Everything below concerns NR1D1. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2025-12-14. Where a claim depends on a specific study, the study is described rather than over-claimed.
SR9009 is frequently discussed in fitness and research-chemical contexts, yet it has no approved medical indication. Regulatory agencies have not authorized it for human use, and it is not a standard prescription drug. Some sports organizations list it as a prohibited substance because of its potential performance-enhancing properties. Published human data are sparse, so claims about its effects in people often rely on animal models or anecdotal reports. Quality and identity of online materials can vary widely.
SR9009 is a synthetic small molecule studied as a REV-ERB agonist. REV-ERBα and REV-ERBβ are nuclear receptors that help regulate circadian rhythms and metabolic gene expression. The compound was identified in academic screening efforts to find synthetic ligands for these receptors. In cell and animal studies, SR9009 alters transcription of genes involved in lipid and glucose metabolism, and it can shift circadian behavior. It is not an approved therapeutic agent.
Mechanistically, SR9009 binds the ligand-binding domain of REV-ERBα/β and enhances recruitment of corepressor complexes. This represses target genes rather than activating them. Because REV-ERB proteins normally compete with ROR proteins at shared response elements, the net effect depends on tissue and timing. Researchers use SR9009 to probe how nuclear receptor signaling links the clock to metabolism, inflammation, and muscle biology. Findings are largely preclinical, and the precise contribution of each receptor subtype remains under study.
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.
The mechanism of action involves binding to REV-ERB receptors and recruiting corepressor complexes, which represses target gene transcription. This contrasts with many nuclear receptor agonists that activate transcription. Downstream effects may include changes in autophagy, mitochondrial biogenesis, and lipid handling, but the precise pathways remain an active area of study. Whether these molecular events translate into meaningful physiological effects in humans is unresolved. Most evidence comes from cultured cells and rodent models rather than human participants.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small-molecule ligand; not a hormone or peptide |
| Molecular formula | C20H24ClN3O4S | Reported for the free base |
| CAS Registry Number | 1379686-30-2 | Unique chemical identifier |
| Common synonyms | SR9009; stenabolic | Stenabolic is informal and not an official name |
| Reported targets | REV-ERBα and REV-ERBβ | Nuclear receptors linked to circadian and metabolic regulation |
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.
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.
Stability depends on physical form, temperature, light exposure, and solvent. Solid SR9009 is generally stored cold and dry, with protection from light to limit degradation. Dimethyl sulfoxide stocks are common for laboratory work, but repeated freeze-thaw cycles can reduce compound integrity. Aqueous solutions may be less stable than organic stocks, and the ethyl ester in the structure can be susceptible to hydrolysis under certain conditions. Researchers typically validate storage conditions and recheck purity before quantitative experiments, especially when using archived material.
Regulatory treatment of SR9009 varies by country and region. It is not approved as a pharmaceutical, and several jurisdictions restrict its sale for human consumption. Some authorities classify it as a research chemical, a prescription-only substance, or a prohibited performance-enhancing agent in sport. Purchasers may encounter certificates of analysis, but these documents do not guarantee identity, purity, or legality. In research settings, institutional safety reviews and controlled procurement help ensure that materials are handled under appropriate oversight. The absence of harmonized rules means that legal status can change and requires verification.
Analytical identification of SR9009 typically relies on liquid chromatography coupled with tandem mass spectrometry. In biological samples, researchers first separate the compound from matrix components using protein precipitation, liquid-liquid extraction, or solid-phase extraction. High-performance liquid chromatography with ultraviolet detection and nuclear magnetic resonance spectroscopy can support structural confirmation of reference materials. Because SR9009 is a small, relatively lipophilic molecule, reverse-phase columns and acidic mobile phases are common. Laboratories often include isotope-labeled internal standards to improve quantification and to correct for ion suppression.
=== Cardiac === Case reports have noted cardiac arrhythmias emerging in relation to trazodone treatment, both in patients with pre-existing mitral valve prolapse and in patients with negative personal and family histories of cardiac disease. QT prolongation has been reported with trazodone therapy. Arrhythmia identified include isolated PVCs, ventricular couplets, and in two patients short episodes (three to four beats) of ventricular tachycardia. Several post-marketing reports have been made of arrhythmia in trazodone-treated patients who have pre-existing cardiac disease and in some patients who did not have pre-existing cardiac disease. Until the results of prospective studies are available, patients with pre-existing cardiac disease should be closely monitored, particularly for cardiac arrhythmias. Trazodone is not recommended for use during the initial recovery phase of myocardial infarction (heart attack). Concomitant administration of drugs that prolong the QT interval or that are inhibitors of CYP3A4 may increase the risk of cardiac arrhythmia.
=== Adverse effects === The most common side effects include too high or too low blood calcium levels, which can lead to headache, diarrhea, vomiting, paraesthesia (unusual sensations like pins and needles), hypoaesthesia (reduced sense of touch), and high calcium levels in the urine. In the US, the FDA label for parathyroid hormone contains a black box warning for osteosarcoma (a malignant bone tumor).
