Everything below concerns REV-ERB. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2025-08-15. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ in preclinical models |
| Molecular formula | C20H24ClN3O4S | Reported for the parent compound |
| CAS Registry Number | 1379686-30-2 | Common identifier in chemical databases |
| Appearance | Off-white to pale yellow solid | Typical research chemical solid |
| Solubility | Soluble in DMSO and ethanol; low in water | Class: small organic molecule |
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.
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.
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.
===== Junior residency (Part I) ===== Duration: 24 to 36 months. Objective: Develop core clinical competencies and foundational knowledge in the chosen specialty. Assessment: Candidates are eligible to sit for the Part I Fellowship Examination after completing this phase.
Bio-Synthesis, Inc. (BSI) is a biotechnology company headquartered in Lewisville, Texas. It is a provider of custom and catalog peptides, custom oligos, antibodies, organic synthesis, and analytical services. Biomedical researchers worldwide in universities, biotech companies, private clinics, and government agencies use products from Bio-Synthesis, Inc. in studies ranging from PCR diagnostics to cancer research and the Human Genome Project.
==== Absorption ==== The absorption of atomoxetine with oral administration is rapid and complete. The drug's absolute bioavailability is 63 to 94%. This is moderated by first-pass metabolism and CYP2D6 status, with poor metabolizers having a bioavailability of 94% and extensive metabolizers having a bioavailability of 63%. Extensive metabolizers are considered to have normal CYP2D6 activity and constitute >90% of people, while poor metabolizers constitute a small minority of up to 7%. The bioavailability of atomoxetine is not different between capsule and solution forms. The time to peak levels of atomoxetine is 1 to 2 hours. It has been reported that the time to peak levels was 1.0 hours in CYP2D6 extensive metabolizers and 2.5 hours in CYP2D6 poor metabolizers. Taking atomoxetine with food does not affect its bioavailability or total exposure but decreases peak levels by 9% with a typical meal and 37% with a standard high-fat breakfast. In addition, food delays the time to peak levels by 3 hours. Atomoxetine exposure increases proportionally with higher doses over a range of 10 to 120 mg orally. Exposure to atomoxetine is proportional to body weight, and hence weight-normalizing dosing is required to produce equivalent exposure. In CYP2D6 poor metabolizers, atomoxetine peak levels are 5- to 6-fold higher and total exposure is 8- to 10-fold higher than in CYP2D6 extensive metabolizers.
== Harvesting and processing == All ECM samples originate from mammalian tissues, such as dermis, pericardium, and small intestinal submucosa (SIS). After explantation from the source, the ECM biomaterial retains some characteristics of the original tissue. The ECM tissues can be harvested from varying stages in the developmental stages in mammalian species such as human, porcine, equine, and bovine. Although they are similarly composed of fibril collagen, the microstructure, specific composition (including presence of non-collagenous protein and glycosaminoglycans and ratio of different types of collagen), physical dimensions and mechanical properties can differ. Depending on the developmental stage of the tissue during which harvesting occurred, the microstructure can vary within an organism. Additionally, keeping in mind the size and shape of the final tissue, the potential of the physical dimensions of the tissue of origin must be considered. Despite this “memory” of the ECM tissue, methods have been engineered so that these innate characteristics can be modified, saved or removed. The modification process varies depending on the material used in clinical setting. Some ECM biomaterials undergo a modification that removes all the cells but leaves the remainder of the other ECM components called decellularization. Another process that can be introduced into the biomaterial is artificial crosslinking. Artificial crosslinking has been shown to stabilize reconstituted collagen, which can rapidly degenerate in vivo.
