A practical reference on LC-MS/MS: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2026-06-11 and is reviewed periodically as new material appears.
Most published work on SR9009 consists of preclinical studies. It is widely sold as a research chemical, a category that does not imply safety, efficacy, or pharmaceutical-grade quality. Sports anti-doping organizations have listed SR9009 as a prohibited substance, and its presence in an athlete sample can lead to sanctions. Legal status differs by country; in several jurisdictions it is not approved for human consumption and may be treated as an unapproved new drug.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
Handling recommendations for SR9009 in a laboratory setting include storing the solid at low temperature, protected from light and moisture. The compound is often dissolved in dimethyl sulfoxide or ethanol for experiments. Solutions should be prepared with appropriate personal protective equipment and disposed of according to local rules. Stability data for long-term storage are limited, so stock solutions are typically kept cold and used within defined periods. Records of preparation date and concentration support reproducibility.
SR9009 is not approved as a medicine by major regulatory agencies. It is commonly sold as a research chemical, a category that may fall outside customary drug approval and quality rules. In sports, the World Anti-Doping Agency lists SR9009 as a prohibited substance. Athletes who use it can face sanctions if it is detected in a sample. Legal status varies by country, and importation may be restricted. Enforcement practices differ across borders.
| Property | Value | Notes |
|---|---|---|
| Common name | SR9009 | Also referred to as Stenabolic in non-scientific contexts. |
| Chemical class | Synthetic small molecule | Not a steroid or peptide hormone. |
| Receptor target | REV-ERBα and REV-ERBβ | Nuclear receptor agonist in preclinical studies. |
| Development status | Investigational | No approved human therapeutic indication. |
| Regulatory attention | Prohibited in sport | Listed by anti-doping authorities. |
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.
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.
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.
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.
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.
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.
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.
Plasmin is a serine protease that acts to dissolve fibrin blood clots. Apart from fibrinolysis, plasmin proteolyses proteins in various other systems: It activates collagenases, some mediators of the complement system, and weakens the wall of the Graafian follicle, leading to ovulation. Plasmin is also integrally involved in inflammation. It cleaves fibrin, fibronectin, thrombospondin, laminin, and von Willebrand factor. Plasmin, like trypsin, belongs to the family of serine proteases. Plasmin is released as a zymogen called plasminogen (PLG) from the liver into the systemic circulation. Two major glycoforms of plasminogen are present in humans - type I plasminogen contains two glycosylation moieties (N-linked to N289 and O-linked to T346), whereas type II plasminogen contains only a single O-linked sugar (O-linked to T346). Type II plasminogen is preferentially recruited to the cell surface over the type I glycoform. Conversely, type I plasminogen appears more readily recruited to blood clots. In circulation, plasminogen adopts a closed, activation-resistant conformation. Upon binding to clots, or to the cell surface, plasminogen adopts an open form that can be converted into active plasmin by a variety of enzymes, including tissue plasminogen activator (tPA), urokinase plasminogen activator (uPA), kallikrein, and factor XII (Hageman factor). Fibrin is a cofactor for plasminogen activation by tissue plasminogen activator. Urokinase plasminogen activator receptor (uPAR) is a cofactor for plasminogen activation by urokinase plasminogen activator.
Electroanalytical methods measure the potential (volts) and/or current (amps) in an electrochemical cell containing the analyte. These methods can be categorized according to which aspects of the cell are controlled and which are measured. The four main categories are potentiometry (the difference in electrode potentials is measured), coulometry (the transferred charge is measured over time), amperometry (the cell's current is measured over time), and voltammetry (the cell's current is measured while actively altering the cell's potential).
==== Antigonadotropic effects ==== EMP at a dosage 280 mg/day has been found to suppress testosterone levels in men into the castrate range (to 30 ng/dL) within 20 days and to the low castrate range (to 10 ng/dL) within 30 days. Similarly, a dosage of 70 mg/day EMP suppressed testosterone levels into the castrate range within 4 weeks.
