If you have been reading about circadian clock and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Updated 2026-07-06. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
| 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. |
Identity and purity of SR9009 samples are usually checked with chromatographic and spectrometric methods. High-performance liquid chromatography can separate the compound from related impurities, while mass spectrometry provides molecular mass confirmation. Nuclear magnetic resonance spectroscopy may be used for structural verification in research settings. No single method proves biological activity, and certificates of analysis should be reviewed alongside raw data. Independent testing is often needed because online products vary widely.
SR9009 stability depends on temperature, moisture, light, and solvent. Solid material is generally kept cool and dry, while solutions may require protection from repeated warming and cooling. Degradation can appear as color changes, precipitate, or new chromatographic peaks. Researchers should follow supplier instructions and their own stability data. Long-term storage conditions for human use have not been established because the compound lacks approved clinical formulation.
Laboratory identification of SR9009 typically relies on chromatographic separation coupled to mass spectrometry, often with ultraviolet detection as a secondary check. Nuclear magnetic resonance spectroscopy can confirm molecular structure when a reference standard is available. Because many suppliers sell the compound as a research chemical, independent identity testing is important for experimental reproducibility. A single retention time is not sufficient proof of identity, especially when related compounds may be present. Purity assessments usually report a percentage based on area normalization.
SR9009 is generally described as poorly soluble in water and more soluble in organic solvents such as dimethyl sulfoxide and ethanol. Stock solutions are commonly prepared in an organic solvent before dilution into an aqueous buffer or vehicle. Precipitation can occur if the organic fraction is reduced too quickly or if the final concentration exceeds the compound's solubility limit. Sonication or gentle warming may aid dissolution in some protocols, but excessive heat can promote degradation. Container material and pH can also influence observed solubility.
For long-term storage, SR9009 is typically kept as a solid at low temperature, protected from moisture and light. Desiccated conditions limit hydrolysis, while opaque containers reduce photochemical breakdown. Solutions are less stable than solids and are often stored frozen in aliquots to avoid repeated freeze-thaw cycles. Stability data are not standardized across all suppliers, so users should rely on certificate-of-analysis information when available. Degradation may appear as color change, precipitate, or decreased chromatographic purity.
== Personal life == Sherman met and married Hildegard Schroeder while they were both graduate students at the University of Iowa, and they had three children: Karen, Marc, and Keith. In addition to his professional activities, he has participated in organizations such as the Boy Scouts of America, the Jewish War Veterans organization, and the Lions Club. Sherman died on December 1, 2023, at the age of 98.
=== EC 2.4.2: Pentosyltransferases === EC 2.4.2.1: purine-nucleoside phosphorylase EC 2.4.2.2: pyrimidine-nucleoside phosphorylase EC 2.4.2.3: uridine phosphorylase EC 2.4.2.4: thymidine phosphorylase EC 2.4.2.5: nucleoside ribosyltransferase EC 2.4.2.6: nucleoside deoxyribosyltransferase EC 2.4.2.7: adenine phosphoribosyltransferase EC 2.4.2.8: hypoxanthine phosphoribosyltransferase EC 2.4.2.9: uracil phosphoribosyltransferase EC 2.4.2.10: orotate phosphoribosyltransferase EC 2.4.2.11: now EC 6.3.4.21 nicotinate phosphoribosyltransferase EC 2.4.2.12: nicotinamide phosphoribosyltransferase EC 2.4.2.13: now EC 2.5.1.6 methionine adenosyltransferase EC 2.4.2.14: amidophosphoribosyltransferase EC 2.4.2.15: guanosine phosphorylase EC 2.4.2.16: urate-ribonucleotide phosphorylase EC 2.4.2.17: ATP phosphoribosyltransferase EC 2.4.2.18: anthranilate phosphoribosyltransferase EC 2.4.2.19: nicotinate-nucleotide diphosphorylase (carboxylating) EC 2.4.2.20: dioxotetrahydropyrimidine phosphoribosyltransferase EC 2.4.2.21: nicotinate-nucleotide—dimethylbenzimidazole phosphoribosyltransferase EC 2.4.2.22: xanthine phosphoribosyltransferase EC 2.4.2.23: This activity has been shown to be catalysed by EC 2.4.2.2, pyrimidine-nucleoside phosphorylase, EC 2.4.2.3, uridine phosphorylase, and EC 2.4.2.4, thymidine phosphorylase.
