A practical reference on REV-ERB: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
Reviewed 2026-08-01. Anything still debated is marked as such rather than presented as settled.
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.
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 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.
SR9009 binds REV-ERB receptors and alters their repressive activity on target genes. This action can change transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. In rodent studies, treated animals have shown changes in muscle oxidative capacity and exercise performance, though effects vary by dose, duration, and model. The precise molecular steps connecting receptor binding to whole-body outcomes are still an active area of investigation. Findings in animals do not automatically translate to humans.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small molecule; not a steroid or peptide. |
| Primary targets | NR1D1 and NR1D2 | Also known as REV-ERBα and REV-ERBβ. |
| Studied routes | Intraperitoneal in rodents | Oral bioavailability in humans is not established. |
| Human approval | No approved therapeutic indication | No recognized clinical use. |
| Key uncertainty | Human physiological effects | Preclinical findings may not translate. |
Storage recommendations for SR9009 reference material typically specify a freezer at -20 °C or lower, with protection from moisture and light. Repeated freeze-thaw cycles can degrade small molecules and introduce variability. Stock solutions in dimethyl sulfoxide are often aliquoted to avoid repeated handling. Stability studies may examine degradation under heat, humidity, and light exposure. The compound's thiophene and nitro groups can participate in reactions that alter analytical signals over time, so such changes affect quantitative results.
Quality control for research materials includes identity confirmation by nuclear magnetic resonance and purity assessment by high-performance liquid chromatography. Mass spectrometry provides molecular weight confirmation and can detect related impurities. Purchasers should request a certificate of analysis that lists lot-specific data. Online products advertised for human use often lack such documentation. Distinguishing legitimate research material from mislabeled or contaminated samples is a recurring challenge in independent testing, and independent laboratories may use orthogonal methods to verify identity.
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.
The experiment showed that C-1 of glycine was found almost exclusively in the glycyl portion of hadacidin while formate, the 3-carbon of serine, and the 2-carbon of glycine were incorporated into both the glycyl and formyl portions of the hydroxamate. N-Hydroxyglycine was incorporated into hadacidin at a rate equal to that for glycine in 3-hr periods and to a much greater extent in longer time periods. N-Hydroxyglycine, but not glycine, brought about a net stimulation of hydroxamate production. Nitroacetic acid, glyoxylic acid oxime, and formylglycine were not rapidly incorporated into hadacidin. Experiments showed that the hydroxylamino oxygen atom of hadacidin is derived from oxygen gas rather than water. The experimental results are consistent with the hypothesis that the biosynthesis of hadacidin occurs by N-oxygenation of glycine to yield N-hydroxyglycine followed by N-formylation to yield the hydroxamate.
== Pharmacokinetics == Plasma picamilon concentrations are generally in the 500–3000 μg/L range during the first few hours after single oral doses of 50–200 mg. It exhibits linear pharmacokinetics with a half-life of 1–2 hours. As discussed previously, the drug undergoes hydrolysis to GABA and nicotinic acid. Urinary excretion of parent drug and the two metabolites accounts for up to 79% of a single dose.
After the expression of the gene product, it may be necessary to purify the expressed protein; however, separating the protein of interest from the great majority of proteins of the host cell can be a protracted process. To make this purification process easier, a purification tag may be added to the cloned gene. This tag could be histidine (His) tag, other marker peptides, or a fusion partners such as glutathione S-transferase or maltose-binding protein. Some of these fusion partners may also help to increase the solubility of some expressed proteins. Other fusion proteins such as green fluorescent protein may act as a reporter gene for the identification of successful cloned genes, or they may be used to study protein expression in cellular imaging.
Sources: en.wikipedia.org
As with all other arteries, the aorta is made up of three layers, the intima, the media, and the adventitia. The intima is in direct contact with the blood inside the vessel, and mainly consists of a layer of endothelial cells on a basement membrane; the media contains connective and muscle tissue, and the vessel is protected on the outside by the adventitia, comprising connective tissue. In an aortic dissection, blood penetrates the intima and enters the media layer. The high pressure rips the tissue of the media apart along the laminated plane splitting the inner two-thirds and the outer one-third of the media apart. This can propagate along the length of the aorta for a variable distance forward or backward. Dissections that propagate towards the iliac bifurcation (with the flow of blood) are called anterograde dissections and those that propagate towards the aortic root (opposite of the flow of blood) are called retrograde dissections. The initial tear is usually within 100 mm of the aortic valve, so a retrograde dissection can easily compromise the pericardium leading to a hemopericardium. Anterograde dissections may propagate all the way to the iliac bifurcation of the aorta, rupture the aortic wall, or recanalize into the intravascular lumen leading to a double-barrel aorta. The double-barrel aorta relieves the pressure of blood flow and reduces the risk of rupture. Rupture leads to hemorrhaging into a body cavity, and prognosis depends on the area of rupture. Retroperitoneal and pericardial ruptures are both possible.
== Genetics == CTD is caused by pathogenic variants in SLC6A8, located at Xq28. Over 60 variants in SLC6A8 have been reported. SLC6A8 contains 13 exons and spreads across 8.5 kb of genomic DNA (gDNA). The presence of hemizygous variants in males and heterozygous variants in females in SLC6A8 provides evidence that CTD is inherited in an X-linked recessive manner. This usually results in hemizygous males having severe symptoms, while heterozygous female carriers tend to have less severe and more varying symptoms.
After a slow start in the final's first two events, after which he found himself 7 points behind the leader in seventh place, he proceeded to dominate the rest of the event with five first place finishes in a row in the final five disciplines, winning the title with an event to spare. In the 2006 World's Strongest Man contest, despite starting the final well, he eventually came second to Phil Pfister after the American won the final five events in a row. Pudzianowski regained his title in 2007, winning the final with one event to spare for a record-breaking third time. In so doing, he joined Jon Pall Sigmarsson and Magnus Ver Magnusson as the only men to win the competition four times. During the 2007 competition, however, Pudzianowski said that his target was to become the only person to win the event five times, and he returned to the 2008 World's Strongest Man the following year to try to achieve his goal. Despite a serious calf injury suffered in the Polish Strongman Championship Cup of 2008 and further exacerbated during the WSM qualifying rounds, Pudzianowski still managed to win his heat and qualify for the final. However, it was clear his dominance of previous years was no longer in effect, as he only won one of the first five events in the final, and finished in fifth in two others. Trailing leader Derek Poundstone with two events to go, Pudzianowski managed to win the Plane Pull despite his injured calf to cut the deficit to just 1 point going into the final event.
The parametrium is the fibrous and fatty connective tissue that surrounds the uterus. This tissue separates the supravaginal portion of the cervix from the bladder. The parametrium lies in front of the cervix and extends laterally between the layers of the broad ligaments. It connects the uterus to other tissues in the pelvis. It is different from the perimetrium, which is the outermost layer of the uterus. The uterine artery and ovarian ligament are located in the parametrium. An associated form of pelvic inflammatory disease is inflammation of the parametrium known as parametritis.
Sources: en.wikipedia.org
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.
REV-ERB receptors generally repress transcription when bound by natural heme. SR9009 is described as an agonist that enhances this repressive activity. The result is altered expression of clock and metabolic genes.
Published controlled human trials are lacking. Some sources cite limited or unofficial reports, but these do not establish safety or efficacy. Claims about human performance effects remain unverified.
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.