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AG 490

NMR下載 COA and HPLC MSDS下載
names：
AG 490, JAK2/3 inhibitor
CAS號：
133550-30-8
MDL Number： MFCD00236452
MF(分子式)： C17H14N2O3 MW(分子量)： 294.3
EINECS: Reaxys Number:4323263
Pubchem ID:253661829 Brand:BIOFOUNT

AG-490（133550-30-8）是酪氨酸激酶抑制劑，其抑制EGFR，Stat-3 和 JAK2/3.Tyrphostin AG490 is a JAK-2 specific inhibitor.

貨品編碼	規(guī)格	純度	價格 (￥)	現(xiàn)價(￥)	特價(￥)	庫存描述	數(shù)量	總計 (￥)
YZM001816-50mg	100mg	99.84%	￥ 1680.00	￥ 1680.00		2-3天	- +	￥ 0.00
YZM001816-10mg	10mg	99.84%	￥ 362.00	￥ 362.00		2-3天	- +	￥ 0.00

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中文別名	AG 490(cas:133550-30-8)；AG-490；AG490；Tyrphostin AG490；Tyrphostin B42；JAK2抑制劑；JAK3抑制劑
英文別名	AG 490, JAK2/3 inhibitor(cas:133550-30-8)
CAS號	133550-30-8
Inchi	InChI=1S/C17H14N2O3/c18-10-14(8-13-6-7-15(20)16(21)9-13)17(22)19-11-12-4-2-1-3-5-12/h1-9,20-21H,11H2,(H,19,22)/b14-8+
InchiKey	TUCIOBMMDDOEMM-RIYZIHGNSA-N
分子式 Formula	C17H14N2O3
分子量 Molecular Weight	294.3
溶解度Solubility	生物體外In Vitro:DMSO溶解度≥ 50 mg/mL(169.89 mM)*"≥" means soluble可溶, but saturation unknown溶解度未知.
性狀	固體粉末,Power
儲藏條件 Storage conditions	-20°C 3 years年 4°C 2 years年 / In solvent溶液中:-80°C 6 months月 -20°C 1 month月

AG-490(CAS:133550-30-8)實驗注意事項：
1.實驗前需戴好防護眼鏡，穿戴防護服和口罩，佩戴手套，避免與皮膚接觸。
2.實驗過程中如遇到有毒或者刺激性物質(zhì)及有害物質(zhì)產(chǎn)生，必要時實驗操作需要手套箱內(nèi)完成以免對實驗人員造成傷害
3.實驗后產(chǎn)生的廢棄物需分類存儲，并交于專業(yè)生物廢氣物處理公司處理，以免造成環(huán)境污染Experimental considerations:
1. Wear protective glasses, protective clothing and masks, gloves, and avoid contact with the skin during the experiment.
2. The waste generated after the experiment needs to be stored separately, and handed over to a professional biological waste gas treatment company to avoid environmental pollution.

產(chǎn)品說明	AG-490(133550-30-8)是酪氨酸激酶的抑制劑，其抑制EGFR，Stat-3和JAK2/3
Introduction	AG90 is a tyrosine kinase inhibitor that inhibitsEGFR,StatandJAK2/3.
Application1
Application2
Application3

AG-490 is a JAK-2 specific inhibitor, which inhibits phosphorylation of EGFR and signal transducer and activator of transcription 3 [STAT-3], and subsequently reduce invasion and adhesion potential of malignant cells.

