freeze-thaw cycle raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
Reviewed 2026-08-01. Anything still debated is marked as such rather than presented as settled.
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.
Detection of SR9009 in biological samples usually relies on liquid chromatography coupled to tandem mass spectrometry. This approach separates the compound from matrix components and identifies it by mass transitions. Because SR9009 can undergo metabolism, laboratories often look for both parent drug and specific metabolites. Sample preparation may involve protein precipitation or solid-phase extraction. Method validation examines sensitivity, carryover, and interference from related substances, and reference standards are required for accurate calibration.
Storage recommendations for SR9009 reference material typically specify a freezer at -20 °C or lower, with protection from moisture and light. Repeated freeze-thaw cycles can degrade small molecules and introduce variability. Stock solutions in dimethyl sulfoxide are often aliquoted to avoid repeated handling. Stability studies may examine degradation under heat, humidity, and light exposure. The compound's thiophene and nitro groups can participate in reactions that alter analytical signals over time, so such changes affect quantitative results.
| 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. |
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.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not an approved medicine and has no established human therapeutic use. The compound appears in scientific literature as a tool for probing circadian and metabolic regulation. Online sellers often label it as a research chemical, sometimes using the nickname Stenabolic. Its chemical identity is distinct from selective androgen receptor modulators, stimulants, and peroxisome proliferator-activated receptor delta agonists. Researchers use it mainly in cell and animal experiments.
At the molecular level, SR9009 binds REV-ERBα and REV-ERBβ and alters their repressive activity on target genes. These nuclear receptors help regulate the circadian clock, lipid synthesis, glucose metabolism, and inflammatory pathways. By changing transcription, the compound can shift the timing or magnitude of downstream metabolic processes in model systems. It does not act through androgen receptors or adenosine receptors, which distinguishes it from several substances sold for athletic performance. Whether the same transcriptional changes occur in humans at tolerable exposures remains an open question because controlled human studies are lacking.
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.
Ardent supporters of Duterte have been labeled as "Diehard Duterte Supporters", alternatively known as "Digong Duterte Supporters", which shares the acronym with the Davao Death Squad (DDS). This label has been applied to the 16 million people who voted for him in the 2016 presidential election. Duterte developed a reputation as a "protector" and "savior" in his hometown of Davao City as mayor of the city for more than two decades. This is despite reports of death squads in the city.
=== Malicious contributions on Wikipedia === In September 2011, Hari admitted that he had edited articles on Wikipedia about himself and journalists with whom he had had disputes. Using a sock puppet account under the name "David r from meth productions", he added false and defamatory claims to articles about journalists including Nick Cohen, Cristina Odone, Francis Wheen, Andrew Roberts, Niall Ferguson and Oliver Kamm, and edited the article about himself "to make him seem one of the essential writers of our times". In July 2011, Cohen wrote about the suspicious Wikipedia editing in The Spectator, prompting the New Statesman journalist David Allen Green to compile evidence that Hari used the identity "David Rose" to pretend to be an editor who was qualified in environmental science. This led to an investigation by the Wikipedia community and "David Rose" was blocked from Wikipedia. Hari published an apology in The Independent, admitting that he had been "David Rose" and writing: "I edited the entries of people I had clashed with in ways that were juvenile or malicious: I called one of them anti-Semitic and homophobic, and the other a drunk. I am mortified to have done this, because it breaches the most basic ethical rule: don't do to others what you don't want them to do to you. I apologise to the latter group unreservedly and totally."
