Everything below concerns Stenabolic. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2025-11-29. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
Laboratory samples of SR9009 are typically supplied as a white to off-white powder. The compound dissolves readily in organic solvents such as dimethyl sulfoxide and ethanol, while its solubility in water is low. Because of this solubility profile, researchers often prepare concentrated stock solutions in an organic solvent before diluting them into aqueous assay buffers. Light exposure, moisture, and repeated freeze-thaw cycles can degrade many small molecules, so handling procedures usually aim to minimize these factors. Purity is commonly checked before use.
Storage conditions for research-grade SR9009 generally involve a freezer at approximately minus twenty degrees Celsius, sometimes lower for long-term preservation. Containers should remain tightly closed and protected from light. Desiccants may be used to limit moisture uptake. Solutions are often stored in aliquots to avoid repeated warming and cooling. Stability data for the compound under various conditions are limited, so laboratories typically follow supplier recommendations and verify performance through periodic analytical checks rather than assuming indefinite stability.
Identity and purity testing for SR9009 commonly uses liquid chromatography coupled with tandem mass spectrometry. This method separates the compound from matrix components and detects it by mass-to-charge transitions, providing sensitive and specific confirmation. Nuclear magnetic resonance spectroscopy can support structural identification, while high-performance liquid chromatography with ultraviolet detection may estimate purity. Because online products labeled as SR9009 may contain other substances or no active compound at all, independent verification is important in research settings. Certificates of analysis are useful but not a substitute for in-house testing.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small molecule; not a steroid or peptide. |
| Primary targets | NR1D1 and NR1D2 | Also known as REV-ERBα and REV-ERBβ. |
| Studied routes | Intraperitoneal in rodents | Oral bioavailability in humans is not established. |
| Human approval | No approved therapeutic indication | No recognized clinical use. |
| Key uncertainty | Human physiological effects | Preclinical findings may not translate. |
REV-ERB proteins typically suppress gene expression by recruiting corepressor complexes to DNA response elements. SR9009 binds these receptors and strengthens that repressive action in cell-based assays. Studies in rodents have reported changes in lipid handling, mitochondrial function, and exercise capacity after treatment. Such findings are often cited as evidence for metabolic effects, but species differences and limited pharmacokinetic data make direct translation to humans uncertain. Researchers continue to examine which effects are robust and which depend on specific experimental conditions.
SR9009 is frequently discussed alongside other REV-ERB ligands, including synthetic agonists and natural heme-related molecules. Its selectivity for REV-ERB over related nuclear receptors has been measured in binding and reporter assays, though off-target activity at higher concentrations is possible. The compound is prohibited in sport by the World Anti-Doping Agency, and it is not approved for any medical use in major jurisdictions. Products sold online may be labeled as research chemicals, and their identity and purity are not guaranteed by regulatory review.
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.
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.
Both testosterone and 5α-DHT are metabolized mainly in the liver. Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively. An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order. Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone. The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile. Only a small fraction (2%) of testosterone is excreted unchanged in the urine. In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively. Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively. Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion. 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.
=== Kidney === Nonsteroidal anti-inflammatory drugs "are associated with adverse renal [kidney] effects caused by the reduction in synthesis of renal prostaglandins" in sensitive persons or animal species, and potentially during long-term use in nonsensitive persons if resistance to side effects decreases with age. However, this side effect cannot be avoided merely by using a COX-2 selective inhibitor because, "Both isoforms of COX, COX-1, and COX-2, are expressed in the kidney...