Congenital hypodysfibrinogenemia is a rare inherited disorder in which low levels (i.e. <150 mg/dl) of immunologically detected plasma fibrinogen are composed at least in part of a dysfunctional fibrinogen. The disorder reflects mutations typically in both inherited fibrinogen genes, one of which produces a dysfunctional fibrinogen, while the other produces low amounts of fibrinogen. The disorder, while having reduced penetrance, is usually more severe than congenital dysfibrinogenemia, but like the latter disorder, causes pathological episodes of bleeding and/or blood clotting.
=== CblE type of homocystinuria === Remethylation of homocysteine to methionine by MTR requires the derivative of cobalamin, methylcobalamin. Cobalamin metabolism is initiated by the endocytosis of cobalamin bound to the plasma protein transcobalamin (II). Cleavage of this complex produces free cobalamin, translocating from lysosome to cytoplasm. Conversion can occur to 5'-deoxyadenosylcobalamin (AdoCbl) activating the mitochondrial enzyme methylmalonly coenzyme A mutase or to methylcobalamin (MeCbl). An error in cobalamin metabolism resulting in decreased MeCbl and unaffected AdoCbl is characteristic of the CblE type of homocystinuria. This complementation is rare with autosomal recessive inheritance. The inherited methionine synthase functional deficiency corresponds to a defect in the reducing system required to activate the MTR enzyme. Symptoms of this condition comprise developmental retardation, megaloblastic anemia, homocystinuria, hypomethioninemia, cerebral atrophy and hyperhomocysteinemia. However, hypomethioninemia remains an inconsistent symptom. Decreased MeCbl alongside normal cobalamin uptake is suggestive of decreased intracellular methionine biosynthesis. Occurring mainly in childhood, 15 pathogenic mutations can be associated with CblE type homocystinuria. Additionally, vascular abnormalities are associated with this defect. Impaired reduction of an oxidised cobalt atom in the active site of MTR is associated with this condition, where enzyme activity can be corrected with reducing agents.
Sources: en.wikipedia.org
By the terms of the 1945 Potsdam Agreement signed by the three victorious Great Powers, the Soviet Union retained most of the territories captured as a result of the Molotov–Ribbentrop Pact of 1939, including western Ukraine and western Belarus, and gained others. Lithuania and the Königsberg area of East Prussia were officially incorporated into the Soviet Union, in the case of the former without the recognition of the Western powers. Poland was compensated with the bulk of Silesia, including Breslau (Wrocław) and Grünberg (Zielona Góra), the bulk of Pomerania, including Stettin (Szczecin), and the greater southern portion of the former East Prussia, along with Danzig (Gdańsk), pending a final peace conference with Germany which eventually never took place. Collectively referred to by the Polish authorities as the "Recovered Territories", they were included in the reconstituted Polish state. With Germany's defeat Poland was thus shifted west in relation to its prewar location, to the area between the Oder–Neisse and Curzon lines, which resulted in a country more compact and with much broader access to the sea.[c] The Poles lost 70% of their pre-war oil capacity to the Soviets, but gained from the Germans a highly developed industrial base and infrastructure that made a diversified industrial economy possible for the first time in Polish history. The flight and expulsion of Germans from what was eastern Germany prior to the war began before and during the Soviet conquest of those regions from the Nazis, and the process continued in the years immediately after the war.
Whose power is to be balanced? Today, no nation or group challenges American power … In fact, should the balance of power operate in its classical form, it would trigger countermoves by states seeking to pose a counterweight to America's expressed ambitions. According to Leffler's exegesis, Bush has invoked a balance of power vocabulary in purpose to integrate the tradition with the hegemonic dilemma. British Orwell Prize-winning policy analyst, Anatol Lieven, comments: In this conception, however, a phrase "was a form of Orwellian doublespeak. The clear intention actually was to be so strong that other countries had no choice but to rally to the side of the United States, concentrating all real power and freedom of action in the hands of America." The surprising rehabilitation of the balance-of-power term in the 2002 NSS "can be accounted for in terms of mythopoetic function that the terminology serves in the document." It keeps alive the traditional concept in a new unipolar world.
