REV-ERB agonist 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 2025-10-07 and is reviewed periodically as new material appears.
SR9009 is often grouped with compounds studied for circadian and metabolic regulation rather than with classical anabolic steroids. Its interactions with nuclear receptors differ from those of androgen receptor ligands, and its proposed mechanisms involve transcriptional control rather than direct hormone signaling. Some sources classify it as a metabolic modulator because of observed effects on energy utilization. The distinction matters for regulation and for interpreting research results across different compound classes.
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.
SR9009 is frequently discussed in fitness and research-chemical contexts, yet it has no approved medical indication. Regulatory agencies have not authorized it for human use, and it is not a standard prescription drug. Some sports organizations list it as a prohibited substance because of its potential performance-enhancing properties. Published human data are sparse, so claims about its effects in people often rely on animal models or anecdotal reports. Quality and identity of online materials can vary widely.
SR9009 is a synthetic small molecule studied as a REV-ERB agonist. REV-ERBα and REV-ERBβ are nuclear receptors that help regulate circadian rhythms and metabolic gene expression. The compound was identified in academic screening efforts to find synthetic ligands for these receptors. In cell and animal studies, SR9009 alters transcription of genes involved in lipid and glucose metabolism, and it can shift circadian behavior. It is not an approved therapeutic agent.
Mechanistically, SR9009 binds the ligand-binding domain of REV-ERBα/β and enhances recruitment of corepressor complexes. This represses target genes rather than activating them. Because REV-ERB proteins normally compete with ROR proteins at shared response elements, the net effect depends on tissue and timing. Researchers use SR9009 to probe how nuclear receptor signaling links the clock to metabolism, inflammation, and muscle biology. Findings are largely preclinical, and the precise contribution of each receptor subtype remains under study.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C20H24ClN3O4S | Reported for the free base |
| Molecular weight | 437.9 g/mol | Calculated from the formula |
| Primary target | REV-ERBα and REV-ERBβ | Nuclear receptors involved in circadian regulation |
| Solubility | Soluble in DMSO and ethanol | Poorly soluble in water |
| Typical storage | -20 °C, desiccated | Protect from light and moisture |
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.
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.
Pharmacokinetic data for SR9009 are limited in published literature. Some reports indicate low oral bioavailability and rapid clearance in animals, which complicates interpretation of exposure and effect. Researchers often use injected routes in preclinical work to achieve measurable systemic levels. Analytical studies rely on mass spectrometry to detect the parent compound and its metabolites. Questions about tissue distribution, active metabolites, and long-term consequences remain open. Species differences in metabolism can affect observed half-life and target engagement.
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 and metabolic gene expression. In laboratory experiments, SR9009 binds these receptors and alters transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. It is not a naturally occurring compound and has no approved therapeutic use. Research interest stems from its ability to modify energy metabolism in cells and animal models.
In rodent studies, SR9009 has been reported to increase mitochondrial content in skeletal muscle and improve exercise endurance under some conditions. These findings led to popular descriptions such as an exercise mimetic, although that term oversimplifies the biology. Effects vary by dose, timing, tissue, and model. The compound's influence on circadian pathways means that time of administration can matter in experiments. Whether similar metabolic changes occur in humans remains largely unexplored in controlled published trials.
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.
The American Academy of Allergy, Asthma & Immunology (AAAAI); American Board of Allergy & Immunology (ABAI) International Society of Internal Medicine Internal Medicine Society of Australia and New Zealand Archived 2016-08-31 at the Wayback Machine The American Board of Internal Medicine Canadian Society of Internal Medicine The American College of Osteopathic Internists American College of Physicians
In the first, the standard and more robust scheme (Figure), Bz (benzoyl) protection is used for A, dA, C, and dC, while G and dG are protected with isobutyryl group. More recently, Ac (acetyl) group is used to protect C and dC as shown in Figure. In the second, mild protection scheme, A and dA are protected with isobutyryl or phenoxyacetyl groups (PAC). C and dC bear acetyl protection, and G and dG are protected with 4-isopropylphenoxyacetyl (iPr-PAC) or dimethylformamidino (dmf) groups. Mild protecting groups are removed more readily than the standard protecting groups. However, the phosphoramidites bearing these groups are less stable when stored in solution. The phosphite group is protected by a base-labile 2-cyanoethyl protecting group. Once a phosphoramidite has been coupled to the solid support-bound oligonucleotide and the phosphite moieties have been converted to the P(V) species, the presence of the phosphate protection is not mandatory for the successful conducting of further coupling reactions.
=== Legal status === Pethidine is in Schedule II of the Controlled Substances Act 1970 of the United States as a Narcotic with ACSCN 9230 with a 6250 kilo aggregate manufacturing quota as of 2014. The free base conversion ratio for salts includes 0.87 for the hydrochloride and 0.84 for the hydrobromide. The A, B, and C intermediates in production of pethidine are also controlled, with ACSCN being 9232 for A (with a 6 gram quota) and 9233 being B (quota of 11 grams) and 9234 being C (6 gram quota). It is listed under the Single Convention for the Control of Narcotic Substances 1961 and is controlled in most countries in the same fashion as is morphine.
