AS-604850PI3Kγ inhibitor,selective and ATP-competitve CAS# 648449-76-7 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 648449-76-7 | SDF | Download SDF |
PubChem ID | 5287855 | Appearance | Powder |
Formula | C11H5F2NO4S | M.Wt | 285.22 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | DMSO : 250 mg/mL (876.52 mM; Need ultrasonic) | ||
Chemical Name | (5Z)-5-[(2,2-difluoro-1,3-benzodioxol-5-yl)methylidene]-1,3-thiazolidine-2,4-dione | ||
SMILES | C1=CC2=C(C=C1C=C3C(=O)NC(=O)S3)OC(O2)(F)F | ||
Standard InChIKey | SRLVNYDXMUGOFI-YWEYNIOJSA-N | ||
Standard InChI | InChI=1S/C11H5F2NO4S/c12-11(13)17-6-2-1-5(3-7(6)18-11)4-8-9(15)14-10(16)19-8/h1-4H,(H,14,15,16)/b8-4- | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
AS-604850 Dilution Calculator
AS-604850 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.5061 mL | 17.5303 mL | 35.0607 mL | 70.1213 mL | 87.6516 mL |
5 mM | 0.7012 mL | 3.5061 mL | 7.0121 mL | 14.0243 mL | 17.5303 mL |
10 mM | 0.3506 mL | 1.753 mL | 3.5061 mL | 7.0121 mL | 8.7652 mL |
50 mM | 0.0701 mL | 0.3506 mL | 0.7012 mL | 1.4024 mL | 1.753 mL |
100 mM | 0.0351 mL | 0.1753 mL | 0.3506 mL | 0.7012 mL | 0.8765 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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AS-604850 is a selective and ATP-competitive PI3Kγ inhibitor (IC50= 2.5 μM), with over 30-fold selectivity for PI3Kδ and PI3Kβ, and 18-fold selectivity over PI3Kα. [1]
PI3K (phosphatidylinositol-4,5-bisphosphate 3-kinase) is a family of enzymes involved in cellular functions such as cell growth, proliferation, differentiation, motility, survival and intracellular trafficking, which in turn are involved in cancer. It plays a key role in PI3K/Akt(PKB)/mTOR pathway.
In rat hepatocytes, AS-604850 pretreatment abolished GCDC-induced phosphorylation of Akt by 50% and inhibited apoptosis by reducing GCDC/TCDC/TLC-induced caspase-3 cleavage. [2] In PI3KCG-/-monocytes and THP-1 (human monocytic cell line), AS-604850 inhibited the PKB phosphorylation activated by MCP-1, it also blocked the MCP-1-mediated chemotaxis in a concentration dependent manner. In RAW264 mouse macrophages, C5a-mediated PKB phosphorylation was inhibited by AS-604850. [1]
In the thioglycollate-induced peritonitis model that induced multiple chemokine in vivo, oral administration of 10 mg/kg AS-604850 showed a 31% decrease of neutrophil recruitment. [1]
References:
1. Camps M, Rückle T, Ji H et al. Blockade of PI3K-gamma suppresses joint inflammation and damage in mouse models of rheumatoid arthritis. Nat Med. 2005 Sep;11(9):936-43.
2. Hohenester S, Gates A, Wimmer R et al. Phosphatidylinositol-3-kinase p110γ contributes to bile salt-induced apoptosis in primary rat hepatocytes and human hepatoma cells. J Hepatol. 2010 Nov;53(5):918-26.
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Role of phosphoinositide 3-kinase IA (PI3K-IA) activation in cardioprotection induced by ouabain preconditioning.[Pubmed:25575882]
J Mol Cell Cardiol. 2015 Mar;80:114-25.
Acute myocardial infarction, the clinical manifestation of ischemia-reperfusion (IR) injury, is a leading cause of death worldwide. Like ischemic preconditioning (IPC) induced by brief episodes of ischemia and reperfusion, ouabain preconditioning (OPC) mediated by Na/K-ATPase signaling protects the heart against IR injury. Class I PI3K activation is required for IPC, but its role in OPC has not been investigated. While PI3K-IB is critical to IPC, studies have suggested that ouabain signaling is PI3K-IA-specific. Hence, a pharmacological approach was used to test the hypothesis that OPC and IPC rely on distinct PI3K-I isoforms. In Langendorff-perfused mouse hearts, OPC was initiated by 4 min of ouabain 10 muM and IPC was triggered by 4 cycles of 5 min ischemia and reperfusion prior to 40 min of global ischemia and 30 min of reperfusion. Without affecting PI3K-IB, ouabain doubled PI3K-IA activity and Akt phosphorylation at Ser(473). IPC and OPC significantly preserved cardiac contractile function and tissue viability as evidenced by left ventricular developed pressure and end-diastolic pressure recovery, reduced lactate dehydrogenase release, and decreased infarct size. OPC protection was blunted by the PI3K-IA inhibitor PI-103, but not by the PI3K-IB inhibitor AS-604850. In contrast, IPC-mediated protection was not affected by PI-103 but was blocked by AS-604850, suggesting that PI3K-IA activation is required for OPC while PI3K-IB activation is needed for IPC. Mechanistically, PI3K-IA activity is required for ouabain-induced Akt activation but not PKCepsilon translocation. However, in contrast to PKCepsilon translocation which is critical to protection, Akt activity was not required for OPC. Further studies shall reveal the identity of the downstream targets of this new PI3K IA-dependent branch of OPC. These findings may be of clinical relevance in patients at risk for myocardial infarction with underlying diseases and/or medication that could differentially affect the integrity of cardiac PI3K-IA and IB pathways.
PI3Kgamma inhibition alleviates symptoms and increases axon number in experimental autoimmune encephalomyelitis mice.[Pubmed:24012746]
Neuroscience. 2013 Dec 3;253:89-99.
Phosphoinositide 3-kinase gamma (PI3Kgamma) is a shared downstream component of chemokine-mediated signaling pathways and regulates migration, proliferation and activation of inflammatory cells. PI3Kgamma has been shown to play a crucial role in regulating inflammatory responses during the progression of several diseases. We investigated the potential function of PI3Kgamma in mediating inflammatory reactions and the development of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). We found that systemic treatment with selective PI3Kgamma inhibitor AS-604850 significantly reduced the number of infiltrated leukocytes in the CNS and ameliorated the clinical symptoms of EAE mice. Treatment with this PI3Kgamma inhibitor enhanced myelination and axon number in the spinal cord of EAE mice. Consistently, we demonstrated that PI3Kgamma deletion in knockout mice mitigates the clinical sign of EAE compared to PI3Kgamma+/+ controls. PI3Kgamma deletion increased the number of axons in the lumbar spinal cord, including descending 5-HT-positive serotonergic fiber tracts. Our results indicate that PI3Kgamma contributes to development of autoimmune CNS inflammation and that PI3Kgamma blockade may provide a great potential for treating patients with MS.