SR9009 raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2026-08-01 and is reviewed periodically as new material appears.
At the molecular level, SR9009 binds REV-ERBα and REV-ERBβ and alters their repressive activity on target genes. These nuclear receptors help regulate the circadian clock, lipid synthesis, glucose metabolism, and inflammatory pathways. By changing transcription, the compound can shift the timing or magnitude of downstream metabolic processes in model systems. It does not act through androgen receptors or adenosine receptors, which distinguishes it from several substances sold for athletic performance. Whether the same transcriptional changes occur in humans at tolerable exposures remains an open question because controlled human studies are lacking.
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, 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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C20H24ClN3O4S | Derived from published structure. |
| Molecular weight | 437.94 g/mol | Calculated value. |
| Appearance | White to off-white solid | Typical for purified research samples. |
| Solubility | DMSO, ethanol; low in water | Class: poorly water-soluble. |
| Typical storage | -20 °C, desiccated, protected from light | Limits degradation. |
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.
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.
Laboratory identification of SR9009 typically relies on chromatographic separation coupled to mass spectrometry, often with ultraviolet detection as a secondary check. Nuclear magnetic resonance spectroscopy can confirm molecular structure when a reference standard is available. Because many suppliers sell the compound as a research chemical, independent identity testing is important for experimental reproducibility. A single retention time is not sufficient proof of identity, especially when related compounds may be present. Purity assessments usually report a percentage based on area normalization.
SR9009 is generally described as poorly soluble in water and more soluble in organic solvents such as dimethyl sulfoxide and ethanol. Stock solutions are commonly prepared in an organic solvent before dilution into an aqueous buffer or vehicle. Precipitation can occur if the organic fraction is reduced too quickly or if the final concentration exceeds the compound's solubility limit. Sonication or gentle warming may aid dissolution in some protocols, but excessive heat can promote degradation. Container material and pH can also influence observed solubility.
For long-term storage, SR9009 is typically kept as a solid at low temperature, protected from moisture and light. Desiccated conditions limit hydrolysis, while opaque containers reduce photochemical breakdown. Solutions are less stable than solids and are often stored frozen in aliquots to avoid repeated freeze-thaw cycles. Stability data are not standardized across all suppliers, so users should rely on certificate-of-analysis information when available. Degradation may appear as color change, precipitate, or decreased chromatographic purity.
=== NICE === The UK's National Institute for Health and Care Excellence (NICE) can pay from £100,000 to £300,000 per QALY (Quality Adjusted Life Year) for treatments of "very rare conditions". This is compared to under £20,000 for non-orphan drugs. In 2015, NICE held consultations with "patient groups, the Department of Health, companies, learned societies, charities and researchers" regarding the appraisal of medicines and other technologies. There was a call for more research into new processes, including:
NRF2, a transcription factor associated with the cellular response to oxidative stress, has been found to be indirectly regulated by O-GlcNAc. KEAP1, an adaptor protein for the cullin 3-dependent E3 ubiquitin ligase complex, mediates the degradation of NRF2; oxidative stress leads to conformational changes in KEAP1 that repress degradation of NRF2. O-GlcNAc modification of KEAP1 at S104 is required for efficient ubiquitination and subsequent degradation of NRF2, linking O-GlcNAc to oxidative stress. Glucose deprivation leads to a reduction in O-GlcNAc and reduces NRF2 degradation. Cells expressing a KEAP1 S104A mutant are resistant to erastin-induced ferroptosis, consistent with higher NRF2 levels upon removal of S104 O-GlcNAc. Elevated O-GlcNAc levels have been associated with diminished synthesis of hepatic glutathione, an important cellular antioxidant. Acetaminophen overdose leads to accumulation of the strongly oxidizing metabolite NAPQI in the liver, which is detoxified by glutathione. In mice, OGT knockout has a protective effect against acetaminophen-induced liver injury, while OGA inhibition with thiamet-G exacerbates acetaminophen-induced liver injury.