In metazoans, small interfering RNAs (siRNAs) processed by Dicer are incorporated into a complex known as the RNA-induced silencing complex or RISC. This complex contains an endonuclease that cleaves perfectly complementary messages to which the siRNA binds. The resulting mRNA fragments are then destroyed by exonucleases. siRNA is commonly used in laboratories to block the function of genes in cell culture. It is thought to be part of the innate immune system as a defense against double-stranded RNA viruses.
Whether food can be addictive is disputed. Neither the DSM-5-TR nor the ICD-11 recognizes a food or eating addiction, and researchers disagree about whether the concept is best framed as an addiction to specific foods, a pattern of disordered eating, or neither. Proponents argue that ultra-processed foods high in refined carbohydrate and fat meet the criteria conventionally used to identify an addictive substance, because processing delivers these nutrients faster and in higher concentrations than they occur in nature. Critics respond that no single constituent has been isolated as the addictive agent, unlike the case for a drug. Most research uses the Yale Food Addiction Scale, which applies the DSM-5 criteria for substance use disorder to eating. Food addiction as measured this way overlaps with, but is not the same as, binge eating disorder: not everyone with an eating disorder screens positive, and not everyone screening positive has a diagnosed eating disorder.
Sources: en.wikipedia.org
== Tissue expression == Alpha-synuclein is a synuclein protein primarily found in neural tissue, making up as much as one percent of all proteins in the cytosol of brain cells. It is expressed highly in neurons within the frontal cortex, hippocampus, striatum, and olfactory bulb, but can also be found in the non-neuronal glial cells. It has been established that alpha-synuclein is extensively localized in the nucleus of mammalian brain neurons, suggesting a role of alpha-synuclein in the nucleus. Synuclein is however found predominantly in the presynaptic termini, in both free or membrane-bound forms, with roughly 15% of synuclein being membrane-bound at any moment in neurons. It has also been shown that alpha-synuclein is localized in neuronal mitochondria. Alpha-synuclein is highly expressed in the mitochondria in olfactory bulb, hippocampus, striatum and thalamus, where the cytosolic alpha-synuclein is also rich. However, the cerebral cortex and cerebellum are two exceptions, which contain rich cytosolic alpha-synuclein but very low levels of mitochondrial alpha-synuclein. It has been shown that alpha-synuclein is localized in the inner membrane of mitochondria, and that the inhibitory effect of alpha-synuclein on complex I activity of the mitochondrial respiratory chain is dose-dependent. Thus, it is suggested that alpha-synuclein in mitochondria is differentially expressed in different brain regions and the background levels of mitochondrial alpha-synuclein may be a potential factor affecting mitochondrial function and predisposing some neurons to degeneration.
Political independence was not necessarily the foreordained outcome of the political turmoil in Spanish America. "There was little interest in outright independence." As historians R.A. Humphreys and John Lynch note, "it is all too easy to equate the forces of discontent or even the forces of change with the forces of revolution." Since "by definition, there was no history of independence until it happened," when Spanish American independence did occur, explanations for why it came about have been sought. The Spanish American Wars of Independence were essentially a power vacuum in the Spanish monarchy that resulting in a rupture that gave rise to new states.
These properties, along with the reduction of oxidative stress and the re-establishment of glutamatergic balance, would lead to an increase in growth factors, such as brain-derived neurotrophic factor (BDNF), and the regulation of neuronal cell death through B-cell lymphoma 2 (BLC-2) expression. Catabolism to cysteine and cystine cannot fully explain the pharmacology of acetylcysteine. Recent work has shown that acetylcysteine can act as a rapid antioxidant via conversion to hydrogen sulfide and hydropersulfides, independent of glutathione elevation. As mentioned before, acetylcysteine clears mucus by opening disulfide bonds.
== Adverse effects == Data from phase II and III clinical trials did not detect any severe adverse effects to setipiprant. The authors were unable to identify any pattern of adverse effects that differ from placebo, including subjective reporting of symptoms and objective laboratory monitoring.
=== Australia === Nando's has been in continuous operation within Australia since 1990, when the first restaurant opened in Tuart Hill in Western Australia. As of August 2021, there were 155 restaurants in Australia; 63 in Victoria, 36 in Western Australia, 30 in Queensland, 16 in New South Wales, four in South Australia, two in the Northern Territory, three in Tasmania and two in the Australian Capital Territory. Per city, there are 59 in Melbourne, 34 in Perth, 20 in Brisbane, 15 in Sydney, four each in Adelaide and the Gold Coast, three in Ipswich, two each in Hobart, Canberra and Darwin and one each in Ballarat, Bunbury, Geelong, Kalgoorlie, Launceston, Newcastle, Rockhampton, Shepparton, the Sunshine Coast, Townsville and Traralgon. There have been various public battles between the parent company and its Australian franchisees.
