DMSO stock 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 2025-12-24 and is reviewed periodically as new material appears.
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.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Common name | SR9009 | Also referred to as Stenabolic in non-scientific contexts. |
| Chemical class | Synthetic small molecule | Not a steroid or peptide hormone. |
| Receptor target | REV-ERBα and REV-ERBβ | Nuclear receptor agonist in preclinical studies. |
| Development status | Investigational | No approved human therapeutic indication. |
| Regulatory attention | Prohibited in sport | Listed by anti-doping authorities. |
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.
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.
SR9009 stability depends on temperature, moisture, light, and solvent. Solid material is generally kept cool and dry, while solutions may require protection from repeated warming and cooling. Degradation can appear as color changes, precipitate, or new chromatographic peaks. Researchers should follow supplier instructions and their own stability data. Long-term storage conditions for human use have not been established because the compound lacks approved clinical formulation.
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.
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.
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.
Vitamin C megadosage is a term describing the consumption or injection of vitamin C in doses comparable to or higher than the amounts produced by the livers of mammals which are able to synthesize vitamin C. An argument for this, although not the actual term, was described in 1970 in an article by Linus Pauling. Briefly, his position was that for optimal health, humans should be consuming at least 2,300 mg/day to compensate for the inability to synthesize vitamin C. The recommendation also fell into the consumption range for gorillas—a non-synthesizing near-relative to humans. A second argument for high intake is that serum ascorbic acid concentrations increase as intake increases until it plateaus at about 190 to 200 micromoles per liter (μmol/L) once consumption exceeds 1,250 milligrams. As noted, government recommendations are a range of 40 to 110 mg/day and normal plasma is approximately 50 μmol/L, so "normal" is about 25% of what can be achieved when oral consumption is in the proposed megadose range. Pauling popularized the concept of high dose vitamin C as prevention and treatment of the common cold in 1970. A few years later he proposed that vitamin C would prevent cardiovascular disease, and that 10 grams/day, initially administered intravenously and thereafter orally, would cure late-stage cancer. Mega-dosing with ascorbic acid has other champions, among them chemist Irwin Stone and the controversial Matthias Rath and Patrick Holford, who both have been accused of making unsubstantiated treatment claims for treating cancer and HIV infection.
The main effect of glaucoma is damage to the optic nerve. Eventually, this damage leads to vision loss, which can deteriorate with time. The underlying cause of open-angle glaucoma remains unclear. Several theories exist on its exact etiology. Intraocular pressure is a function of the production of liquid aqueous humor by the ciliary processes of the eye, and its drainage through the trabecular meshwork. Aqueous humor flows from the ciliary processes into the posterior chamber, bounded posteriorly by the lens and the zonules of Zinn, and anteriorly by the iris. It then flows through the pupil of the iris into the anterior chamber, bounded posteriorly by the iris and anteriorly by the cornea. From here, the trabecular meshwork drains aqueous humor via the scleral venous sinus (Schlemm's canal) into scleral plexuses and general blood circulation. In open/wide-angle glaucoma, flow is reduced through the trabecular meshwork due to the degeneration and obstruction of the trabecular meshwork, whose original function is to absorb the aqueous humor. Loss of aqueous humor absorption leads to increased resistance and thus a chronic, painless buildup of pressure in the eye. In primary angle-closure glaucoma, the iridocorneal angle is narrowed or completely closed, obstructing the flow of aqueous humor to the trabecular meshwork for drainage. This is usually due to the forward displacement of the iris against the cornea, resulting in angle closure. This accumulation of aqueous humor causes an acute increase in pressure and damage to the optic nerve.
=== Abnormal collagen === Abnormal collagen fibrils are often found in diabetes. Due to increased levels of lysyl oxidase, collagen increases cross-linking. This thickens the basement membrane, another hallmark of NL.
=== Imaging studies === In some cases, imaging studies may be used to assess the extent of organ involvement and damage. For example, chest x-rays or CT scans can identify lung involvement in diseases like rheumatoid arthritis or systemic lupus erythematosus, while an MRI can reveal inflammation or damage in the brain and spinal cord in multiple sclerosis.
