This is a working overview of REV-ERB agonist, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-07-08. Anything still debated is marked as such rather than presented as settled.
Regulatory and sporting contexts treat SR9009 as a prohibited substance in many elite competitions. Its presence on banned lists reflects concerns about performance enhancement and unknown long-term safety. Analytical chemists have developed methods to detect the parent compound and its metabolites in urine and blood. Literature discussions distinguish between in vitro potency, animal pharmacology, and anecdotal human reports. The latter are difficult to verify because products sold online may lack purity or contain different compounds.
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, lipid metabolism, and inflammatory gene expression. In cell and animal experiments, SR9009 alters transcription of clock-controlled genes and metabolic pathways. The compound is not a hormone and does not resemble classical steroid structures. Its activity depends on binding to the ligand-binding domain of REV-ERB, where it can modify corepressor recruitment.
Research interest in SR9009 grew from studies of circadian biology and metabolic disease. Preclinical reports describe effects on exercise capacity, muscle metabolism, and blood lipid levels in rodents, but these findings come from controlled laboratory settings. The compound has low oral bioavailability in animals, which limits systemic exposure after swallowing. Investigators often use injected routes in experiments to achieve measurable plasma concentrations. Human clinical data are sparse, no approved therapeutic product exists, and whether animal effects translate to humans remains an open question.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ in preclinical models |
| Molecular formula | C20H24ClN3O4S | Reported for the parent compound |
| CAS Registry Number | 1379686-30-2 | Common identifier in chemical databases |
| Appearance | Off-white to pale yellow solid | Typical research chemical solid |
| Solubility | Soluble in DMSO and ethanol; low in water | Class: small organic molecule |
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.
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.
=== Cancer === Inflammation orchestrates the microenvironment around tumours, contributing to proliferation, survival and migration. Cancer cells use selectins, chemokines and their receptors for invasion, migration and metastasis. On the other hand, many cells of the immune system contribute to cancer immunology, suppressing cancer. Molecular intersection between receptors of steroid hormones, which have important effects on cellular development, and transcription factors that play key roles in inflammation, such as NF-κB, may mediate some of the most critical effects of inflammatory stimuli on cancer cells. This capacity of a mediator of inflammation to influence the effects of steroid hormones in cells is very likely to affect carcinogenesis. On the other hand, due to the modular nature of many steroid hormone receptors, this interaction may offer ways to interfere with cancer progression, through targeting of a specific protein domain in a specific cell type. Such an approach may limit side effects that are unrelated to the tumor of interest, and may help preserve vital homeostatic functions and developmental processes in the organism. There is some evidence from 2009 to suggest that cancer-related inflammation (CRI) may lead to accumulation of random genetic alterations in cancer cells.
Light, however, does not guarantee that a proplastid will develop into a chloroplast. Whether a proplastid develops into a chloroplast some other kind of plastid is mostly controlled by the nucleus and is largely influenced by the kind of cell it resides in.
=== Transamination === Urea undergoes transamination. For example, treatment with anilinium gives both N-phenylurea and N,N'-diphenylurea. N-Methylurea can be prepared by a similar acid-catalyzed pathway.
Thus, truly comprehensive or 'deep' proteome analyses must assess proteoforms. There are two general approaches to proteome analysis - bottom up (BUP or shotgun) and top down (TDP). The former, a peptide-centric or proteogenomic approach, infers (often with quite limited data) the identities of canonical protein sequences by correlation with existing databases, mostly derived from genome sequencing projects. In contrast, TDP can, in theory, yield comprehensive proteome analyses at the level of proteoforms provided the methods used effectively address the full breadth of species in a proteome.
