This is a working overview of SR9009, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-05-10. Anything still debated is marked as such rather than presented as settled.
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.
Physicochemical behavior influences handling. SR9009 is described as a solid with limited aqueous solubility, so organic solvents such as dimethyl sulfoxide or ethanol are common in research stock solutions. Aqueous dilution can produce precipitates if the organic content is too low. Light, heat, and repeated freeze-thaw cycles may affect stability. Storage recommendations usually specify a desiccated freezer environment protected from light, but exact stability data depend on the formulation and matrix.
Detection in biological samples can be complicated by rapid metabolism and low circulating concentrations. Some studies report phase I and phase II metabolites, and analytical methods may need to target those species in addition to the parent compound. Immunoassays are not broadly available, so mass spectrometry remains the main confirmatory approach. For anti-doping testing, laboratories look for SR9009 and its metabolites using validated LC-MS methods. Open questions include how long metabolites remain detectable and how different routes of administration alter detection windows.
In laboratory settings, SR9009 is typically characterized by liquid chromatography–mass spectrometry (LC-MS) or high-performance liquid chromatography with ultraviolet detection (HPLC-UV). These methods can confirm identity and estimate purity, but they require reference standards for accurate quantification. Because SR9009 is not a licensed pharmaceutical, no harmonized pharmacopeial monograph exists. Laboratories often validate in-house methods for matrices such as plasma, urine, or cell culture media. Sample preparation may involve protein precipitation or liquid-liquid extraction before analysis.
| 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 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 binds REV-ERB receptors and alters their repressive activity on target genes. This action can change transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. In rodent studies, treated animals have shown changes in muscle oxidative capacity and exercise performance, though effects vary by dose, duration, and model. The precise molecular steps connecting receptor binding to whole-body outcomes are still an active area of investigation. Findings in animals do not automatically translate to humans.
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.
Quality control for research materials includes identity confirmation by nuclear magnetic resonance and purity assessment by high-performance liquid chromatography. Mass spectrometry provides molecular weight confirmation and can detect related impurities. Purchasers should request a certificate of analysis that lists lot-specific data. Online products advertised for human use often lack such documentation. Distinguishing legitimate research material from mislabeled or contaminated samples is a recurring challenge in independent testing, and independent laboratories may use orthogonal methods to verify identity.
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.
Laboratory studies often administer SR9009 by injection because oral absorption appears poor in rodents. Reported pharmacokinetic properties include rapid metabolism and low systemic exposure after oral dosing. Human pharmacokinetic data are sparse, so absorption, distribution, metabolism, and excretion in people are not well defined. Some research explores related REV-ERB compounds with improved drug-like properties. Regulatory approval for any REV-ERB agonist as a human medicine has not been granted to date.
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.
For services to Education. Donna Jones. Team Leader, Ministry of Defence. For services to Defence. Janet Elizabeth Kay. Kinship Carer, Kinship. For services to Children and Families. Professor Simon Edward Kenny. National Clinical Director for Children and Young People, NHS England and Consultant Paediatric Surgeon, Alder Hey Children's Hospital. For services to Paediatric Surgery. Professor Bienvenido Arturo Langa Ferreira. Consultant Psychiatrist, NHS Lanarkshire. For services to Vulnerable People in Scotland. Nicholas David Leader. Lately Governor, HM Prison Berwyn. For Public Service. Kathryn Maria Leahy. Director of Operations, Heathrow Airport. For services to Aviation Transport and to Major Events. Cathryn Lee. Chief Executive, Alzheimer's Society. For services to Charity. Janet Legrand, KC. Lately Chair of Trustees, The Children's Society. For services to Young People. Carl Anthony Les. Leader, North Yorkshire Council. For services to Local Government. Philip John Loach, QFSM. Lately Chief Fire Officer, West Midlands Fire and Rescue Service. For services to Fire and Rescue. Dr. William Patrick James Lockhart. Deputy Director, International Biodiversity and Wildlife, Department for Environment, Food and Rural Affairs. For services to the Environment. Antony Craig Lockley. Director of Strategy and Assistant Chief Executive, Blackpool Council. For services to Local Government. Professor Mark Logan, FRSE. Chief Entrepreneurial Adviser to the Scottish Government. For services to the Economy. Sally-Ann Loudon.
