Everything below concerns REV-ERB. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-08-01. 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.
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 studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.
| 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. |
Analytical chemists detect SR9009 with liquid chromatography-tandem mass spectrometry, commonly abbreviated LC-MS/MS. Sample preparation may involve protein precipitation, liquid-liquid extraction, or solid-phase extraction before analysis. Laboratories can target the parent compound or its metabolites, depending on the matrix and the purpose of testing. Anti-doping methods require sensitive and specific assays because concentrations in biological samples can be low. Reference standards and validated methods are essential for reliable identification and quantification.
Regulatory agencies have not approved SR9009 for human therapeutic use. It is typically sold as a research chemical with labels stating that it is not for human consumption. The World Anti-Doping Agency prohibits the substance in sport, generally under the category of non-approved substances. Customs and national laws may restrict importation, sale, or possession. Product quality and legal status can vary by country and vendor, and therapeutic claims are not permitted in regulated advertising because the compound lacks approval.
=== Invention === In 1966 (1966) Sato Foods Industries Co., Ltd. invented alcohol pulverization. Sato is a food additives and seasoning manufacturer in Aichi Prefecture in Japan. (ja:佐藤食品工業 (愛知県)) A year later, in 1967, Sato began production and sales of various kinds of "high content alcohol powder Alcock" ("高含度アルコール粉末「アルコック」"). On 15 January 1974, a practical manufacturing process for alcohol powder was patented by Sato. Sato has patented the process in 17 countries around the world. In the 1970s Sato began promoting powdered alcohol in the United States. Test sales began in 1977 under the trade name "SureShot". The product "Palcohol" was announced for future release in the U.S. in 2015. In Turkey, on November 21, 1973, a former chemist named İsmail Serin invented a powdered version of rakı, a traditional Turkish anise-flavored alcoholic beverage.
==== MeSH D13.570.230 – deoxyribonucleosides ==== MeSH D13.570.230.229 – deoxyadenosines MeSH D13.570.230.229.075 – cladribine MeSH D13.570.230.229.105 – dideoxyadenosine MeSH D13.570.230.229.650 – puromycin aminonucleoside MeSH D13.570.230.329 – deoxycytidine MeSH D13.570.230.329.100 – bromodeoxycytidine MeSH D13.570.230.329.950 – zalcitabine MeSH D13.570.230.329.950.500 – lamivudine MeSH D13.570.230.360 – deoxyguanosine MeSH D13.570.230.430 – deoxyuridine MeSH D13.570.230.430.196 – bromodeoxyuridine MeSH D13.570.230.430.432 – floxuridine MeSH D13.570.230.430.609 – idoxuridine MeSH D13.570.230.500 – dideoxynucleosides MeSH D13.570.230.500.090 – didanosine MeSH D13.570.230.500.105 – dideoxyadenosine MeSH D13.570.230.500.850 – stavudine MeSH D13.570.230.500.925 – zalcitabine MeSH D13.570.230.500.925.500 – lamivudine MeSH D13.570.230.500.950 – zidovudine MeSH D13.570.230.677 – pentostatin MeSH D13.570.230.855 – thymidine MeSH D13.570.230.855.875 – stavudine MeSH D13.570.230.855.900 – trifluridine MeSH D13.570.230.855.950 – zidovudine
=== Kenny Kilbane === Kenny Kilbane (Conor MacNeill) is a VP on Pierpoint's FX desk, and Yasmin's line manager. Throughout the first season, Kenny subjects Yasmin to repeated bullying and verbal abuse in the workplace, which he often blames on his alcoholism. In one case, Yasmin brings Kenny to a client dinner she arranged with her family friend Maxim Alonso, but Kenny embarrasses her when he orders a stripper to perform a lap dance on Yasmin in front of her disgusted clients. On RIF day, however, Kenny's boss Hilary Wyndham advises that Yasmin not report his behavior during her interview, suggesting that being a "team player" would help her career prospects. In series 2, Kenny returns to work following a long stint in rehab during the COVID-19 pandemic, noticeably kinder to his colleagues and vocal about his commitment to self-improvement and repentance. Yasmin, though still uncomfortable around Kenny, invites him to another client dinner, which ends up going well after Kenny and the client bond over both attending AA. When Yasmin announces her departure from the FX desk for a role in private wealth management (PWM), Kenny takes her aside and offers a sincere, tearful apology for his past behavior. Later, however, new FX hire Venetia Berens reports to Kenny that CPS client Nicole Craig sexually assaulted her, and that Yasmin dismissed her concerns. Kenny confronts Yasmin about her response, but Yasmin berates him for his hypocrisy given his own history of abusive conduct towards her, and brands him a narcissist lording his sobriety over others.
Sources: en.wikipedia.org
=== Behavioral reinforcement of food intake === It is well-characterized that activating the growth hormone secretagogue receptor with ghrelin induces an orexigenic state, or general feeling of hunger. However, ghrelin may also play a role in behavioral reinforcement. Studies in animal models, found that food intake increased when ghrelin was specifically administered to just the ventral tegmental area (VTA), a brain area that uses dopamine signaling to reinforce behavior. In fact, the more ghrelin administered, the more food the rodent consumed. This is called a dose-dependent effect. Building on this, it was found that there are growth hormone secretagogue receptors in the VTA and that ghrelin acts on the VTA through these receptors. Current studies, furthermore, suggest that the VTA may contain dimers of GHS-R1a and dopamine receptor type 2 (DRD2). If these two receptors do indeed form dimers, this would somehow link ghrelin signaling to dopaminergic signaling.
In business and investing, a megacap stock (also mega-cap or mega cap) is a stock whose market capitalization (market cap) is among the very largest. These are stocks of the largest publicly traded companies in the world. The market capitalization of a stock is the total value of the shares outstanding, calculated as (shares outstanding x share price). Stocks with large market caps, but smaller than megacaps, instead fall within the large-cap segment of the stock market. There is no official definition of, or full consensus agreement about, the exact market cap cutoff value for a stock to qualify as megacap, and it may vary internationally. However, for the 2020s US market, a minimum market cap value of $200 billion is often cited. Index providers, investment funds, and investment managers may have other definitions.
As the leader of the Cure Alzheimer's Fund's Alzheimer's Genome Project, Tanzi several other AD genes, most notably, CD33, reported in 2008 with Lars Bertram, in the American Journal of Human Genetics. In that study, Tanzi reported the first family-based genome-wide association study of AD, which most notably to the identification of the first innate immune microglial AD gene, CD33, which encodes a cell-surface receptor on monocytes and microglia. In 2013, Tanzi and Dr. Ana Griciuc first reported in Neuron that increased expression of CD33 in microglial cells in AD brain and showed that a protective CD33 gene variant was associated with reductions in CD33 expression and Abeta levels in AD brain. Importantly, they showed CD33 inhibits microglial phagocytosis and clearance of Abeta and induces pro-inflammatory cytokine release leading to neuroinflammation. They also elucidated the molecular mechanism by which sialic acid binds to CD33 to induce neuroinflammation. In a follow-up study published in Neuron in 2019, Tanzi and Griciuc compared the neuroinflammatory effects of the CD33 gene to another AD-associated innate immune gene, TREM2. Knockout of CD33 in AD mice attenuated amyloid-beta pathology and improved cognition while knockout of TREM2 led to opposite effects. They then showed that TREM2 functions downstream of CD33 and that crosstalk between CD33 and TREM2 involves the neuroinflammation-related IL-1beta/IL-1RN axis cluster.
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.
It is a synthetic compound studied as an agonist of REV-ERB nuclear receptors. It is not an approved medicine and has mainly been examined in laboratory and animal research.