Everything below concerns HPLC-UV. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2025-08-31. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Regulatory treatment of SR9009 reflects its investigational status. The compound has no approved human therapeutic indication, and sports authorities prohibit its use. It appears on anti-doping lists as a non-approved substance or metabolic modulator, depending on the list version. Products sold online as research chemicals are not quality-controlled medicines, so their identity and purity can differ from the label. Such products may also contain unlisted compounds, which complicates both testing and safety assessment.
Scientific discussion of SR9009 often separates animal evidence from human anecdote. Rodent studies provide controlled data on endurance, metabolism, and gene expression, but they use specific strains, doses, and treatment durations. Human reports are mostly uncontrolled and cannot establish cause and effect. Open questions include oral bioavailability, tissue distribution, metabolic stability, and long-term effects. Review articles generally call for more rigorous pharmacokinetic and safety research before any clinical use could be considered.
Analytical methods for SR9009 typically rely on liquid chromatography coupled with tandem mass spectrometry. The technique can separate the parent compound from related substances and detect low concentrations in biological matrices. Urine and blood are common samples in anti-doping testing, while in vitro studies may use cell culture media. Rapid metabolism and low expected concentrations make method validation important for reliable identification. Exact metabolite patterns can vary by species and are not fully mapped.
| 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 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.
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.
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.
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.
APEKTx1 is a highly selective blocker of the voltage-gated potassium channel Kv1.1 with no effect on other tested potassium channels (Kv1.2, Kv1.3, Kv1.4, Kv1.5, Kv1.6, Shaker IR, Kv2.1, Kv3.1, Kv4.2 and Kv4.3). APEKTx1 selectively blocks Kv1.1 channels with an IC50 value of 0.9 nM, which makes it between a 700 to 3000 times more potent inhibitor than the two known sea anemone peptides targeted against Kv channels (kalicludines and SHTX II). APEKTx1 is thought to interact with Kv1.1 through the aliphatic residue alanine (A352), an acidic residue glutamate (E353), and an aromatic residue tyrosine (Y379), as a mutation in these sites causes a loss in affinity of the toxin for Kv1.1. These residues are located in the H5-loop between the S5 and S6 domains and are part of the channel’s pore. In addition, APEKTx1 acts as a potent trypsin inhibitor (Kd= 124 nM), probably a competitive one. However, trypsin inhibition is more potent (as it has a higher affinity) in BPTI, which can be explained by the presence of Phe13 and Pro19 in APEKTx1, causing an unfavorable interaction.
There are at least three known isoforms of this protein in humans produced by alternative splicing: isoform 1, of length 442 amino acids, isoform 2 of length 261 amino acids and isoform 3 of length 169 amino acids. MIPOL1 contains two coiled-coil domains in its C-terminus at positions 107 – 212 and 253 – 435 (shown in Fig.1). A bipartite nuclear localization signal is predicted at position 128 – 143. The following post-translational modifications are predicted using bioinformatics tools for MIPOL1. Multiple phosphorylation sites are predicted for this protein, that are conserved in close orthologs, including a Casein kinase 1 (CK1) site, three Casein kinase 2 (CK2) sites, and three NEK2 sites. The exact structure of the MIPOL1 has not yet been characterized. Homology-based and de novo predictions of its tertiary structure suggest that it may consist of inter-twined alpha helices, forming coiled-coil domains (see Fig.4.).
In 1998, Cryo Interactive Entertainment released Philip K. Dick's Ubik, a tactical action/strategy video game very loosely based on the book. The game allowed players to act as Joe Chip and train combat squads into missions against the Hollis Corporation. The game was available for PlayStation and for Microsoft Windows and was not a significant commercial success.
In 2024, The Wall Street Journal reported that big AI companies have begun negotiations with the US nuclear power providers to provide electricity to the data centres. In March 2024, Amazon purchased a Pennsylvania nuclear-powered data centre for US$650 million. In September 2024, Microsoft announced an agreement with Constellation Energy to re-open the Three Mile Island nuclear power plant to provide Microsoft with 100% of all electric power produced by the plant for 20 years. Reopening the plant, which suffered a partial nuclear meltdown of its Unit 2 reactor in 1979, will require Constellation to get through strict regulatory processes which will include extensive safety scrutiny from the US Nuclear Regulatory Commission. If approved (this will be the first ever US re-commissioning of a nuclear plant), over 835 megawatts of power – enough for 800,000 homes – will be produced. The cost for re-opening and upgrading is estimated at US$1.6 billion and is dependent on tax breaks for nuclear power contained in the 2022 US Inflation Reduction Act. As of 2024, the US government and the state of Michigan have been investing almost US$2 billion to reopen the Palisades nuclear reactor on Lake Michigan. Closed since 2022, the plant was scheduled to be reopened in October 2025. After the last approval in September 2023, Taiwan suspended the approval of data centres north of Taoyuan with a capacity of more than 5 MW in 2024, due to power supply shortages. Taiwan aims to phase out nuclear power by 2025.
