This is a working overview of SR9009, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2025-10-27 and is reviewed periodically as new material appears.
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.
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.
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 |
|---|---|---|
| Common name | SR9009 | Also marketed informally as Stenabolic |
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ |
| Molecular formula | C24H30ClN3O4S | Approximate molecular weight 492 g/mol |
| CAS Registry Number | 1379686-30-2 | Identifier for the parent compound |
| Regulatory status | Not approved for human use | Prohibited in sport by WADA |
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.
In laboratory settings, SR9009 is commonly identified by its molecular structure and its interaction with REV-ERB receptors. Vendors may list it under synonyms such as Stenabolic or REV-ERB agonist, but those names do not define purity or identity. Analytical confirmation typically uses high-performance liquid chromatography with ultraviolet detection or liquid chromatography–mass spectrometry. A reference standard is needed to compare retention time and mass spectrum, because the compound can be confused with related research chemicals.
Handling practices for SR9009 focus on minimizing degradation and contamination. The solid is generally stored desiccated at or below -20 °C, protected from light and moisture. Stock solutions are often prepared in dimethyl sulfoxide or ethanol, then aliquoted to avoid repeated freeze–thaw cycles. Aqueous solubility is low, so formulations for animal studies may require cosolvents or suspending agents. Personnel should follow institutional chemical safety procedures, because toxicological data for humans are incomplete.
Regulatory status varies by country and intended use. Major drug agencies have not granted marketing authorization for SR9009 as a medicine, and it is not listed as a controlled substance in many jurisdictions. It is often sold as a research chemical, a category that may fall outside pharmaceutical manufacturing rules. Buyers should verify local laws and supplier documentation, including certificates of analysis. The lack of standardized quality controls raises concerns about identity, purity, and actual content in products marketed online.
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.
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.
On 1 March, the PAF conducted airstrikes in Kabul with locals reporting hearing sounds of explosions and gunfire in several parts of Kabul, including Darulaman, and areas near the airport and Kārte Naw. According to residents, Pakistani fighter aircraft began patrolling and conducting intermittent strikes at about 20:30 local time on 28 February; explosions and gunfire were reported until about 06:00 the following morning. Residents also report hearing sound of explosions and gunfire around Shash Darak neighborhood. Shash Darak is home to several Afghan government and intelligence facilities, including Directorate 40 of the Taliban's intelligence service and offices of the Urban Development Ministry. Afghanistan's Ministry of Defense said that air-defense fire had been directed at Pakistani aircraft over Kabul and advised residents not to be alarmed. Later that day, the PAF carried out airstrikes on Bagram Airfield. According to local Afghan sources, the airstrikes were carried out by at least three aircraft, with several explosions being heard. Taliban officials claimed Pakistan's fighter jets attempted to bomb the base but were repelled by anti-aircraft fire and that no damage was sustained. However, satellite imagery published by The New York Times showed a hangar and two warehouses at the base had been destroyed. Pakistani officials later confirmed the strike on Bagram and said it also destroyed military supplies and an unknown number of Black Hawks, C-130 and Super Tucanos on the airfield.
Prompt chaining: A sequence where the output of one step serves as the input for the next. Routing: Directing an input to a specialized downstream task or tool. Parallelization: The simultaneous execution of multiple tasks. Sequential processing: A fixed, linear progression of tasks through a predefined pipeline. Planner-critic: An iterative pattern where one agent generates a proposal and another evaluates it to provide feedback for refinement.
This rearrangement demonstrates that similar to the Michaelis–Menten equation, the maximal rate of reaction depends on the proportion of the enzyme population interacting with its substrate. fraction of the enzyme population bound by substrate
== Activation == MOR can mediate acute changes in neuronal excitability via suppression of presynaptic release of GABA. Activation of the MOR leads to different effects on dendritic spines depending upon the agonist, and may be an example of functional selectivity at the μ-receptor. The physiological and pathological roles of these two distinct mechanisms remain to be clarified. Perhaps, both might be involved in opioid addiction and opioid-induced deficits in cognition. Activation of the μ-opioid receptor by an agonist such as morphine causes analgesia, sedation, slightly reduced blood pressure, itching, nausea, euphoria, decreased respiration, miosis (constricted pupils), and decreased bowel motility often leading to constipation. Some of these effects, such as analgesia, sedation, euphoria, itching and decreased respiration, tend to lessen with continued use as tolerance develops. Miosis and reduced bowel motility tend to persist; little tolerance develops to these effects. The canonical MOR1 isoform is responsible for morphine-induced analgesia, whereas the alternatively spliced MOR1D isoform (through heterodimerization with the gastrin-releasing peptide receptor) is required for morphine-induced itching.
Sources: en.wikipedia.org
=== Food additives === Potassium sodium tartrate (KNaC4H4O6, Rochelle salt) is a main constituent of some varieties of baking powder; it is also used in the silvering of mirrors. Potassium bromate (KBrO3) is a strong oxidizer (E924), used to improve dough strength and rise height. Potassium bisulfite (KHSO3) is used as a food preservative, for example in wine and beer-making (but not in meats). It is also used to bleach textiles and straw, and in the tanning of leathers.