=== Category:EC 5.2 (cis-trans-isomerases) === Category:EC 5.2 FKBP: FKBP1A FKBP1B FKBP2 FKBP3 FKBP4 FKBP5 FKBP6 FKBP8 FKBP9 FKBP10 FKBPL Cyclophilin Parvulin Prolyl isomerase 2-chloro-4-carboxymethylenebut-2-en-1,4-olide isomerase Beta-carotene isomerase Farnesol 2-isomerase Furylfuramide isomerase Linoleate isomerase Maleate isomerase Maleylacetoacetate isomerase Maleylpyruvate isomerase Parvulin Photoisomerase Prolycopene isomerase Prolyl isomerase Retinal isomerase Retinol isomerase Zeta-carotene isomerase
Sources: en.wikipedia.org
Chlorpromazine is a very effective antagonist of D2 dopamine receptors and similar receptors, such as D3 and D5. Unlike most other drugs of this genre, it also has a high affinity for D1 receptors. Blocking these receptors causes diminished neurotransmitter binding in the forebrain, resulting in many different effects. Dopamine, unable to bind with a receptor, causes a feedback loop that causes dopaminergic neurons to release more dopamine. Therefore, upon first taking the drug, patients will experience an increase in dopaminergic neural activity. Eventually, dopamine production in the neurons will drop substantially and dopamine will be removed from the synaptic cleft. At this point, neural activity decreases greatly; the continual blockade of receptors only compounds this effect. Chlorpromazine acts as an antagonist (blocking agent) on different postsynaptic and presynaptic receptors:
5 October The New York Times summarizes those awarded Nobel Prizes in the Sciences for the year 2022: Physiology or Medicine (October 3): Svante Pääbo for discoveries involving genomes of extinct hominins Physics (October 4): Alain Aspect, John F. Clauser and Anton Zeilinger for work in quantum technology Chemistry (October 5): Carolyn R. Bertozzi, Morten Meldal and K. Barry Sharpless for studies on click chemistry and bioorthogonal chemistry. Scientists report the discovery of ongoing transfer of mitochondrial DNA into DNA in the cell nucleus. Previously, nuclear-mitochondrial segments (NUMT) were thought to have arisen only long ago. 66 thousand whole-genome sequences indicate this currently occurs as frequent as once in every ~4,000 human births. Researchers outline the large potentials and benefits of marine algae-based aquaculture for the development of a future healthy and sustainable food system. Scientists demonstrate the use of organoids for the study of brain development, identifying and investigating genetic switches that have a significant impact on it using single-cell transcriptome readouts.
==== Iron import in some cancer cells ==== Iron can also enter cells via CD44 in complexes bound to hyaluronic acid during epithelial–mesenchymal transition (EMT). In this process, epithelial cells transform into mesenchymal cells with detachment from the basement membrane, to which they’re normally anchored, paving the way for the newly differentiated motile mesenchymal cells to begin migration away from the epithelial layer. While EMT plays a crucial role in physiological processes like implantation, where it enables the embryo to invade the endometrium to facilitate placental attachment, its dysregulation can also fuel the malignant spread of tumors empowering them to invade surrounding tissues and establish distant colonies (metastasis). Malignant cells often exhibit a heightened demand for iron, fueling their transition towards a more invasive mesenchymal state. This iron is necessary for the expression of mesenchymal genes, like those encoding transforming growth factor beta (TGF-β), crucial for EMT. Notably, iron’s unique ability to catalyze protein and DNA demethylation plays a vital role in this gene expression process. Conventional iron uptake pathways, such as those using the transferrin receptor 1 (TfR1), often prove insufficient to meet these elevated iron demands in cancer cells. As a result, various cytokines and growth factors trigger the upregulation of CD44, a surface molecule capable of internalizing iron bound to the hyaluronan complex.
Sources: en.wikipedia.org
Crick's view of the relationship between science and religion continued to play a role in his work as he made the transition from molecular biology research into theoretical neuroscience. Crick asked in 1998 "and if some of the Bible is manifestly wrong, why should any of the rest of it be accepted automatically? ... And what would be more important than to find our true place in the universe by removing one by one these unfortunate vestiges of earlier beliefs?" In 2003 he was one of 22 Nobel laureates who signed the Humanist Manifesto.
== Research == Ritanserin was tested in clinical trials for depression, anxiety, schizophrenia, and migraine. It was also found to improve sleep in human volunteers. It reached phase 3 clinical trials for major depressive disorder prior to the discontinuation of its development. Some of the safety liabilities that led to its discontinuation of ritanserin for treatment of insomnia have led to its potential repurposing in the field of oncology. Specifically, it acts as a potent inhibitor of diacylglycerol kinase alpha (DGKα). As such, it may be used to treat certain types of glioblastoma and melanoma. It has also been used as a reference compound to identify putatively more selective and potent DGKα inhibitors to treat these forms of cancer as well as possibly others.
== Parent isotope source == 99Mo can be obtained by the neutron activation (n,γ reaction) of 98Mo in a high-neutron-flux reactor. However, the most frequently used method is through fission of uranium-235 in a nuclear reactor. While most reactors currently engaged in 99Mo production use highly enriched uranium-235 targets, proliferation concerns have prompted some producers to transition to low-enriched uranium targets. The target is irradiated with neutrons to form 99Mo as a fission product (with 6.1% yield). Molybdenum-99 is then separated from unreacted uranium and other fission products in a hot cell.
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.
Liquid chromatography-tandem mass spectrometry is a common approach. It can detect the parent compound and its metabolites in biological matrices.