This is a working overview of REV-ERB agonist, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2025-12-26. Anything still debated is marked as such rather than presented as settled.
Regulatory treatment of SR9009 reflects its investigational status. The compound has no approved human therapeutic indication, and sports authorities prohibit its use. It appears on anti-doping lists as a non-approved substance or metabolic modulator, depending on the list version. Products sold online as research chemicals are not quality-controlled medicines, so their identity and purity can differ from the label. Such products may also contain unlisted compounds, which complicates both testing and safety assessment.
Scientific discussion of SR9009 often separates animal evidence from human anecdote. Rodent studies provide controlled data on endurance, metabolism, and gene expression, but they use specific strains, doses, and treatment durations. Human reports are mostly uncontrolled and cannot establish cause and effect. Open questions include oral bioavailability, tissue distribution, metabolic stability, and long-term effects. Review articles generally call for more rigorous pharmacokinetic and safety research before any clinical use could be considered.
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, lipid metabolism, and inflammatory gene expression. In cell and animal experiments, SR9009 alters transcription of clock-controlled genes and metabolic pathways. The compound is not a hormone and does not resemble classical steroid structures. Its activity depends on binding to the ligand-binding domain of REV-ERB, where it can modify corepressor recruitment.
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.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Not approved for human use | Investigational status in most countries |
| Sports status | Prohibited by WADA | Classified as non-approved or metabolic modulator |
| Common analytical method | LC-MS/MS | Used for trace detection in biological samples |
| Typical test matrices | Urine and blood | Sample choice depends on testing program |
| Human trial data | None published | Effects and safety are not established |
Identity and purity of SR9009 samples are usually checked with chromatographic and spectrometric methods. High-performance liquid chromatography can separate the compound from related impurities, while mass spectrometry provides molecular mass confirmation. Nuclear magnetic resonance spectroscopy may be used for structural verification in research settings. No single method proves biological activity, and certificates of analysis should be reviewed alongside raw data. Independent testing is often needed because online products vary widely.
SR9009 stability depends on temperature, moisture, light, and solvent. Solid material is generally kept cool and dry, while solutions may require protection from repeated warming and cooling. Degradation can appear as color changes, precipitate, or new chromatographic peaks. Researchers should follow supplier instructions and their own stability data. Long-term storage conditions for human use have not been established because the compound lacks approved clinical formulation.
SR9009 is supplied as a solid research chemical, often in milligram quantities. Laboratories typically weigh it in a controlled environment because fine powders can disperse. Stock solutions are commonly prepared in dimethyl sulfoxide and stored in small aliquots to reduce freeze-thaw cycles. Personal protective equipment and chemical fume hoods are standard when handling unknown or potent compounds. These practices address laboratory safety rather than human use.
=== Cardiovascular diseases === Cardiovascular disease is the leading cause of death in the world. Ischemic heart disease develops when stenosis and occlusion of coronary arteries develops, leading to reduced perfusion of the cardiac tissue. Induction of neovascularization of ischemic cardiac tissues therefore has therapeutic potential.
=== Pharmacodynamics === 3-MeO-PCP has a Ki of 20 nM for the PCP site of the NMDA receptor, which is higher than PCP or any other anisyl substition of PCP. It has secondary activity at multiple other receptors, with a Ki of 216 nM for the serotonin transporter (SERT), and 42 nM for the sigma σ1 receptor. It does not bind to the norepinephrine or dopamine transporter, nor to the sigma σ2 receptor (Ki >10,000 nM). Based on structural similarity to 3-HO-PCP, it was initially expected that 3-MeO-PCP may have opioid activity. However, radioligand binding assays confirmed that the drug lacks significant activity at μ-, δ-, or κ-opioid receptors.
=== Medications === Certain medications can cause either weight loss or weight gain. Side effects are often listed for each medication and should be considered when attempting to manage a person's weight. Semaglutide is an anti-obesity drug that is also used for blood sugar control.
