en · de · es · fr · pt
field-notes.peptides3626.com › Data › Background And Receptor Pharmacology — Explained

Background And Receptor Pharmacology — Explained

By Editorial Desk · published 2025-10-06 · last reviewed 2025-11-01 · Data

REV-ERB agonist is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.

Updated 2025-11-01. Numbers and descriptions here follow the published literature rather than marketing material.

Background and Receptor Pharmacology

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.

Analytical Detection and Storage

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.

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.

Sr9009 at a glance

PropertyValueNotes
Chemical classSynthetic REV-ERB agonistBinds REV-ERBα and REV-ERBβ in preclinical models
Molecular formulaC20H24ClN3O4SReported for the parent compound
CAS Registry Number1379686-30-2Common identifier in chemical databases
AppearanceOff-white to pale yellow solidTypical research chemical solid
SolubilitySoluble in DMSO and ethanol; low in waterClass: small organic molecule

Background and Mechanism

SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not an approved medicine and has no established human therapeutic use. The compound appears in scientific literature as a tool for probing circadian and metabolic regulation. Online sellers often label it as a research chemical, sometimes using the nickname Stenabolic. Its chemical identity is distinct from selective androgen receptor modulators, stimulants, and peroxisome proliferator-activated receptor delta agonists. Researchers use it mainly in cell and animal experiments.

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.

Related pages on this site

Analytical Detection and Stability

Analytical identification of SR9009 typically relies on liquid chromatography coupled with tandem mass spectrometry. In biological samples, researchers first separate the compound from matrix components using protein precipitation, liquid-liquid extraction, or solid-phase extraction. High-performance liquid chromatography with ultraviolet detection and nuclear magnetic resonance spectroscopy can support structural confirmation of reference materials. Because SR9009 is a small, relatively lipophilic molecule, reverse-phase columns and acidic mobile phases are common. Laboratories often include isotope-labeled internal standards to improve quantification and to correct for ion suppression.

Stability depends on physical form, temperature, light exposure, and solvent. Solid SR9009 is generally stored cold and dry, with protection from light to limit degradation. Dimethyl sulfoxide stocks are common for laboratory work, but repeated freeze-thaw cycles can reduce compound integrity. Aqueous solutions may be less stable than organic stocks, and the ethyl ester in the structure can be susceptible to hydrolysis under certain conditions. Researchers typically validate storage conditions and recheck purity before quantitative experiments, especially when using archived material.

Regulatory treatment of SR9009 varies by country and region. It is not approved as a pharmaceutical, and several jurisdictions restrict its sale for human consumption. Some authorities classify it as a research chemical, a prescription-only substance, or a prohibited performance-enhancing agent in sport. Purchasers may encounter certificates of analysis, but these documents do not guarantee identity, purity, or legality. In research settings, institutional safety reviews and controlled procurement help ensure that materials are handled under appropriate oversight. The absence of harmonized rules means that legal status can change and requires verification.

Further detail

=== Alternating tangential flow (ATF) === A diaphragm pump is used to produce an alternating tangential flow, helping to dislodge retained particles and prevent membrane fouling. Repligen is the largest producer of ATF systems.

=== Brust-Schiffrin method === This method was discovered by Brust and Schiffrin in the early 1990s, and can be used to produce gold nanoparticles in organic liquids that are normally not miscible with water (like toluene). It involves the reaction of a chlorauric acid solution with tetraoctylammonium bromide (TOAB) solution in toluene and sodium borohydride as an anti-coagulant and a reducing agent, respectively. Here, the gold nanoparticles will be around 5–6 nm. NaBH4 is the reducing agent, and TOAB is both the phase transfer catalyst and the stabilizing agent. TOAB does not bind to the gold nanoparticles particularly strongly, so the solution will aggregate gradually over the course of approximately two weeks. To prevent this, one can add a stronger binding agent, like a thiol (in particular, alkanethiols), which will bind to gold, producing a near-permanent solution. Alkanethiol protected gold nanoparticles can be precipitated and then redissolved. Thiols are better binding agents because there is a strong affinity for the gold-sulfur bonds that form when the two substances react with each other. Tetra-dodecanthiol is a commonly used strong binding agent to synthesize smaller particles. Some of the phase transfer agent may remain bound to the purified nanoparticles, this may affect physical properties such as solubility. In order to remove as much of this agent as possible, the nanoparticles must be further purified by soxhlet extraction.