=== Phase 2 === AB-2004 – microbiome modulator Acamprosate (AOP-2020; Campral; SF-679/SF-775; SF-999) – unknown / GABAA receptor positive allosteric modulator and ionotropic glutamate NMDA receptor antagonist Alogabat (RG-7816, RG7816, RO-7017773; GABA-A-α5 PAM) – GABAA α5 subunit-containing receptor positive allosteric modulator Arbaclofen ((R)-baclofen; STX-209) – GABAB receptor agonist Cannabidiol (CBD; Epidiolex) – cannabinoid receptor modulator, other actions Cannabidiol transdermal patch/gel (Zygel; ZYN-002) – cannabinoid receptor modulator, other actions Cannabidivarin (CBDV; GWP-42006) – non-intoxicating cannabinoid receptor modulator, other actions CP-101 – bacteria relacement and gastrointestinal microbiome modulator JNJ-42165279 (JNJ-5279) – fatty acid amide hydrolase (FAAH) inhibitor Non-racemic MDMA (ALA-002; 70–80% (R)-MDMA, 20–30% (S)-MDMA) – serotonin, norepinephrine, and dopamine releasing agent, weak serotonin 5-HT2A, 5-HT2B, 5-HT2C receptor agonist, entactogen, and weak psychedelic hallucinogen Oxytocin (intranasal potentiated oxytocin; TI-001, TI-114, TNX-1900, TNX-2900) – oxytocin receptor agonist Pitolisant (Wakix; tiprolisant) – histamine H3 receptor inverse agonist Racemetirosine (DL-α-methyltyrosine; L1-79) – tyrosine hydroxylase inhibitor Suramin (IV suramin; PAX-101/PAX-102) – DNA synthesis inhibitor and anti-purinergic agent Zolmitriptan modified-release (ML-004, ML004) – serotonin 5-HT1B and 5-HT1D receptor agonist
=== Type I Diabetes === It is thought that high glucagon levels and lack of insulin production are the main triggers for the metabolic issues associated with Type I diabetes, in particular maintaining normal blood glucose levels, formation of ketone bodies, and formation of urea. One finding of note is that the glucagon response to hypoglycemia is completely absent in patients with Type I diabetes. Consistently high glucagon concentrations in the blood can lead to diabetic ketoacidosis, which is when ketones from lipid breakdown build up in the blood, which can lead to dangerously low blood glucose levels, low potassium levels, and in extreme cases cerebral edema. It has been proposed that the reason for the high levels of glucagon found in the plasma of patients with Type I diabetes is the absence of beta cells producing insulin and the reciprocal effect this has on delta cells and the secretion of somatostatin.
=== House of Tirol === Albert I (–1078), Count of Eurasburg Albert II (1078–1101), maybe son of Albert I Albert III (1101–1165), son of Albert II Berthold I (1165–1180), son of Albert II Berthold II (1180–1181), son of Berthold I Henry I (1181–1202), son of Berthold I Albert IV (1202–1253), son of Henry I Male line extinct.
Sources: en.wikipedia.org
It is a synthetic compound studied as an agonist of REV-ERB nuclear receptors. It is not an approved medicine and has mainly been examined in laboratory and animal research.
No. It is a small molecule that binds nuclear receptors involved in circadian regulation. Its classification differs from anabolic steroids or peptide hormones.
Published human clinical trial data are lacking. Most safety and activity information comes from preclinical models, so effects in people remain uncertain.
Its legal status depends on the country and intended use. It is not an approved medicine in major jurisdictions. In sport, it is prohibited by anti-doping rules.