This is a working overview of SR9009, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2025-11-24 and is reviewed periodically as new material appears.
Analytical identification and purity assessment often use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Liquid chromatography–tandem mass spectrometry is used to detect and quantify SR9009 in biological matrices, including urine and blood, for anti-doping or pharmacokinetic studies. Nuclear magnetic resonance spectroscopy can confirm molecular structure. Stability depends on form and storage: the solid is generally more stable than solutions, and repeated freeze–thaw cycles may degrade samples. Purity is typically reported as a percentage from a certificate of analysis.
Regulatory treatment of SR9009 varies by country and context. It is not approved as a therapeutic drug by agencies such as the United States Food and Drug Administration or the European Medicines Agency. Sports authorities list it as a prohibited substance; the World Anti-Doping Agency classifies it among hormone and metabolic modulators. Legal status for personal possession or sale differs across jurisdictions, and some countries may restrict it under analog or research chemical laws. Buyers who seek verified material often rely on independent laboratory testing because online product labels may not match contents.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.
Most published work on SR9009 consists of preclinical studies. It is widely sold as a research chemical, a category that does not imply safety, efficacy, or pharmaceutical-grade quality. Sports anti-doping organizations have listed SR9009 as a prohibited substance, and its presence in an athlete sample can lead to sanctions. Legal status differs by country; in several jurisdictions it is not approved for human consumption and may be treated as an unapproved new drug.
| Property | Value | Notes |
|---|---|---|
| Appearance | White to off-white powder | Common supplier description |
| Solubility | Soluble in DMSO and ethanol | Low solubility in water |
| Typical storage | −20 °C, desiccated, dark | For research samples |
| Analytical method | LC-MS/MS | Used for detection and quantification |
| Regulatory status | Prohibited in sport | WADA metabolic modulator class |
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.
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.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ, also called NR1D1 and NR1D2. These receptors help regulate circadian rhythms and metabolic gene programs. The compound was developed for laboratory research, not as an approved therapeutic. Its identity is distinct from steroid hormones and selective androgen receptor modulators. Scientific interest centers on how REV-ERB activation changes gene expression in cells and animal models.
At the molecular level, SR9009 binds the ligand-binding domain of REV-ERB and strengthens recruitment of corepressor proteins such as NCoR and HDAC3. This increases repression of target genes, including Bmal1 and other clock-controlled and metabolic genes. In rodent studies, such changes have been linked to altered lipid handling, glucose metabolism, and energy expenditure. The precise chain of events between receptor binding and whole-body effects remains an active area of research. Findings in animals do not automatically translate to humans.
Laboratory studies often administer SR9009 by injection because oral absorption appears poor in rodents. Reported pharmacokinetic properties include rapid metabolism and low systemic exposure after oral dosing. Human pharmacokinetic data are sparse, so absorption, distribution, metabolism, and excretion in people are not well defined. Some research explores related REV-ERB compounds with improved drug-like properties. Regulatory approval for any REV-ERB agonist as a human medicine has not been granted to date.
Butorphanol is a morphinan-type synthetic agonist–antagonist opioid analgesic developed by Bristol-Myers. Butorphanol is most closely structurally related to levorphanol. Butorphanol is available as the tartrate salt in injectable, tablet, and intranasal spray formulations. The tablet form is only used in dogs, cats and horses due to low bioavailability in humans. It was patented in 1971 and approved for medical use in 1979.
== Chemistry == Selegiline is a substituted phenethylamine and amphetamine derivative. It is also known as (R)-(–)-N,α-dimethyl-N-(2-propynyl)phenethylamine, (R)-(–)-N-methyl-N-2-propynylamphetamine, or N-propargyl-L-methamphetamine. Selegiline (L-deprenyl) is the enantiopure levorotatory enantiomer of the racemic mixture deprenyl, whereas D-deprenyl is the dextrorotatory enantiomer. Selegiline is a derivative of levomethamphetamine (L-methamphetamine), the levorotatory enantiomer of the psychostimulant and sympathomimetic agent methamphetamine (N-methylamphetamine), with a propargyl group attached to the nitrogen atom of the molecule. Selegiline is a small-molecule compound, with the molecular formula C13H17N and a low molecular weight of 187.281 g/mol. It has high lipophilicity, with an experimental log P of 2.7 and predicted log P values of 2.9 to 3.1. Pharmaceutically, selegiline is used almost always as the hydrochloride salt, though the free base form has also been used. At room temperature, selegiline hydrochloride is a white to near white crystalline powder. Selegiline hydrochloride is freely soluble in water, chloroform, and methanol.
14 February – A study reviews educational content of 18,400 universities worldwide, finding higher education is not transitioning from fossil fuels to renewable energy curricula, failing to meet the growing demand for a clean energy workforce. On 26 February, a study analyzing funding sources and activities of two prominent academic centers delineates animal agriculture industry entrenchment in academia through support of industry-supported research and policy advocacy amid potential unfavorable policies.
Sources: en.wikipedia.org
Researchers cautioned against causal interpretation from this study, citing confounding effects, methodological concerns and a 2020 meta-analysis of randomized controlled trials which showed no increased risk.