=== EC 1.14.99 Miscellaneous === EC 1.14.99.1: prostaglandin-endoperoxide synthase EC 1.14.99.2: kynurenine 7,8-hydroxylase EC 1.14.99.3: Now EC 1.14.14.18, heme oxygenase (biliverdin-producing) EC 1.14.99.4: progesterone monooxygenase EC 1.14.99.5: Now EC 1.14.19.1, stearoyl-CoA 9-desaturase EC 1.14.99.6: Now EC 1.14.19.2, acyl-[acyl-carrier-protein] desaturase EC 1.14.99.7: Transferred to EC 1.14.13.132, squalene monooxygenase EC 1.14.99.8: Now included with EC 1.14.14.1 unspecific monooxygenase EC 1.14.99.9: Now classified as EC 1.14.14.19, steroid 17α-monooxygenase EC 1.14.99.10: Now EC 1.14.14.16, steroid 21-monooxygenase EC 1.14.99.11: estradiol 6β-monooxygenase EC 1.14.99.12: 4-androstene-3,17-dione monooxygenase EC 1.14.99.13: Now EC 1.14.13.23, 3-hydroxybenzoate 4-monooxygenase EC 1.14.99.14: Now EC 1.14.14.197, progesterone 11α-monooxygenase EC 1.14.99.15: 4-methoxybenzoate monooxygenase (O-demethylating) EC 1.14.99.16: Now EC 1.14.13.72, methylsterol monooxygenase EC 1.14.99.17: Now EC 1.14.16.5, glyceryl-ether monooxygenase EC 1.14.99.18: deleted EC 1.14.99.19: Now classified as EC 1.14.19.77, plasmanylethanolamine desaturase EC 1.14.99.20: phylloquinone monooxygenase (2,3-epoxidizing) EC 1.14.99.21: Latia-luciferin monooxygenase (demethylating) EC 1.14.99.22: ecdysone 20-monooxygenase EC 1.14.99.23: 3-hydroxybenzoate 2-monooxygenase EC 1.14.99.24: steroid 9α-monooxygenase EC 1.14.99.25: Now EC 1.14.19.3, linoleoyl-CoA desaturase EC 1.14.99.26: 2-hydroxypyridine 5-monooxygenase EC 1.14.99.27: Now classified as EC 1.17.3.4, juglone 3-monooxygenase EC 1.14.99.28: Now EC 1.14.14.84, linalool 8-monooxygenase EC 1.14.99.29: deoxyhypusine monooxygenase EC 1.14.99.30: Now EC 1.3.5.6, 9,9′-dicis-ζ-carotene desaturase. EC 1.14.99.31: Now classified as EC 1.14.19.24, myristoyl-CoA 11-(E) desaturase EC 1.14.99.32: Now classified as EC 1.14.19.5, acyl-CoA 11-(Z)-desaturase EC 1.14.99.33: Now EC 1.14.19.39, acyl-lipid Δ12-acetylenase EC 1.14.99.34: monoprenyl isoflavone epoxidase EC 1.14.99.35: thiophene-2-carbonyl-CoA monooxygenase EC 1.14.99.36: Now classified as EC 1.13.11.63, β-carotene 15,15′-dioxygenase EC 1.14.99.37: Now EC 1.14.14.176, taxadiene 5α-hydroxylase EC 1.14.99.38: cholesterol 25-hydroxylase EC 1.14.99.39: ammonia monooxygenase EC 1.14.99.40: Now EC 1.13.11.79, 5,6-dimethylbenzimidazole synthase EC 1.14.99.41: Now EC 1.13.11.75, all-trans-8′-apo-β-carotenal 15,15′-oxygenase EC 1.14.99.42: Now EC 1.13.11.84, crocetin dialdehyde synthase EC 1.14.99.43: Now EC 1.14.14.134, β-amyrin 24-hydroxylase EC 1.14.99.44: diapolycopene oxygenase EC 1.14.99.45: Now EC 1.14.14.158, carotene ε-monooxygenase EC 1.14.99.46: pyrimidine oxygenase EC 1.14.99.47: (+)-larreatricin hydroxylase EC 1.14.99.48: heme oxygenase (staphylobilin-producing) EC 1.14.99.49: Now EC 1.14.15.31, 2-hydroxy-5-methyl-1-naphthoate 7-hydroxylase EC 1.14.99.50: γ-glutamyl hercynylcysteine S-oxide synthase EC 1.14.99.51: hercynylcysteine S-oxide synthase EC 1.14.99.52: L-cysteinyl-L-histidinylsulfoxide synthase EC 1.14.99.53: lytic chitin monooxygenase EC 1.14.99.54: lytic cellulose monooxygenase (C1-hydroxylating) EC 1.14.99.55: lytic starch monooxygenase EC 1.14.99.56: lytic cellulose monooxygenase (C4-dehydrogenating) EC 1.14.99.57: heme oxygenase (mycobilin-producing) EC 1.14.99.58: heme oxygenase (biliverdin-IX-β and δ-forming) EC 1.14.99.59: tryptamine 4-monooxygenase EC 1.14.99.60: 3-demethoxyubiquinol 3-hydroxylase EC 1.14.99.61: cyclooctat-9-en-7-ol 5-monooxygenase EC 1.14.99.62: cyclooctatin synthase EC 1.14.99.63: β-carotene 4-ketolase EC 1.14.99.64: zeaxanthin 4-ketolase EC 1.14.99.65: 4-amino-L-phenylalanyl-[CmlP-peptidyl-carrier-protein] 3-hydroxylase EC 1.14.99.66: [histone H3]-N6,N6-dimethyl-L-lysine4 FAD-dependent demethylase EC 1.14.99.67: α-N-dichloroacetyl-p-aminophenylserinol N-oxygenase EC 1.14.99.68: 4-aminobenzoate N-oxygenase EC 1.14.99.69: tRNA 2-(methylsulfanyl)-N6-isopentenyladenosine37 hydroxylase

