If you have been reading about SR9009 and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Last reviewed on 2026-05-25. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
SR9009 is generally described as poorly soluble in water and more soluble in organic solvents such as dimethyl sulfoxide and ethanol. Stock solutions are commonly prepared in an organic solvent before dilution into an aqueous buffer or vehicle. Precipitation can occur if the organic fraction is reduced too quickly or if the final concentration exceeds the compound's solubility limit. Sonication or gentle warming may aid dissolution in some protocols, but excessive heat can promote degradation. Container material and pH can also influence observed solubility.
For long-term storage, SR9009 is typically kept as a solid at low temperature, protected from moisture and light. Desiccated conditions limit hydrolysis, while opaque containers reduce photochemical breakdown. Solutions are less stable than solids and are often stored frozen in aliquots to avoid repeated freeze-thaw cycles. Stability data are not standardized across all suppliers, so users should rely on certificate-of-analysis information when available. Degradation may appear as color change, precipitate, or decreased chromatographic purity.
| 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 |
Laboratory samples of SR9009 are typically supplied as a white to off-white powder. The compound dissolves readily in organic solvents such as dimethyl sulfoxide and ethanol, while its solubility in water is low. Because of this solubility profile, researchers often prepare concentrated stock solutions in an organic solvent before diluting them into aqueous assay buffers. Light exposure, moisture, and repeated freeze-thaw cycles can degrade many small molecules, so handling procedures usually aim to minimize these factors. Purity is commonly checked before use.
Storage conditions for research-grade SR9009 generally involve a freezer at approximately minus twenty degrees Celsius, sometimes lower for long-term preservation. Containers should remain tightly closed and protected from light. Desiccants may be used to limit moisture uptake. Solutions are often stored in aliquots to avoid repeated warming and cooling. Stability data for the compound under various conditions are limited, so laboratories typically follow supplier recommendations and verify performance through periodic analytical checks rather than assuming indefinite stability.
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.
80. Levothyroxine. Drugs and Lactation Database (LactMed®) [Internet]. Bethesda (MD): National Institute of Child Health and Human Development; 2006–. 2026 Sep 15. Levothyroxine (T4) is a normal component of human milk. Limited data on exogenous replacement doses of levothyroxine during breastfeeding indicate no adverse effects in infants. The American Thyroid Association recommends that subclinical and overt hypothyroidism should be treated with levothyroxine in lactating women seeking to breastfeed.[1] Adequate levothyroxine treatment during lactation may normalize milk production in hypothyroid lactating mothers with low milk supply, but does not return milk lipids to normal. Mothers taking levothyroxine because of gestational hypothyroidism may have lower exclusive breastfeeding rates rates at 1 month and increased early formula supplementation.[2] Levothyroxine dosage requirement may be increased in the postpartum period compared to prepregnancy requirements in patients with Hashimoto’s thyroiditis.[3]
=== Rutherfordium and dubnium === During the height of the Cold War, teams from the Soviet Union and the United States independently created rutherfordium and dubnium. The naming and credit for synthesis of these elements remained unresolved for many years, but eventually, shared credit was recognized by IUPAC/IUPAP in 1992. In 1997, IUPAC decided to give dubnium its current name, honoring the city of Dubna where the Russian team worked since American-chosen names had already been used for many existing synthetic elements, while the name rutherfordium (chosen by the American team) was accepted for element 104.
Insulin detemir, sold under the brand name Levemir among others, is a long-acting modified form of medical insulin used to treat both type 1 and type 2 diabetes. It is used by injection under the skin. It is effective for up to 24 hours. Common side effects include low blood sugar, allergic reactions, pain at the site of injection, and weight gain. Use in pregnancy and breastfeeding appears safe. It works by increasing the amount of glucose that tissues take in and decreasing the amount of glucose made by the liver. Insulin detemir was approved for medical use in the European Union in June 2004, and in the United States in June 2005. It is on the World Health Organization's List of Essential Medicines. In 2023, it was the 153rd most commonly prescribed medication in the United States, with more than 3 million prescriptions. Novo Nordisk is discontinuing production of insulin detemir, with supplies in the UK expected to run out in December 2026.
, is the probability, after time t, that there is a base j at a given position, conditional on there being a base i in that position at time 0. When the model is time reversible, this can be performed between any two sequences, even if one is not the ancestor of the other, if you know the total branch length between them. The asymptotic properties of Pij(t) are such that Pij(0) = δij, where δij is the Kronecker delta function. That is, there is no change in base composition between a sequence and itself. At the other extreme,
Sources: pubmed.ncbi.nlm.nih.gov
Besides recommendations for infant vaccinations and boosters, many specific vaccines are recommended for other ages or for repeated injections throughout life – most commonly for measles, tetanus, influenza, and pneumonia. Pregnant women are often screened for continued resistance to rubella. As of 2011, the human papillomavirus vaccine was recommended in the US, and, as of 2009, in the UK. Vaccine recommendations for the elderly concentrate on pneumonia and influenza, which are more deadly to that group. In 2006, a vaccine was introduced against shingles, a disease caused by the chickenpox virus, which usually affects the elderly. Scheduling and dosing of a vaccination may be tailored to the level of immunocompetence of an individual and to optimize population-wide deployment of a vaccine when its supply is limited, e.g. in the setting of a pandemic.
