This is a working overview of research chemical, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-08-01. Anything still debated is marked as such rather than presented as settled.
SR9009 is frequently discussed alongside other REV-ERB ligands, including synthetic agonists and natural heme-related molecules. Its selectivity for REV-ERB over related nuclear receptors has been measured in binding and reporter assays, though off-target activity at higher concentrations is possible. The compound is prohibited in sport by the World Anti-Doping Agency, and it is not approved for any medical use in major jurisdictions. Products sold online may be labeled as research chemicals, and their identity and purity are not guaranteed by regulatory review.
SR9009 is a synthetic small molecule that acts on the nuclear receptors REV-ERBα and REV-ERBβ. These receptors are part of the circadian clock machinery and normally repress transcription of certain target genes. In laboratory research, SR9009 is used as a chemical tool to study how REV-ERB activity influences metabolism, inflammation, and daily biological rhythms. The compound is not an approved medicine, and its effects in humans remain largely uncharacterized. It is often described as an investigational agent rather than a therapeutic product.
Physicochemical behavior influences handling. SR9009 is described as a solid with limited aqueous solubility, so organic solvents such as dimethyl sulfoxide or ethanol are common in research stock solutions. Aqueous dilution can produce precipitates if the organic content is too low. Light, heat, and repeated freeze-thaw cycles may affect stability. Storage recommendations usually specify a desiccated freezer environment protected from light, but exact stability data depend on the formulation and matrix.
Detection in biological samples can be complicated by rapid metabolism and low circulating concentrations. Some studies report phase I and phase II metabolites, and analytical methods may need to target those species in addition to the parent compound. Immunoassays are not broadly available, so mass spectrometry remains the main confirmatory approach. For anti-doping testing, laboratories look for SR9009 and its metabolites using validated LC-MS methods. Open questions include how long metabolites remain detectable and how different routes of administration alter detection windows.
| Property | Value | Notes |
|---|---|---|
| Common name | SR9009 | Also marketed informally as Stenabolic |
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ |
| Molecular formula | C24H30ClN3O4S | Approximate molecular weight 492 g/mol |
| CAS Registry Number | 1379686-30-2 | Identifier for the parent compound |
| Regulatory status | Not approved for human use | Prohibited in sport by WADA |
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.
Sulfur–sulfur bonds are a structural component used to stiffen rubber, similar to the disulfide bridges that rigidify proteins. In the most common type of industrial "curing" or hardening and strengthening of natural rubber, elemental sulfur is heated with the rubber to the point that chemical reactions form disulfide bridges between isoprene units of the polymer. This process, patented in 1843, made rubber a major industrial product, especially in automobile tires. Because of the heat and sulfur, the process was named vulcanization, after the Roman god of the forge and volcanism.
Tenkaonian Goren Nashi (テンカオ星人ゴレン・ナシ, Tenkao Seijin Goren Nashi) and Tenkaonian Yam Tomukun (テンカオ星人ヤム・トムクン, Tenkao Seijin Yamu Tomukun): Namunan's partners of the same species who are killed by Chou San. Goren Nashi is voiced by Seiji Fujita (藤田 清二, Fujita Seiji), who also portrays his human form; Yam Tomukun is portrayed by Minoru Nanaeda (七枝 実, Nanaeda Minoru). Mikean Clord (マイク星人クロード, Maiku Seijin Kurōdo): A vine-themed criminal from Planet Mike who is charged with several counts of mass murder and inhuman experimentation stemming from his stealing young women's nutrients to cure his sister Teresa, who is dating Hoji. Despite learning of Clord's goal and being initially torn over allowing him to continue, Hoji ultimately deletes him before he can kill another group of young women. Clord is voiced by Yuuki Tsujimoto (辻本 祐樹, Tsujimoto Yūki), who also portrays his human form. Aladonian Gyanjava (アラドン星人ギャンジャバ, Aradon Seijin Gyanjaba): A cricket-themed bank robber from Planet Aladon who is charged with burglary and child abduction, having killed Yaako's parents to take advantage of her natural ability to manipulate locks. After requesting Agent Abrella's help to access the Deka Base's systems, Yaako betrays Gyanjava and helps the Dekarangers foil his latest robbery. Gyanjava dons a Muscle Gear to evade capture and judgement before piloting a Kaijuki called Cannon Gladiator 4 (キャノングラディエーター4, Kaijūki Kyanon Guradiētā Fō) to crush the Dekarangers, only to be thwarted and judged by Deka Bike Robo.
== Pharmacodynamics == Liraglutide is an acylated glucagon-like peptide-1 (GLP-1) receptor agonist, derived from human GLP-1-(7-37), a less common form of endogenous GLP-1. It reduces meal-related hyperglycemia (for 24 hours after administration) by increasing insulin secretion (only) when required by increasing glucose levels, delaying gastric emptying, and suppressing prandial glucagon secretion. Liraglutide leads to insulin release in pancreatic beta cells in the presence of elevated blood glucose. This insulin secretion subsides as glucose concentrations decrease and approach euglycemia (normal blood glucose level). It also decreases glucagon secretion in a glucose-dependent manner and delays gastric emptying. Unlike endogenous GLP-1, liraglutide is stable against metabolic degradation by peptidases, with a plasma half-life of 13 hours.
