SR9009 raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2026-08-01 and is reviewed periodically as new material appears.
Because REV-ERB receptors are core clock components, SR9009 has been examined for effects on daily rhythms as well as metabolism. Research has explored whether the compound can shift or reinforce circadian gene expression in tissues such as liver and muscle. Some studies report improved metabolic markers in obese or diabetic mice, while others show context-dependent responses. Questions remain about which effects are direct, which are secondary to timing, and how they might differ across species.
SR9009 is a synthetic small molecule studied as an agonist of REV-ERB nuclear receptors. REV-ERB alpha and REV-ERB beta help regulate circadian rhythms and metabolic gene expression. In laboratory research, SR9009 has been used to probe how these receptors affect skeletal muscle, liver, and adipose tissue. The compound was identified in academic drug-discovery work and is often described in scientific literature by its chemical name and research code. It is not an approved medicine, and human clinical data remain limited or absent.
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.
Preclinical reports describe effects on exercise endurance, mitochondrial content, and lipid profiles in rodents, but these findings come from specific experimental conditions. Many studies use high doses or delivery methods that may not translate directly to human use. SR9009 has been reported to have low oral bioavailability and a short half-life, which complicates interpretation of oral dosing studies. It is not established as safe or effective for any indication. Literature discussions often separate its pharmacological mechanism from unverified claims made in fitness and supplement markets.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small-molecule nuclear receptor ligand |
| Appearance | Off-white to pale yellow solid | Typical for research-grade powder |
| Solubility class | Soluble in DMSO; low water solubility | Common stock solutions use organic solvent |
| Typical stock solvent | Dimethyl sulfoxide | Used for laboratory assays |
| Common analytical method | HPLC with UV or mass detection | Used for identity and purity checks |
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.
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.
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 supplied as a solid research chemical, often in milligram quantities. Laboratories typically weigh it in a controlled environment because fine powders can disperse. Stock solutions are commonly prepared in dimethyl sulfoxide and stored in small aliquots to reduce freeze-thaw cycles. Personal protective equipment and chemical fume hoods are standard when handling unknown or potent compounds. These practices address laboratory safety rather than human use.
Identity and purity of SR9009 samples are usually checked with chromatographic and spectrometric methods. High-performance liquid chromatography can separate the compound from related impurities, while mass spectrometry provides molecular mass confirmation. Nuclear magnetic resonance spectroscopy may be used for structural verification in research settings. No single method proves biological activity, and certificates of analysis should be reviewed alongside raw data. Independent testing is often needed because online products vary widely.
SR9009 stability depends on temperature, moisture, light, and solvent. Solid material is generally kept cool and dry, while solutions may require protection from repeated warming and cooling. Degradation can appear as color changes, precipitate, or new chromatographic peaks. Researchers should follow supplier instructions and their own stability data. Long-term storage conditions for human use have not been established because the compound lacks approved clinical formulation.
At the regulatory site, the binding of a ligand may elicit amplified or inhibited protein function. The binding of a ligand to an allosteric site of a multimeric enzyme often induces positive cooperativity, that is the binding of one substrate induces a favorable conformation change and increases the enzyme's likelihood to bind to a second substrate. Regulatory site ligands can involve homotropic and heterotropic ligands, in which single or multiple types of molecule affects enzyme activity respectively. Enzymes that are highly regulated are often essential in metabolic pathways. For example, phosphofructokinase (PFK), which phosphorylates fructose in glycolysis, is largely regulated by ATP. Its regulation in glycolysis is imperative because it is the committing and rate limiting step of the pathway. PFK also controls the amount of glucose designated to form ATP through the catabolic pathway. Therefore, at sufficient levels of ATP, PFK is allosterically inhibited by ATP. This regulation efficiently conserves glucose reserves, which may be needed for other pathways. Citrate, an intermediate of the citric acid cycle, also works as an allosteric regulator of PFK.
Enzymatic specificity provides useful insight into enzyme structure, which ultimately determines and plays a role in physiological functions. Specificity studies also may provide information of the catalytic mechanism. Specificity is important for novel drug discovery and the field of clinical research, with new drugs being tested for its specificity to the target molecule in various rounds of clinical trials. Drugs must contain as specific as possible structures in order to minimize the possibility of off-target affects that would produce unfavorable symptoms in the patient. Drugs depend on the specificity of the designed molecules and formulations to inhibit particular molecular targets. Novel drug discovery progresses with experiments involving highly specific compounds. For example, the basis that drugs must successfully be proven to accomplish is both the ability to bind the target receptor in the physiological environment with high specificity and also its ability to transduce a signal to produce a favorable biological effect against the sickness or disease that the drug is intended to negate.