=== Hyperglycemia hyperosmolar state (HHS) === hyperosmolar non-ketotic state (HONK) or Hyperglycemia hyperosmolar state (HHS) is an acute complication sharing many symptoms with DKA, but an entirely different origin and different treatment. Oppositely, the prevalence of HHS is common in individuals with T2D. Furthermore, it showcases approximately ten times greater mortality rate than the observed in DKA. Both DKA and HHS occur when insulin becomes less effective, either due to a shortage of insulin secretion ( as in DKA), or lack of proper insulin action (as in HHS). For a person with very high blood glucose levels (usually considered to be above 30 mmol/L (600 mg/dL), that will result in osmotic diuresis, water is osmotically drawn out of cells into the blood and the kidneys eventually begin to dump glucose into the urine. This results in a loss of water (which contains electrolytes and glucose) that will increase blood osmolarity. If the fluid is not replaced, by mouth or intravenously, will ultimately result in dehydration (which in HHS typically becomes worse than DKA). Also causes electrolyte imbalances which are always dangerous. A decline in consciousness levels is primarily attributed to an increase in plasma osmolality. Lethargy may ultimately progress to a coma which is more common in T2D than T1D. HHS, unlike DKA, does not result in significant ketosis and acidosis, or there may be only a very minimal. This is because the presence of a small quantity of insulin suppresses the release of counterregulatory hormones and limits the production of ketones.
Sources: en.wikipedia.org
== Medical uses == In the EU, opicapone is indicated as adjunctive therapy to preparations of levodopa/ DOPA decarboxylase inhibitors (DDCI) in adults with Parkinson's disease and end-of-dose motor fluctuations who cannot be stabilised on those combinations. In the US, opicapone is indicated as adjunctive treatment to levodopa/carbidopa in people with Parkinson's disease (PD) experiencing "off" episodes. The COMT inhibitor opicapone is used as an additive to a combination of levodopa and a DOPA decarboxylase inhibitor to treat patients with Parkinson's disease experiencing end-of-dose motor fluctuations, if they cannot be stabilised with this drug combination.
Clocks, watches, and instruments dating from the first half of the 20th century, often in military applications, may have been painted with radioactive luminous paint. They are usually no longer luminous; this is not due to radioactive decay of the radium (which has a half-life of 1600 years) but to the fluorescence of the zinc sulfide fluorescent medium being worn out by the radiation from the radium. Originally appearing as white, most radium paint from before the 1960s has tarnished to yellow over time. The radiation dose from an intact device is usually only a hazard when many devices are grouped together or if the device is disassembled or tampered with.
At higher doses, it can induce psychosis, rhabdomyolysis, and cerebral hemorrhage. Methamphetamine is known to have a high potential for abuse and addiction. Recreational use of methamphetamine may result in psychosis or lead to post-acute-withdrawal syndrome, a withdrawal syndrome that can persist for months beyond the typical withdrawal period. Unlike amphetamine and cocaine, methamphetamine is neurotoxic to humans, damaging both dopamine and serotonin neurons in the central nervous system (CNS). Unlike the long-term use of amphetamine in prescription doses, which may improve certain brain regions in individuals with ADHD, there is evidence that methamphetamine causes brain damage from long-term use in humans; this damage includes adverse changes in brain structure and function, such as reductions in gray matter volume in several brain regions and adverse changes in markers of metabolic integrity.
Daniel Levy (political analyst); analyst, commentator, author, journalist, former advisor to Israeli government; formerly Israeli negotiator Taba summit and Oslo 2 peace process; current president of U.S./Middle East Project (USMEP); among founders of J Street; son of Lord Michael Levy; was World Chairman of World Union of Jewish Students in Jerusalem; served in Israel Defense Forces (IDF) as non-commissioned officer; worked as head of Jerusalem Affairs unit under Minister Haim Ramon; served as advisor to Justice Minister Yossi Beilin; served as an Israeli negotiator in peace talks with Palestinian leaders during his IDF years under Israeli Prime Ministers Yitzhak Rabin and Ehud Barak; was lead drafter of 2003 Geneva Initiative along with Ghaith al-Omari; current president of the U.S./Middle East Project He previously headed the Middle East and North Africa program at the European Council on Foreign Relations from 2012 to 2016. He has also worked at the director level on the New America Foundation's Middle East Task Force and as a fellow with the Century Foundation.
