If you have been reading about REV-ERB and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Updated 2026-03-18. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small-molecule nuclear receptor ligand |
| Appearance | Off-white to pale yellow solid | Typical for research-grade powder |
| Solubility class | Soluble in DMSO; low water solubility | Common stock solutions use organic solvent |
| Typical stock solvent | Dimethyl sulfoxide | Used for laboratory assays |
| Common analytical method | HPLC with UV or mass detection | Used for identity and purity checks |
In laboratory settings, SR9009 is typically characterized by liquid chromatography–mass spectrometry (LC-MS) or high-performance liquid chromatography with ultraviolet detection (HPLC-UV). These methods can confirm identity and estimate purity, but they require reference standards for accurate quantification. Because SR9009 is not a licensed pharmaceutical, no harmonized pharmacopeial monograph exists. Laboratories often validate in-house methods for matrices such as plasma, urine, or cell culture media. Sample preparation may involve protein precipitation or liquid-liquid extraction before analysis.
Physicochemical behavior influences handling. SR9009 is described as a solid with limited aqueous solubility, so organic solvents such as dimethyl sulfoxide or ethanol are common in research stock solutions. Aqueous dilution can produce precipitates if the organic content is too low. Light, heat, and repeated freeze-thaw cycles may affect stability. Storage recommendations usually specify a desiccated freezer environment protected from light, but exact stability data depend on the formulation and matrix.
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.
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.
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.
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.
UPMC Kildare Hospital is a 39-bed private hospital located in County Kildare, Ireland (founded in 1985 as Clane General Hospital). UPMC acquired the hospital in November 2019 in partnership with the Institute of Eye Surgery.
=== Itching === Itching tends not to be a severe problem when opioids are used for pain relief, but antihistamines are useful for counteracting itching when it occurs. Non-sedating antihistamines such as fexofenadine are often preferred as they avoid increasing opioid induced drowsiness. However, some sedating antihistamines such as orphenadrine can produce a synergistic pain relieving effect permitting smaller doses of opioids be used. Consequently, several opioid/antihistamine combination products have been marketed, such as Meprozine (meperidine/promethazine) and Diconal (dipipanone/cyclizine), and these may also reduce opioid induced nausea.
The support can be a synthetic resin, a biopolymer or an inorganic polymer such as (mesoporous) silica or a zeolite. Entrapment involves inclusion of an enzyme in a polymer network (gel lattice) such as an organic polymer or a silica sol-gel, or a membrane device such as a hollow fiber or a microcapsule. Entrapment requires the synthesis of the polymeric network in the presence of the enzyme. The third category involves cross-linking of enzyme aggregates or crystals, using a bifunctional reagent, to prepare carrier-free macroparticles. The use of a carrier inevitably leads to ‘dilution of activity’, owing to the introduction of a large portion of non-catalytic ballast, ranging from 90% to >99%, which results in lower space-time yields and productivities. Moreover, immobilization of an enzyme on a carrier often leads to a substantial loss of activity, especially at high enzyme loadings. Consequently, there is an increasing interest in carrier-free immobilized enzymes, such as cross-linked enzyme crystals (CLECs) and cross-linked enzyme aggregates (CLEAs) that offer the advantages of highly concentrated enzyme activity combined with high stability and low production costs owing to the exclusion of an additional (expensive) carrier.
The increase in γGCS causes an increased production of arsenite triglutathionine (As(SG)3) an important adduct that is taken up by either multidrug associated protein 1 (MRP1) or MRP2 which remove the arsenic out of the cell and into bile for excretion. This adduct can also decompose back into inorganic arsenic. Of particular note in the excretion of arsenic is the multiple methylation steps that take place which may increase the toxicity of arsenic due to MMeAsIII being a potent inhibitor of glutathione peroxidase, glutathione reductase, pyruvate dehydrogenase, and thioredoxin reductase.