== Epidemiology == Nickel allergy is the most common contact allergy in industrialized countries, affecting around 8% to 19% of adults and 8% to 10% of children. Women are affected 4–10 times as frequently as men. Nickel allergy is estimated to affect 4% of men and 16% of women worldwide. In southern European countries, nickel allergy is more common than in northern countries, 16% versus 10%. The results are similar in the USA.
Sources: en.wikipedia.org
In a study looking at gene polymorphisms of GPX1 and other oxidative stress genes in relation to prevalence of Type 2 diabetes mellitus, Banerjee, et al., found that while no association was found in expression of most GPX1 polymorphisms and risk of Type 2 diabetes mellitus, having the C allele of GPX1 led to a 1.362 times higher risk of the disease, highlighting the importance of finding individuals in the population with this gene variant to help treat them early on. Recent work by Alan M. Diamond and colleagues has shown that allelic variations of GPX1, like the codon 198 polymorphism that results in leucine or proline and an increase in alanine repeat codons, can result in different localization levels in MCF-7 human breast carcinoma cells. For instance, the allele expressing the leucine-198 polymorphism and 7 alanine repeats generates GPX-1 localization that is disproportionately in the cytoplasm as compared to other allelic variants. To further understand the effects of these variants on GPX-1 function, mutant GPX-1 with mitochondrial localization sequences were generated and the GPX-1 infused cells were analyzed for their response to oxidative stress, energy metabolism and cancer-associated signaling molecules. Ultimately, GPX-1 variants heavily influenced cellular biology, suggesting that different GPX-1 variants affect cancer risk differently.
== Medical uses == Tiratricol is indicated for the treatment of peripheral thyrotoxicosis in people with monocarboxylate transporter 8 (MCT8) deficiency (Allan-Herndon-Dudley syndrome), from birth. Thyrotoxicosis in MCT8 deficiency is caused by a mutation (change) in the gene that provides instructions for making a protein called MCT8. This protein normally transports the thyroid hormone T3 into cells of various tissues and organs, including those of the brain. Due to the gene mutation, MCT8 does not work properly and so T3 cannot enter the brain cells, causing problems with brain and muscle development. It also leads to a buildup of T3 in other parts of the body, causing problems due to too much thyroid hormone (hyperthyroidism). Tiratricol, is very similar to T3 but it does not need MCT8 to move in and out of cells. Tiratricol is therefore expected to enter the body’s cells in people with MCT8 deficiency and replace the missing T3 hormone. This helps restore normal thyroid hormone activity in the body and reduce symptoms of peripheral thyrotoxicosis. MCT8 deficiency is a rare genetic disorder that primarily affects males. The condition is caused by a faulty gene that provides instructions for making the MCT8 transporter, a critical protein responsible for carrying thyroid hormone into the brain. Because thyroid hormone cannot cross the blood-brain barrier without the MCT8 transporter, the brain receives too little of this hormone, while excessive levels of the hormone build up in the bloodstream.
Emmanuelle Charpentier and Jennifer A Doudna won the 2020 prize in chemistry “for the development of a method for genome editing.” Charpentier and Doudna are the first women to share the Nobel Prize in chemistry.
Carnivore protoparvovirus 1 is a species of parvovirus that infects carnivorans. It causes a highly contagious disease in both dogs and cats separately. The disease is generally divided into two major genogroups: the group of the classical feline panleukopenia virus (FPLV), and the group of the canine parvovirus type 2 (CPV-2), which appeared in the 1970s. Belonging to the family Parvoviridae, FPLV have linear, single-stranded DNA (ssDNA) genomes. This agent is one of the smallest animal viruses, barely 18 to 20 nm in diameter. Like other parvovirus genomes, it has hairpin structures at both ends of its genome: 3-genome Y-type structure and 5-terminal U-shaped structure, making it challenging to amplify the full-length genome of parvovirus despite its small size. Sequences in the genome show a high degree of nucleotide conservation in the VP2 gene after over 90 years since it has emerged; the VP2 gene codes for the capsid protein VP2, a main structural protein, which determines the major mutations during the evolution of CPV. FPLV is known to infect all wild and domestic members of the felid (cat) family worldwide. It is a highly contagious, severe infection that causes gastrointestinal, immune system, and nervous system disease. Its primary effect is to decrease the number of white blood cells, causing the disease known as feline panleukopenia. Although it was once thought that only FPLV caused panleukopenia in cats, it has been confirmed that a feline panleukopenia illness can be caused by CPV 2a, 2b, and 2c. FPLV is commonly referred to as:
== Career == From 1967 to 1972, Chrestensen served as production manager of his family's horticultural business in Erfurt. The firm was subsequently nationalized, and from 1972 to 1990 he worked as production manager of the East German state enterprise VEB Erfurter Blumensamen.Following German reunification, from 1990 to 2010 he served as co-managing director of the reconstituted Erfurt seed and plant-breeding company N. L. Chrestensen. From 1990 to 2010, Chrestensen also served as president of the Thuringian Chamber of Industry and Commerce (Industrie- und Handelskammer Thüringen). In that role, he was a co-founder of the Erfurt chamber of commerce after reunification and advocated for Erfurt's inclusion as a stop on Germany's Intercity-Express (ICE) high-speed rail network.