AG490 inhibits the activation of Stat-3 by selectively blocking JAK2. AG490 is used to selectively inhibit JAK/Stat-3 activation. At a dose of 10 μM, Stat-3 phosphorylation is decreased by >95% and cell viability is maintained. AG490 at a dose of 10 μM results in >95% decrease in pStat-3 in EGF-stimulated A431 cells with no effect on Stat-3 mass. AG-490 is a potent inhibitor of the JAK3/STAT, JAK3/AP-1, and JAK3/MAPK pathways and their cellular consequences. AG-490 abolishes IL-2-inducible [³H]thymidine incorporation in a dose-dependent manner, displaying an IC₅₀ of 25 μM. AG-490 potently inhibits IL-2-mediated proliferation in T cells, results distinct from previous studies that showed this agent induced apoptosis in ALL cells while exerting apparently no effects on the growth of mitogen-stimulated normal T cells

警示圖
危險性	warning
危險性警示	Not available
安全聲明	H303吞入可能有害+H313皮膚接觸可能有害+H2413吸入可能對身體有害
安全防護	P264處理后徹底清洗+P280戴防護手套/穿防護服/戴防護眼罩/戴防護面具+P305如果進入眼睛+P351用水小心沖洗幾分鐘+P338取出隱形眼鏡（如果有）并且易于操作,繼續(xù)沖洗+P337如果眼睛刺激持續(xù)+P2393獲得醫(yī)療建議/護理
備注	實驗過程中防止吸入、食入，做好安全防護

Demethoxycurcumin was superior to temozolomide in the inhibition of the growth of glioblastoma stem cells in vivo. Leng L;Zhong X;Sun G;Qiu W;Shi L Tumour Biol. 2016 Oct 18. [Epub ahead of print]

JAK2/STAT3 activation by melatonin attenuates the mitochondrial oxidative damage induced by myocardial ischemia/reperfusion injury. Yang Y;Duan W;Jin Z;Yi W;Yan J;Zhang S;Wang N;Liang Z;Li Y;Chen W;Yi

Dowlati A, et al. Combined inhibition of epidermal growth factor receptor and JAK/STAT pathways results in greater growth inhibition in vitro than single agent therapy. Mol Cancer Ther. 2004 Apr;3(4):

Davoodi-Semiromi A, et al. The tyrphostin agent AG490 prevents and reverses type 1 diabetes in NOD mice. PLoS One. 2012;7(5):e36079.

Cheppudira BP, et al. Anti-hyperalgesic effects of AG490, a Janus kinase inhibitor, in a rat model of inflammatory pain. Biomed Rep. 2015 Sep;3(5):703-706.

Regulation and mechanism of leptin on lipid metabolism in ovarian follicle cells from yellow catfish Pelteobagrus fulvidraco.
Zhang LH;Tan XY;Wu K;Zhuo MQ;Song YF;Chen QL Gen Comp Endocrinol. 2015 Oct 1;222:116-23. doi: 10.1016/j.ygcen.2015.06.008. Epub 2015 Jun 25.
The present study was conducted to determine the effect of leptin on lipid metabolism in ovarian follicle cells of yellow catfish Pelteobagrus fulvidraco. For that purpose, primary ovarian follicle cells were isolated from yellow catfish, cultured and subjected to different treatments (control, 0.1% DMSO, 500ng/ml leptin, 500ng/ml leptin plus 100μM wortmannin, 500ng/ml leptin plus 50nM AG490, respectively) for 48h. Intracellular triglyceride (TG) content, the activities (CPT I, FAS, G6PD, and 6PGD) and/or expression level of several enzymes (CPT I, FAS, G6PD, 6PGD, ACCa and ACCb), as well as the mRNA expression of transcription factors (PPARα, PPARγ and SREBP-1) involved in lipid metabolism were determined. Recombinant human leptin (rt-hLEP) incubation significantly reduced intracellular TG content, activities and mRNA levels of FAS, G6PD and 6PGD, SREBP-1 and PPARγ, but enhanced activity and mRNA level of CPT I, PPARα and ACCa. Specific inhibitors AG490 and wortmannin of JAK-STAT and IRS-PI3K signaling pathways prevented leptin-induced changes, indicating that JAK-STAT and IRS-PI3K signaling pathways were involved in the process of leptin-induced changes of lipid metabolism. Based on these observations above, for the first time, our study indicated that leptin reduced lipid deposition by activating lipolysis and suppressing lipogenesis in ovarian follicles of yellow catfish, and both JAK-STAT and IRS-PI3K signaling pathways were involved in the changes of leptin-induced lipid metabolism.

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