Sources: en.wikipedia.org
The order offered sickness and death insurance, assuring its members would be buried by Jewish law and become good American citizens. Order of United Hebrew Brothers - Founded in 1915. in 1917 was reported to have 1,800 members and 12 lodges in New York City. Orders stated objectives included promoting social intercourse, discussions of subjects relating to their community, and acting upon them. Provided free burials, helped members in distress, and encouraged enrollment in the Postal Life Insurance Company. United Order of True Sisters - Founded by Henrietta Bruckman, wife of a prominent New York doctor, with 12 other ladies to assist Hebrew housewives. Had 5,991 members in 21 lodges in 1918. Had 12,000 members in 1995. Headquarters in New York. National structure called "Grand Lodge". Has degrees, secret ritual regalia, etc. Originally German-speaking, the first English lodge was organized in 1892, by 1918 German language was "essentially discontinued in all lodges". Although originally a benevolent society for sick and widows, by the late 1970s, had become primarily a philanthropic group, particularly with cancer-related causes. The United Order True Sister Inc, Cancer Service created in 1947, contributes $300,000 a year to cancer patients and specialized care hospitals in 13 and Israel. Workmen's Circle
== History == Although genetics has its roots back in the 19th century with the work of the Bohemian monk Gregor Mendel and other pioneering scientists, human genetics emerged later. It started to develop, albeit slowly, during the first half of the 20th century. Mendelian (single-gene) inheritance was studied in a number of important disorders such as albinism, brachydactyly (short fingers and toes), and hemophilia. Mathematical approaches were also devised and applied to human genetics. Population genetics was created. Medical genetics was a late developer, emerging largely after the close of World War II (1945) when the eugenics movement had fallen into disrepute. The Nazi misuse of eugenics sounded its death knell. Shorn of eugenics, a scientific approach could be used and was applied to human and medical genetics. Medical genetics saw an increasingly rapid rise in the second half of the 20th century and continues in the 21st century.
== 3-Dimensional proximity-based technology (YoctoReactor technology) == The YoctoReactor (yR) is a 3D proximity-driven approach which exploits the self-assembling nature of DNA oligonucleotides into 3, 4 or 5-way junctions to direct small molecule synthesis at the center of the junction. Figure 5 illustrates the basic concept with a 4-way DNA junction.
Flight has enabled bats to become one of the most widespread groups of mammals, being found nearly everywhere apart from polar regions, some remote islands and the very tops of mountains. Species diversity is greater in tropical areas than temperate ones. Bats are about 66% of all mammalian individuals, despite being just 10% of the total biomass of wild terrestrial mammals. Different species select different habitats during different seasons, including ocean coasts, mountains, rainforests and deserts, but they require suitable roosts. Bat roosts can be found in hollows, crevices, foliage, and even human-made structures and include "tents" the bats construct with leaves; megabats generally roost in trees. Bats are usually nocturnal but are known to exhibit diurnal behaviour in temperate regions during summer to make up for insufficient nighttime feeding and where there is little predatory threat from birds. In temperate areas, some bats migrate to winter hibernation dens, usually caves and mines, where they pass into torpor during the cold weather, never waking and relying on their stored fat. Similarly, tropical bats go through aestivation during periods of prolonged heat and dryness. Bats rarely fly in rain, possibly because being wet costs them more energy and raindrops interfere with their echolocation. They do appear to surf storm fronts when travelling to give birth in warmer temperatures.
== Corneal cross-linking == In 2002, Hafezi's clinical and research interests turned to the cornea. He became a corneal specialist, and his work helped develop the principles of corneal collagen cross-linking (CXL) and translate CXL from a laboratory into a clinical setting, initially for the treatment of keratoconus. Hafezi's combination of basic science knowledge combined with clinical, surgical experience of CXL has led him to become one of the world's leading experts on both keratoconus and cross-linking technology. The impact of CXL on the treatment of keratoconus is hard to underestimate: today, CXL considered to be the treatment of choice for progressive keratoconus and corneal ectasias, reducing the need for corneal transplantation by half. Hafezi continued to work to expand the number of people who could benefit from CXL. Briefly, the original CXL method, termed the Dresden Protocol, involves removing the central 8–10 mm of the corneal epithelium of adult patients with corneas thicker than 400 μm, and applying 0.1% riboflavin solution to the cornea for 30 minutes before, and at 5-minute intervals during 365 nm UV-A irradiation of the corneal surface at an irradiance of 3 mW/cm2. Hafezi has helped push the boundaries, pioneering CXL in children with keratoconus, the use of hypoosmolar riboflavin solutions to treat people with thin (≤400 μm) corneas. and using CXL to treat post-LASIK ectasia. The knowledge Hafezi accrued from this work led to him becoming a leading international expert on corneal ectasia in general and keratoconus in particular.
Sources: en.wikipedia.org
It is a synthetic REV-ERB agonist used mainly in preclinical research. It is not an approved medicine for human use.
It binds to REV-ERBα and REV-ERBβ, nuclear receptors involved in circadian and metabolic gene regulation. This can alter transcription of genes related to lipid and glucose metabolism in experimental models.
No controlled human trials have established that effect. Endurance findings come primarily from rodent studies, and human responses remain unknown.
SR9009 is a synthetic compound investigated as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is used in preclinical research on circadian rhythm and metabolism. It is not an approved drug.