Sources: en.wikipedia.org
== Track listing == "Too Cold To Snow" – 4:42 "Demons In The Scenery" – 3:48 "No Window" – 4:21 "I Spy" – 4:12 "Wreckage" – 3:16 "Demons Die" – 3:30 "Word For Word" – 3:43 "Nerve" – 4:07 "My Baby Only Cares For Me" – 3:30 "Senseless Sentences" – 4:20 "Divine" – 4:09 "Lucky Breaks" – 4:08 "Grace" – 5:02 "Harry: Walkies" - 0:09
=== Brain injury === There are similarities in what happens in the brain over time in Parkinson's disease and after a traumatic brain injury (TBI). PD is a progressive disorder, while TBI is an acute event that can be followed by both short- and long-term changes. Mechanisms common to both include changes in protein regulation, increased protein misfolding, protein aggregation, inflammation, and neurodegeneration. A history of TBI is reported as a risk factor for developing PD, but how mechanisms interact and whether TBI affects PD onset, development or progression are unclear.
In the fields of medicine, biotechnology, and pharmacology, drug discovery is the process by which new drugs are discovered. Historically, drugs were discovered by identifying the active ingredient from traditional remedies or by serendipitous discovery. Later chemical libraries of synthetic small molecules, natural products, or extracts were screened in intact cells or whole organisms to identify substances that have a desirable therapeutic effect in a process known as classical pharmacology. Since sequencing of the human genome which allowed rapid cloning and synthesis of large quantities of purified proteins, it has become common practice to use high throughput screening of large compound libraries against isolated biological targets which are hypothesized to be disease-modifying in a process known as reverse pharmacology. Hits from these screens are then tested in cells and then in animals for efficacy. Even more recently, scientists have been able to understand the shape of biological molecules at the atomic level and to use that knowledge to design (see drug design) drug candidates. Modern drug discovery involves the identification of screening hits, medicinal chemistry, and optimization of those hits to increase the affinity, selectivity (to reduce the potential of side effects), efficacy/potency, metabolic stability (to increase the half-life), and oral bioavailability. Once a compound that fulfills all of these requirements has been identified, it will begin the process of drug development prior to clinical trials.
The BioBricks assembly standard was described and introduced by Tom Knight in 2003 and it has been constantly updated since then. Currently, the most commonly used BioBricks standard is the assembly standard 10, or BBF RFC 10. BioBricks defines the prefix and suffix sequences required for a DNA part to be compatible with the BioBricks assembly method, allowing the joining of all DNA parts which are in the BioBricks format. The prefix contains the restriction sites for EcoRI, NotI and XBaI, while the suffix contains the SpeI, NotI and PstI restriction sites. Outside of the prefix and suffix regions, the DNA part must not contain these restriction sites. To join two BioBrick parts together, one of the plasmids is digested with EcoRI and SpeI while the second plasmid is digested with EcoRI and XbaI. The two EcoRI overhangs are complementary and will thus anneal together, while SpeI and XbaI also produce complementary overhangs which can also be ligated together. As the resulting plasmid contains the original prefix and suffix sequences, it can be used to join with more BioBricks parts. Because of this property, the BioBricks assembly standard is said to be idempotent in nature. However, there will also be a "scar" sequence (either TACTAG or TACTAGAG) formed between the two fused BioBricks.
=== Pharmacokinetics === Oxprenolol is a lipophilic beta blocker which passes the blood–brain barrier more easily than hydrophilic beta blockers. As such, it is associated with a higher incidence of CNS-related side effects than beta blockers with more hydrophilic molecules such as atenolol, sotalol, and nadolol. The brain-to-blood ratio of oxprenolol in humans has been found to be 50:1. For comparison, the brain-to-blood ratio of the highly lipophilic propranolol was 15:1 to 26:1 and of the hydrophilic atenolol was 0.2:1.
Sources: en.wikipedia.org
SR9009 is a synthetic small molecule studied as an agonist of the REV-ERB nuclear receptors. It is not an approved medicine, and its effects in humans are not well characterized.
No. It is a synthetic ligand that binds nuclear receptors, not a steroid or peptide hormone. Its activity depends on receptor binding rather than endocrine secretion.
Clinical evidence is limited. Most published data come from cell and animal experiments. Human safety and efficacy remain uncertain.
No. It is an investigational compound without approved therapeutic indications. It is sold for research purposes only in many jurisdictions.