DMSO stock 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 2025-12-21. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Analytical methods for SR9009 typically rely on liquid chromatography coupled with tandem mass spectrometry. The technique can separate the parent compound from related substances and detect low concentrations in biological matrices. Urine and blood are common samples in anti-doping testing, while in vitro studies may use cell culture media. Rapid metabolism and low expected concentrations make method validation important for reliable identification. Exact metabolite patterns can vary by species and are not fully mapped.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic small molecule | Studied as a REV-ERB agonist |
| Molecular formula | C20H24ClN3O4S | Reported for the neutral compound |
| Appearance | Off-white to pale yellow solid | Typical research-grade material |
| Solubility | Sparingly soluble in water | Soluble in solvents such as DMSO |
| Common synonyms | SR9009; Stenabolic | Stenabolic is an informal alias |
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.
Laboratory samples of SR9009 are typically handled as research chemicals rather than pharmaceuticals. Suppliers usually state that the material is for research use only and not for human or veterinary administration. Storage recommendations generally call for a freezer at approximately −20 °C, protection from light, and a desiccated environment. The solid is often described as a white to off-white powder. Solubility is commonly reported in organic solvents such as dimethyl sulfoxide and ethanol, with low solubility in water.
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.
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.
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. It is not an approved medicine and has no established human therapeutic use. The compound appears in scientific literature as a tool for probing circadian and metabolic regulation. Online sellers often label it as a research chemical, sometimes using the nickname Stenabolic. Its chemical identity is distinct from selective androgen receptor modulators, stimulants, and peroxisome proliferator-activated receptor delta agonists. Researchers use it mainly in cell and animal experiments.
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.
=== Proteogenomics === In what is now commonly referred to as proteogenomics, peptides identified with mass spectrometry are used for improving gene annotations (for example, gene start sites) and protein annotations. Parallel analysis of the genome and the proteome facilitates discovery of post-translational modifications and proteolytic events, especially when comparing multiple species.
Ergometrine, which is a minor constituent representing up to 8% of total alkaloids, is known to produce psychedelic effects only in higher amounts (2–10 mg) than those in typical doses of morning glory seeds and hence is thought to not contribute to the effects of the seeds either. Moreover, ergometrine is present in Ipomoea tricolor and Argyreia nervosa but not in Ipomoea corymbosa. Isoergine being responsible for the hallucinogenic effects of morning glory seeds is also supported by animal studies. According to Alexander Shulgin in his 1997 book TiHKAL (Tryptamines I Have Known and Loved) however, both ergine and isoergine are "probably correctly dismissed" as not contributing to the effects of morning glory seeds. The poorly-stable lysergic acid hydroxyethylamides (LSHs) might alternatively be involved in the psychedelic effects of morning glory seeds per Shulgin.
=== β+ decay and electron capture === In 1934, Frédéric and Irène Joliot-Curie bombarded aluminium with alpha particles to effect the nuclear reaction 42He + 2713Al → 3015P + 10n, and observed that the product isotope 3015P emits a positron identical to those found in cosmic rays (discovered by Carl David Anderson in 1932). This was the first example of β+ decay (positron emission), which they termed artificial radioactivity since 3015P is a short-lived nuclide which does not exist in nature. In recognition of their discovery, the couple were awarded the Nobel Prize in Chemistry in 1935. The theory of electron capture was first discussed by Gian-Carlo Wick in a 1934 paper, and then developed by Hideki Yukawa and others. K-electron capture was first observed in 1937 by Luis Alvarez, in the nuclide 48V. Alvarez went on to study electron capture in 67Ga and other nuclides.
Sources: en.wikipedia.org
"Chinese Communists have been moving ahead the last 10 years. India has been making some progress, but if India does not succeed with her 450 million people, if she can't make freedom work, then people around the world are going to determine, particularly in the underdeveloped world, that the only way they can develop their resources is through the Communist system." Relations took a nosedive when India annexed the Portuguese colony of Goa in 1961, in which the Kennedy administration condemned the armed action of the Indian government and demanded that all Indian forces be unconditionally withdrawn from Goan soil, at the same time, cutting all foreign aid appropriation to India by 25 percent. In response, Menon, now the Minister of Defence, lectured Kennedy on the importance of US-Soviet compromise and dismissed the admonishments of Kennedy and Stevenson as "vestige(s) of Western imperialism". The Kennedy administration openly supported India during the 1962 Sino-Indian war and considered the Chinese action as "blatant Chinese Communist aggression against India". The United States Air Force flew in arms, ammunition and clothing supplies to the Indian troops and the United States Navy sent the USS Kitty Hawk aircraft carrier from the Pacific Ocean to India, though it was recalled before it reached the Bay of Bengal since the crisis had passed. In a May 1963 National Security Council meeting, the United States discussed contingency planning that could be implemented in the event of another Chinese aggression on India.
== Cause == This disorder is caused by a mutation in a gene, TANGO2, which codes for protein Transport and golgi organization 2 homolog, and its located on chromosome 22. According to one study, exons 3-9 are frequently deleted in people of European origin and Hispanic ethnicity, although in Hispanic ethnicity c.460G>A (which is expressed as p.Gly154Arg, which means that on position 154, glycine is changed to arginine) is also frequent. Also, people with 22q11.2DS (DiGeorge syndrome) are at risk of developing this disorder because of hemizygosity (which means that they express only one copy of that gene, consequently chances of getting this disorder is higher).
Emerging evidence suggests that the gut microbiome may also provide predictive information for response to immune checkpoint blockade. In a multi-regional study 674 patients with resected high-risk melanoma receiving adjuvant immune checkpoint blockade, pre-treatment gut bacterial markers were associated with recurrence, with prediction performing best when patients were compared within groups matched for overall gut microbiome composition, suggesting that microbiome-based biomarkers may be informative but context dependent. PD-1 and PD-L1 inhibitors are closely related to CTLA4 (cytotoxic T-lymphocyte-associated protein 4) inhibitors, such as ipilimumab. PD-1 and CTLA-4 are both expressed on activated T cells, but at different phases of immune response. Current clinical trials are evaluating anti-PD-1 and PD-L1 drugs in combination with other immunotherapy drugs blocking LAG3, B7-H3, KIR, OX40, PARP, CD27, and ICOS.
Sources: en.wikipedia.org
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.
No. SR9009 is frequently mislabeled as a SARM in online discussions, but it does not target androgen receptors. Its known mechanism involves REV-ERB nuclear receptors and circadian-metabolic gene regulation.
Human clinical data are very limited. There is no approved human use, and safety and efficacy in people are not established. Most evidence comes from preclinical models, so effects observed in animals may not apply to humans.
No. It is an investigational compound without approved therapeutic indications. It is sold for research purposes only in many jurisdictions.