SR9009 is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Last reviewed on 2025-08-04. Where a claim depends on a specific study, the study is described rather than over-claimed.
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, 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.
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 |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ in preclinical models |
| Molecular formula | C20H24ClN3O4S | Reported for the parent compound |
| CAS Registry Number | 1379686-30-2 | Common identifier in chemical databases |
| Appearance | Off-white to pale yellow solid | Typical research chemical solid |
| Solubility | Soluble in DMSO and ethanol; low in water | Class: small organic molecule |
SR9009 is a synthetic small molecule developed as an agonist of the nuclear receptors REV-ERBα (NR1D1) and REV-ERBβ (NR1D2). These receptors help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, SR9009 alters transcription of genes involved in lipid metabolism, inflammation, and mitochondrial function. It is not an approved medicine, and its pharmacological profile in humans remains largely uncharacterized. The compound is frequently discussed in the context of circadian biology and metabolic research rather than clinical use.
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.
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.
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.
The purified compound (penicillin F) was isolated in 1940 by a research team led by Howard Florey and Ernst Boris Chain at the University of Oxford. Fleming first used the purified penicillin to treat streptococcal meningitis in 1942. The 1945 Nobel Prize in Physiology or Medicine was shared by Chain, Fleming and Florey. Several semisynthetic penicillins are effective against a broader spectrum of bacteria: these include the antistaphylococcal penicillins, aminopenicillins, and antipseudomonal penicillins.
In June 2013, two biosimilar versions (Inflectra and Remsima) were submitted for approval in the European Union, by Hospira and Celltrion Healthcare respectively. Both had a positive opinion from European Medicines Agency's (EMA) Committee for Medicinal Products for Human Use (CHMP) for sale in the European Union (EU). Celltrion obtained marketing authorization approval (MAA) from 27 EU countries and 3 EEA (European Economic Area) countries by September 2013. Inflectra was approved for use in the European Union in September 2013, and Remsima was approved for use in the European Union in October 2013. In Japan, Celltrion received marketing authorization for Remsima from Japan's Ministry of Health, Labour and Welfare (MHLW) in July 2014. In India, Epirus Biopharmaceuticals obtained approval to produce biosimilar infliximab under the brand name "Infimab" (trail name BOW015). The US Food and Drug Administration (FDA) approved Celltrion/Hospira/Pfizer's Inflectra (infliximab-dyyb) in April 2016. The FDA approved Samsung Bioepis Co., Ltd.'s Renflexis (infliximab-abda) in April 2017. Biogen released another biosimilar, Flixabi, which was approved in Germany, the UK, and the Netherlands. Flixabi was approved for use in the European Union in May 2016. In December 2017, Ixifi (infliximab-qbtx) was approved in the United States. Zessly was approved for use in the European Union in May 2018. In December 2019, Avsola (infliximab-axxq) was approved in the United States. Avsola was approved for medical use in Canada in March 2020.
==== Codon models ==== Codon models describe the evolution of protein-coding nucleic acid sequences. The simplest codon model, MG, estimates one parameter: nonsynonymous/synonymous mutation ratio. The more complex GY also estimates transition/transversion rate ratios. Both of these are mechanistic models. They can be expanded by the addition of rate parameters. Empirical codon models directly describe the odds of one non-stop codon (61 in the standard code) being replaced by another, making them similar to amino acid exchangability matrices. By their construction, they are tied to the genetic code found in the data used to construct them. They can also be combined with a mechanistic model by multiplying the two estimated rates, adding back the ability to adapt to the data being processed.
== Annexation == Gqozo refused to participate in the negotiations to agree to a post-apartheid constitution for South Africa, and initially threatened to boycott the first non-racial elections. This became unsustainable, and in March 1994, Ciskei government workers went on strike for fear of losing their job security and pensions in the post-apartheid era. The police then mutinied, prompting Gqozo to resign on 22 March. The Transitional Executive Council (TEC) appointed two administrators, who took control of the homeland to ensure security until the elections could be held the following month. The TEC also blocked the South African government from deploying the paramilitary Internal Stability Unit (ISU) of the South African Police force, as the unit was suspected of fomenting violence in other parts of the country after the Ciskei military had threatened to open fire on the ISU if it entered the territory. On 27 April 1994, Ciskei and all of the other homelands were reincorporated into South Africa, after the first post-apartheid elections. Along with Transkei, Ciskei became part of the new Eastern Cape Province, with its capital becoming the capital of the new province, and the former territory of the Ciskei forming parts of the Buffalo City Metropolitan Municipality, the Chris Hani District Municipality, and the Amathole District Municipality—as of 2016.
Sources: en.wikipedia.org
== External links == What is a WW domain? Ranganathan lecture on statistical coupling analysis (audio included) Protein folding — a step closer? - A summary of the Ranganathan lab's SCA-based design of artificial yet functional WW domains.
==== FY2026 proposed elimination ==== In the FY2026 President's Budget, released in mid-2025, the Trump administration proposed eliminating NCCIH entirely, along with three other NIH institutes, as part of a plan to consolidate NIH's 27 institutes and centers into eight and cut the overall NIH budget by approximately 40%. Congress rejected the proposed cuts on a bipartisan basis. The FY2026 appropriations package provided NIH with $48.7 billion in discretionary funding, an increase of $415 million over FY2025, and did not include the proposed consolidation or elimination of any NIH institutes or centers. NCCIH funding for FY2026 remained unchanged from FY2025.
A relatively short-range dating technique is based on the decay of uranium-234 into thorium-230, a substance with a half-life of about 80,000 years. It is accompanied by a sister process, in which uranium-235 decays into protactinium-231, which has a half-life of 32,760 years. While uranium is water-soluble, thorium and protactinium are not, and so they are selectively precipitated into ocean-floor sediments, from which their ratios are measured. The scheme has a range of several hundred thousand years. A related method is ionium–thorium dating, which measures the ratio of ionium (thorium-230) to thorium-232 in ocean sediment.
Sources: en.wikipedia.org
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.
No. It is a synthetic ligand that binds nuclear receptors, not a steroid or peptide hormone. Its activity depends on receptor binding rather than endocrine secretion.
Clinical evidence is limited. Most published data come from cell and animal experiments. Human safety and efficacy remain uncertain.
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.