In 1886, Eugen Goldstein observed rays in gas discharges under low pressure that traveled away from the anode and through channels in a perforated cathode, opposite to the direction of negatively charged cathode rays (which travel from cathode to anode). Goldstein called these positively charged anode rays "Kanalstrahlen"; the standard translation of this term into English is "canal rays". Wilhelm Wien found that strong electric or magnetic fields deflected the canal rays and, in 1899, constructed a device with perpendicular electric and magnetic fields that separated the positive rays according to their charge-to-mass ratio (Q/m). Wien found that the charge-to-mass ratio depended on the nature of the gas in the discharge tube. English scientist J. J. Thomson later improved on the work of Wien by reducing the pressure to create the mass spectrograph.
The WPB placed penicillin under a wartime allocation system on 16 July 1943. All supplies were designated for use by the armed forces and the Public Health Service. Penicillin production in the United States ramped up from 800 million Oxford units in the first half of 1943 to 20 billion units in the second half. The US government built six production plants at a cost of $7.6 million (equivalent to $139 million in 2025). These were sold after the war to the companies that operated them for $3.4 million (equivalent to $56 million in 2025). Another sixteen plants were built by the private sector for $22.6 million (equivalent to $413 million in 2025), although $14.5 million (equivalent to $265 million in 2025) was approved for accelerated depreciation under which the cost could be written off in five years instead of the usual twelve to fifteen. US penicillin production rose from 21 billion units in 1943, to 1,663 billion units in 1944 and an estimated 6,852 billion units in 1945. By June 1944, Pfizer alone was producing 70 billion units per month. Monthly production dropped off after July 1945 due to a shortage of corn-steep liquor. The price offered by the CMR for a million units fell from $200 in 1943 (equivalent to $4,000 in 2025), which was below its manufacturing cost, to $6 in 1945 (equivalent to $107 in 2025). The chairman of the NRC committee on chemotherapy, Chester Keefer, was responsible for administering the equitable distribution of penicillin for civilian use on behalf of the CMR.
Sources: en.wikipedia.org
There are many mountains named after the breast because they resemble it in appearance and so are objects of religious and ancestral veneration as a fertility symbol and of well-being. In Asia, there was "Breast Mountain", which had a cave where the Buddhist monk Bodhidharma (Da Mo) spent much time in meditation. Other such breast mountains are Mount Elgon on the Uganda–Kenya border; Beinn Chìochan and the Maiden Paps in Scotland; the Bundok ng Susong Dalaga ('Maiden's breast mountains') in Talim Island, Philippines, the twin hills known as the Paps of Anu (Dá Chích Anann or 'the breasts of Anu'), near Killarney in Ireland; the 2,086 m high Tetica de Bacares or La Tetica in the Sierra de Los Filabres, Spain; Khao Nom Sao in Thailand, Cerro Las Tetas in Puerto Rico; and the Breasts of Aphrodite in Mykonos, among many others. In the United States, the Teton Range is named after the French word for 'nipple'.
==== United Kingdom ==== In the United Kingdom, MDMA was made illegal in 1977 by a modification order to the existing Misuse of Drugs Act 1971. Although MDMA was not named explicitly in this legislation, the order extended the definition of Class A drugs to include various ring-substituted phenethylamines. The drug is therefore illegal to sell, buy, or possess without a licence in the UK. Penalties include a maximum of seven years and/or unlimited fine for possession; life and/or unlimited fine for production or trafficking. Some researchers such as David Nutt have criticized the scheduling of MDMA, which he determined to be a relatively harmless drug. An editorial he wrote in the Journal of Psychopharmacology, where he compared the risk of harm for horse riding (1 adverse event in 350) to that of ecstasy (1 in 10,000) resulted in his dismissal, leading to the resignation of several of his colleagues from the ACMD.
=== Development === Development of the film was announced on 20 December 2008, although writer Alex Garland had begun working on the script in 2006. British studio DNA Films produced the film, and partnered with sales agency IM Global to sell the worldwide distribution rights. By May 2010, this partnership saw IM Global and its owner Reliance Big Pictures agree to co-finance the 3-D project with a $45 million production budget, and a schedule to begin filming in Johannesburg, South Africa in late 2010. Pete Travis was named as the film's director and Garland, Andrew Macdonald and Allon Reich would produce it. Duncan Jones had previously been offered the role of director. In a 2010 interview, Jones said that his vision for the film was unconventional—describing it as weird, dark, and funny—and it did not mesh well with Garland's script. In September 2010, it was reported that the film would be titled Dredd. Pre-production commenced on 23 August 2010 at Cape Town Film Studios in Cape Town, South Africa. During the 2010 San Diego Comic-Con in July, Urban confirmed that he had been offered the role of Judge Dredd, and on 18 August 2010, it was reported that Urban had the role. In September 2010, it was announced that Thirlby would play Dredd's telepathic rookie Cassandra Anderson. In the same month during the Toronto International Film Festival, the film attracted $30 million in worldwide pre-sales to distributors in 90% of theatrical markets. The sales included a $7 million deal with British distributor Entertainment Film Distributors.
Sources: en.wikipedia.org
SR9009 is a synthetic compound investigated as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is used in preclinical research on circadian rhythm and metabolism. It is not an approved drug.
No. It has no approved medical indication, and human safety and efficacy data are limited. It appears in research chemical markets and is banned by some sports authorities.
Natural ligands include heme and certain metabolites; SR9009 is a synthetic small molecule with higher potency and selectivity in some assays. Its effects depend on cell type and timing. It is not a naturally occurring compound.
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.