Rather than finding homologous proteins from different species, a new Tag/Catcher pair was developed from SpyTag/SpyCatcher with minimal mutations. SpyTag I3W (AW) reacts with SpyCatcher F77V, F94A (BVA) but minimally with SpyCatcher, whereas SpyCatcher F77V, F94A can react with both SpyTag I3W and SpyTag. However, the cross-reactivity of SpyCatcher F77V, F94A with both SpyTag versions may limit its utility as a new Tag/Catcher pair. A different chemistry can be exploited for protein ligation: the discovery of an intramolecular ester bond formation in Clostridium perfringens cell-surface adhesin protein Cpe0147 led to the development of another Tag/Catcher pair with Cpe0147565–587 as the Tag and Cpe0147439–563 as the Catcher. The ester bond formed between Thr-Gln is irreversible, however by mutating the Thr to Ser, the Ser-Gln ester bond is reversible with a change of pH.
== Louisiana Secretary of Revenue (1996–1999) == Following his first stint in state government, Kennedy returned to private law practice until 1996. That year, he was appointed secretary of the state Department of Revenue in the cabinet of Governor Mike Foster. Despite having political differences with Kennedy during his time in Roemer's administration, Foster selected Kennedy for the position and later endorsed him for the U.S. Senate. Kennedy stepped down as secretary in April 1999 and was replaced by Brett Crawford.
Sources: en.wikipedia.org
However, the failure of D2 dopamine receptor antagonism, or dopamine receptor dysfunction, do not fully explain the presenting symptoms and signs of NMS, as well as the occurrence of NMS with atypical antipsychotic drugs with lower D2 dopamine activity. This has led to the hypothesis of sympathoadrenal hyperactivity (results from removing tonic inhibition from the sympathetic nervous system) as a mechanism for NMS. Release of calcium is increased from the sarcoplasmic reticulum with antipsychotic usage. This can result in increased muscle contractility, which can play a role in the breakdown of muscle, muscle rigidity, and hyperthermia. Some antipsychotic drugs, such as typical antipsychotics, are known to block dopamine receptors; other studies have shown that when drugs supplying dopamine are withdrawn, symptoms similar to NMS present themselves. In support of the sympathoadrenal hyperactivity model, it has been hypothesized that a defect in calcium regulatory proteins within the sympathetic neurons may bring about the onset of NMS. This model of NMS strengthens its suspected association with malignant hyperthermia in which NMS may be regarded as a neurogenic form of this condition which itself is linked to defective calcium-related proteins. There is also thought to be considerable overlap between malignant catatonia and NMS in their pathophysiology, the former being idiopathic and the latter being the drug-induced form of the same syndrome.
The process of blending gives the end product a consistent taste, as batches of tobacco grown in different regions may change in flavor profile from year to year due to different environmental conditions. Modern cigarettes produced after the 1950s, although composed mainly of shredded tobacco leaf, use a significant quantity of tobacco processing byproducts in the blend. Each cigarette's tobacco blend is made mainly from the leaves of flue-cured brightleaf, burley tobacco, and oriental tobacco. These leaves are selected, processed, and aged prior to blending and filling. The processing of brightleaf and burley tobaccos for tobacco leaf "strips" produces several byproducts such as leaf stems, tobacco dust, and tobacco leaf pieces ("small laminate"). To improve the economics of producing cigarettes, these byproducts are processed separately into forms where they can then be added back into the cigarette blend without a marked change in the cigarette's quality. The most common tobacco byproducts include:
=== Trivehexin precursor === Like most precursors used for radiolabeling with radioactive metal cations, Trivehexin is composed of a dedicated complex ligand (a so-called chelator) for kinetically inert binding of the 68GaIII ion, and the bioligand(s) for binding to αvβ6-integrin. The chelator comprised in Trivehexin is a triazacycloalkane with 3 phosphinic acid substituents, with the basic structure 1,4,7-triazacyclononane-1,4,7-triphosphinate (frequently abbreviated TRAP). The αvβ6-integrin binding molecular unit is a cyclic nonapeptide with the amino acid sequence cyclo(YRGDLAYp(NMe)K) (INN: relitegatide). In the Trivehexin molecule, three of these cyclopeptides are attached by covalent bonds to a single TRAP chelator core. Since TRAP possesses three equivalent carboxylic acids for conjugation of other molecular units via amide formation, Trivehexin is a C3-symmetrical molecule with its three peptide bioligands being fully equivalent. The peptides are attached to the chelator core via the terminal amine group of the side chains of N-methyl lysine. Actually, the conjugation is not done by amide bonding directly, but involves prior functionalization of the peptide with a short molecular extension (a linker) bearing a terminal alkyne, and of TRAP with three linkers bearing terminal azides. These components are assembled by means of copper(I) catalyzed alkyne-azide cycloaddition (CuAAC, also known as Huisgen reaction, a Click chemistry reaction), giving rise to the three 1,3-triazole linkages in the 68Ga-Trivehexin structure.
Sources: en.wikipedia.org
SR9009 is a synthetic research compound that binds and modulates the nuclear receptors REV-ERBα and REV-ERBβ. It is used in laboratory studies of circadian biology and metabolism, not as an approved medicine. It is also known by the informal name Stenabolic.
No. SR9009 has not been approved as a therapeutic drug in the United States, European Union, or other major markets. Human safety and efficacy data are very limited. Its presence in consumer products does not imply regulatory approval.
The World Anti-Doping Agency lists SR9009 as a prohibited substance because it can alter gene expression and metabolic pathways relevant to performance. The ban applies at all times, not only during competition. Detection relies on laboratory methods such as mass spectrometry.
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.