Sources: en.wikipedia.org
== Career == Working first in the Physical Chemistry Laboratory, he moved to the Dunn Nutritional Laboratory, and in 1938 moved to Wool Industries Research Institution in Leeds. He was head of the biochemistry division of Boots Pure Drug Company from 1946 to 1948, when he joined the Medical Research Council. There, he was appointed head of the physical chemistry division of the National Institute for Medical Research in 1952, and was chemical consultant from 1956 to 1959. He specialised in biochemistry, in some aspects of vitamins E and B2, and in techniques that laid the foundation for several new types of chromatography. He developed partition chromatography whilst working on the separation of amino acids, and later developed gas-liquid chromatography with Anthony T. James. Amongst many honours, he received his Nobel Prize in 1952. After his retirement from the University of Sussex, he was visiting professor at both the University of Houston in Texas and the EPFL (École Polytechnique Fédérale de Lausanne) in Switzerland. He published far fewer papers than the typical Nobel winners—only 70 in all—but his ninth paper contained the work that would eventually win him the Nobel Prize. The University of Houston dropped him from its chemistry faculty in 1979 (when he was 69 years old) because he was not publishing enough.
== Etymology == The genus name, Rotheca, seemingly comes from the Malaysian words "cheriga", which means small, and "thekku", which means teak. The species epithet comes from the French word "myriades", which means ten thousand, and a Latinization of the Greek "oides", which means to see. Some say that the species epithet came about because it resembles another species in Myrica, so the name refers to the leaf shape. 'Ugandense' is a cultivar of this species which shows purplish-blue flowers with flashy stamens. It was originally named Clerodendrum myricoides 'Ugandense', but a 1998 study led to its current status as Rotheca myricoides 'Ugandense".
== Management == PMOS has no cure, and management focuses on relief of symptoms. Treatment usually involves lifestyle changes such as diet and exercise of moderate intensity. Metabolic issues can further be treated with metformin or GLP-1 receptor agonists. For women with a BMI over 35, bariatric surgery may be an option. Combined oral contraceptives are especially effective and used as the first line of treatment to reduce acne and hirsutism and regulate the menstrual cycle. Other typical acne treatments and hair removal techniques may be used. First-line treatment for fertility issues uses ovulation induction with clomiphene or letrozole. As PMOS is associated with psychological disorders and cardiovascular risk, screening for both is recommended.
== External links == Official website of the Essendon Football Club Official website of the Australian Football League Archived 22 February 2011 at the Wayback Machine 2012 Season scores and results at AFL Tables 2012 Essendon player statistics at AFL Tables
Sources: en.wikipedia.org
=== Career === On 22 December 1884, Thomson was appointed Cavendish Professor of Physics at the University of Cambridge. This appointment caused considerable surprise; candidates such as Osborne Reynolds and Richard Glazebrook were older and more experienced in laboratory work, whereas Thomson was known for his work as a mathematician—being recognised as an exceptional talent. Thomson was knighted in 1908 and appointed to the Order of Merit in 1912. At Oxford, he gave the 1914 Romanes Lecture titled The Atomic Theory. In 1918, he became Master of Trinity College, Cambridge, a position he held until his death on 30 August 1940. His ashes rest in Westminster Abbey, near the graves of Isaac Newton and his former student, Ernest Rutherford. Rutherford succeeded him as Cavendish Professor. Six of Thomson's research assistants and junior colleagues (Charles Glover Barkla, Niels Bohr, Max Born, William Henry Bragg, Owen Willans Richardson and Charles Thomson Rees Wilson) won the Nobel Prize in Physics, and two (Francis William Aston and Ernest Rutherford) won the Nobel Prize in Chemistry. Thomson's son, George Paget Thomson, won the 1937 Nobel Prize in Physics for proving the wave-like properties of electrons.
MrMed is an online pharmacy for super-specialty medicines based in India. It was founded by Devashish Singh and Saurab Jain and has its headquarters in Chennai. In 2022, the company received an award from the Government of Tamil Nadu for its contributions to healthcare.
