This is a working overview of REV-ERB agonist, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2025-11-12 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.
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.
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.
| 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. |
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.
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.
SR9009 is a synthetic small molecule developed as a REV-ERB agonist. It binds to REV-ERBα and REV-ERBβ, nuclear receptors that help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, the compound alters lipid and glucose handling and influences skeletal muscle oxidative capacity. Its exact effects in humans remain largely uncharacterized because controlled clinical trials have not been reported. The molecule is frequently described in preclinical literature as a metabolic modulator.
Research interest in SR9009 grew from studies showing improved running endurance in mice after short treatment periods. Those experiments linked the compound to increased mitochondrial content and fatty acid oxidation in muscle, but the findings come from animal models and specific dosing schedules. Independent replication has been limited, and the pathways connecting REV-ERB activation to exercise performance are still being mapped. Whether similar responses occur in humans is an open question.
SR9009 is a synthetic small molecule that acts on the nuclear receptors REV-ERBα and REV-ERBβ. These receptors are part of the circadian clock machinery and normally repress transcription of certain target genes. In laboratory research, SR9009 is used as a chemical tool to study how REV-ERB activity influences metabolism, inflammation, and daily biological rhythms. The compound is not an approved medicine, and its effects in humans remain largely uncharacterized. It is often described as an investigational agent rather than a therapeutic product.
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.
Hypoglycemia due to a tumor of the pancreas or elsewhere is usually curable by surgical removal. Most of these tumors are benign. Streptozotocin is a specific beta cell toxin and has been used to treat insulin-producing pancreatic carcinoma. Hyperinsulinism due to diffuse overactivity of beta cells, such as in many of the forms of congenital hyperinsulinism, and more rarely in adults, can often be treated with diazoxide or a somatostatin analog called octreotide. Diazoxide is given by mouth, octreotide by injection or continuous subcutaneous pump infusion. When congenital hyperinsulinism is due to focal defects of the insulin-secretion mechanism, surgical removal of that part of the pancreas may cure the problem. In more severe cases of persistent congenital hyperinsulinism unresponsive to drugs, a near-total pancreatectomy may be needed to prevent continuing hypoglycemia. Even after pancreatectomy, continuous glucose may be needed in the form of gastric infusion of formula or dextrose. High dose glucocorticoid is an older treatment used for presumptive transient hyperinsulinism but incurs side effects with prolonged use.
== Signs and symptoms == Signs and symptoms of Huntington's disease most commonly become noticeable between the ages of 30 and 50 years, but they can begin at any age and present as a triad of motor, cognitive, and psychiatric symptoms. When developed in an early stage, it is known as juvenile Huntington's disease. In 50% of cases, the psychiatric symptoms appear first. These can precede the motor symptoms by many years. Disease progression is often described in early stages, middle stages and late stages with an earlier prodromal phase. In the early stages, subtle personality changes, problems in cognition and physical skills, irritability and mood swings occur, all of which may go unnoticed. Almost everyone with HD eventually exhibits similar physical symptoms, but the onset, progression, and extent of cognitive and behavioral symptoms vary significantly between individuals. The most characteristic initial physical symptoms are jerky, random and uncontrollable movements called chorea. Many people are not aware of their involuntary movements, or impeded by them. Chorea may be initially exhibited as general restlessness, small unintentionally initiated or uncompleted motions, lack of coordination, or slowed saccadic eye movements. These minor motor abnormalities usually precede more obvious signs of motor dysfunction by at least three years. The clear appearance of symptoms such as rigidity, writhing motions, or abnormal posturing appear as the disorder progresses. These are signs that the system in the brain that is responsible for movement has been affected.
==== Electric and magnetic fields ==== External fields are the most common directors of self-assembly. Electric and magnetic fields allow induced interactions to align the particles. The fields take advantage of the polarizability of the nanoparticle and its functional groups. When these field-induced interactions overcome random Brownian motion, particles join to form chains and then assemble. At more modest field strengths, ordered crystal structures are established due to the induced dipole interactions. Electric and magnetic field direction requires a constant balance between thermal energy and interaction energies.
PT-00114, also known as TCAP-1, is a corticotropin-releasing hormone (CRH) inhibitor which is under development for the treatment of generalized anxiety disorder, major depressive disorder, opioid-related disorders, post-traumatic stress disorder (PTSD), and mood disorders. It is taken by subcutaneous injection. The drug is a synthetic analogue of the teneurin C-terminal associated peptides (TCAP) and is a 41-amino acid peptide. It has been reported to produce anxiolytic-like effects in animals, among other effects. PT-00114 is under development by Protagenic Therapeutics and Charles River Laboratories. As of August 2025, it is in phase 1/2 clinical trials for generalized anxiety disorder, major depressive disorder, opioid-related disorders, and PTSD and is in phase 1 trials for mood disorders. It is or was also under development for the treatment of other anxiety and depressive disorders as well as of impulse control disorders and neurodegenerative disorders, but no recent development has been reported for these indications.
isomerase Any of a class of enzymes which catalyze the conversion of a molecule from one isomer to another, such that the product of the reaction has the same molecular formula as the original substrate but differs in the connectivity or spatial arrangement of its atoms.
