purity testing raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2026-05-14 and is reviewed periodically as new material appears.
Pharmacokinetic data for SR9009 are limited in published literature. Some reports indicate low oral bioavailability and rapid clearance in animals, which complicates interpretation of exposure and effect. Researchers often use injected routes in preclinical work to achieve measurable systemic levels. Analytical studies rely on mass spectrometry to detect the parent compound and its metabolites. Questions about tissue distribution, active metabolites, and long-term consequences remain open. Species differences in metabolism can affect observed half-life and target engagement.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic small-molecule REV-ERB agonist | Not a hormone or natural product |
| Primary targets | REV-ERBα and REV-ERBβ | Nuclear receptors involved in circadian and metabolic regulation |
| Appearance | White to off-white solid | Typical for purified research samples |
| Solubility | Soluble in DMSO and ethanol; low water solubility | Laboratory solubility depends on solvent and purity |
| Common synonyms | SR9009; Stenabolic | Stenabolic is a colloquial name, not a formal chemical name |
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.
Because REV-ERB receptors are core clock components, SR9009 has been examined for effects on daily rhythms as well as metabolism. Research has explored whether the compound can shift or reinforce circadian gene expression in tissues such as liver and muscle. Some studies report improved metabolic markers in obese or diabetic mice, while others show context-dependent responses. Questions remain about which effects are direct, which are secondary to timing, and how they might differ across species.
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.
Identity and purity testing for SR9009 commonly uses liquid chromatography coupled with tandem mass spectrometry. This method separates the compound from matrix components and detects it by mass-to-charge transitions, providing sensitive and specific confirmation. Nuclear magnetic resonance spectroscopy can support structural identification, while high-performance liquid chromatography with ultraviolet detection may estimate purity. Because online products labeled as SR9009 may contain other substances or no active compound at all, independent verification is important in research settings. Certificates of analysis are useful but not a substitute for in-house testing.
Laboratory samples of SR9009 are typically supplied as a white to off-white powder. The compound dissolves readily in organic solvents such as dimethyl sulfoxide and ethanol, while its solubility in water is low. Because of this solubility profile, researchers often prepare concentrated stock solutions in an organic solvent before diluting them into aqueous assay buffers. Light exposure, moisture, and repeated freeze-thaw cycles can degrade many small molecules, so handling procedures usually aim to minimize these factors. Purity is commonly checked before use.
Korea is believed to be the first country in Asia that acupuncture spread to outside of China. Within Korea there is a legend that acupuncture was developed by emperor Dangun, though it is more likely to have been brought into Korea from a Chinese colonial prefecture in 514 AD. Acupuncture use was commonplace in Korea by the 6th century. It spread to Vietnam in the 8th and 9th centuries. As Vietnam began trading with Japan and China around the 9th century, it was influenced by their acupuncture practices as well. China and Korea sent "medical missionaries" that spread traditional Chinese medicine to Japan, starting around 219 AD. In 553, several Korean and Chinese citizens were appointed to re-organize medical education in Japan and they incorporated acupuncture as part of that system. Japan later sent students back to China and established acupuncture as one of five divisions of the Chinese State Medical Administration System. Acupuncture began to spread to Europe in the second half of the 17th century. Around this time, Willem ten Rhijne, a physician working for the Dutch East India Company, met Japanese acupuncture practitioners and later encouraged Europeans to further investigate it. He published the first in-depth description of acupuncture for the European audience and created the term "acupuncture" in his 1683 work De Acupunctura. France was an early adopter among the West due to the influence of Jesuit missionaries, who brought the practice to French clinics in the 16th century.