== History == Scott Reismanis, a website developer from Melbourne, Australia, first pursued web development as a hobby, creating two websites dedicated to video games. Afterwards, he purchased the ChaosRealm.com domain and formed the Realm Network. The network comprised over twenty websites, one of which was ModDB's predecessor, ModRealm. Launched in 1998, ModRealm was initially dedicated to Counter-Strike cheat codes before becoming a modding website. The website became defunct in December 2001, when its network was shut down after its hosting service, Playnet, filed for bankruptcy. Reismanis was motivated to start a new website by the difficulty of searching for mods on the then-dominant search engine, AltaVista, much less mods released to the public. He began ModDB's development in January 2002, following IMDb's structure in the process. The website was launched as Mod Database in June 2002. It differed from his earlier websites in that its articles were managed by the community, not only the website's founder. By January 2005, ModDB listed 49,539 members and 2,191 mods. In 2006, the ModDB team launched AddonDB, whose aim was to list additional content for games not applicable under the category of game modifications. This includes models, skins and maps. Just one year into service, it was merged into ModDB.

Sources: en.wikipedia.org

Background from the literature

As well as with dim sum, many Chinese drink their tea with snacks such as nuts, plums, dried fruit (in particular jujube), small sweets, melon seeds, and waxberry. China was the earliest country to cultivate and drink tea, which is enjoyed by people from all social classes. Tea processing began after the Qin and Han dynasties. The different types of Chinese tea include red (known as "black tea" outside of East Asia), white, green, yellow, oolong, and black (often called "dark tea" in English to differentiate it from "black tea"). Chinese tea is often classified into several different categories according to the variety of the tea plant from which it is sourced, the region in which it is grown, and the method of production used. Flavored and scented teas originated in China. Jasmine, osmanthus, chrysanthemum, and ginseng are popular varieties. Historically, compressed tea dominated and powdered tea known as matcha would be made from it. This was later supplanted by loose-leaf tea. Fermented tea drinks like kombucha are believed to originate in China, but kombucha is now better known outside of China than within the country. There are four major tea plantation regions: Jiangbei, Jiangnan, Huanan and the southwestern region. Well known types of green tea include Longjing, Huangshan Maofeng, Bilochun, Putuofeng Cha, and Liu'an Guapian. China is the world's largest exporter of green tea. One of the most ubiquitous accessories in modern China, after a wallet or purse and an umbrella, is a double-walled insulated glass thermos with tea leaves in the top behind a strainer.

