AG-490 - CAS 133550-30-8
Catalog number: B0084-164022
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C17H14N2O3
Molecular Weight:
294.31
COA:
Inquire
Targets:
EGFR
Description:
Tyrphostin AG490 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.
Ordering Information
Catalog Number Size Price Stock Quantity
B0084-164022 25 mg $248 In stock
B0084-164022 50 mg $448 In stock
Bulk Inquiry
Purity:
0.98
Appearance:
Light yellow to yellow Solid
Synonyms:
Tyrphostin AG 490.
MSDS:
Inquire
InChIKey:
TUCIOBMMDDOEMM-RIYZIHGNSA-N
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+
Canonical SMILES:
C1=CC=C(C=C1)CNC(=O)C(=CC2=CC(=C(C=C2)O)O)C#N
1.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 D;Yu S J Pineal Res. 2013 Oct;55(3):275-86. doi: 10.1111/jpi.12070. Epub 2013 Jun 25.
Ischemia/reperfusion injury (IRI) is harmful to the cardiovascular system and causes mitochondrial oxidative stress. Numerous data indicate that the JAK2/STAT3 signaling pathway is specifically involved in preventing myocardial IRI. Melatonin has potent activity against IRI and may regulate JAK2/STAT3 signaling. This study investigated the protective effect of melatonin pretreatment on myocardial IRI and elucidated its potential mechanism. Perfused isolated rat hearts and cultured neonatal rat cardiomyocytes were exposed to melatonin in the absence or presence of the JAK2/STAT3 inhibitor AG490 or JAK2 siRNA and then subjected to IR. Melatonin conferred a cardio-protective effect, as shown by improved postischemic cardiac function, decreased infarct size, reduced apoptotic index, diminished lactate dehydrogenase release, up-regulation of the anti-apoptotic protein Bcl2, and down-regulation of the pro-apoptotic protein Bax. AG490 or JAK2 siRNA blocked melatonin-mediated cardio-protection by inhibiting JAK2/STAT3 signaling. Melatonin exposure also resulted in a well-preserved mitochondrial redox potential, significantly elevated mitochondrial superoxide dismutase (SOD) activity, and decreased formation of mitochondrial hydrogen peroxide (H2 O2 ) and malondialdehyde (MDA), which indicates that the IR-induced mitochondrial oxidative damage was significantly attenuated.
2.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.
3.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]
Temozolomide (TMZ) is widely used in the treatment of glioblastoma multiforme (GBM) as it can effectively inhibit the growth of GBM for some months; however, this cancer type is still incurable. The existence of glioma stem cells (GSCs) is thought to be responsible for the invariable recurrence of GBM after treatment, but GSCs are insensitive to TMZ. Our recent research showed that demethoxycurcumin (DMC), a component of curcumin, was superior to TMZ in its ability to inhibit proliferation and induce apoptosis of GSCs in vitro. In addition, the combined treatment of TMZ + DMC induced more obvious anti-GSC effects. However, in this study, no obvious synergistic anti-GSC effects of TMZ + DMC were found in vivo, while DMC was still superior to TMZ with respect to growth inhibition of GSCs in vivo. Furthermore, immunohistochemistry for proliferating cell nuclear antigen (PCNA) showed that such inhibitory effects were mainly related to the inhibition of cell proliferation rather than to apoptosis. However, a high concentration of DMC (50 mg/kg) alone or combined with TMZ could also induce approximately 10 % of the cells to undergo apoptosis according to a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay.
Molecular Weight Calculator Molarity Calculator Solution Dilution Calculator

Related EGFR Products


CAS 848942-61-0 AZD-8931

AZD-8931
(CAS: 848942-61-0)

Sapitinib, also known as AZD-8931, is an erbB receptor tyrosine kinase inhibitor with potential antineoplastic activity. AZD8931 binds to and inhibits erbB tyro...

CAS 481-74-3 Chrysophanol

Chrysophanol
(CAS: 481-74-3)

Chrysophanic acid (Chrysophanol) is a natural anthraquinone with anticancer activity in EGFR-overexpressing SNU-C5 human colon cancer cells. Chrysophanic acid p...

ZD-4190
(CAS: 413599-62-9)

ZD-4190, a substituted 4-anilinoquinazoline, is a potent, orally available inhibitor of the vascular endothelial cell growth factor receptor 2 (VEGFR2) and of e...

CAS 610798-31-7 Icotinib

Icotinib
(CAS: 610798-31-7)

Icotinib Hydrochloride (BPI-2009H), or Icotinib, is a highly selective, first generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI).

CAS 1374640-70-6 Rociletinib

Rociletinib
(CAS: 1374640-70-6)

Rociletinib is a third-generation irreversible kinase inhibitor of epidermal growth factor receptor (EGFR). Rociletinib was shown to inhibit the proliferation o...

CAS 139087-53-9 AG 494

AG 494
(CAS: 139087-53-9)

AG-494 is a EGFR (epidermal growth factor receptor) kinase inhibitor with IC50 value of 0.7 μM. It is selective over ErbB2, PDGFR and insulin receptor kinase (I...

CAS 205923-56-4 Cetuximab

Cetuximab
(CAS: 205923-56-4)

EGF816 mesylate
(CAS: 1508250-72-3)

EGF816 mesylate is the mesylate salt of EGF816 which is a covalent mutant-selective EGFR inhibitor and potently inhibits the T790M.

Chemical Structure

CAS 133550-30-8 AG-490

Quick Inquiry

Verification code

Featured Items