The short version of LC-MS/MS fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2025-12-01 and is reviewed periodically as new material appears.
Analytical chemists detect SR9009 with liquid chromatography-tandem mass spectrometry, commonly abbreviated LC-MS/MS. Sample preparation may involve protein precipitation, liquid-liquid extraction, or solid-phase extraction before analysis. Laboratories can target the parent compound or its metabolites, depending on the matrix and the purpose of testing. Anti-doping methods require sensitive and specific assays because concentrations in biological samples can be low. Reference standards and validated methods are essential for reliable identification and quantification.
Regulatory agencies have not approved SR9009 for human therapeutic use. It is typically sold as a research chemical with labels stating that it is not for human consumption. The World Anti-Doping Agency prohibits the substance in sport, generally under the category of non-approved substances. Customs and national laws may restrict importation, sale, or possession. Product quality and legal status can vary by country and vendor, and therapeutic claims are not permitted in regulated advertising because the compound lacks approval.
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.
Identity and purity testing for SR9009 commonly uses liquid chromatography coupled with tandem mass spectrometry. This method separates the compound from matrix components and detects it by mass-to-charge transitions, providing sensitive and specific confirmation. Nuclear magnetic resonance spectroscopy can support structural identification, while high-performance liquid chromatography with ultraviolet detection may estimate purity. Because online products labeled as SR9009 may contain other substances or no active compound at all, independent verification is important in research settings. Certificates of analysis are useful but not a substitute for in-house testing.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Not approved for human use | Research-use-only status in many markets |
| WADA status | Prohibited in sport | Generally listed as a non-approved substance |
| Detection technique | LC-MS/MS | Common for urine and blood analysis |
| Common alias | Stenabolic | Informal market nickname, not a pharmacopoeial name |
| Purity check | HPLC or LC-UV | Independent certificate of analysis is typical |
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.
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.
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.
Alison Elizabeth Larter (born February 28, 1976), is an American actress and former model. She portrayed fictional model Allegra Coleman in a 1996 Esquire magazine hoax and took on guest roles on several television shows in the 1990s. Her film debut in Varsity Blues (1999) was followed by a role in the horror film House on Haunted Hill (1999). She portrayed Clear Rivers in the Final Destination franchise (2000–2003) establishing her as a scream queen. Larter played supporting roles in Legally Blonde (2001), Jay and Silent Bob Strike Back (2001), and the romantic comedy A Lot Like Love (2005), and main roles in the Bollywood movie Marigold (2007) and the thriller Obsessed (2009). She achieved wider recognition for playing the dual roles of Niki Sanders and Tracy Strauss on the science fiction drama series Heroes (2006–2010) on NBC, and for portraying video game heroine Claire Redfield in three films of the Resident Evil film series (2007–2016). Larter costars as Angela Norris in the Paramount+ drama series Landman (2024). As of April 2017, Larter's films have grossed over $1.31 billion worldwide. Her presence in the media is reinforced by her appearances in lists compiled by Maxim, FHM, and Stuff as well as People's "Best Dressed List" in 2007. She published a cookbook, Kitchen Revelry: A Year of Festive Menus from My Home to Yours, in September 2013.
== Gene == The COL3A1 gene is located on the long (q) arm of chromosome 2 at 2q32.2, between positions 188974372 and 189012745. The gene has 51 exons and is approximately 40 kbp long. The COL3A1 gene is in tail-to-tail orientation with a gene for another fibrillar collagen, namely COL5A2. Two transcripts are generated from the gene using different polyadenylation sites. Although alternatively spliced transcripts have been detected for this gene, they are the result of mutations; these mutations alter RNA splicing, often leading to the exclusion of an exon or use of cryptic splice sites. The resulting defective protein is the cause of a severe, rare disease, the vascular type of Ehlers-Danlos syndrome (vEDS). These studies have also provided important information about RNA splicing mechanisms in multi-exon genes.
Sausage casing, also known as sausage skin or simply casing, is the material that encloses the filling of a sausage. Natural casings are made from animal intestines or skin; artificial casings, introduced in the early 20th century, are made of collagen and cellulose. The material is then shaped via a continuous extrusion process—producing a single sausage casing of indefinite length—which is then cut into desired lengths, usually while the extrusion process continues.
Solvent extraction may also be used to separate out the thorium and uranium, by dissolving the resultant filter cake in nitric acid. The presence of titanium hydroxide is deleterious as it binds thorium and prevents it from dissolving fully.
Sources: en.wikipedia.org
As an antagonist at ionotropic AMPA, NMDA and Kainate glutamate receptors in the concentration range of 0.1-2.5 mM. As a noncompetitive antagonist at the glycine site of the NMDA receptor. As an antagonist of the α7 nicotinic acetylcholine receptor. However, recently (2011) direct recording of α7 nicotinic acetylcholine receptor currents in adult (noncultured) hippocampal interneurons by the Cooper laboratory validated a 2009 study that failed to find any blocking effect of kynurenic acid across a wide range of concentrations, thus suggesting that in noncultured, intact preparations from adult animals there is no effect of kynurenic acid on α7 nicotinic acetylcholine receptor currents. As a ligand for the orphan G protein-coupled receptor GPR35. As an agonist for the G protein-coupled receptor HCAR3.