Sources: en.wikipedia.org
ASBMB Avanti Award for Lipid Research (1998) Elected to the American Academy of Arts and Sciences (1999) Heinrich Wieland Prize for Lipid Research (2000) Elected to the National Academy of Sciences (2001) Caledonian Prize from the Royal Society of Edinburgh (2002) Pezcoller-AACR International Award for Cancer Research (2005) Rolf Luft Award of the Karolinska Institute (2009) Pasrow Prize for Cancer Research (2011) Breakthrough Prize in Life Sciences (2013) Jacobaeus Prize for Diabetes Research, from the Karolinska Institute (2013) Elected to the Institute of Medicine of the National Academies (2014) AACR Princess Takamatsu Memorial Lectureship (2015) Ross Prize in Molecular Medicine (2015) Canada Gairdner International Award (2015) Elected to European life sciences academy EMBO (2015) The Association of American Cancer Institutes Distinguished Scientist Award (2015) Thomson Reuter's "The World's Most Influential Scientific Minds 2015". The Wolf Prize in Medicine (2016) The Hope Funds Award of Excellence in Basic Science (2016) Louisa Gross Horwitz Prize (2019) He appeared in the 60 Minutes program "Is sugar toxic?".
=== Development === Under the code names JNJ-39823277 and TPI-1062, tianeptine was previously under development for the treatment of major depressive disorder in the United States and Belgium. Phase I clinical trials were completed in Belgium and the United States in May and June 2009, respectively. For unclear reasons development of tianeptine was discontinued in both countries in January 2012. In October 2023, Tonix Pharmaceuticals announced that it had discontinued its development of tianeptine as a monotherapy for major depressive disorder after disappointing phase-2 clinical trial results. An ongoing clinical trial, sponsored by the New York Psychiatric Institute, is examining tianeptine's use in treatment-resistant depression. U.S. National Poison Data System data on tianeptine showed a nationwide increase in tianeptine exposure calls and calls related to abuse and misuse during 2014–2017.
=== Amino acid metabolism === Transaminases break down amino acids with PLP as a cofactor. The proper activity of these enzymes is crucial for the process of moving amine groups from one amino acid to another. To function as a transaminase coenzyme, PLP bound to a lysine of the enzyme then binds to a free amino acid via formation of a Schiff's base. The process then dissociates the amine group from the amino acid, releasing a keto acid, then transfers the amine group to a different keto acid to create a new amino acid. Serine racemase which synthesizes the neuromodulator D-serine from its enantiomer is a PLP-dependent enzyme. PLP is a coenzyme needed for the proper function of the enzymes cystathionine synthase and cystathionase. These enzymes catalyze reactions in the catabolism of methionine. Part of this pathway (the reaction catalyzed by cystathionase) also produces cysteine. Selenomethionine is the primary dietary form of selenium. PLP is needed as a cofactor for the enzymes that allow selenium to be used from the dietary form. PLP also plays a cofactor role in releasing selenium from selenohomocysteine to produce hydrogen selenide, which can then be used to incorporate selenium into selenoproteins. PLP is required for the conversion of tryptophan to niacin, so low vitamin B6 status impairs this conversion.
Allied technological cooperation during World War II List of aircraft of the United Kingdom in World War II List of aircraft of World War II List of fighter aircraft List of military aircraft of the United States
Sources: en.wikipedia.org
SR9009 is a synthetic research compound that binds and modulates the nuclear receptors REV-ERBα and REV-ERBβ. It is used in laboratory studies of circadian biology and metabolism, not as an approved medicine. It is also known by the informal name Stenabolic.
No. SR9009 has not been approved as a therapeutic drug in the United States, European Union, or other major markets. Human safety and efficacy data are very limited. Its presence in consumer products does not imply regulatory approval.
The World Anti-Doping Agency lists SR9009 as a prohibited substance because it can alter gene expression and metabolic pathways relevant to performance. The ban applies at all times, not only during competition. Detection relies on laboratory methods such as mass spectrometry.
It is usually detected by LC-MS or HPLC-UV against a reference standard. In biological matrices, metabolite targeting can improve detection. No universal immunoassay is widely available.