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Analytical And Handling Considerations — 2026 Update

By Editorial Desk · published 2026-01-30 · last reviewed 2026-03-17 · Wiki

Everything below concerns REV-ERB agonist. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.

Updated 2026-03-17. Numbers and descriptions here follow the published literature rather than marketing material.

Analytical and Handling Considerations

Laboratory identification of SR9009 typically relies on chromatographic separation coupled to mass spectrometry, often with ultraviolet detection as a secondary check. Nuclear magnetic resonance spectroscopy can confirm molecular structure when a reference standard is available. Because many suppliers sell the compound as a research chemical, independent identity testing is important for experimental reproducibility. A single retention time is not sufficient proof of identity, especially when related compounds may be present. Purity assessments usually report a percentage based on area normalization.

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.

Mechanism and Preclinical Findings

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.

Sr9009 at a glance

PropertyValueNotes
AppearanceWhite to off-white powderVisual inspection is not sufficient for identity.
SolubilitySoluble in DMSO and ethanolLow solubility in water; stock solutions use organic solvent.
Storage-20°C, desiccated, protected from lightLimits hydrolysis and photodegradation.
Analytical methodHPLC-UV/MSUsed for identity and purity assessment.
SynonymsSR9009, StenabolicNaming varies by supplier.

Background and Receptor Mechanism

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.

At the molecular level, SR9009 binds the ligand-binding domain of REV-ERB and strengthens recruitment of corepressor proteins such as NCoR and HDAC3. This increases repression of target genes, including Bmal1 and other clock-controlled and metabolic genes. In rodent studies, such changes have been linked to altered lipid handling, glucose metabolism, and energy expenditure. The precise chain of events between receptor binding and whole-body effects remains an active area of research. Findings in animals do not automatically translate to humans.

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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.

Reference notes

The isotopes of nickel range in mass number from 48 (48Ni) to 82 (82Ni). Natural nickel is composed of five stable isotopes, 58Ni, 60Ni, 61Ni, 62Ni and 64Ni, of which 58Ni is the most abundant (68.077% natural abundance). Nickel-62 has the highest binding energy per nucleon of any nuclide: 8.7946 MeV/nucleon. Its binding energy is greater than both 56Fe and 58Fe, more abundant nuclides often incorrectly cited as having the highest binding energy. Though this would seem to predict nickel as the most abundant heavy element in the universe, the high rate of photodisintegration of nickel in stellar interiors causes iron to be by far the most abundant. Nickel-60 is the daughter product of the extinct radionuclide 60Fe (half-life 2.6 million years). Due to the long half-life of 60Fe, its persistence in materials in the Solar System may generate observable variations in the isotopic composition of 60Ni. Therefore, the abundance of 60Ni in extraterrestrial material may give insight into the origin of the Solar System and its early history. At least 26 nickel radioisotopes have been characterized; the most stable are 59Ni with half-life 76,000 years, 63Ni (100 years), and 56Ni (6 days). All other radioisotopes have half-lives less than 60 hours and most these have half-lives less than 30 seconds. This element also has one meta state. Radioactive nickel-56 is produced by the silicon burning process and later set free in large amounts in Type Ia supernovae.

This article incorporates public domain material from The World Factbook (2025 ed.). CIA. (country: Honk Kong) Hong Kong from BBC News Key Development Forecasts for Hong Kong from International Futures Hong Kong in Transition (1995–2020) Archived 20 March 2025 at the Wayback Machine, an open access photographic archive of recent Hong Kong history Government

Symptoms depend on the type and severity of thalassemia. Carriers of thalassemia genes may have no symptoms (thalassemia minor) or very mild symptoms with occasional crisis (thalassemia intermedia); individuals who are homozygous for the mutation have severe and life threatening symptoms (thalassemia major). Individuals with beta-thalassemia major usually present within the first two years of life with symptomatic severe anemia, poor growth, and skeletal abnormalities. Untreated thalassemia major eventually leads to death, usually by heart failure. Those with beta-thalassemia intermedia (those who are compound heterozygotes for the beta thalassemia mutation) usually present later in life with mild to moderate symptoms of anemia. Beta thalassemia trait (beta thalassemia minor) involves heterozygous inheritance of a beta-thalassemia mutation. Individuals usually have microcytosis with mild anemia; they are usually asymptomatic or have mild symptoms. Beta thalassemia minor can also present as beta-thalassemia silent carriers; those who inherit a beta thalassemic mutation but have no hematologic abnormalities or symptoms. Individuals with thalassemia thalassemia major and intermedia (to a lesser extent) are susceptible to health complications that involve the spleen (hypersplenism) and gallstones (due to hyperbilirubinemia from peripheral hemolysis). Additional symptoms of beta-thalassemia major or intermedia include the classic symptoms of anemia including fatigue, developmental delay in childhood, leg ulcers, and organ failure.

