This is a working overview of nuclear receptor, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-04-10 and is reviewed periodically as new material appears.
REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.
Most published work on SR9009 consists of preclinical studies. It is widely sold as a research chemical, a category that does not imply safety, efficacy, or pharmaceutical-grade quality. Sports anti-doping organizations have listed SR9009 as a prohibited substance, and its presence in an athlete sample can lead to sanctions. Legal status differs by country; in several jurisdictions it is not approved for human consumption and may be treated as an unapproved new drug.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
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.
| Property | Value | Notes |
|---|---|---|
| Common name | SR9009 | Also referred to as Stenabolic in non-scientific contexts. |
| Chemical class | Synthetic small molecule | Not a steroid or peptide hormone. |
| Receptor target | REV-ERBα and REV-ERBβ | Nuclear receptor agonist in preclinical studies. |
| Development status | Investigational | No approved human therapeutic indication. |
| Regulatory attention | Prohibited in sport | Listed by anti-doping authorities. |
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.
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 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.
SR9009 is a synthetic small molecule that acts on the nuclear receptors REV-ERBα and REV-ERBβ. These receptors are part of the circadian clock machinery and normally repress transcription of certain target genes. In laboratory research, SR9009 is used as a chemical tool to study how REV-ERB activity influences metabolism, inflammation, and daily biological rhythms. The compound is not an approved medicine, and its effects in humans remain largely uncharacterized. It is often described as an investigational agent rather than a therapeutic product.
=== Transcriptional variants === So far, three different transcription variants (TVs) have been described for CK1δ in humans (Homo sapiens), mice (Mus musculus), and rats (Rattus norvegicus), which are highly homologous. The alignment of all CK1δ sequences of all organisms shows a high homology in the first 399 amino acids, except for position 381. While the human transcription variants are using isoleucine, the mouse and rat sequences incorporate a valine instead. The only exception is rat TV3, which is also transcribing its nucleotide sequence into an isoleucine. After position 399, three different general structures can be observed. The first variant consists of 415 amino acids across all three organisms and is called TV1 in human and rat, while the murine counterpart is named CRAa. The shortest group of sequences consists of 409 amino acids: TV2 in humans and rats, CRAc in mice. The longest variant consists of 428 amino acids in rat (TV3) and mice (CRAb), while the human (TV3) variant is missing the second to last amino acid (threonine), resulting in a protein of a length of 427 amino acids. The various transcription variants are based on a different usage of the exons that are encoding for CSNK1D. The whole gene consists of eleven different exons and is located in humans on chromosome 17 at position 17q25.3. CSNK1D has a length of 35kb and is overlapping with the gene Slc16a3. The intersecting part is exon 11, which is located downstream of exon 10. However, it does not interfere with Slc16a3 since it is located in a non-coding area.
=== Non-neuronal Control === Non-neuronal control has been found to be indirect paracrine regulation through ions, hormones, and neurotransmitters. Zinc, insulin, serotonin, γ-aminobutyric acid, and γ-hydroxybutyrate, all of which are released by beta cells in the pancreas, have been found to suppress glucagon production in alpha cells. Delta cells also release somatostatin which has been found to inhibit glucagon secretion. Zinc is secreted at the same time as insulin by the beta cells in the pancreas. It has been proposed to act as a paracrine signal to inhibit glucagon secretion in alpha cells. Zinc is transported into both alpha and beta cells by the zinc transporter ZnT8. This protein channel allows zinc to cross the plasma membrane into the cell. When ZnT8 is under-expressed, there is a marked increase in glucagon secretion. When ZnT8 is over-expressed, there is a marked decrease in glucagon secretion. The exact mechanism by which zinc inhibits glucagon secretion is not known. Insulin has been shown to function as a paracrine signal to inhibit glucagon secretion by the alpha cells. However, this is not through a direct interaction. It appears that insulin functions to inhibit glucagon secretion through activation of delta cells to secrete somatostatin. Insulin binds to SGLT2 causing an increased glucose uptake into delta cells. SGLT2 is a sodium and glucose symporter, meaning that it brings glucose and sodium ions across the membrane at the same time in the same direction.
=== Cathedral === Aquileia Cathedral is a flat-roofed basilica that was erected by Patriarch Poppo in 1031 on the site of an earlier church and rebuilt in the Gothic style by Patriarch Marquard of Randeck (1365–1381).
Crystal violet stains both Gram positive and Gram negative organisms. Treatment with alcohol removes the crystal violet colour from gram negative organisms only. Safranin as counterstain is used to colour the gram negative organisms that got decolorised by alcohol. While ex vivo, many cells continue to live and metabolize until they are "fixed". Some staining methods are based on this property. Those stains excluded by the living cells but taken up by the already dead cells are called vital stains (e.g. trypan blue or propidium iodide for eukaryotic cells). Those that enter and stain living cells are called supravital stains (e.g. New Methylene Blue and brilliant cresyl blue for reticulocyte staining). However, these stains are eventually toxic to the organism, some more so than others. Partly due to their toxic interaction inside a living cell, when supravital stains enter a living cell, they might produce a characteristic pattern of staining different from the staining of an already fixed cell (e.g. "reticulocyte" look versus diffuse "polychromasia"). To achieve desired effects, the stains are used in very dilute solutions ranging from 1:5000 to 1:500000 (Howey, 2000). Note that many stains may be used in both living and fixed cells.