Sources: en.wikipedia.org
Aflatoxins – originating from Aspergillus parasiticus and Aspergillus flavus. They are frequently found in tree nuts, peanuts, maize, sorghum and other oilseeds, including corn and cottonseeds. The pronounced forms of aflatoxins are those of B1, B2, G1, and G2, amongst which Aflatoxin B1 predominantly targets the liver, which will result in necrosis, cirrhosis, and carcinoma. Other forms of aflatoxins exist as metabolites such as Aflatoxin M1. In the US, the acceptable level of total aflatoxins in foods is less than 20 μg/kg, except for Aflatoxin M1 in milk, which should be less than 0.5 μg/kg. The European union has more stringent standards, set at 10 μg/kg in cereals and cereal products. These references are also adopted in other countries. Altertoxins – are those of alternariol (AOH), alternariol methyl ether (AME), altenuene (ALT), altertoxin-1 (ATX-1), tenuazonic acid (TeA), and radicinin (RAD), originating from Alternaria spp. Some of the toxins can be present in sorghum, ragi, wheat and tomatoes. Some research has shown that the toxins can be easily cross-contaminated between grain commodities, suggesting that manufacturing and storage of grain commodities is a critical practice. Citrinin Citreoviridin Cyclopiazonic acid Cytochalasins Ergot alkaloids / ergopeptine alkaloids – ergotamine Fumonisins – Crop corn can be easily contaminated by the fungi Fusarium moniliforme, and its fumonisin B1 will cause leukoencephalomalacia (LEM) in horses, pulmonary edema syndrome (PES) in pigs, liver cancer in rats and esophageal cancer in humans.
Morgan Freeman at IMDb Morgan Freeman at the Internet Broadway Database Morgan Freeman at the Internet Off-Broadway Database Morgan Freeman on Charlie Rose Morgan Freeman collected news and commentary at The New York Times Morgan Freeman collected news and commentary at The Guardian Appearances on C-SPAN
In October 2025, GSK announced it had acquired the rights to a prostate cancer drug developed by Syndivia, a French biotechnology company, for £268 million. In January 2026, GSK agreed to acquire Rapt Therapeutics in a deal valued at $2.2 billion. In January 2026, Alteogen Inc. entered into an exclusive license agreement with Tesaro, Inc., a subsidiary of GSK, allowing Tesaro to acquire world-wide rights to use ALT-B4, Alteogen's novel hyaluronidase utilising Hybrozyme technology, for the development and commercialisation of a subcutaneous formulation of dostarlimab, a programmed death receptor-1 (PD-1) blocking antibody. In February 2026, GlaxoSmithKline announced an agreement to acquire Canada-based biopharmaceutical firm 35Pharma for $950 million in cash. The deal includes the early-stage drug HS235 for pulmonary arterial hypertension and related conditions. In June 2026, GSK announced it was acquiring Nuvalent, an American biopharmaceutical company, for $10.6 billion. Subject to regulatory and shareholder approval, if complete, the deal will be its largest in more than 10 years.
Sources: en.wikipedia.org
It is a synthetic compound that acts as an agonist at REV-ERBα and REV-ERBβ. It is used mainly as a research chemical to study circadian and metabolic pathways. It is not approved for human therapeutic use.
REV-ERB receptors generally repress transcription when bound by natural heme. SR9009 is described as an agonist that enhances this repressive activity. The result is altered expression of clock and metabolic genes.
Published controlled human trials are lacking. Some sources cite limited or unofficial reports, but these do not establish safety or efficacy. Claims about human performance effects remain unverified.
Research-grade SR9009 is typically stored frozen at about minus twenty degrees Celsius, protected from light and moisture. Stock solutions are often kept in aliquots to avoid repeated freeze-thaw cycles. Specific storage conditions should follow the supplier's documentation.