=== Japanese volunteers === Many former Imperial Japanese Army soldiers fought alongside the Việt Minh—perhaps as many as 5,000 volunteered their services throughout the war. These Japanese soldiers had stayed behind in Indochina after World War II concluded in 1945. The occupying British authorities then repatriated most of the rest of the 50,000 Japanese troops back to Japan. For those that stayed behind, supporting the Việt Minh became a more attractive idea than returning to a defeated and occupied homeland. In addition the Việt Minh had minimal experience in warfare or government so the advice of the Japanese was welcome. Some of the Japanese were ex-Kenpeitai who were wanted for questioning by Allied authorities. Giap arranged for them all to receive Vietnamese citizenship and false identification papers. Some Japanese were captured by the Việt Minh during the last months of World War II and were recruited into their ranks. Most of the Japanese officers who stayed served as military instructors for the Việt Minh forces, most notably at the Quảng Ngãi Army Academy. They imparted necessary conventional military knowledge – such as how to conduct assaults, night attacks, company/battalion level exercises, commanding, tactics, navigation, communications and movements. A few, however, actively led Vietnamese forces into combat. The French also identified eleven Japanese nurses and two doctors working for the Việt Minh in northern Vietnam in 1951. The Yasukuni Shrine commemorates a number of Japanese involved in the First Indochina War.
== Isoforms == Like 95% of human genes, TP53 encodes multiple proteins, collectively known as the p53 isoforms. These vary in size from 3.5 to 43.7 kDa. Since their initial discovery in 2005, 12 human p53 isoforms have been identified: p53α, p53β, p53γ, ∆40p53α, ∆40p53β, ∆40p53γ, ∆133p53α, ∆133p53β, ∆133p53γ, ∆160p53α, ∆160p53β, and ∆160p53γ. Isoform expression is tissue-dependent, and p53α is never expressed alone. The isoforms differ by the inclusion or exclusion of specific domains. Some, such as Δ133p53β/γ and Δ160p53α/β/γ, lack the transactivation or proline-rich domains and are deficient in apoptosis induction, illustrating the functional diversity of TP53. Isoforms are generated through multiple mechanisms:
Sources: en.wikipedia.org
Furthermore, it has been observed in many retrospective longitudinal studies that corticosteroid treatment does not seem to significantly prolong survival of the native liver or transplant-free survival.
=== Enzyme induction and inhibition === The duration and intensity of pharmacological action of most lipophilic drugs are determined by the rate they are metabolized to inactive products. The Cytochrome P450 monooxygenase system (CYP) is a crucial pathway in this regard. In general, anything that increases the rate of metabolism (e.g., enzyme induction) of a pharmacologically active metabolite will decrease the duration and intensity of the drug action. The opposite is also true, as in enzyme inhibition. However, in cases where an enzyme is responsible for metabolizing a pro-drug into a drug, enzyme induction can accelerate this conversion and increase drug levels, potentially causing toxicity. For example, chemotherapy prodrugs like cyclophosphamide (CPA) and ifosfamide (Ifex), which are initially inactive, become toxic as they are metabolized into cytotoxic compounds (such as phosphoramide mustard and chloroacetaldehyde) primarily from liver enzymes CYP2B6 and CYP3A4. Co-administration of a strong CYP inducer, such as phenytoin or rifampicin, accelerates metabolism and increases the rate of bioactivation which causes a higher concentration of cytotoxic metabolites that may lead to higher toxicity. This drug–drug interaction may enhance the risk of adverse effects, most notably severe myelosuppression and hemorrhagic cystitis.
== Higher-energy collisional dissociation == Higher-energy collisional dissociation (HCD) is a CID technique specific to the orbitrap mass spectrometer in which fragmentation takes place external to the trap. HCD was formerly known as higher-energy C-trap dissociation. In HCD, the ions pass through the C-trap and into the HCD cell, an added multipole collision cell, where dissociation takes place. The ions are then returned to the C-trap before injection into the orbitrap for mass analysis. HCD does not suffer from the low mass cutoff of resonant-excitation (CID) and therefore is useful for isobaric tag–based quantification as reporter ions can be observed. Despite the name, the collision energy of HCD is typically in the regime of low energy collision induced dissociation (less than 100 eV).
=== Pharmacodynamics === Dextromethorphan acts as an NMDA receptor antagonist, σ1 receptor agonist, and serotonin–norepinephrine reuptake inhibitor, among other actions, while bupropion acts as a norepinephrine–dopamine reuptake inhibitor and nicotinic acetylcholine receptor negative allosteric modulator. Bupropion is also a potent inhibitor of CYP2D6, and thereby inhibits the metabolism of dextromethorphan. Dextromethorphan/bupropion has less activity as an NMDA receptor antagonist than dextromethorphan alone. This is because bupropion is a potent CYP2D6 inhibitor and prevents the bioactivation of dextromethorphan into dextrorphan, a much more potent NMDA receptor antagonist and weaker serotonin reuptake inhibitor than dextromethorphan itself. The mechanism of action of dextromethorphan/bupropion in the treatment of depression is unknown, although the preceding pharmacological actions are assumed to be involved.
Sources: en.wikipedia.org
Legality depends on the country and the intended use. In many places it is not approved as a medicine and may be sold only as a research chemical. Importation or possession can be restricted, and sports organizations prohibit it.
Anti-doping laboratories typically use LC-MS/MS to detect SR9009 or its metabolites in urine or blood. The exact assay depends on the laboratory and the testing program. Detection can be challenging because the compound may be rapidly metabolized and present at low levels.
Stenabolic is an informal nickname used in online fitness and research-chemical markets, not an official drug name. It likely references reported effects on endurance in rodent studies. The nickname does not imply approval or proven human benefit.
Research-grade SR9009 is typically stored frozen at about minus twenty degrees Celsius, protected from light and moisture. Stock solutions are often kept in aliquots to avoid repeated freeze-thaw cycles. Specific storage conditions should follow the supplier's documentation.