Unlike TTP, no deficient ADAMTS13 activity nor anti-ADAMTS13 antibody was found indicating a thrombotic microangiopathy of different underlying cause. If IV Opana abuse is acknowledged, supportive care, instead of therapeutic plasma exchange could be considered. In January 2015, the first HIV outbreak linked to abuse of prescription opioid drugs was identified by the Indiana State Department of Health (ISDH), in the small, rural community of Scott County in southeastern Indiana. ISDH launched an investigation into this HIV outbreak when 11 individuals were confirmed positive for HIV with ties tracing back to the same community. Three months into this investigation, ISDH diagnosed a total of 135 people with HIV, with the numbers still increasing. The cause of this outbreak has been linked to the sharing of needles between opioid abusers, which in some cases, involves sharing needles with up to nine different partners. In late March 2015, reports indicated Austin, Indiana, was the center of an outbreak of HIV caused by oxymorphone use as an injectable recreational drug. The outbreak required emergency action by state officials. The NPR podcast "embedded" episode of 31 March 2016 was an in-depth account of a visit to oxymorphone abusers in Austin, Indiana. In 2016, the street price of oxymorphone was reported to be US$140. The common opioid of abuse in this outbreak has been identified as Opana ER, a time-released oxymorphone pain killer formulated to be resistant to crushing, manufactured by Endo Pharmaceuticals.
Sources: en.wikipedia.org
== Treatment == Nifedipine and amlodipine, which are vasodilators in the class of drugs known as calcium channel blockers, may be used as treatments. Vasodilation may reduce pain, facilitate healing, and prevent recurrences. Vasodilators are typically available in an oral pill but can be compounded into a topical formula. Diltiazem, another vasodilator, is also sometimes used.
In contrast with this limited scope, MOFs exhibit more diverse coordination geometries, polytopic linkers, and ancillary ligands (F−, OH−, H2O among others). It is also difficult to obtain zeolites with pore sizes larger than 1 nm, which limits the catalytic applications of zeolites to relatively small organic molecules (typically no larger than xylenes). Furthermore, mild synthetic conditions typically employed for MOF synthesis allow direct incorporation of delicate functionalities into the framework structures. Such a process would not be possible with zeolites or other microporous crystalline oxide-based materials because of the harsh conditions typically used for their synthesis (e.g., calcination at high temperatures to remove organic templates). Metal–organic framework MIL-101 is one of the most used MOFs for catalysis incorporating different transition metals such as Cr. However, the stability of some MOF photocatalysts in aqueous medium and under strongly oxidizing conditions is low. Zeolites still cannot be obtained in enantiopure form, which precludes their applications in catalytic asymmetric synthesis.
It could also reflect steric and chemical properties that had another effect on the codon during its evolution. Amino acids with similar physical properties also tend to have similar codons, reducing the problems caused by point mutations and mistranslations. Three main hypotheses address the origin of the genetic code. Many models belong to one of them or to a hybrid:
On 12 August 1990, Saddam "propose[d] that all cases of occupation, and those cases that have been portrayed as occupation, in the region, be resolved simultaneously". He called for Israel to withdraw from occupied territories in Palestine, Syria, and Lebanon, Syria to withdraw from Lebanon, and "mutual withdrawals by Iraq and Iran and arrangement for the situation in Kuwait." He called for a replacement of US troops, that mobilized in Saudi Arabia, with "an Arab force", as long as that force did not involve Egypt. He requested an "immediate freeze of all boycott and siege decisions" and a normalization of relations with Iraq. Bush was strongly opposed to any "linkage" between Iraq's occupation of Kuwait and the Palestinian issue. On 23 August, Saddam appeared on state television with Western hostages to whom he had refused exit visas. In the video, he asks a British boy, Stuart Lockwood, whether he is getting his milk, and goes on to say, through his interpreter, "We hope your presence as guests here will not be for too long. Your presence here, and in other places, is meant to prevent the scourge of war." Another Iraqi proposal communicated was delivered to US national security advisor Brent Scowcroft by an unidentified Iraqi official. The official communicated that Iraq would "withdraw from Kuwait and allow foreigners to leave" provided the UN lifted sanctions, allowed "guaranteed access to the Persian Gulf through the Kuwaiti islands of Bubiyan and Warbah", and allowed Iraq to "gain full control of the Rumaila oil field that extends slightly into Kuwaiti territory".
Sources: en.wikipedia.org
SR9009 is a synthetic REV-ERB agonist used in laboratory research. It is not an approved drug, and its effects in humans are not well characterized. It is often sold as a research chemical under the name Stenabolic.
No. SR9009 targets the nuclear receptors REV-ERBα and REV-ERBβ, not the androgen receptor. This mechanism differs from selective androgen receptor modulators and from exercise mimetics that act on PPARδ.
Published evidence is mainly preclinical, using cell cultures and animal models. Controlled human trials are not well documented in the public literature. Claims about human performance or health effects therefore remain unsupported by robust clinical data.
SR9009 is a synthetic research compound that activates the REV-ERBα and REV-ERBβ nuclear receptors. It is not an approved drug and has no established human therapeutic use. Most published biological data come from cell and rodent studies.