NR1D2 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.
Updated 2026-06-25. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small-molecule ligand; not a hormone or peptide |
| Molecular formula | C20H24ClN3O4S | Reported for the free base |
| CAS Registry Number | 1379686-30-2 | Unique chemical identifier |
| Common synonyms | SR9009; stenabolic | Stenabolic is informal and not an official name |
| Reported targets | REV-ERBα and REV-ERBβ | Nuclear receptors linked to circadian and metabolic regulation |
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.
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.
=== Proteomics === Analysis of proteins can be done by either using top-down or bottom-up approach. However, better sequence coverage is provided by top-down analysis. Combination of ECD with FTICR MS has resulted in popularity of this approach. It has also helped in determining the multiple modification sites in intact proteins. Native electron capture dissociation (NECD) was used to study cytochrome c dimer and has been recently used to elucidate iron-binding channels in horse spleen ferritin.
=== Other vapors === Although both oxygen and water vapor represent the most studied permeants in food packaging applications, other gases such as carbon dioxide (CO2) and nitrogen (N2) have also great relevance in the preservation of food products. In fact, N2 and CO2 have been employed in modified atmosphere packaging (MAP) technology, to establish the correct conditions inside the package's headspace to lessen food spoiling.
Following independence on 15 August 1947, Jawaharlal Nehru served as prime minister of the Dominion of India, remaining caretaker until 1951, shortly after India became a republic in 1950. Led by Nehru, the Congress won the 1951, 1957, and 1962 general elections comfortably. After Nehru died in May 1964, Lal Bahadur Shastri became prime minister. Shastri died in January 1966, shortly after signing the Tashkent Peace Declaration. The Congress chose Indira Gandhi as prime minister, leading the party to election victories in 1967 and 1971. In 1975, she declared a state of emergency, suspending civil liberties, which led to Congress being voted out in 1977. Congress returned to power in 1980. Following a military operation at the Golden Temple in Amritsar, Indira Gandhi was assassinated on 31 October 1984. Indira Gandhi's son, Rajiv Gandhi, succeeded her and won the late 1984 elections. During the general election campaign of 1991, Rajiv Gandhi was assassinated by a Sri Lankan Tamil separatist. Congress emerged from the elections as the largest party, and P. V. Narasimha Rao formed a minority government that completed a full five-year term. After the 1999 elections, the BJP's Atal Bihari Vajpayee led a National Democratic Alliance (NDA) coalition and became the first non-Congress prime minister to complete a five-year term. The NDA was defeated in 2004 by the Congress-led United Progressive Alliance (UPA). Manmohan Singh served as prime minister with external support, returning with increased, independent numbers in 2009.
By 2016, regeneration had been operationalised and induced by four main techniques: regeneration by instrument; regeneration by materials; regeneration by 3D printing; and regeneration by drugs. By 2016, regeneration by instrument, regeneration by materials and by regeneration drugs had been generally operationalised in vivo (inside living tissues), while regeneration by 3D printing had been generally operationalised in vitro (inside the lab) in order to create and prepare tissue for transplantation.
Sources: en.wikipedia.org
==== Drugs ==== The ability to maintain functional telomeres may be one mechanism that allows cancer cells to grow in vitro for decades. Telomerase activity is necessary to preserve many cancer types and is inactive in somatic cells, creating the possibility that telomerase inhibition could selectively repress cancer cell growth with minimal side effects. If a drug can inhibit telomerase in cancer cells, the telomeres of successive generations will progressively shorten, limiting tumor growth. Telomerase is a good biomarker for cancer detection because about 85% of human cancer cells express high levels of it. Telomerase activity can be identified by its catalytic protein domain (hTERT). hTERT is believed to be the rate-limiting step in telomerase activity, and as a consequence, increased hTERT expression is associated with elevated telomerase activity in many cancer types. Various cancer cells and fibroblasts transformed with hTERT cDNA have high telomerase activity, while somatic cells do not. Cells testing positive for hTERT have positive nuclear signals. Epithelial stem cell tissue and its early daughter cells are the only noncancerous cells in which hTERT can be detected. Since hTERT expression is dependent only on the number of tumor cells within a sample, the amount of hTERT indicates the severity of cancer. The expression of hTERT can also be used to distinguish benign tumors from malignant tumors. Malignant tumors have higher hTERT expression than benign tumors.