==== Warning signs ignored ==== From 2005 to 2006, an agent, Jiang Weisuo, from Shaanxi Jinqiao Dairy Company in northern China reportedly publicly discussed his fears about unauthorised substances being added to competitors' milk. His complaints to regulators and dairy makers in 2005 and 2006 never yielded any result; his story was picked up by China Central Television, who ran a report, complete with footage of adulteration in progress, yet the Shaanxi Quality and Technical Supervision Bureau said they failed to find evidence of wrongdoing. The bulletin board of the Administration of Quality Supervision, Inspection and Quarantine (AQSIQ) indicated a rare occurrence of kidney stones in children–all causally traced to Sanlu milk formula–was flagged by at least one member of the public in June 2008 and by a urologist in a paediatric hospital on 24 July 2008. Neither received definitive replies. The paediatrician, who specifically asked the AQSIQ to refer his observations to epidemiologists, was asked to refer his query to the health department. In June, Jiangsu media reported a two-month surge in the number of babies diagnosed with kidney disease; in July, a parent of a sick baby in Hunan questioned Sanlu's powdered milk and complained to the AQSIQ. Gansu Province sent a report to the Ministry of Health on 16 July to alert that one local hospital had identified an increase in the incidence of kidney ailments among babies in the months earlier, and that most victims had consumed Sanlu's baby formula. The health ministry sent investigators to Gansu in early August.
Dengue fever becomes more virulent during a second infection by means of antibody-dependent enhancement. After the first infection, macrophages display antibodies on their cell membranes specific to the dengue virus. By attaching to these antibodies, dengue viruses from a second infection are better able to infect the macrophages, thus reducing the immune system's ability to fight off infection.
Sources: en.wikipedia.org
Minor histocompatibility antigen (also known as MiHA) are peptides presented on the cellular surface of donated organs that are known to give an immunological response in some organ transplants. They cause problems of rejection less frequently than those of the major histocompatibility complex (MHC). Minor histocompatibility antigens (MiHAs) are diverse, short segments of proteins and are referred to as peptides. These peptides are normally around 9-12 amino acids in length and are bound to both the major histocompatibility complex (MHC) class I and class II proteins. Peptide sequences can differ among individuals and these differences arise from SNPs in the coding region of genes, gene deletions, frameshift mutations, or insertions. About a third of the characterized MiHAs come from the Y chromosome. Prior to becoming a short peptide sequence, the proteins expressed by these polymorphic or diverse genes need to be digested in the proteasome into shorter peptides. These endogenous or self peptides are then transported into the endoplasmic reticulum with a peptide transporter pump called TAP where they encounter and bind to the MHC class I molecule. This contrasts with MHC class II molecules's antigens which are peptides derived from phagocytosis/endocytosis and molecular degradation of non-self entities' proteins, usually by antigen-presenting cells. MiHA antigens are either ubiquitously expressed in most tissue like skin and intestines or restrictively expressed in the immune cells.
This response is activated by the binding of complement proteins to carbohydrates on the surfaces of microbes, or to antibodies that have attached to these microbes, which creates a cell signal that triggers a rapid killing response, whose speed is significantly amplified after sequential proteolytic activation of complement protease molecules, controlled by positive feedback. The cascade results in the production of peptides that attract immune cells; increase vascular permeability; and opsonize the surface of a pathogen, marking it for destruction. Complement binding can also kill cells directly by disrupting their plasma membrane via a membrane attack complex.
Creatine transporter deficiency (CTD) is an inborn error of creatine metabolism in which creatine is not properly transported to the brain and muscles due to defective creatine transporters. CTD is an X-linked disorder caused by mutation in SLC6A8. SLC6A8 is located at Xq28. Hemizygous males with CTD express speech and behavior abnormalities, intellectual disabilities, development delay, seizures, and autistic behavior. Heterozygous females with CTD generally express fewer, less severe symptoms. CTD is one of three different types of cerebral creatine deficiency (CCD). The other two types of CCD are guanidinoacetate methyltransferase (GAMT) deficiency and L-arginine:glycine amidinotransferase (AGAT) deficiency. Clinical presentation of CTD is similar to that of GAMT and AGAT deficiency. CTD was first identified in 2001 with the presence of a hemizygous nonsense change in SLC6A8 in a male patient.
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.
Liquid chromatography with mass spectrometry is a common approach. Ultraviolet detection and nuclear magnetic resonance can support identification when suitable standards are available.