Sources: en.wikipedia.org
=== Secret peace discussions, opposition to troop withdrawals === In June 1969, the former Defense Secretary Clark Clifford published an article in Foreign Affairs calling for the withdraw of 100,000 U.S. troops from Vietnam by the end of 1969 and all by the end of 1970. Influenced by Laird, Nixon announced the immediate withdraw of 25,000 U.S. troops from Vietnam, saying: "I would hope that we could beat Mr. Clifford's timetable". Kissinger was opposed to the withdrawal, which he predicted would mean the immediate collapse of South Vietnam. On 4 August 1969, Kissinger met secretly with Xuân Thủy at the Paris apartment of Jean Sainteny to discuss peace. Sainteny was a former French colonial official sympathetic to Vietnamese nationalism who had offered to serve as an honest broker. Kissinger had been hoping to see Tho rather than Thuy. Kissinger repeated the American offer of "mutual withdrawal" of U.S. and North Vietnamese forces from South Vietnam, which Thủy rejected, while Thủy demanded a new government in Saigon, which Kissinger rejected. Kissinger had a low opinion of North Vietnam, saying "I can't believe that a fourth-rate power like North Vietnam doesn't have a breaking point". Kissinger was opposed to the strategy of Vietnamization, expressing some doubt about the ability of the ARVN (Army of the Republic of Vietnam-i.e. the South Vietnamese Army) to hold the field, causing much tension with Defense Secretary Laird who was deeply committed to Vietnamization. In September 1969, Kissinger, in a memo, advised Nixon against "de-escalation", saying that keeping U.S.
== Testing procedure == A niacin test strip is similar in appearance to a pH test strip. It is small, thin, rectangular, and white in color. Water is placed onto the culture plate and touched with a test strip for 15–20 minutes inside a small, sterile tube. If excess amounts of niacin are detected, the liquid inside the tube will turn yellow, a positive test. If the liquid in the tube is clear, there are no excess amounts of niacin and the test is negative. A positive niacin test does not necessarily indicate the presence of M. tuberculosis because other Mycobacterium species can test positive for excess niacin. Along with each batch of specimens being tested, a positive control of M. tuberculosis and a negative control with no organism will be included. If the positive control tests negative, there was probably an error with the batch, and likewise for a negative test showing positive. Because lab samples that are determined to be acid-fast bacilli are possibly M. tuberculosis, a biosafety level 3 organism, all niacin tests must be conducted in a biosafety cabinet with a full gown, respirator, gloves, and sealed laboratory to ensure the safety of the laboratory technician performing the test. All tests must also be conducted with sterile technique.
«Феназепам» (Phenazepam) tablets 0.5, 1 and 2.5 mg, solution for intramuscular and intravenous injection 1 mg/mL (0.1%) «Элзепам» (Elzepam) tablets 0.5 and 1 mg, solution for intramuscular and intravenous injection 1 mg/mL (0.1%) «Фензитат» (Phenzitat) tablets 0.5 and 1 mg «Фенорелаксан» (Phenorelaxan) tablets 0.5 and 1 mg, solution for intramuscular and intravenous injection 1 mg/mL (0.1%) «Транквезипам» (Trankvezipam) tablets 0.5 and 1 mg, solution for intramuscular and intravenous injection 1 mg/mL (0.1%) «Фезипам» (Phezipam) tablets 0.5 and 1 mg (not to be confused with «Фезам» (Phezam) which contains cinnarizine/piracetam) «Фезанеф» (Phezanef) tablets 1 mg
=== Neurotoxicity === Selegiline has been reported to protect against the damage caused by the potent dopaminergic and/or noradrenergic neurotoxins 6-hydroxydopamine (6-OHDA), N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4), and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in animals. Conversely, selegiline is ineffective in protecting against the serotonergic and noradrenergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). Selegiline has also been reported to protect against methylenedioxymethamphetamine (MDMA)-induced serotonergic neurotoxicity in rodents. The serotonergic neurotoxicity of MDMA appears to be dependent on release of dopamine and its subsequent metabolism by MAO-B within serotonergic neurons into hydroxyl radicals, which is blocked by MAO-B inhibition. Likewise, selegiline prevented the serotonergic neurotoxicity of a combination of methylenedioxyaminoindane (MDAI) and dextroamphetamine. Conversely, selegiline failed to reduce the serotonergic neurotoxicity caused by fenfluramine and either did not affect or potentiated the serotonergic neurotoxicity caused by para-chloroamphetamine (PCA). In addition, findings are mixed and conflicting on whether selegiline prevents amphetamine- and methamphetamine-induced dopaminergic neurotoxicity in rodents. Although MAO-B-selective doses of selegiline protect against MDMA-induced serotonergic neurotoxicity in rodents, combination of amphetamines like MDMA with MAOIs, including selegiline, can produce serious complications, including serotonin syndrome, hypertensive crisis, and death.
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.
SR9009 is a synthetic small molecule studied as an agonist of the REV-ERB nuclear receptors. It is not an approved medicine, and its effects in humans are not well characterized.