== Further reading == Rogers, Andrew W (1979). Techniques of Autoradiography (3rd ed.). New York: Elsevier North Holland. ISBN 978-0-444-80063-3. "Patent US4101780 Treating silver with a radioactive sulfur compound such as thiourea or derivatives". Google Patents. Retrieved 26 June 2014.
Nobody's done that before." In February 2012, the Smithsonian National Museum of American History announced that Ayyadurai had donated "a trove of documents and code" related to EMAIL. Initially, the museum—inaccurately—cited the program as one of the first to include the now common "subject and body fields, inboxes, outboxes, cc, bcc, attachments, and others. He based these elements directly off of the interoffice mail memos the doctors had been using for years, in hopes of convincing people to actually use the newfangled technology." Ayyadurai's claims drew editorial clarifications and corrections, as well as criticism from industry observers. In a followup to its acquisition announcement, the Smithsonian stated that it was not claiming that Ayyadurai had invented email, but rather that the materials were historically notable for other reasons related to trends in computer education and the role of computers in medicine. The Smithsonian statement distinguished Ayyadurai's achievement by noting that historians in the field, "have largely focused on the use of large networked computers, especially those linked to the ARPANET in the early 1970s". The statement observed that Ayyadurai's approach instead "focused on communications between linked computer terminals in an ordinary office situation".
A 2016 WHO report found that formaldehyde from second-hand vapor was around 20% greater compared to background air levels. Normal usage of e-cigarettes generates very low levels of formaldehyde. Different power settings reached significant differences in the amount of formaldehyde in the e-cigarette vapor across different devices. Later-generation e-cigarette devices can create greater amounts of carcinogens. Some later-generation e-cigarettes let users increase the volume of vapor by adjusting the battery output voltage. Depending on the heating temperature, the carcinogens in the e-cigarette vapor may surpass the levels of cigarette smoke. E-cigarettes devices using higher voltage batteries can produce carcinogens including formaldehyde at levels comparable to cigarette smoke. The later-generation and "tank-style" devices with higher voltages (5.0 V) could produce formaldehyde at comparable or greater levels than in cigarette smoke. A 2015 study hypothesized from the data that at high voltage (5.0 V), a user, "vaping at a rate of 3 mL/day, would inhale 14.4 ± 3.3 mg of formaldehyde per day in formaldehyde-releasing agents." The 2015 study used a puffing machine showed that a third-generation e-cigarette turned on to the maximum setting would create levels of formaldehyde between five and 15 times greater than with cigarette smoke.
Sources: en.wikipedia.org
==== Effects on the immune system ==== Morphine has long been known to act on receptors expressed in cells of the central nervous system resulting in pain relief and analgesia. In the 1970s and '80s, evidence suggesting that people addicted to opioids show an increased risk of infection (such as increased pneumonia, tuberculosis, and HIV/AIDS) led scientists to believe that morphine may also affect the immune system. This possibility increased interest in the effect of chronic morphine use on the immune system. The first step in determining that morphine may affect the immune system was to establish that the opioid receptors known to be expressed on cells of the central nervous system are also expressed on cells of the immune system. One study successfully showed that dendritic cells, part of the innate immune system, display opioid receptors. Dendritic cells are responsible for producing cytokines, which are the tools for communication in the immune system. This same study showed that dendritic cells chronically treated with morphine during their differentiation produce more interleukin-12 (IL-12), a cytokine responsible for promoting the proliferation, growth, and differentiation of T-cells (another cell of the adaptive immune system) and less interleukin-10 (IL-10), a cytokine responsible for promoting a B-cell immune response (B cells produce antibodies to fight off infection). This regulation of cytokines appears to occur via the p38 MAPKs (mitogen-activated protein kinase)-dependent pathway.
=== United States === In the United States, there are certain prerequisites that need to be completed before individuals can apply at either of the two programs of study approved by the National Denturist Association USA. The prerequisites vary from prior work experience to related education in the dental field. On successful completion of the selected courses, individuals are then required to complete a jurisdiction, written and clinical examination offered by each legislated state. Upon successful completion of the examination, individuals can register with each legislated state and the National Denturist Association USA to practice legally as a denturist.
=== No development reported === Bupropion (Wellbutrin) – norepinephrine–dopamine reuptake inhibitor (NDRI) and nicotinic acetylcholine receptor negative allosteric modulator EX-597 (KDS-4103; ORG-231295; URB-597) – fatty acid amide hydrolase (FAAH) inhibitor Guanfacine extended-release (Connexyn; Intuniv; Intuniv XR; S-877503; SHP-503; SPD-503) – α2-adrenergic receptor agonist
Sources: en.wikipedia.org
Legality depends on the country and the intended use. In many places it is sold as a research chemical, but sports and medicine regulations restrict it.
Detection commonly uses liquid chromatography–tandem mass spectrometry. This method can identify the compound in urine or blood at low concentrations.
Typical guidance is −20 °C, dry, and protected from light. Solutions should be aliquoted and limited freeze–thaw cycles should be used.
It is a synthetic compound studied as an agonist of REV-ERB nuclear receptors. It is not an approved medicine and has mainly been examined in laboratory and animal research.