NR1D1 is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Last reviewed on 2025-02-24. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
Identity and purity testing for SR9009 commonly uses liquid chromatography coupled with tandem mass spectrometry. This method separates the compound from matrix components and detects it by mass-to-charge transitions, providing sensitive and specific confirmation. Nuclear magnetic resonance spectroscopy can support structural identification, while high-performance liquid chromatography with ultraviolet detection may estimate purity. Because online products labeled as SR9009 may contain other substances or no active compound at all, independent verification is important in research settings. Certificates of analysis are useful but not a substitute for in-house testing.
| Property | Value | Notes |
|---|---|---|
| Common name | SR9009 | Also marketed informally as Stenabolic |
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ |
| Molecular formula | C24H30ClN3O4S | Approximate molecular weight 492 g/mol |
| CAS Registry Number | 1379686-30-2 | Identifier for the parent compound |
| Regulatory status | Not approved for human use | Prohibited in sport by WADA |
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.
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.
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.
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.
thio-phosphorylated derivatives of resorcinols and calixarenes; studying thio-phosphorylated unsaturated compounds using petrochemical and wood-chemical feedstock; generation and theoretical study of phosphabetains and their derivatives (phosphonium salts, carboxyl-containing metal complexes); searching for liquid growth-boosting fertilizer compounds based on microelements. The following majors are currently offered to students: 04.03.01 Chemistry, Bachelor's degree program; 04.05.01 Fundamental and Applied Chemistry, Specialist Degree program; 04.04.01 Chemistry, Master's degree program; 44.03.01 Pedagogical Education, Bachelor's degree program. The following master's degree programs are offered by the Institute in the academic year 2015–2016:
European Union officials, European ministers and Commissioner (Tonio) Borg set up an urgent meeting in Brussels on 13 February 2013 on how to contain the horse meat scandal that exposed flaws in European control systems on food safety, and to formulate an action plan. Following the meeting, EU agriculture ministers announced a three-month coordinated control plan of DNA testing of processed meat across the European Union. The plan, adopted 19 February 2013, called for 2,500 random tests on processed food for horse DNA and 4,000 for phenylbutazone (bute), beginning in March 2013, with initial results announced on 15 April 2013. The Hague-based Europol would handle the co-ordination of investigations among national authorities, as well as any raids on premises and arrests on suspicion of criminal conspiracy to defraud.
Prior to the Air Pollution Control Act of 1955, little headway was made to initiate this air pollution reform. U.S. cities Chicago and Cincinnati first established smoke ordinances in 1881. In 1904, Philadelphia passed an ordinance limiting the amount of smoke in flues, chimneys, and open spaces. The ordinance imposed a penalty if not all smoke inspections were passed. It was not until 1947 that California authorized the creation of Air Pollution Control Districts in every county of the state.
Following subcutaneous injection, albiglutide reaches highest blood concentrations after three to five days. Steady-state concentrations are achieved after three to five weeks. The substance is most likely broken down by protease enzymes to small peptides and amino acids. Being resistant to dipeptidyl peptidase-4 (DPP-4), the enzyme that breaks down GLP-1, albiglutide has a biological half-life of five (4–7) days, which is considerably longer than the older GLP-1 analogs exenatide and liraglutide. This allows for a once-weekly administration, unlike liraglutide but like the extended-release form of exenatide. Albiglutide is a peptide consisting of 645 proteinogenic amino acids with 17 disulfide bridges. Amino acids 1–30 and 31–60 constitute two copies of modified human GLP-1, the alanine at position 2 having been exchanged for a glycine for better DPP-4 resistance. The remaining sequence is human albumin. The complete sequence is
Sources: en.wikipedia.org
Signal transduction is realized by activation of specific receptors and consequent production/delivery of second messengers, such as Ca2+ or cAMP. These molecules operate as signal transducers, triggering intracellular cascades and in turn amplifying the initial signal. Two main signal transduction mechanisms have been identified, via nuclear receptors, or via transmembrane receptors. In the first one, first messenger cross through the cell membrane, binding and activating intracellular receptors localized at nucleus or cytosol, which then act as transcriptional factors regulating directly gene expression. This is possible due to the lipophilic nature of those ligands, mainly hormones. In the signal transduction via transmembrane receptors, the first messenger binds to the extracellular domain of transmembrane receptor, activating it. These receptors may have intrinsic catalytic activity or may be coupled to effector enzymes, or may also be associated to ionic channels. Therefore, there are four main transmembrane receptor types: G protein coupled receptors (GPCRs), tyrosine kinase receptors (RTKs), serine/threonine kinase receptors (RSTKs), and ligand-gated ion channels (LGICs). Second messengers can be classified into three classes:
The following classification system for transmembrane solute transporters has been constructed in the TCDB. Three families of ABC exporters are defined by their evolutionary origins. ABC1 exporters evolved by intragenic triplication of a 2 TMS precursor (TMS = transmembrane segment. A "2 TMS" protein has 2 transmembrane segments) to give 6 TMS proteins. ABC2 exporters evolved by intragenic duplication of a 3 TMS precursor, and ABC3 exporters evolved from a 4 TMS precursor which duplicated either extragenicly to give two 4 TMS proteins, both required for transport function, or intragenicly to give 8 or 10 TMS proteins. The 10 TMS proteins appear to have two extra TMSs between the two 4 TMS repeat units. Most uptake systems (all except 3.A.1.21) are of the ABC2 type, divided into type I and type II by the way they handle nucleotides. A special subfamily of ABC2 importers called ECF use a separate subunit for substrate recognition. ABC1 (InterPro: IPR036640): ABC2 (InterPro: IPR000412 [partial]): ABC3 (InterPro: IPR003838):
ACC Synthase is 450-516 amino acid long sequence depending on the species of plant from which it is extracted. Though it is comparable in the species in which it is found, its COOH-terminal domain is more variable, leading to differences such as oligomerization. The COOH-terminal domain is responsible for oligomerization. In most ACC Synthase producing cells, ACC Synthase exists as a dimer. However, in some we find a monomer ("which is more active and efficient [than its dimer counterpart"). The structure of ACS has been largely determined via X-ray crystallography. Conservation of the residues in ACS's catalytic domain and sequence homology suggest that ACS catalyzes the synthesis of ACC in a similar fashion as other enzymes that require PLP as a cofactor. However, unlike many other PLP-dependent enzymes, Lys (278) is not the only residue that interacts with the substrate. The proximity of the electronegative oxygen from Tyr (152) to the C-γ-S bond suggests a crucial role in the formation of ACC. X-ray crystallography with aminoethoxyvinylglycine (AVG) a competitive inhibitor confirmed Tyrosine's role in the γ elimination. As of late 2007, 6 structures have been solved for this class of enzymes, with PDB accession codes PDB: 1B8G, PDB: 1IAX, PDB: 1IAY, PDB: 1M4N, PDB: 1M7Y, and PDB: 1YNU.
Sources: en.wikipedia.org
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.
No. SR9009 has not been approved as a therapeutic drug in the United States, European Union, or other major markets. Human safety and efficacy data are very limited. Its presence in consumer products does not imply regulatory approval.
The World Anti-Doping Agency lists SR9009 as a prohibited substance because it can alter gene expression and metabolic pathways relevant to performance. The ban applies at all times, not only during competition. Detection relies on laboratory methods such as mass spectrometry.
Research-grade SR9009 is typically stored frozen at about minus twenty degrees Celsius, protected from light and moisture. Stock solutions are often kept in aliquots to avoid repeated freeze-thaw cycles. Specific storage conditions should follow the supplier's documentation.