This is in part due to the myriad job titles used to describe them, including clinical physiologists, medical physicists, and clinical biochemists, which generally mean the public and other healthcare workers assume clinical scientists to be medically qualified doctors, due to the sometimes complex nature of the role.
== Solid phase peptide synthesis == The established method for the production of synthetic peptides is known as solid phase peptide synthesis (SPPS). Pioneered by Robert Bruce Merrifield, SPPS allows facile assembly of a target peptide by stepwise addition of amino acids while the growing peptide chain is attached to a macroscopically insoluble solvent-swollen beaded resin support.
==== In adults ==== In 2022, the UK National Institute for Health and Care Excellence (NICE) recommended that antidepressants be offered as a first-line treatment for moderate to severe depression, but for mild depression, non-drug interventions are preferred unless the patient chooses medication. They recommended that antidepressants should not be routinely offered for mild depression and should generally be used only if non-drug treatments fail or the patient prefers medication. In a 2018 review, all 21 studied antidepressants were more effective than placebo for major depressive disorder. The commonly used definition of antidepressant "response" as a 50% symptom reduction dichotomizes continuous data, which methodologists note can inflate effect sizes, exaggerate drug–placebo differences, and may not reliably indicate clinical significance. A large FDA trial analysis found that SSRIs and other antidepressants produced only modest average benefits over placebo, with about 15% of patients experiencing a substantial drug-specific response. SSRIs and other antidepressants may have average treatment effects that fall below the minimal important difference on common depression outcome measures, leaving their clinical significance in acute moderate-to-severe depression uncertain. There is no consistent evidence that depression is caused by lowered serotonin activity or concentrations, with some data suggesting that long-term antidepressant use may reduce serotonin levels.
Sources: en.wikipedia.org
Chasing the Scream: The First and Last Days of the War on Drugs was published in the UK on January 15th, 2015, followed by the US on January 20th the same month. Chasing the Scream critiques the global prohibition of illicit narcotics. Hari argued that most addictions are functional responses to experiences and a lack of healthy supportive relationships, rather than a simple biological need for a particular substance. Due to the previous scandals, Hari put the audio of some interviews conducted for Chasing the Scream online. Writer Jeremy Duns criticised instances where quotes were inaccurately transcribed or misrepresented, stating that out of a sample of dozens of clips, "in almost all cases, words in quotes had been changed or omitted without being noted, often for no apparent purpose, but in several cases to subtly change the narrative." In a review for New Matilda, Michael Brull expressed reservations about Hari's citational practices and highlighted contradictions between the narrative in Chasing the Scream and a 2009 article by Hari. For newer UK editions, the subtitle has been changed: Chasing the Scream: The Search for the Truth About Addiction.
== Criteria == The King's College criteria were described in a seminal publication in 1989 by J.G. O'Grady and colleagues from King's College School of Medicine. 588 patients with acute liver failure who presented to King's College Hospital from 1973 to 1985 were assessed retrospectively to determine if there were particular clinical features or tests that correlated poorly with prognosis. The criteria were stratified into acetaminophen and non-acetaminophen causes of acute liver failure, due to the different operating characteristics of parameters correlating with prognosis in the two causes.
== Initiation == Initiation of translation in bacteria involves the assembly of the components of the translation system, which are: the two ribosomal subunits (50S and 30S subunits); the mature mRNA to be translated; the tRNA charged with N-formylmethionine (the first amino acid in the nascent peptide); guanosine triphosphate (GTP) as a source of energy, and the three bacterial initiation factors IF1, IF2, and IF3, which help the assembly of the initiation complex. Variations in the mechanism can be anticipated. The ribosome has three active sites: the A site, the P site, and the E site. The A site is the point of entry for the aminoacyl tRNA (except for the first aminoacyl tRNA, which enters at the P site). The P site is where the peptidyl tRNA is formed in the ribosome. And the E site which is the exit site of the now uncharged tRNA after it gives its amino acid to the growing peptide chain.
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.
It is usually detected by LC-MS or HPLC-UV against a reference standard. In biological matrices, metabolite targeting can improve detection. No universal immunoassay is widely available.