Whenever the player is caught, they must either fight off the citizens and police force through combat, or use stealth to sneak around the town and hide from pursuers. Furthermore, the player-character will suffer withdrawal effects from coming off Joy, impacting their health and thirst, as well as highly raising the suspicion meter of enemies. Should the player-character take too much damage from enemies or the environment, they will have to restart at a recent checkpoint. Optionally, the game allows the player to enable permadeath, requiring them to restart the game should the player-character die. The player must also account for their clothing; outside the Garden District where wastrels live, if the player-character is caught wearing a torn suit no matter if they take their Joy, they will be hunted down by the residents. Some pieces of clothing allow a player to conform in restricted areas, disarm traps in broad daylight without a fuss, or take honey from bees without being stung to death.
Sources: en.wikipedia.org
1993/288) National Health Service Trusts (Originating Capital Debt) Order 1993 (S.I. 1993/289) Council Tax (Alteration of Lists and Appeals) Regulations 1993 (S.I. 1993/290) Non-Domestic Rating (Alteration of Lists and Appeals) Regulations 1993 (S.I. 1993/291) Valuation and Community Charge Tribunals (Amendment) Regulations 1993 (S.I. 1993/292) A65 Trunk Road (Manor Park Improvement) Order 1993 (S.I. 1993/293) A65 Trunk Road (Denton Bridge to Black Bull Farm) (De-Trunking) Order 1993 (S.I. 1993/294) Family Proceedings (Amendment) Rules 1993 (S.I. 1993/295) Lands Tribunal for Scotland (Amendment) (Fees) Rules 1993 (S.I. 1993/296) Scottish Land Court (Fees) Order 1993 (S.I. 1993/297) Lyon Court and Office Fees (Variation) Order 1993 (S.I. 1993/298)
=== Embryology === In vertebrates and invertebrate chordates, RA has a pivotal role during development. Altering levels of endogenous RA signaling during early embryology, either too low or too high, leads to birth defects, including congenital vascular and cardiovascular defects. Of note, fetal alcohol spectrum disorder encompasses congenital anomalies, including craniofacial, auditory, and ocular defects, neurobehavioral anomalies and mental disabilities caused by maternal consumption of alcohol during pregnancy. It is proposed that in the embryo there is competition between acetaldehyde, an ethanol metabolite, and retinaldehyde (retinal) for aldehyde dehydrogenase activity, resulting in a retinoic acid deficiency, and attributing the congenital birth defects to the loss of RA activated gene activation. In support of this theory, ethanol-induced developmental defects can be ameliorated by increasing the levels of retinol or retinal. As for the risks of too much RA during embryogenesis, the prescription drugs tretinoin (all-trans-retinoic acid) and isotretinoin (13-cis-retinoic acid), used orally or topically for acne treatment, are labeled with boxed warnings for pregnant women or women who may become pregnant, as they are known human teratogens.
=== Start date and nomenclature === No consensus exists as to when the French Revolutionary Wars ended and the Napoleonic Wars began. Possible dates include 9 November 1799, when Bonaparte seized power on 18 Brumaire, the date according to the Republican Calendar then in use; 18 May 1803, when Britain and France ended the one short period of peace between 1792 and 1814; or 2 December 1804, when Bonaparte crowned himself Emperor. British historians occasionally refer to the nearly continuous period of warfare from 1792 to 1815 as the Great French War, or as the final phase of the Anglo-French Second Hundred Years' War, spanning the period 1689 to 1815. Historian Mike Rapport (2013) suggested using the term "French Wars" to unambiguously describe the entire period from 1792 to 1815. In France, the Napoleonic Wars are generally integrated with the French Revolutionary Wars: Les guerres de la Révolution et de l'Empire. German historiography may count the War of the Second Coalition (1798/9–1801/2), during which Napoleon had seized power, as the Erster Napoleonischer Krieg ("First Napoleonic War"). In Dutch historiography, it is common to refer to the 7 major wars between 1792 and 1815 as the Coalition Wars (coalitieoorlogen), referring to the first two as the French Revolution Wars (Franse Revolutieoorlogen).
== P == Palladin Plastin p30 PAK (p21-activated Kinase) Plectin p47PHOX Parvin (actopaxin) Prefoldin p53 PASK (Proline, Alanine rich Ste20 related Kinase) Presenilin I p58 Phalloidin (not a protein; a small cyclic peptide) Profilin p185neu Ponticulin Protein kinase C Porin P.IB Prk1p (actin regulating kinase)
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 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.