Naja christyi (formerly Boulengerina christyi), commonly known as the Congo water cobra or Christy's water cobra, is a species of venomous snakes belonging to the family Elapidae. The species is native to Sub-Saharan Africa. This species was formerly in the genus Boulengerina, but more recent research by Wallach et al. has shown that Boulengerina is actually a subgenus and Boulengerina christyi is a synonym of Naja christyi. This species has no known subspecies.
== Clinical significance == Mutations of the CELA1 gene were suspected to be associated with diffuse nonepidermolytic palmoplantar keratoderma (diffuse NEPPK). However the suspected sequence variant was fully functional and did not strongly associate with the disease. More recently, a specific mutation in the KRT6C gene has been linked to some cases of diffuse NEPPK. A possible polymorphism of the CELA1 gene coding this protein was found. On a secondary structure level, this polymorphism manifests itself in an excision of a short sequence of CELA1. The disappeared sequence carries the key amino acid residues Val-227 and Thr-239, which contribute to the substrate specificity of elastase I (highlighted in Figure 3), as well as five of the eight amino acids involved in the primary contact of the elafin(inhibitor)/elastase complex formation. These observations imply that the sequence variant might modify the substrate specificity of the enzyme and abolish the inhibitor binding capability. Though there were no obvious pathogenic epidermal abnormalities associated with the truncated ELA1 variant, it is possible that carriers of the polymorphism may be at greater risk of developing the common skin diseases such as psoriasis and eczema (genetic and histologic studies will be required to investigate the role of ELA1 in these common epidermal disorders.).
Sources: en.wikipedia.org
== Special populations == Undernutrition is an important determinant of maternal and child health, accounting for more than a third of child deaths and more than 10 percent of the total global disease burden according to 2008 studies.
=== Family record book (1877) === The loss of Parisian civil records largely influenced the creation of the family record book in 1877, introduced by a circular from Jules Simon, President of the Council and Minister of the Interior. The circular explicitly referenced the Commune’s destruction, stating that “family record books will serve as a third deposit of civil records entrusted to individuals and will provide valuable information should registers be destroyed.” The law of April 5, 1884, concerning municipal organization, required town halls to budget for the costs of family record books.
=== Covalent catalysis === Many enzymes including serine protease, cysteine protease, protein kinase and phosphatase evolved to form transient covalent bonds between them and their substrates to lower the activation energy and allow the reaction to occur. This process can be divided into 2 steps: formation and breakdown. The former step is rate-limit step while the later step is needed to regenerate intact enzyme. Nucleophilic catalysis: This process involves the donation of electrons from the enzyme's nucleophile to a substrate to form a covalent bond between them during the transition state. The strength of this interaction depends on two aspects.: the ability of the nucleophilic group to donate electrons and the electrophile to accept them. The former one is mainly affected by the basicity(the ability to donate electron pairs) of the species while the later one is in regard to its pKa. Both groups are also affected by their chemical properties such as polarizability, electronegativity and ionization potential. Amino acids that can form nucleophile including serine, cysteine, aspartate and glutamine. Electrophilic catalysis: The mechanism behind this process is exactly same as nucleophilic catalysis except that now amino acids in active site act as electrophile while substrates are nucleophiles. This reaction usually requires cofactors as the amino acid side chains are not strong enough in attracting electrons.
Sources: en.wikipedia.org
SR9009 is a synthetic compound investigated as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is used in preclinical research on circadian rhythm and metabolism. It is not an approved drug.
No. It has no approved medical indication, and human safety and efficacy data are limited. It appears in research chemical markets and is banned by some sports authorities.
Natural ligands include heme and certain metabolites; SR9009 is a synthetic small molecule with higher potency and selectivity in some assays. Its effects depend on cell type and timing. It is not a naturally occurring compound.
It is a synthetic REV-ERB agonist used mainly in preclinical research. It is not an approved medicine for human use.