Everything below concerns circadian rhythm. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2025-09-14. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
| 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. |
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.
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.
Analytical methods for SR9009 typically rely on liquid chromatography coupled with tandem mass spectrometry. The technique can separate the parent compound from related substances and detect low concentrations in biological matrices. Urine and blood are common samples in anti-doping testing, while in vitro studies may use cell culture media. Rapid metabolism and low expected concentrations make method validation important for reliable identification. Exact metabolite patterns can vary by species and are not fully mapped.
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.
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.
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.
internal carotid the supratrochlear artery to the midline forehead. The supratrochlear artery is a branch of the ophthalmic branch of the internal carotid artery. the supraorbital artery to the lateral forehead and scalp as far up as the vertex. The supraorbital artery is a branch of the ophthalmic branch of the internal carotid artery. external carotid the superficial temporal artery gives off frontal and parietal branches to supply much of the scalp the occipital artery which runs posteriorly to supply much of the posterior aspect of the scalp the posterior auricular artery, a branch of the external carotid artery, ascends behind the auricle to supply the scalp above and behind the auricle. Because the walls of the blood vessels are firmly attached to the fibrous tissue of the superficial fascial layer, cut ends of vessels here do not readily retract; even a small scalp wound may bleed profusely. Venous drainage The veins of the scalp accompany the arteries and thus have similar names, e.g. Supratrochlear and supraorbital veins, which unite at the medial angle of the eye, and form the angular vein, which further continues as the facial vein. The superficial temporal vein descends in front of the tragus, enters the parotid gland, and then joins the maxillary vein to form the retromandibular vein. The anterior part of it unites with the facial vein to form the common facial vein, which drains into jugular vein, and ultimately to the subclavian vein. The occipital vein terminates to the sub-occipital plexus.
In addition to the myoglobinuria, two other mechanisms contribute to kidney impairment: low blood pressure leads to constriction of the blood vessels and therefore a relative lack of blood flow to the kidney, and finally, uric acid may form crystals in the tubules of the kidneys, causing obstruction. Together, these processes lead to acute tubular necrosis, the destruction of the cells of the tubules. Glomerular filtration rate falls, and the kidney is unable to perform its normal excretory functions. This disrupts electrolyte regulation, leading to a further rise in potassium levels, and interferes with vitamin D processing, further worsening the low calcium levels.
=== April to June: Allied discussions === Balfour met Weizmann at the Foreign Office on 22 March 1917; two days later, Weizmann described the meeting as being "the first time I had a real business talk with him". Weizmann explained at the meeting that the Zionists had a preference for a British protectorate over Palestine, as opposed to an American, French or international arrangement; Balfour agreed, but warned that "there may be difficulties with France and Italy". The French position in regard to Palestine and the wider Syria region during the lead up to the Balfour Declaration was largely dictated by the terms of the Sykes–Picot Agreement and was complicated from 23 November 1915 by increasing French awareness of the British discussions with the Sherif of Mecca. Prior to 1917, the British had led the fighting on the southern border of the Ottoman Empire alone, given their neighbouring Egyptian colony and the French preoccupation with the fighting on the Western Front that was taking place on their own soil. Italy's participation in the war, which began following the April 1915 Treaty of London, did not include involvement in the Middle Eastern sphere until the April 1917 Agreement of Saint-Jean-de-Maurienne; at this conference, Lloyd George had raised the question of a British protectorate of Palestine and the idea "had been very coldly received" by the French and the Italians. In May and June 1917, the French and Italians sent detachments to support the British as they built their reinforcements in preparation for a renewed attack on Palestine.
Sources: en.wikipedia.org
Stephen G. Weber is a professor of chemistry and clinical translational science at the University of Pittsburgh. He researches analytical separations theory and its application, and has developed "green" techniques for molecular recognition and microextractions. He is particularly interested in the identification of peptides and dipeptides, and their effects on neurochemistry. He has received a number of awards, including the 2016 Dal Nogare Award for "contributions to the fundamental understanding of the chromatographic process".