=== Acquisition and merging of Novartis' vaccine business === In October 2014, Novartis announced its intention to sell its influenza vaccine business, including its development pipeline, to CSL for $275 million. CSL merged it into its BioCSL operation. In November 2015, BioCSL rebranded the combined business with Novartis Influenza Vaccines as Seqirus [Sek-eer-us], creating the world's second-largest influenza vaccine company. In August 2017, the business announced it would acquire Calimmune and its stem cell therapy platform. Completed in 2018, Seqirus's plant in Holly Spring, NC was funded with $59 million from the U.S. government. in June 2020, CSL announced it would exercise its right to acquire Vitaeris. In December 2021, the business announced it would acquire Swiss drugmaker, Vifor Pharma AG, for $11.7 billion. In August 2022, CSL rebranded all of its divisions to start with the CSL name. Therefore, the divisions became CSL Behring, CSL Plasma, CSL Seqirus, and CSL Vifor.
Until about the time of the Meiji Restoration in 1868, cattle were used only as draught animals, in agriculture, forestry, mining and transport, and as a source of fertilizer. Milk consumption was unknown, and – for cultural and religious reasons – meat was not eaten. Cattle were highly prized and valuable, too expensive for a poor farmer to buy. Japan was effectively isolated from the rest of the world from 1635 until 1854; there was no possibility of the intromission of foreign genes to the cattle population during this time. In western Japan during the Edo period (1603–1867), superior cattle were produced by aggressive inbreeding, and the superior bloodlines were called "tsuru" (蔓, lit. 'vine'), and cattle with superior bloodlines (tsuru-ushi, lit. 'vine cattle') were traded at high prices. Famous tsuru include the Takenotani tsuru (Okayama Prefecture), Bokura tsuru (Shimane Prefecture), Iwakura tsuru (Hiroshima Prefecture), and Shusuke tsuru (Hyōgo Prefecture). In Japan, where meat eating was frowned upon and the use of milk was not widespread, cows in the Edo period were primarily work cattle that plowed the fields, so a good cow in this period meant one that was healthy and obedient.
The strong homology seen in the insulin sequence of diverse species suggests that it has been conserved across much of animal evolutionary history. The C-peptide of proinsulin, however, differs much more among species; it is also a hormone, but a secondary one. Insulin is produced and stored in the body as a hexamer (a unit of six insulin molecules), while the active form is the monomer. The hexamer is about 36000 Da in size. The six molecules are linked together as three dimeric units to form symmetrical molecule. An important feature is the presence of zinc atoms (Zn2+) on the axis of symmetry, which are surrounded by three water molecules and three histidine residues at position B10. The hexamer is an inactive form with long-term stability, which serves as a way to keep the highly reactive insulin protected, yet readily available. The hexamer-monomer conversion is one of the central aspects of insulin formulations for injection. The hexamer is far more stable than the monomer, which is desirable for practical reasons; however, the monomer is a much faster-reacting drug because diffusion rate is inversely related to particle size. A fast-reacting drug means insulin injections do not have to precede mealtimes by hours, which in turn gives people with diabetes more flexibility in their daily schedules. Insulin can aggregate and form fibrillar interdigitated beta-sheets. This can cause injection amyloidosis, and prevents the storage of insulin for long periods.
Sources: en.wikipedia.org
No. It is an investigational compound without approved therapeutic indications. It is sold for research purposes only in many jurisdictions.
Sports authorities prohibit it because it is not approved for human use and has potential performance-enhancing effects. It appears on anti-doping lists under non-approved or metabolic modulator categories.
Detection usually uses liquid chromatography-tandem mass spectrometry. The method targets the parent compound or its metabolites in urine or blood.
SR9009 is a synthetic small molecule studied as an agonist of the REV-ERB nuclear receptors. It is not an approved medicine, and its effects in humans are not well characterized.