Sources: en.wikipedia.org
== Structure == Delta hexatoxin Hv1 is a tightly folded polypeptide that contains a chain of 42 amino acid residues and has the chemical formula C206H318N58O60S9. The amino acid sequence of delta hexatoxin Hv1 is:The tertiary structure of δ-ACTX-Hv1 contains a core β region that is made up of the residues Cys1–Cys8, Cys14–Val21, and Ser30–Ser33, with Tyr22–Gly29 protruding outwards. The β region has a three-stranded antiparallel β sheet comprising Asn6–Trp7 (β1), Met18–Val21 (β2), and Ser30–Ser33 (β3). The C-terminal end of the short β1 is held in place by a bifurcated hydrogen bond between the Cys8 amide proton and the carbonyl oxygens of the two residues preceding β strand 3 (Gln28 and Gly29). The β region also contains type II β turns at Lys3–Asn6 and Cys15–Met18 with a rare cis peptide bond at Cys16–Met 17. The nonpolar C-terminal 310 helix formed by Ile35–Lys41, bordering Lys40 and Lys41 and connecting to β region with a disulphide bond next to a β turn. The β region contains hydrophobic cysteine sidechains bordered by a lysine sidechain.Three of the four disulphide bonds form the ICK. The structure of the cystine knot motif found in versutoxin is similar to the one found in gurmarin, a 35-residue plant polypeptide used to test the inhibition of sweet taste receptors.
The reactions that follow the formation of FKA consist of the aromatization and functionalization stages. FKA is subjected to two rounds of hydroxylation catalyzed by two distinct P450 monooxygenases forming flavokermesic acid and kermesic acid, respectively. Whether these monooxygenases are oxygen or flavin dependent is to be determined. The first monooxygenation occurs in the central aromatic ring carbon, C10 while the second occurs in the C4 position. The final attachment of a carbohydrate onto the C2 position C-glycosylation reaction is catalyzed by a UDP-glucose dependent membrane bound glucosyltransferase. The order of the last two steps has not been determined due to lack of experimental kinetic data.
Valve struggled to find a publisher, as many believed Half-Life was too ambitious for a first-time developer. Sierra On-Line signed Valve for a one-game deal as it was interested in making a 3D action game, especially one based on the Quake engine. Sierra gave Valve an advance of around $1 million in exchange for 30% of the revenue and 100% of the intellectual property; the rest of development was funded by Newell and Harrington. Valve first showed Half-Life in early 1997; it was a success at E3 that year, where Valve demonstrated the animation and artificial intelligence. Novel features of the artificial intelligence included fear and pack behavior. Valve aimed for a November 1997 release to compete with Quake II. By September 1997, the team found that, while they had built some innovative aspects in weapons, enemies, and level design, the game was not fun and there was little design cohesion. Playtesting produced "lukewarm" responses. Sierra would not agree to extra funding, so Newell took out a loan to fund additional development to rework the game and delay its release date. Valve took a novel approach of assigning a small team to build a prototype level containing every element in the game and then spent a month iterating on the level. When the rest of the team played the level, which the designer Ken Birdwell described as "Die Hard meets Evil Dead", they agreed to use it as a baseline. The team developed three theories about what made the level fun.
Sources: en.wikipedia.org
=== Biofilm === Biofilm is one of the most common reasons for delayed healing in pressure ulcers. Biofilm occurs rapidly in wounds and stalls healing by keeping the wound inflamed. Frequent debridement and antimicrobial dressings are needed to control the biofilm. Infection prevents the healing of pressure ulcers. Signs of pressure ulcer infection include slow or delayed healing and pale granulation tissue. Signs and symptoms of systemic infection include fever, pain, redness, swelling, warmth of the area, and purulent discharge. Additionally, infected wounds may have a gangrenous smell, be discolored, and may eventually produce more pus. In order to eliminate this problem, it is imperative to apply antiseptics at once. Hydrogen peroxide (a near-universal toxin) is not recommended for this task as it increases inflammation and impedes healing. Cleaning the open wound with hypochlorous acid is helpful. Dressings with cadexomer iodine, silver, or honey have been shown to penetrate bacterial biofilms. Systemic antibiotics are not recommended in treating local infection in a pressure ulcer, as it can lead to bacterial resistance. They are only recommended if there is evidence of advancing cellulitis, bony infection, or bacteria in the blood.
