Everything below concerns REV-ERB. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-04-10. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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 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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic small-molecule REV-ERB agonist | Not a hormone or natural product |
| Primary targets | REV-ERBα and REV-ERBβ | Nuclear receptors involved in circadian and metabolic regulation |
| Appearance | White to off-white solid | Typical for purified research samples |
| Solubility | Soluble in DMSO and ethanol; low water solubility | Laboratory solubility depends on solvent and purity |
| Common synonyms | SR9009; Stenabolic | Stenabolic is a colloquial name, not a formal chemical name |
Detection of SR9009 in biological samples usually employs liquid chromatography coupled with tandem mass spectrometry. This method can identify the parent compound and sometimes metabolites in urine or blood. Because exposure can be low and clearance may be rapid, sample timing and limits of detection matter. Laboratories validate assays for sensitivity and specificity. Results are interpreted alongside chain-of-custody and quality-control records. Urine is the common matrix for anti-doping analysis, while blood may be used in research settings.
Handling recommendations for SR9009 in a laboratory setting include storing the solid at low temperature, protected from light and moisture. The compound is often dissolved in dimethyl sulfoxide or ethanol for experiments. Solutions should be prepared with appropriate personal protective equipment and disposed of according to local rules. Stability data for long-term storage are limited, so stock solutions are typically kept cold and used within defined periods. Records of preparation date and concentration support reproducibility.
Laboratory samples of SR9009 are typically supplied as a white to off-white powder. The compound dissolves readily in organic solvents such as dimethyl sulfoxide and ethanol, while its solubility in water is low. Because of this solubility profile, researchers often prepare concentrated stock solutions in an organic solvent before diluting them into aqueous assay buffers. Light exposure, moisture, and repeated freeze-thaw cycles can degrade many small molecules, so handling procedures usually aim to minimize these factors. Purity is commonly checked before use.
Storage conditions for research-grade SR9009 generally involve a freezer at approximately minus twenty degrees Celsius, sometimes lower for long-term preservation. Containers should remain tightly closed and protected from light. Desiccants may be used to limit moisture uptake. Solutions are often stored in aliquots to avoid repeated warming and cooling. Stability data for the compound under various conditions are limited, so laboratories typically follow supplier recommendations and verify performance through periodic analytical checks rather than assuming indefinite stability.
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.
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.
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There have been several structures solved for this class of enzymes, given PDB accession codes, and published in peer-reviewed journals. At least 4 such structures have been solved using pig enzymes: PDB: 1OHV, PDB: 1OHW, PDB: 1OHY, PDB: 1SF2, and at least 4 such structures have been solved in Escherichia coli: PDB: 1SFF, PDB: 1SZK, PDB: 1SZS, PDB: 1SZU. There are actually some differences between the enzyme structure for these organisms. E. coli enzymes of GABA-T lack an iron-sulfur cluster that is found in the pig model. Amino acid residues found in the active site of 4-aminobutyrate transaminase include Lys-329, which are found on each of the two subunits of the enzyme. This site will also bind with a pyridoxal 5'- phosphate co-enzyme. Aminooxyacetic acid Gabaculine Phenelzine Phenylethylidenehydrazine (PEH) Rosmarinic acid Valproic acid Vigabatrin 4-Aminobutyrate+Transaminase at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Pearl PL, Parviz M, Hodgeman R, Gibson KM, Reimschisel T (2015). "GABA-transaminase deficiency". MedLink Neurology.
In May 1952, Raymond Gosling, a graduate student working under the supervision of Rosalind Franklin, took an X-ray diffraction image, labeled as "Photo 51", at high hydration levels of DNA. This photo was given to Watson and Crick by Maurice Wilkins and was critical to their obtaining the correct structure of DNA. Franklin told Crick and Watson that the backbones had to be on the outside. Before then, Linus Pauling, and Watson and Crick, had erroneous models with the chains inside and the bases pointing outwards. Franklin's identification of the space group for DNA crystals proved her correct. In February 1953, Linus Pauling and Robert Corey proposed a model for nucleic acids containing three intertwined chains, with the phosphates near the axis, and the bases on the outside. Watson and Crick completed their model, which is now accepted as the first correct model of the double helix of DNA. On 28 February 1953 Crick interrupted patrons' lunchtime at The Eagle pub in Cambridge, England to announce that he and Watson had "discovered the secret of life".
A pilot comparison using the same 24 h repeat protocol found multiple-sclerosis patients showed day-2 VO₂ and workload shifts that overlapped CFS, undermining “uniqueness.” Repeat-CPET reliability studies in cardiac, pulmonary and multiple sclerosis cohorts report intra-individual variation of 4-7 % for VO₂-peak; several CFS papers cite falls in the 7-12 % range—just outside that noise band and within confidence limits of small samples. A 2015 PLoS One analysis explicitly questioned the sensitivity of CPET change-scores in fatiguing illness. On top of that PEM itself has been claimed to exist in cancer-related fatigue, however this study did not differentiate between PEM and exercise intolerance.