Glycogen storage diseases may show transient exercise-induced alkalosis (high pH), hyperammonemia, and myogenic hyperuricemia. During a non-ischemic forearm exercise test, in GSDs the plasma lactate typically fails to rise (and may fall below resting levels); except for a few GSDs such as phosphoglucomutase deficiency (GSD-XIV), deficiency of functioning myophosphorylase-a (autosomal dominant PYGM), phosphorylase-b kinase deficiency (GSD-IXd), and Pompe disease (GSD-II) where lactate production is normal. In myoadenylate deaminase deficiency (AMPD1 deficiency), there is no rise in ammonia. Some fatty acid oxidation disorders show lactic acidosis, hypoketotic hypoglycaemia and hyperammonemia, while others are asymptomatic. Differentiating between different types of metabolic myopathies can be difficult due to the similar symptoms of each type such as myoglobinuria and exercise intolerance. It has to be determined whether the patient has fixed (static) or exercise-induced (dynamic) manifestations; and if exercise-related, what kind of exercise, before extensive exercise-related lab testing is done to determine the underlying cause. Adequate knowledge is required of the body's bioenergetic systems, including:
Sources: en.wikipedia.org
Offshore Group Newcastle make oil platforms. Sage Group, who produce accounting software, are based at Hazlerigg at the northern end of the Newcastle bypass. Northern Rock, which became a bank in 1997 and was taken over by Virgin Money in November 2011, and the Newcastle Building Society are based in Gosforth. The Gosforth-based bakery Greggs now has over 1,500 shops. The Balliol Business Park in Longbenton contains Procter & Gamble research and global business centres and a tax credits call centre for HMRC, and is the former home of Findus UK. The Government National Insurance Contributions Office in Longbenton, demolished and replaced in 2000, had a 1 mile (1.6 km) long corridor. Be-Ro and the Go-Ahead Group bus company are in central Newcastle. Nestlé use the former Rowntrees chocolate factory on the east of the A1. BAE Systems Land & Armaments in Scotswood, formerly Vickers-Armstrongs, is the main producer of British Army tanks such as the Challenger 2. A Rolls-Royce apprentice training site is next door. Siemens Energy Service Fossil make steam turbines at the CA Parsons Works in South Heaton. Sir Charles Parsons invented the steam turbine in 1884, and developed an important local company. Domestos, a product whose main ingredient is sodium hypochlorite, was originated in Newcastle in 1929 by William Handley, and was distributed from the area for many years. Clarke Chapman is next to the A167 in Gateshead. The MetroCentre, the largest shopping centre in Europe, is in Dunston.
Some hydrothermal vents form roughly cylindrical chimney structures. These form from minerals that are dissolved in the vent fluid. When the superheated water contacts the near-freezing sea water, the minerals precipitate out to form particles which add to the height of the stacks. Some of these chimney structures can reach heights of 60 m (200 ft). An example of such a towering vent was "Godzilla", a structure on the Pacific Ocean deep seafloor near Oregon that rose to 40 m (130 ft) before it fell over in 1996.
African American Cultural Complex Contemporary Art Museum of Raleigh Gregg Museum of Art & Design at North Carolina State University Haywood Hall House & Gardens Marbles Kids Museum North Carolina Museum of Art North Carolina Museum of History North Carolina Museum of Natural Sciences North Carolina Sports Hall of Fame City of Raleigh Museum J. C. Raulston Arboretum Joel Lane House Mordecai Plantation Pope House Museum
==== MeSH D06.472.040 – adrenal cortex hormones ==== MeSH D06.472.040.502 – 17-ketosteroids MeSH D06.472.040.502.112 – androstenedione MeSH D06.472.040.502.195 – androsterone MeSH D06.472.040.502.497 – estrone MeSH D06.472.040.502.583 – etiocholanolone MeSH D06.472.040.502.620 – dehydroepiandrosterone MeSH D06.472.040.502.620.300 – dehydroepiandrosterone sulfate MeSH D06.472.040.585 – hydroxycorticosteroids MeSH D06.472.040.585.353 – 11-hydroxycorticosteroids MeSH D06.472.040.585.353.118 – aldosterone MeSH D06.472.040.585.353.237 – corticosterone MeSH D06.472.040.585.353.476 – hydrocortisone MeSH D06.472.040.585.353.500 – 18-hydroxycorticosterone MeSH D06.472.040.585.353.825 – tetrahydrocortisol MeSH D06.472.040.585.478 – 17-hydroxycorticosteroids MeSH D06.472.040.585.478.195 – cortisone MeSH D06.472.040.585.478.225 – cortodoxone MeSH D06.472.040.585.478.392 – hydrocortisone MeSH D06.472.040.585.478.782 – tetrahydrocortisol MeSH D06.472.040.585.478.865 – tetrahydrocortisone MeSH D06.472.040.585.611 – desoxycorticosterone MeSH D06.472.040.585.611.400 – 18-hydroxydesoxycorticosterone MeSH D06.472.040.585.745 – pregnenolone MeSH D06.472.040.585.745.500 – 17-alpha-hydroxypregnenolone
Sources: en.wikipedia.org
It is a synthetic compound studied as an agonist of REV-ERB nuclear receptors. It is not an approved medicine and has mainly been examined in laboratory and animal research.
No. It is a small molecule that binds nuclear receptors involved in circadian regulation. Its classification differs from anabolic steroids or peptide hormones.
Published human clinical trial data are lacking. Most safety and activity information comes from preclinical models, so effects in people remain uncertain.
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.