mimetic, although that term oversimplifies the biology. Effects vary by dose, timing, tissue, and model. The compound's influence on circadian pathways means that time of administration can matter in experiments. Whether similar metabolic changes occur in humans remains largely unexplored in controlled published trials.
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.
== Use == The juice is drinkable, yet not palatable in its pure form due to its bitter taste. The bitterness diminishes as the hemp juice is mixed with fruit or vegetable juices. The hemp juice simultaneously heightens the fruity, savory and sweet taste of juices and foods in general. Therefore hemp juice is often used in drinks, certain food dishes, seasoning, food supplements, medical products as well as cosmetics. The press remnants can also be used as food supplements.
== Clinical significance == Impaired NO production is involved in the pathogenesis of several diseases such as hypertension, preeclampsia, diabetes mellitus, obesity, erectile dysfunction, and migraine. In this regard, a large number of studies showed that polymorphisms in NOS3 gene affect the susceptibility to these diseases. Although NOS3 is a highly polymorphic gene, three genetic polymorphisms in this gene have been widely studied: the single nucleotide polymorphisms (SNPs) g.-786T>C (where "g." denotes genomic change which results in a Glu298Asp change in the coded protein), located in NOS3 promoter and in exon 7, respectively, and the variable number of tandem repeats (VNTR) characterized by 27 bp repeat in intron 4. The C allele for the g.-786T>C polymorphism, which results in reduced eNOS expression and NO production, was associated with increased risk for hypertension, preeclampsia, diabetic nephropathy, and retinopathy, migraine, and erectile dysfunction. The presence of 'Asp' allele for the Glu298Asp polymorphism reduces eNOS activity, and was associated with higher susceptibility to hypertension, preeclampsia, diabetes mellitus, migraine, and erectile dysfunction. The VNTR in intron 4 affects eNOS expression, and the susceptibility to hypertension, preeclampsia, obesity, and diabetes mellitus. Growing evidence supports the association of diseases with NOS3 haplotypes (combination of alleles in close proximity, within a DNA block). This approach may be more informative than the analysis of genetic polymorphisms one by one.
== Downloadable content == The game's downloadable content (DLC) are playable stories that follow some of the residents in Wellington Wells that occur before, during, or after the main survivors' journey. They Came From Below: The first DLC story which follows lovers Roger Bacon and James Maxwell, two houseboys who are in search of their superior Dr. Faraday (who created Wellington Wells' technology) in an underground facility populated with hostile robots. The player, controlling Roger, fights with a futuristic raygun that can kill robot enemies or interact with special buttons (which can convert to a mace for melee combat). Roger also acquires a satellite device (which was shown in Arthur's story) capable of moving mechanisms or terrain, and a stopwatch-like "ChronoBomb" that can slow time. The story starts with Roger returning home from a shopping trip to discover Dr. Faraday's laboratory in ruins, and arriving just in time to discover Faraday falling through a portal in her laboratory. He quickly rouses James, who has been knocked unconscious, spurring the couple to attempt to find Dr. Faraday. After discovering a hatch located below the stairs to a hidden shelter, Roger and James discover a massive facility beneath Faraday's lab populated with hostile robots who speak in Faraday's voice. Roger make his way through the facility while James uses the blueprints to guide him via radio in an attempt to locate Faraday and stop the robot menace.
==== Luspatercept ==== Luspatercept is a drug used to treat anemia in adults with β-thalassemia, it can improve the maturation of red blood cells and reduce the need for frequent blood transfusions. It is administered by injection every three weeks. Luspatercept was authorised for use in the US in 2019 and by the European Medicines Agency in 2020.
Sources: en.wikipedia.org
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=== Immune functions === Vitamin A deficiency has been linked to compromised resistance to infectious diseases. In countries where early childhood vitamin A deficiency is common, vitamin A supplementation public health programs initiated in the 1980s were shown to reduce the incidence of diarrhea and measles, and all-cause mortality. Vitamin A deficiency also increases the risk of immune system over-reaction, leading to chronic inflammation in the intestinal system, stronger allergic reactions and autoimmune diseases. Lymphocytes and monocytes are types of white blood cells of the immune system. Lymphocytes include natural killer cells, which function in innate immunity, T cells for adaptive cellular immunity and B cells for antibody-driven adaptive humoral immunity. Monocytes differentiate into macrophages and dendritic cells. Some lymphocytes migrate to the thymus where they differentiate into several types of T cells, in some instances referred to as "killer" or "helper" T cells and further differentiate after leaving the thymus. Each subtype has functions driven by the types of cytokines secreted and organs to which the cells preferentially migrate, also described as trafficking or homing. Retinoic acid (RA) triggers receptors in bone marrow, resulting in generation of new white blood cells. RA regulates proliferation and differentiation of white blood cells, the directed movement of T cells to the intestinal system, and to the up- and down-regulation of lymphocyte function.
=== Start date and nomenclature === No consensus exists as to when the French Revolutionary Wars ended and the Napoleonic Wars began. Possible dates include 9 November 1799, when Bonaparte seized power on 18 Brumaire, the date according to the Republican Calendar then in use; 18 May 1803, when Britain and France ended the one short period of peace between 1792 and 1814; or 2 December 1804, when Bonaparte crowned himself Emperor. British historians occasionally refer to the nearly continuous period of warfare from 1792 to 1815 as the Great French War, or as the final phase of the Anglo-French Second Hundred Years' War, spanning the period 1689 to 1815. Historian Mike Rapport (2013) suggested using the term "French Wars" to unambiguously describe the entire period from 1792 to 1815. In France, the Napoleonic Wars are generally integrated with the French Revolutionary Wars: Les guerres de la Révolution et de l'Empire. German historiography may count the War of the Second Coalition (1798/9–1801/2), during which Napoleon had seized power, as the Erster Napoleonischer Krieg ("First Napoleonic War"). In Dutch historiography, it is common to refer to the 7 major wars between 1792 and 1815 as the Coalition Wars (coalitieoorlogen), referring to the first two as the French Revolution Wars (Franse Revolutieoorlogen).
== P == Palladin Plastin p30 PAK (p21-activated Kinase) Plectin p47PHOX Parvin (actopaxin) Prefoldin p53 PASK (Proline, Alanine rich Ste20 related Kinase) Presenilin I p58 Phalloidin (not a protein; a small cyclic peptide) Profilin p185neu Ponticulin Protein kinase C Porin P.IB Prk1p (actin regulating kinase)
It is often observed that several compounds are found to have some degree of activity, and if these compounds share common chemical features, one or more pharmacophores can then be developed. At this point, medicinal chemists will attempt to use structure–activity relationships (SAR) to improve certain features of the lead compound:
Sources: en.wikipedia.org
SR9009 is a synthetic research compound that acts on REV-ERB nuclear receptors. It is not approved for human use and is sold only as a research chemical. Its effects have been studied mainly in cells and rodents.
It binds REV-ERB alpha and REV-ERB beta and changes the expression of genes tied to metabolism and circadian rhythm. These changes can affect mitochondria and energy use in animal models. The exact chain from receptor binding to physiological outcome is still being mapped.
No reliable human trials show that SR9009 improves athletic performance. Some rodent studies report endurance changes, but these results are not proof of human benefit. Its use in sport is prohibited, and quality and safety data are lacking.
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.