Sources: en.wikipedia.org
leukotriene A4 + glutathione This enzyme belongs to the family of lyases, specifically the class of carbon-sulfur lyases. The systematic name of this enzyme class is leukotriene-C4 glutathione-lyase (leukotriene-A4-forming). Other names in common use include leukotriene C4 synthetase, LTC4 synthase, LTC4 synthetase, leukotriene A4:glutathione S-leukotrienyltransferase, (7E,9E,11Z,14Z)-(5S,6R)-5,6-epoxyicosa-7,9,11,14-tetraenoate:glutathione leukotriene-transferase, (epoxide-ring-opening), (7E,9E,11Z,14Z)-(5S,6R)-6-(glutathion-S-yl)-5-hydroxyicosa-7,9,11,14-tetraenoate glutathione-lyase (epoxide-forming). This enzyme participates in arachidonic acid metabolism.
Despite increased ties to the Latin American left, the Castillo Administration has maintained cordial, if not friendly, relations with the US. Relations began when the US State Department denied Keiko's claims of electoral fraud in the 2021 Peruvian general election. Afterward, relations were further normalized under former Foreign Minister Héctor Béjar, when both countries agreed to hold bilateral meetings every 6 months. Additionally, the US pledged cooperation in vaccines, and aid for the poorest regions of Peru. Relations with the US have been maintained after the resignation of Héctor Béjar. Castillo has also renewed Peru's agreement with USAID for another 5 years. This decision has been protested by a congressman from his party, who accused USAID of being an "accomplice in all the coups in Latin America and a spy agency within our homeland." On 23 October 2021, Castillo gave a speech at the FOLAC 2021, organized by the chambers of commerce of the US and Latin American countries. Castillo stated that "it is a propitious moment to consolidate the strong ties of friendship and cooperation with the United States. We have a new opportunity."
Ac-Aib-Pro-Aib-Ala-Aib-Ala-Gln-Aib-Val-Aib-Gly-Leu-Aib-Pro-Val-Aib-Aib-Glu-Gln-Phl where Ac = acetyl, Phl = phenylalaninol, and Aib = 2-Aminoisobutyric acid. In cell membranes, it forms voltage-dependent ion channels by aggregation of four to six molecules.
=== Ukraine === The epidemic of HIV/AIDS in Ukraine is quickly growing and was the reason for research into opioid agonist therapies (OAT) in the country as a means to curb the spread of HIV. Ukraine has the highest rate of HIV in Europe at 1.2% and most of the spread of HIV in Ukraine is primarily through people who inject drugs and secondarily through these drug users sexual partners. In 2016, opioid agonist therapies were only being given to 2.7% of the 346,000 people who inject drugs in Ukraine. OAT utilized Buprenorphine starting in 2004 and Methadone in 2008. However, due to the cost of OAT, government regulation prohibits the number of patients that can receive such therapies at a time, meaning a new patient can enter only after another has left. From 2010 to 2013 this number patients remained at a ceiling of roughly 9,000 patients throughout the country. As of 2016 OAT for these 9,000 patients is being administered only by narcologists at 174 licensed treatment centers.
=== Biosynthesis === The biosynthesis of the rapamycin core is accomplished by a type I polyketide synthase (PKS) in conjunction with a nonribosomal peptide synthetase (NRPS). The domains responsible for the biosynthesis of the linear polyketide of rapamycin are organized into three multienzymes, RapA, RapB, and RapC, which contain a total of 14 modules (figure 1). The three multienzymes are organized such that the first four modules of polyketide chain elongation are in RapA, the following six modules for continued elongation are in RapB, and the final four modules to complete the biosynthesis of the linear polyketide are in RapC. Then, the linear polyketide is modified by the NRPS, RapP, which attaches L-pipecolate to the terminal end of the polyketide, and then cyclizes the molecule, yielding the unbound product, prerapamycin.
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.
No. It is an investigational compound without approved therapeutic indications. It is sold for research purposes only in many jurisdictions.