=== Temporal lobe epilepsy === Epilepsy of the mesial temporal lobe is associated with HHV-6 infection. Within this region of the brain exists three structures: the amygdala, hippocampus, and parahippocampal gyrus. Mesial temporal lobe epilepsy (MTLE) is the most common form of chronic epilepsy and its underlying mechanism is not fully understood. Researchers consistently report having found HHV-6 DNA in tissues that were removed from patients with MTLE. Studies have demonstrated a tendency for HHV-6 to aggregate in the temporal lobe, with the highest concentrations in astrocytes of the hippocampus. However, one group of researchers ultimately concluded that HHV-6 may not be involved in MTLE related to mesial temporal sclerosis.
dimer A molecular aggregate consisting of two subunits. The term is often used to describe a protein complex composed of two proteins, either the same protein (a homodimer) or different proteins (a heterodimer); or to an individual protein composed of two polypeptides. Compare monomer, trimer, and tetramer.
== Evolution == LCRs are very interesting from a micro and macro evolutionary perspective. They may be generated by DNA slippage, recombination and repair. Thus, they are linked to recombination hotspots and may even possibly facilitate cross-over. By originating from genetic instability, they may cause, at the DNA level, a certain region of the protein to expand or contract and even cause frame-shifts (phase-variants) that affect microbial pathogenicity or provide raw material for evolution. Most intriguingly, they may provide a window into the very early evolution of life. During early evolution, when only few amino acids were available and the primary genetic code was still expanding its repertoire, the first proteins were assumed to be short, repetitive and therefore, of low complexity. Thus, modern LCRs could represent primordial aspects of the evolution towards the protein world and may provide clues about the functions of the early proto-peptides. Most studies have focused on the evolution, functional and structural role of eukaryotic LCRs. However, a comprehensive study of prokaryotic LCRs from many diverse prokaryotic lineages provides a unique opportunity to understanding the origin, evolution and nature of these regions. Due to the high effective population size and short generation times of prokaryotes, the de novo emergence of a mildly or moderately deleterious amino acid repeat or LCR should quickly be filtered out by strong selective forces.
Sources: en.wikipedia.org
A researcher at Texas AgriLife Research reported in 2012 that incorporating two genes from spinach into citrus trees improved resistance to citrus greening disease in greenhouse trials. Field tests by Southern Gardens Citrus of oranges with the spinach genes in Florida are ongoing. A resistant variety of mandarin orange called 'Bingo' has been bred at the University of Florida. Some other varieties have a partial tolerance to the disease.
=== Football field (length) === A football field is often used as a comparative measurement of length when talking about distances that may be hard to comprehend when stated in terms of standard units. An American football field is usually understood to be 100 yards (91 m) long, though it is technically 120 yards (110 m) when including the two 10 yd (9.1 m) long end zones. The field is 160 ft (53 yd; 49 m) wide. An association football pitch may vary within limits of 90–120 m (98–131 yd) in length and 45–90 m (49–98 yd) in width. The recommended field size is 105 m × 68 m (115 yd × 74 yd) for major competitions such as the FIFA World Cup, UEFA European Championship and UEFA Champions League. A Canadian football field is 65 yd (59 m) wide and 150 yd (140 m) long, including two 20 yd (18 m) long end zones.
Dynamic allele-specific hybridization (DASH) genotyping takes advantage of the differences in the melting temperature in DNA that results from the instability of mismatched base pairs. The process can be vastly automated and encompasses a few simple principles. In the first step, a genomic segment is amplified and attached to a bead through a PCR reaction with a biotinylated primer. In the second step, the amplified product is attached to a streptavidin column and washed with NaOH to remove the unbiotinylated strand. An allele-specific oligonucleotide is then added in the presence of a molecule that fluoresces when bound to double-stranded DNA. The intensity is then measured as temperature is increased until the melting temperature (Tm) can be determined. A SNP will result in a lower than expected Tm. Because DASH genotyping is measuring a quantifiable change in Tm, it is capable of measuring all types of mutations, not just SNPs. Other benefits of DASH include its ability to work with label free probes and its simple design and performance conditions.
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.
Liquid chromatography–mass spectrometry is common for identity and purity checks. High-performance liquid chromatography with ultraviolet detection can also be used. Both methods require a suitable reference standard.