=== EC 1.5.99 With unknown physiological acceptors === EC 1.5.99.1: Now EC 1.5.8.3, sarcosine dehydrogenase EC 1.5.99.2: Now EC 1.5.8.4, dimethylglycine dehydrogenase EC 1.5.99.3: L-pipecolate dehydrogenase EC 1.5.99.4: nicotine dehydrogenase EC 1.5.99.5: methylglutamate dehydrogenase EC 1.5.99.6: spermidine dehydrogenase EC 1.5.99.7: Now EC 1.5.8.2, trimethylamine dehydrogenase EC 1.5.99.8: Now EC 1.5.5.2, proline dehydrogenase EC 1.5.99.9: transferred to EC 1.5.98.1, methylenetetrahydromethanopterin dehydrogenase EC 1.5.99.10: Now EC 1.5.8.1, dimethylamine dehydrogenase EC 1.5.99.11: transferred to EC 1.5.98.2, 5,10-methylenetetrahydromethanopterin reductase EC 1.5.99.12: cytokinin dehydrogenase EC 1.5.99.13: D-proline dehydrogenase EC 1.5.99.14: 6-hydroxypseudooxynicotine dehydrogenase EC 1.5.99.15: dihydromethanopterin reductase (acceptor)
== Further reading == Brandoni, Diego; Scillato Yané, Gustavo J.; Miño Boilini, Ángel R.; Favotti, Emmanuel (2016). "Los Tardigrada (Mammalia, Xenarthra) de Argentina: diversidad, evolución y biogeografía" (PDF). Contribuciones del MACN. _: 263–274. Retrieved 2018-10-08. Cuvier, G. (1796): Notice sur le squelette d'une très grande espèce de quadrupède inconnue jusqu'à présent, trouvé au Paraguay, et déposé au cabinet d'histoire naturelle de Madrid. Magasin encyopédique, ou Journal des Sciences, des Lettres et des Arts (1): 303–310; (2): 227–228. De Iuliis, G. & Cartelle, C. (1999): A new giant megatheriine ground sloth (Mammalia: Xenarthra: Megatheriidae) from the late Blancan to early Irvingtonian of Florida. Zool. J. Linn. Soc. 127(4): 495–515. Harrington, C.R. (1993): Yukon Beringia Interpretive Center - Jefferson's Ground Sloth. Retrieved 2008-JAN-24. Hogan, C.M. (2008): Cueva del Milodon, Megalithic Portal. Retrieved 2008-APR-13 Kurtén, Björn and Anderson, Elaine (1980): Pleistocene Mammals of North America. Columbia University Press, New York. ISBN 0-231-03733-3 McKenna, Malcolm C. & Bell, Susan K. (1997): Classification of Mammals Above the Species Level. Columbia University Press, New York. ISBN 0-231-11013-8 Nowak, R.M. (1999): Walker's Mammals of the World (Vol. 2). Johns Hopkins University Press, London. White, J.L. (1993): Indicators of locomotor habits in Xenarthrans: Evidence for locomotor heterogeneity among fossil sloths. Journal of Vertebrate Paleontology, 13(2): 230–242. White, J.L.; MacPhee, R.D.E. (2001).
=== Allegations of patent infringement on mRNA technology (2022) === In August 2022, Moderna announced that it will sue Pfizer and its partner BioNTech for infringing its patent on the mRNA technology. In May 2024, the European Patent Office upheld the validity of Moderna's EP949 patent, one of the two patents asserted against Pfizer and BioNTech.