Cholera toxins: encoded by CTX phages, virulent Vibrio cholerae strains require lysogenic conversion by CTX phage infection Several botulinum toxins (BoNTs): Type C and D BoNTS have been shown to be encoded by clostridial phages and are produced by Clostridium botulinum strains harboring these phage genes Shiga toxins: encoded by lambdoid phages, mainly produced by lysogenic shiga-toxin producing strains of E. coli (STEC) Diphtheria toxins: encoded by corynephage ß, produced by lysogenic Corynebacterium diphtheriae strains infected with corynephage ß Several staphylococci toxins (staphylokinase (SAK), staphylococcal enterotoxin A (SEA), exfoliative toxin (ETA), Panton–Valentine leucocidin (PVL), and other enterotoxins): toxins that are phage-encoded and produced by lysogenic converted strains of the staphylococci group.
Sources: en.wikipedia.org
1. Int J Pharm Compd. 2026 Jul-Aug;30(4):329-336. Synthetic Peptides in Pharmacy Compounding: Analysis of PCAC Recommendations and Industry Safety Standards. Willis J(1), Vu N(2)(3). Author information: (1)University of Oklahoma College of Pharmacy. (2)ARL Bio Pharma, Oklahoma City, Oklahoma. Nvu@arlok.com. (3)University of Oklahoma College of Pharmacy, Oklahoma City, Oklahoma. Compounded peptides have quickly moved from a niche topic to a growing area of interest among patients and prescribers. These products are promoted for a wide range of uses, including tissue repair, inflammation, metabolic health, and healthy aging. This article examines the proposed uses of these peptides, the concerns raised during the review, and the practical implications for compounders. Copyright© by International Journal of Pharmaceutical Compounding, Inc.
== Distribution == The labeled [18F]FDG compound has a relatively short shelf life which is determined largely by the physical decay of fluorine-18 with a half-life of 109.8 minutes, or slightly less than two hours. Still, this half-life is sufficiently long to allow shipping the compound to remote PET scanning facilities, in contrast to other medical radioisotopes like carbon-11 with a half-life of ~20 minutes. Due to transport regulations for radioactive compounds, delivery is normally done by specially licensed road transport, but means of transport may also include dedicated small commercial jet services. Transport by air allows expanding the distribution area around a [18F]FDG production site to deliver the compound to PET scanning centres within a 1–3-hour flight time. Recently, on-site cyclotrons with integral shielding and portable chemistry stations for making [18F]FDG have accompanied PET scanners to remote hospitals. This technology holds some promise in the future, for replacing some of the scramble to transport [18F]FDG from site of manufacture to site of use.
== Historical consequences == The history of tolbutamide has had a lasting effect on medicine and the pharmaceutical industry. Patients today are still diagnosed with prediabetes, many of them managing to delay the onset of diabetes through dietary and lifestyle changes, but many also have the option to take metformin, which demonstrated a 31% reduction in three-year incidence of development of diabetes relative to placebo. While impressive, the lifestyle-modification arm of that same trial demonstrated a 58% reduction.
Metabolism and biosynthesis of serotonin. Pyridoxal phosphate is a cofactor of aromatic L-amino acids decarboxylase. This allows for conversion of 5-hydroxytryptophan (5-HTP) into serotonin (5-HT). This reaction takes place in serotonergic neurons. Metabolism and biosynthesis of histamine. Pyridoxal phosphate is a cofactor of L-histidine decarboxylase. This allows for conversion of histidine into histamine. This reaction takes place in Golgi apparatus in mast cells and in basophils. Next, histamine is stored in granularity in mast cells as a complex with acid residues of heparin proteoglycan while in basophils as a complex with chondroitine sulfate. Metabolism and biosynthesis of GABA (γ-aminobutyric acid). Pyridoxal phosphate is a cofactor of glutamic acid decarboxylase (GAD). This allows for conversion of glutamate into GABA. Reaction takes place in cytoplasm of termination of GABA-ergic neurons, therefore vitamin B6 deficiency may cause epileptic seizures in children. Pyridoxal phosphate also participates in the oxidative deamination of GABA, where it is a cofactor of GABA aminotransferase. Metabolism of ornithine. Pyridoxal phosphate is a cofactor of ornithine decarboxylase. It is therefore associated with the synthesis of polyamines; crucial compounds associated with cell growth and proliferation. Transamination. Pyridoxal phosphate takes part in decomposition and synthesis of amino acids, fats, and carbohydrates, and in the biosynthesis of hormones, neurotransmitters, and heme.
Sources: pubmed.ncbi.nlm.nih.gov
It is a synthetic research compound that activates REV-ERB nuclear receptors. It is not an approved drug or dietary supplement. Most information comes from cell and animal studies.
It binds REV-ERBα and REV-ERBβ and changes transcription of metabolic genes. This can affect circadian rhythm, lipid use, and mitochondrial function. The full downstream effects are still under study.
No. Some rodent studies show increased endurance, but controlled human trials are lacking. Claims about human performance are not established by published evidence.
SR9009 is a synthetic research compound that binds and modulates the nuclear receptors REV-ERBα and REV-ERBβ. It is used in laboratory studies of circadian biology and metabolism, not as an approved medicine. It is also known by the informal name Stenabolic.