Sources: en.wikipedia.org
Control of endemic diseases: This program aims at modifying the existing means of control measures and introducing more recent methods to achieve a more effective yet less expensive control scheme without any harmful environmental impact, through the employment of molecular biology in vaccine production and biological control of the parasites and their intermediate hosts. Moreover, studying the role of the community and intensifying its active participation are prerequisites. Diagnosis of endemic diseases: This program is directed to the study, assessment and modification of all diagnostic measures utilizing the most advanced technologies. The diagnosis varies from clinical and laboratory techniques to field studies (prevalence, ecological and socioeconomic implications). Morbidity changes of endemic diseases: This program aims at studying the pathogenesis and the pathological changes caused by endemic diseases on different body systems. Management of endemic diseases: This program evaluates both the current and advanced therapeutic measures and assess their efficacy and side effects. It includes the different medical and surgical management procedures of diseases and their complications. Studies on partial hepatectomy, liver regeneration and transplantation are items of this program. Innovation in Applied Medical Sciences Any innovations or patency in relevant research fields at TBRI are encouraged and supported.
== Synthesis == Clicked peptide polymers are prepared by the azide-alkyne Huisgen cycloaddition also called the click reaction; which is commonly used in bioconjugation reactions to link molecules together with a stable triazole bridge. Peptide based polymers are produced from a cycloaddition variant of step-growth polymerization. The monomers used in this polymerization are oligopeptides with terminal azide and terminal alkyne groups
==== Preventive measures ==== In August 2010, Purdue Pharma reformulated their long-acting oxycodone line, marketed as OxyContin, using a polymer, Intac, to make the pills more difficult to crush or dissolve in water to reduce non-medical use of OxyContin. Inactive ingredients/excipients are butylated hydroxytoluene (BHT), hypromellose, polyethylene glycol 400, polyethylene oxide, magnesium stearate, and titanium dioxide. The FDA approved relabeling the reformulated version as abuse-resistant in April 2013. Pfizer manufactures a preparation of short-acting oxycodone, marketed as Oxecta, which contains inactive ingredients, referred to as tamper-resistant Aversion Technology. Approved by the FDA in the U.S. in June 2011, the new formulation, while not being able to deter oral recreational use, makes crushing, chewing, snorting, or injecting the opioid impractical because of a change in its chemical properties.
== Function == Membrane-Bound RAGE (mRAGE): mRAGE acts as a cellular receptor capable of activating inflammatory and oxidative stress pathways in response to ligand binding. The receptor's structure, which includes the ligand-binding domain, transmembrane segment, and cytoplasmic tail, is critical for these functions. The wide variety of ligands that interact with mRAGE contributes to its involvement in multiple pathological states, such as diabetes, neurodegeneration, and cardiovascular diseases. Soluble RAGE (sRAGE): On the other hand, sRAGE functions as a decoy receptor. It circulates in the bloodstream and binds RAGE ligands, thereby preventing them from activating mRAGE on the cell surface. By neutralizing these ligands, sRAGE reduces RAGE-mediated cellular activation and inflammation. Elevated levels of sRAGE are considered to have a protective effect in inflammatory diseases by limiting the activity of harmful ligands. The balance between mRAGE and sRAGE levels is thought to influence disease outcomes. An excess of mRAGE is often associated with inflammation and disease progression, whereas higher concentrations of sRAGE may be beneficial in mitigating inflammatory responses.
=== Post-SNL, 30 Rock, and film career === After leaving the cast of SNL in 2003, Morgan starred in his own sitcom, The Tracy Morgan Show, debuting in 2003. The show was subsequently canceled after one season. During the same year, he was featured on an episode of Punk'd in which his car was towed from valet parking.
Sources: en.wikipedia.org
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.
No. It is a synthetic ligand that binds nuclear receptors, not a steroid or peptide hormone. Its activity depends on receptor binding rather than endocrine secretion.
Clinical evidence is limited. Most published data come from cell and animal experiments. Human safety and efficacy remain uncertain.
SR9009 is a synthetic research compound that activates the REV-ERBα and REV-ERBβ nuclear receptors. It is not an approved drug and has no established human therapeutic use. Most published biological data come from cell and rodent studies.