Lurasidone is taken by mouth and should be taken with a meal of at least 350 calories to ensure maximum absorption. It has an estimated absorption rate of 9 to 19%. Studies have shown that when lurasidone is taken with food, absorption increases about twofold. Peak blood plasma concentrations are reached after one to three hours. About 99% of the circulating substance are bound to plasma proteins. Efficacy data for lurasidone have been evaluated for doses of 20 mg to 120 mg daily. In schizophrenia, lurasidone has a recommended dose range of 40-160 mg. In bipolar depression, lurasidone has a slightly lower recommended dose range of 20-120 mg. Lurasidone is extensively metabolised by CYP3A4 leading to contraindication of both strong inhibitors as well as strong inducers of this enzyme, but has negligible affinity to other cytochrome P450 enzymes. It is transported by P-glycoprotein and ABCG2 and also inhibits these carrier proteins in vitro. It also inhibits the solute carrier protein SLC22A1, but no other relevant transporters. Main metabolism pathways are oxidative N-dealkylation between the piperazine and cyclohexane rings, hydroxylation of the norbornane ring, and S-oxidation.:59 Other pathways are hydroxylation of the cyclohexane ring and reductive cleavage of the isothiazole ring followed by S-methylation. The two relevant active metabolites are the norbornane hydroxylation products called ID-14283 and ID-14326, the former reaching pharmacologically relevant blood plasma concentrations.
Sources: en.wikipedia.org
=== Toxicity of trivalent arsenicals === Enzymes and receptors that contain thiol or sulfhydryl functional groups are actively targeted by arsenite (III) metabolites. These sulfur-containing compounds are normally glutathione and the amino acid cysteine. Arsenite derivatives generally have higher binding affinity compared to the arsenate metabolites. These bindings restrict activity of certain metabolic pathways. For example, pyruvate dehydrogenase (PDH) is inhibited when monomethylarsonous acid (MMAIII) targets the thiol group of the lipoic acid cofactor. PDH is a precursor of acetyl-CoA, thus the inhibition of PDH eventually limits the production of ATP in electron transport chain, as well as the production of gluconeogenesis intermediates.
In 2017, Ice-T signed a petition to Congress for criminal-justice reform. His 1994 book, The Ice Opinion, was largely focused on his view on politics. Writing in the aftermath of the 1992 Los Angeles riots, he was one of the only rappers who criticized the targeting of Koreans by some Black rioters. On June 5, 2008, Ice-T joked that he would be voting for John McCain in the 2008 American elections, speculating that his past affiliation with Body Count could hurt Barack Obama's chances if he endorsed him, so he would choose instead to ruin McCain's campaign by saying he supported him. In 2015, Ice-T said that he admired Obama "just for the simple fact he took the shot and went all the way to be president" and included Obama in the list of people who he would like to have for a dream dinner party. On September 22, 2022, Ice-T narrated an advertisement for the Foundation for Individual Rights and Expression.
=== Synthesis and modification === Synthesis of the subunits occurs in the cytosol. Folding of the β-subunit is thought to be aided by the chaperone CCT (chaperonin containing tailless-complex polypeptide 1), which also prevents aggregation of folded subunits. A second chaperone, PhLP (phosducin-like protein), binds to the CCT/Gβ complex, and is phosphorylated, allowing CCT to dissociate and Gγ to bind. Finally, PhLP is released, exposing the binding site for Gα, allowing for formation of the final trimer at the endoplasmic reticulum, where it is targeted to the plasma membrane. Gγ subunits are known to be prenylated (covalently modified by the addition of lipid moieties) prior to addition to Gβ, which itself has not been found to be modified. This prenylation is thought to be involved in directing the interaction of the subunit both with membrane lipids and other proteins.
elementary reaction Any chemical reaction in which one or more chemical species react directly to form products in a single reaction step and with a single transition state, i.e. without any intermediates. Contrast stepwise reaction.
Sources: en.wikipedia.org
It is a synthetic research compound that activates REV-ERB nuclear receptors. It is not an approved drug or dietary supplement. Most information comes from cell and animal studies.
It binds REV-ERBα and REV-ERBβ and changes transcription of metabolic genes. This can affect circadian rhythm, lipid use, and mitochondrial function. The full downstream effects are still under study.
No. Some rodent studies show increased endurance, but controlled human trials are lacking. Claims about human performance are not established by published evidence.
SR9009 is a synthetic REV-ERB agonist used in laboratory research. It is not an approved drug, and its effects in humans are not well characterized. It is often sold as a research chemical under the name Stenabolic.