Sources: en.wikipedia.org

Notes from published material

== Biosynthesis == FAD plays a major role as an enzyme cofactor along with flavin mononucleotide, another molecule originating from riboflavin. Bacteria, fungi and plants can produce riboflavin, but other eukaryotes, such as humans, have lost the ability to make it. Therefore, humans must obtain riboflavin, also known as vitamin B2, from dietary sources. Riboflavin is generally ingested in the small intestine and then transported to cells via carrier proteins. Riboflavin kinase (EC 2.7.1.26) adds a phosphate group to riboflavin to produce flavin mononucleotide, and then FAD synthetase attaches an adenine nucleotide; both steps require ATP. Bacteria generally have one bi-functional enzyme, but archaea and eukaryotes usually employ two distinct enzymes. Current research indicates that distinct isoforms exist in the cytosol and mitochondria. It seems that FAD is synthesized in both locations and potentially transported where needed.

TAAR1 also couples G-protein alpha subunit G13; when triggered by amphetamine, this pathway activates Ras homolog A (RhoA) and its downstream protein kinase, Rho-associated coiled-coil kinase (ROCK), an effect that internalizes both DAT and the neuronal glutamate transporter EAAT3. Transporter internalization via TAAR1's G13-coupled pathway is transient because Gs-cAMP-PKA signaling functionally inhibits RhoA's downstream activity; once intracellular cAMP sufficiently accumulates, PKA is activated and phosphorylates RhoA, thereby terminating ROCK-mediated transporter internalization. In addition to presynaptic actions that regulate DAT, TAAR1 activation exerts a somatodendritic inhibitory influence on midbrain dopamine neurons by reducing their firing rate via G protein-coupled inwardly-rectifying potassium channels, an effect that is expected to reduce action potential-dependent (vesicular) dopamine release into the synaptic cleft. Amphetamine's effect on intracellular calcium is associated with DAT phosphorylation through Ca2+/calmodulin-dependent protein kinase II alpha (CAMKIIα), in turn producing dopamine efflux. Because conventional PKC isoforms can be activated by Ca2+ and diacylglycerol, elevated intracellular calcium can promote PKC-dependent DAT phosphorylation independent of TAAR1.

== External links == The Nuclear Science web portal Nucleonica The Karlsruhe Nuclide Chart National Nuclear Data Center Portal to large repository of free data and analysis programs from NNDC National Isotope Development Center Coordination and management of the production, availability, and distribution of isotopes, and reference information for the isotope community Isotope Development & Production for Research and Applications (IDPRA) U.S. Department of Energy program for isotope production and production research and development International Atomic Energy Agency Homepage of International Atomic Energy Agency (IAEA), an Agency of the United Nations (UN) Atomic Weights and Isotopic Compositions for All Elements Static table, from NIST (National Institute of Standards and Technology) Atomgewichte, Zerfallsenergien und Halbwertszeiten aller Isotope Exploring the Table of the Isotopes at the LBNL Current isotope research and information isotope.info Emergency Preparedness and Response: Radioactive Isotopes by the CDC (Centers for Disease Control and Prevention) Chart of Nuclides Archived 2018-10-10 at the Wayback Machine Interactive Chart of Nuclides (National Nuclear Data Center) Interactive Chart of the nuclides, isotopes and Periodic Table Archived 2008-09-30 at the Wayback Machine The LIVEChart of Nuclides – IAEA with isotope data. Annotated bibliography for isotopes from the Alsos Digital Library for Nuclear Issues The Valley of Stability (video) – a virtual "flight" through 3D representation of the nuclide chart, by CEA (France)

Sources: en.wikipedia.org

Frequently asked questions

How is SR9009 detected in laboratory samples?

Liquid chromatography with mass spectrometry is a common approach. Ultraviolet detection and nuclear magnetic resonance can support identification when suitable standards are available.

How should SR9009 be stored?

The solid is generally kept cold, dry, and protected from light. Solutions are often frozen in single-use aliquots to reduce repeated freeze-thaw cycles.

What does research chemical grade mean?

It indicates a material sold for laboratory study, not for human use. The label does not guarantee pharmaceutical purity, sterility, or regulatory approval.

What is SR9009?

It is a synthetic compound that acts as an agonist at REV-ERBα and REV-ERBβ. It is used mainly as a research chemical to study circadian and metabolic pathways. It is not approved for human therapeutic use.

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