A practical reference on mitochondrial biogenesis: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2026-03-22 and is reviewed periodically as new material appears.
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 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.
| 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. |
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 a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ, also called NR1D1 and NR1D2. These receptors help regulate circadian rhythms and metabolic gene programs. The compound was developed for laboratory research, not as an approved therapeutic. Its identity is distinct from steroid hormones and selective androgen receptor modulators. Scientific interest centers on how REV-ERB activation changes gene expression in cells and animal models.
At the molecular level, SR9009 binds the ligand-binding domain of REV-ERB and strengthens recruitment of corepressor proteins such as NCoR and HDAC3. This increases repression of target genes, including Bmal1 and other clock-controlled and metabolic genes. In rodent studies, such changes have been linked to altered lipid handling, glucose metabolism, and energy expenditure. The precise chain of events between receptor binding and whole-body effects remains an active area of research. Findings in animals do not automatically translate to humans.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. These receptors help regulate circadian rhythms and metabolic gene expression. In laboratory experiments, SR9009 binds these receptors and alters transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. It is not a naturally occurring compound and has no approved therapeutic use. Research interest stems from its ability to modify energy metabolism in cells and animal models.
In rodent studies, SR9009 has been reported to increase mitochondrial content in skeletal muscle and improve exercise endurance under some conditions. These findings led to popular descriptions such as an exercise mimetic, although that term oversimplifies the biology. Effects vary by dose, timing, tissue, and model. The compound's influence on circadian pathways means that time of administration can matter in experiments. Whether similar metabolic changes occur in humans remains largely unexplored in controlled published trials.
=== Nervous system === Prenatal exposure of BaP in rats is known to affect learning and memory in rodent models. Pregnant rats eating BaP were shown to negatively affect the brain function in the late life of their offspring. At a time when synapses are first formed and adjusted in strength by activity, BaP diminished NMDA receptor-dependent nerve cell activity measured as mRNA expression of the NMDA NR2B receptor subunit.
== Reconstitution == The ILEA was reformed by the Local Government Act 1985 which reconstituted it as a standalone body corporate and a directly elected authority. The replacement body came into existence before the abolition of the special committee of the GLC and was known as the Inner London Interim Education Authority until it came into its powers on 1 April 1986. In the May 1986 elections, each Inner London Parliamentary constituency elected two members of the ILEA. Labour won easily.
Tea is the most consumed manufactured drink in the world, equalling all others combined, including coffee, soft drinks, and alcohol. Most tea consumed outside East Asia is produced on large plantations in the hilly regions of India and Sri Lanka and is destined to be sold to large businesses. Opposite this large-scale industrial production are many small "gardens," sometimes minuscule plantations, that produce highly sought-after teas prized by gourmets. India is the world's largest tea-drinking nation, although the per capita consumption of tea remains a modest 750 grams (26 oz) per person every year. Turkey, with 2.5 kilograms (5 lb 8 oz) of tea consumed per person per year, is the world's greatest per capita consumer.
Sources: en.wikipedia.org
The production of pure alkali metals is somewhat complicated due to their extreme reactivity with commonly used substances, such as water. From their silicate ores, all the stable alkali metals may be obtained the same way: sulfuric acid is first used to dissolve the desired alkali metal ion and aluminium(III) ions from the ore (leaching), whereupon basic precipitation removes aluminium ions from the mixture by precipitating it as the hydroxide. The remaining insoluble alkali metal carbonate is then precipitated selectively; the salt is then dissolved in hydrochloric acid to produce the chloride. The result is then left to evaporate and the alkali metal can then be isolated. Lithium and sodium are typically isolated through electrolysis from their liquid chlorides, with calcium chloride typically added to lower the melting point of the mixture. The heavier alkali metals, however, are more typically isolated in a different way, where a reducing agent (typically sodium for potassium and magnesium or calcium for the heaviest alkali metals) is used to reduce the alkali metal chloride. The liquid or gaseous product (the alkali metal) then undergoes fractional distillation for purification. Most routes to the pure alkali metals require the use of electrolysis due to their high reactivity; one of the few which does not is the pyrolysis of the corresponding alkali metal azide, which yields the metal for sodium, potassium, rubidium, and caesium and the nitride for lithium. Lithium salts have to be extracted from the water of mineral springs, brine pools, and brine deposits.
siRNAs can be incorporated into a RNA-induced transcriptional silencing (RITS) complex. An active RITS complex will trigger the formation of heterochromatin around DNA matching the siRNA, effectively silencing the genes in that region of the DNA.
Mahathir criticised the awarding of import permits for foreign cars, which he claimed were causing Proton's domestic sales to suffer, and attacked Abdullah for cancelling the construction of a second causeway between Malaysia and Singapore. Mahathir complained that his views were not getting sufficient airing by the Malaysian press. In response, he began writing a column for Malaysiakini and starting his own blog. He unsuccessfully sought election from his local party division to be a delegate to UMNO's general assembly in 2006, where he planned to initiate a challenge to Abdullah's leadership. Mahathir had previously missed the UMNO General Assembly twice since 2006 for health reasons. After the 2008 election, in which UMNO lost its two-thirds majority in parliament, Mahathir resigned from the party. When Abdullah was replaced by his deputy Najib Razak in 2009, Mahathir re-joined the party and urged all former members to follow his move. Before the 2013 general election, Mahathir promised to keep the government in check and ensure it fulfilled its manifesto promises, vowing to protest and fight against it if it failed.
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 REV-ERB agonist used mainly in preclinical research. It is not an approved medicine for human use.