In early February, the North Korean government took severe measures to block the spread of COVID-19. Rodong Sinmun, the Workers' Party of Korea newspaper, reported that the customs officials at the port of Nampo were performing disinfection activities, including placing imported goods in quarantine. All international flights and railway services were suspended in early February, and connections by sea and road were largely closed over the following weeks. In February, wearing face masks was obligatory, and visiting public places such as restaurants was forbidden. Ski resorts and spas were closed, and military parades, marathons, and other public events were cancelled. Schools were closed throughout the country; university students in Pyongyang from elsewhere in the country were confined to their dormitories. Although South Korean media reported the epidemic had spread to North Korea, the WHO said there were no indications of cases there. On 18 February, Rodong Sinmun, the official newspaper of North Korea's ruling party, quoted a public health official reiterating that there had been "no confirmed case of the new coronavirus so far". The WHO prioritised aid for North Korea, including the shipment of protective equipment and supplies. The Daily NK reported information from an informant inside North Korea's military on 9 March, stating that 180 soldiers had died in January and February from complications of "high fevers stemming from pneumonia, tuberculosis, asthma or colds", while about 3,700 soldiers were under quarantine.
==== South Korea ==== Dubu plays an important part in Korean cuisine. Tofu is often pan-fried and served as banchan with a dipping sauce. It is also used in many soups. Cubes of firm tofu can be seasoned with soy sauce, garlic, and other ingredients before pan-frying. A dish of tofu cubes simmered with similar spicy seasoning is called dubu-jorim. Dubu-kimchi features blanched tofu served in rectangular slices around the edges of a plate with pan-fried kimchi. This is a popular food to accompany alcoholic drinks (anju). Soft, unpressed sun-dubu is used as the main ingredient of sundubu-jjigae (soft tofu stew), while other soups and stews such as doenjang-guk (soybean paste soup), doenjang-jjigae (soybean paste stew), and kimchi-jjigae (kimchi stew) tend to have diced firm tofu in them. As in many other East Asian countries, tofu is also enjoyed in a hot pot dish called dubu-jeongol (tofu hot pot).
== Causes == Type 1 diabetes is caused by the destruction of β-cells—the only cells in the body that produce insulin—and the consequent progressive insulin deficiency. Without insulin, the body cannot respond effectively to increases in blood sugar. Due to this, people with untreated diabetes have persistent hyperglycemia. In 70–90% of cases, β-cells are destroyed by one's own immune system, for reasons that are not entirely clear. The best-studied components of this autoimmune response are β-cell-targeted autoantibodies that begin to develop in the months or years before symptoms arise. Typically, antibodies against insulin or the protein GAD65,are the first to develop, followed by antibodies against the proteins IA-2, IA-2β, and/or ZNT8. People with a higher level of these antibodies, especially those who develop them earlier in life, are at higher risk for developing symptomatic type 1 diabetes. The trigger for the development of these antibodies remains unclear. Several explanatory theories have been put forward, and the cause may involve genetic susceptibility, a diabetogenic trigger, and/or exposure to an antigen. The remaining 10–30% of patients with type 1 diabetes have β-cell destruction but no sign of autoimmunity; this is called idiopathic type 1 diabetes (its cause is unknown).
Sources: en.wikipedia.org
SR9009 is a synthetic research compound that acts on REV-ERB nuclear receptors. It is not approved for human use and is sold only as a research chemical. Its effects have been studied mainly in cells and rodents.
It binds REV-ERB alpha and REV-ERB beta and changes the expression of genes tied to metabolism and circadian rhythm. These changes can affect mitochondria and energy use in animal models. The exact chain from receptor binding to physiological outcome is still being mapped.
No reliable human trials show that SR9009 improves athletic performance. Some rodent studies report endurance changes, but these results are not proof of human benefit. Its use in sport is prohibited, and quality and safety data are lacking.
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.