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Of tyrosine kinase inhibitor

Akin C. Brockow K. D Ambrosio C. et al Effects of tyrosine kinase inhibitor SXI571 on human mast cells bearing wild-type or mutated c-kit. Exp Hem-atol 2003 31 686-692. [Pg.124]

Sorenson RL, Brelje TC and Roth C. 1994. Effect of tyrosine kinase inhibitors on islets of Langerhans evidence for tyrosine kinases in the regulation of insulin secretion. Endocrinology 134(4)4975—1978. [Pg.174]

Ozvegy-Laczka C, Elegedus T, Varady G et al. High-affinity interaction of tyrosine kinase inhibitors with the ABCG2 multi drug transporter. Mol Pharmacol 2004 65 1485-1495. [Pg.125]

Fry DW, Bridges AJ, Denny WA et al. Specific, irreversible inactivation of the epidermal growth factor receptor and erbB2, by a new class of tyrosine kinase inhibitor. Proc Natl Acad Sci USA 1998 95 12022-12027. [Pg.125]

Klumpen HJ et al (2011) Moving towards dose individualization of tyrosine kinase inhibitors. Cancer Treat Rev 37(4) 251-260... [Pg.240]

Bouchet S et al (2010) Therapeutic drug monitoring of tyrosine-kinase inhibitors in the treatment of chronic myelogenous leukaemia interests and limits. Therapie 65 213-218... [Pg.241]

Recently Shi et al. (239) reported the synthesis of a 432-member focused hbrary LIO as a source of tyrosine kinase inhibitors using benzylidene malononitriles, or tyr-phostins, as structural motifs to design the library. Both the general tyrphostin structure (7.61) and an example of an active compound on a specific tyrosine kinase (7.62) are reported in Fig. 7.37. [Pg.315]

Donato NJ, Talpaz M (2000) Clinical use of tyrosine kinase inhibitors Therapy for chronic myelogenous leukemia and other cancers. Clin Cancer Res 6 2965-2966... [Pg.139]

Comparative QSAR study of tyrosine kinase inhibitors 01CRV2573. [Pg.28]

Tyrosine phosphorylation of plasmalemmal receptors or other proteins provides high-affinity binding sites for src homology 2 (SH2)-containing proteins and represents a key targeting mechanism for enzyme translocation. Several groups of tyrosine kinase inhibitors are currently available and have been shown to interfere with enzyme translocation. [Pg.310]

Tyrosine kinases have been implicated in Ca +-sensitization largely as the result of the inhibitory effects of tyrosine kinase inhibitors, genistein and vanadate, and the correlation between tyrosine phosphorylation and vanadate- or agonist-induced contractions (Di Salvo et al. 1993a,b, 1994, 1997 Steusloff et al. 1995). However, the tyrosine-phosphorylated proteins have yet to be directly linked to a known contractile regulatory mechanism i.e., MLCK, SMPP-IM) and evaluation of the relationships between tyrosine phosphorylation and modulation of Ca +-sensitization of contraction in intact muscle is somewhat complicated by concurrent changes in cytosolic Ca (Di Salvo et al. 1994,1997), possibly as the result of activation of PLC-y (Marrero et al. 1994) or Gaq.n (Umemori et al. 1997). [Pg.217]

Piontek M, Hengels KJ, Porschen R, Strohmeyer G. Anti proliferative effect of tyrosine kinase inhibitors in epidermal growth factor-stimulated growth of human gastric cancer cells. Anticancer Res 1993 13 2119-2123. [Pg.93]

Arora A, Scholar EM (2005) Role of tyrosine kinase inhibitors in cancer therapy. J Pharmacol Exp Ther 315 971-979... [Pg.212]

Shah RR, Morganroth J (2015) Update on cmdiovasculm safety of tyrosine kinase inhibitors with a special focus on QT interval, left ventricular dysfunction and overall risk/benefit. Drug Saf 38 693-710... [Pg.220]

Systobc dysfunction and heart failure are some of the most common cardiovascular side effects of tyrosine kinase inhibitors. This may occur because the pathways that are involved in the survival of cancer cells also appear to be involved in the survival of some normal cells (Chen et al. 2011). The tyrosine kinase inhibitors include molecules that target mie or a few tyrosine kinases to those that target multiple tyrosine kinases. Although targeting multiple kinases may add efficacy, this also increases the likelihood for inducing toxicities. The toxicities that are observed appear to be on-target, i.e., directly related to the type of tyrosine kinase that is inhibited. [Pg.425]

Scheme 16.25 Two syntheses of tyrosine kinase inhibitor that showcase the efficiency of C-H functionaiization in poiyaryiated imidazoie synthesis. Scheme 16.25 Two syntheses of tyrosine kinase inhibitor that showcase the efficiency of C-H functionaiization in poiyaryiated imidazoie synthesis.
In 2010, Mural and Shibahara successfully synthesized the same target via sequential C-H arylation of imidazole using their own catalytic system (Scheme 16.25b) [49a]. They discovered that cationic palladium species [Pd(phen)2](PFg)2 (phen = 1,10-phenanthroline) is more effective than neutral palladium catalysts for the C-H arylation of 1,3-azoles and, in order to demonstrate the utility of their catalyst, the synthesis of tyrosine kinase inhibitor was carried out. Their synthesis... [Pg.530]

Synthesis of tat-davilactone B Clavilactones A, D, and B 20 are potent kinase inhibitors against Ret/ptcl and epidermal growth factor receptor (EGF-R) tyrosine kinases. As such, they represent a new structural class of tyrosine kinase inhibitors, which are key enzymes modulating the... [Pg.1046]


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See also in sourсe #XX -- [ Pg.15 , Pg.447 , Pg.449 ]




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