After the Netherlands in World War II in 1945, Korvezee returned to Delft, initially serving as a curator and, from 1948, as a lecturer in theoretical chemistry. Although an expert in radioactivity, she had no role in the planning of the reactor center later built on the university's grounds. When the chair became vacant following Scheffer's retirement, Korvezee was passed over once more. In 1954, the Department of Chemical Technology created an extraordinary professorship for her in the emerging field of theoretical chemistry largely regarded as compensation for the chairs she had earlier missed. Her appointment on 14 April 1954, making her the first female professor at Delft, received extensive press coverage. As a full professor, however, she retained the salary of her former lectureship. As professor, Korvezee supervised doctoral and master's students and published more than forty scientific works before 1940, many co-authored with fellow female assistants. She was a member of the Association of Women with an Academic Education (VVAO), though she was never actively involved in the women's movement despite being widely regarded as a feminist figure.
Helices observed in proteins can range from four to over forty residues long, but a typical helix contains about ten amino acids (about three turns). In general, short polypeptides do not exhibit much α-helical structure in solution, since the entropic cost associated with the folding of the polypeptide chain is not compensated for by a sufficient amount of stabilizing interactions. In general, the backbone hydrogen bonds of α-helices are considered slightly weaker than those found in β-sheets, and are readily attacked by the ambient water molecules. However, in more hydrophobic environments such as the plasma membrane, or in the presence of co-solvents such as trifluoroethanol (TFE), or isolated from solvent in the gas phase, oligopeptides readily adopt stable α-helical structure. Furthermore, crosslinks can be incorporated into peptides to conformationally stabilize helical folds. Crosslinks stabilize the helical state by entropically destabilizing the unfolded state and by removing enthalpically stabilized "decoy" folds that compete with the fully helical state. It has been shown that α-helices are more stable, robust to mutations and designable than β-strands in natural proteins, and also in artificially designed proteins.
Sources: en.wikipedia.org
The LCPO method uses a linear approximation of the two-body problem for a quicker analytical calculation of ASA. The approximations used in LCPO result in an error in the range of 1-3 Ų. In 2011, a method was presented that calculates ASA fast and analytically using a power diagram. Accessible surface area is often used when calculating the transfer free energy required to move a biomolecule from an aqueous solvent to a non-polar solvent, such as a lipid environment. The LCPO method is also used when calculating implicit solvent effects in the molecular dynamics software package AMBER. It is recently suggested that (predicted) accessible surface area can be used to improve prediction of protein secondary structure.
An aldehyde tag is a short peptide tag that can be further modified to add fluorophores, glycans, PEG (polyethylene glycol) chains, or reactive groups for further synthesis. A short, genetically-encoded peptide with a consensus sequence LCxPxR is introduced into fusion proteins, and by subsequent treatment with the formylglycine-generating enzyme (FGE), the cysteine of the tag is converted to a reactive aldehyde group. This electrophilic group can be targeted by an array of aldehyde-specific reagents, such as aminooxy- or hydrazide-functionalized compounds.
An organic compound is a chemical whose molecules contain carbon. Carbon is abundant in the Sun, stars, comets, and in the atmospheres of most planets of the Solar System. Organic compounds are relatively common in space, formed by "factories of complex molecular synthesis" which occur in molecular clouds and circumstellar envelopes, and chemically evolve after reactions are initiated mostly by ionizing radiation. Purine and pyrimidine nucleobases including guanine, adenine, cytosine, uracil, and thymine, as well as sugars, have been found in meteorites. These could have provided the materials for DNA and RNA to form on the early Earth. The amino acid glycine was found in material ejected from comet Wild 2; it had earlier been detected in meteorites. Comets are encrusted with dark material, thought to be a tar-like organic substance formed from simple carbon compounds under ionizing radiation. A rain of material from comets could have brought such complex organic molecules to Earth. During the Late Heavy Bombardment, meteorites may have delivered up to five million tons of organic prebiotic elements to Earth per year. Currently 40,000 tons of cosmic dust falls to Earth each year.
Sources: en.wikipedia.org
SR9009 is a synthetic research compound that acts on REV-ERB nuclear receptors. It is not approved for human use and is sold only as a research chemical. Its effects have been studied mainly in cells and rodents.
It binds REV-ERB alpha and REV-ERB beta and changes the expression of genes tied to metabolism and circadian rhythm. These changes can affect mitochondria and energy use in animal models. The exact chain from receptor binding to physiological outcome is still being mapped.
No reliable human trials show that SR9009 improves athletic performance. Some rodent studies report endurance changes, but these results are not proof of human benefit. Its use in sport is prohibited, and quality and safety data are lacking.
SR9009 is a synthetic REV-ERB agonist used in laboratory research. It is not an approved drug, and its effects in humans are not well characterized. It is often sold as a research chemical under the name Stenabolic.