23090Th + n → 23190Th + γ β−→25.5 h 23191Pa ( α→3.28 × 104 y 22789Ac ) 23191Pa + n → 23291Pa + γ β−→1.3 d 23292U α→69 y 232U by itself is not particularly harmful, but quickly decays to produce the strong gamma emitter 208Tl. (232Th follows the same decay chain, but its much longer half-life means that the quantities of 208Tl produced are negligible.) These impurities of 232U make 233U easy to detect and dangerous to work on, and the impracticality of their separation limits the possibilities of nuclear proliferation using 233U as the fissile material. 233Pa has a relatively long half-life of 27 days and a high cross section for neutron capture. Thus it is a neutron poison: instead of rapidly decaying to the useful 233U, a significant amount of 233Pa converts to 234U and consumes neutrons, degrading the reactor efficiency. To avoid this, 233Pa is extracted from the active zone of thorium molten salt reactors during their operation, so that it does not have a chance to capture a neutron and will only decay to 233U. The irradiation of 232Th with neutrons, followed by its processing, needs to be mastered before these advantages can be realised. Because this requires more advanced technology than the uranium and plutonium fuel cycle, research continues in this area. Others cite the low commercial viability of the thorium fuel cycle: the international Nuclear Energy Agency predicts that the thorium cycle will never be commercially viable while uranium is available in abundance—a situation which may persist "in the coming decades".
Sources: en.wikipedia.org
=== Brand names === As of 2018, the combination is marketed under several brand names, including Efficib, Janmet, Januet, Janumet, Jznumet, Ristaben Met, Ristfor, Siglimet, Sitamet, Sitar-M, Sliptin-M, Treviamet, Velmetia, Istamet, Emsita, Sitaglyn, Sitazit-M, and Zaxoran.
There is great variation in the carbon isotope composition of amino acids within a single organism. In cyanobacteria, Macko et al. observed a ~30‰ range in δ13C values amongst the amino acids. Amino acids produced from the same precursors also had widely varying compositions. It is difficult to explain these trends because of limited data on the kinetic isotope effects associated with reactions that synthesize amino acid carbon skeletons. Nevertheless, some insights can be gained by applying the logic above to the reaction networks responsible for amino acid biosynthesis. Consider the amino acids synthesized from pyruvate. Pyruvate is produced during glycolysis and can be decarboxylated by pyruvate dehydrogenase to generate acetyl groups. These acetyl groups enter the citric acid cycle as acetyl-CoA or can be used to synthesize lipids. There is a large kinetic isotope effect associated with this reaction, so the remaining pyruvate pool becomes enriched in 13C relative to the acetyl groups. This enriched pyruvate can be transaminated to produce alanine. In the experiments by Macko et al., alanine indeed had a δ13C value slightly higher than that of cyanobacterial photosynthate. Valine is synthesized by the addition of a 13C depleted acetyl group to pyruvate. Consistent with this mechanism, Takano et al. found valine to be depleted in 13C relative to alanine in anaerobic methanotrophic archaea. However, in cyanobacteria, Macko et al. observed a higher δ13C value for valine than alanine.
which gives the area in terms of the diagonals p, q and the sides a, b, c, d of the tangential quadrilateral. The area can also be expressed in terms of just the four tangent lengths. If these are e, f, g, h, then the tangential quadrilateral has the area
=== Huntington's disease === Huntington's disease is a hyperkinetic movement basal ganglia disease caused by lack of normal inhibitory inputs from medium spiny neurons of the basal ganglia. This poses the opposite effects of those associated with Parkinson's disease, including inappropriate activation of upper motor neurons. As with the GABAergic mechanisms observed in relation to Parkinson's disease, a GABA agonist injected into the substantia nigra pars reticulata decreases inhibition of upper motor neurons, resulting in ballistic involuntary motor movements, similar to symptoms of Huntington's disease.
=== Learning and memory === A study at the European Neuroscience Institute-Goettingen (Germany) found that fear extinction-induced IGF2/IGFBP7 signalling promotes the survival of 17- to 19-day-old newborn hippocampal neurons. This suggests that therapeutic strategies that enhance IGF2 signalling and adult neurogenesis might be suitable to treat diseases linked to excessive fear memory such as PTSD. The same group has found that IGFBP7 levels are increased in Alzheimer's disease and regulated via DNA methylation. Elevation of IGFBP7 in wild type mice causes memory impairment. Blocking IGFBP7 function in mice that develop Alzheimer's disease-like memory impairment restores memory function. These data suggest that IGFBP7 is a critical regulator of memory consolidation and might be used as biomarker for Alzheimer's disease. Targeting IGFBP7 could be a novel therapeutic avenue for the treatment of Alzheimer's disease patients.
Sources: en.wikipedia.org
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.
No. It is a small molecule that binds nuclear receptors involved in circadian regulation. Its classification differs from anabolic steroids or peptide hormones.
Published human clinical trial data are lacking. Most safety and activity information comes from preclinical models, so effects in people remain uncertain.
Liquid chromatography with mass spectrometry is a common approach. Ultraviolet detection and nuclear magnetic resonance can support identification when suitable standards are available.