Azidophenylalanine (4-azido-L-phenylalanine) is an unnatural amino acid derivative of L-phenylalanine, featuring an azide group at the para position of the phenyl ring. It is a bioorthogonal click-chemistry reagent that can be genetically incorporated into proteins via expanded genetic code techniques for site-specific labeling and functionalization. The compound serves as a vibrational reporter for local protein environments due to its azide group and is used in photo-crosslinking for protein interaction studies.

The human body's immune response to a surgically-implanted foreign object (prosthetic breast, cardiac pacemaker, orthopedic prosthesis) is to biologically isolate the foreign object with a capsule of tightly-woven collagen fibres. Afterwards, the capsular contracture occurs over time when the thickened, collagen-fibre capsule has compressed inwards, against the breast-implant with great mechanical pressure that deforms and breaks the implant, and so disfigures the breast; the causes of capsular contracture include bacterial contamination, shell-rupture of the medical device, leakage of the prosthetic filler-material, and hematoma. The prosthetic-breast implantation surgeries that have a low-rate of capsular contractures include surgical approaches that feature the submuscular emplacement of the breast-implant and the use of breast implants with a textured surface; limited handling of the breast implants before the surgery, limited contact with and handling of the skin of the implant-pocket, and irrigation of the surgical site with antibiotic solutions. To correct a capsular contraction, the plastic surgeon realises an open capsulotomy procedure to loosen and release the collagen-fibre capsule from the implant-pocket, for removal and replacement with a new model of prosthetic breast. Moreover, non-surgical therapies for treating collagen-fibre capsules include massage, external ultrasonic therapy, pharmaceutic therapy with leukotriene pathway inhibitor medications, and Diapulse therapy (Pulsed Electromagnetic Field Therapy, PEMFT).

Sources: en.wikipedia.org

Further detail

== History and name == The name leukotriene, introduced by Swedish biochemist Bengt Samuelsson in 1979, comes from the words leukocyte and triene (indicating the compound's three conjugated double bonds). What would be later named leukotriene C, "slow reaction smooth muscle-stimulating substance" (SRS) was originally described between 1938 and 1940 by Feldberg and Kellaway. The researchers isolated SRS from lung tissue after a prolonged period following exposure to snake venom and histamine.

== Early life == Daveigh Elizabeth Chase-Schwallier was born on July 24, 1990, in Las Vegas, Nevada, to Cathy Chase and John David Schwallier. She was young when her parents divorced. Each remarried, and she grew up with several half-siblings, including a younger half-brother named Cade. Chase later used her mother's maiden name professionally. She subsequently relocated with her mother to Albany, Oregon, where she performed in local talent shows and pageants. Her early vocal performances were centered on country music, for which she won a national vocal competition during her childhood. During a stay in Los Angeles, Chase began attending casting calls and booking minor roles, including national television advertising spots at age seven for the Campbell's Soup Company. Chase appeared in a regional theatrical production of the musical Utah! at the Tuacahn Amphitheatre in 1998, sharing the role of Norma Sanderson. She credited this stage experience with refining her live singing ability and performance presence.

== Early life and education == He was born in St. Paul, Minnesota on May 28, 1911. Nier showed an early ability in mathematics and science, coupled with an aptitude for craft and mechanical work. Nier's German immigrant parents had little education or financial resources but their determination for his development meant that he was able to attend the nearby University of Minnesota. Though he graduated in electrical engineering in 1931, the lack of engineering jobs during the Great Depression encouraged him to take up graduate study in physics.

Sources: en.wikipedia.org

Frequently asked questions

What is SR9009?

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.

Is SR9009 a hormone?

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.

What is known about human use?

Clinical evidence is limited. Most published data come from cell and animal experiments. Human safety and efficacy remain uncertain.

How is SR9009 measured?

Liquid chromatography-tandem mass spectrometry is a common approach. It can detect the parent compound and its metabolites in biological matrices.

Network