ライフサイエンスコーパス: kinase inhibitor

1 ously unknown targets of a receptor tyrosine kinase inhibitor.

2 actor receptor (EGFR)-directed oral tyrosine kinase inhibitor.

3 -S6 and restored sensitivity to the tyrosine kinase inhibitor.

4 tinib is a selective, potent Bruton tyrosine-kinase inhibitor.

5 n of TJ proteins, which was blocked by a Rho-kinase inhibitor.

6 have superior efficacy versus selective HER2 kinase inhibitors.

7 t IL-6, the IL-6 receptor (IL-6R), and Janus kinase inhibitors.

8 pt, favoring the development of high-potency kinase inhibitors.

9 ications for the design of therapeutic LRRK2 kinase inhibitors.

10 romal tumour is highly resistant to tyrosine kinase inhibitors.

11 ibition of ternary CDK8 complexes by type II kinase inhibitors.

12 (ALL) have improved with the use of tyrosine kinase inhibitors.

13 lds promise for the development of selective kinase inhibitors.

14 those with resistance to commonly used ABL1 kinase inhibitors.

15 biology or developing conformation-specific kinase inhibitors.

16 , dasatinib and bosutinib, are multitargeted kinase inhibitors.

17 ons can be targeted successfully by tyrosine-kinase inhibitors.

18 e used to develop allosteric, DDR1-specific, kinase inhibitors.

19 gies are needed to treat tumors resistant to kinase inhibitors.

20 enhanced selectivity relative to competitive kinase inhibitors.

21 cated in the resistance to BRAF and MAPK/ERK kinase inhibitors.

22 d cells when IL7 was added together with the kinase inhibitors.

23 kyballs as a novel class of non-receptor Src kinases inhibitors.

24 e of Jdp2, a complex of the cyclin-dependent kinase inhibitor 1 (p21(Cip1)) and Nrf2 bound to antioxi

25 es expression of p(21CIP1) (cyclin-dependent kinase inhibitor 1), and p(27KIP1) (cyclin-dependent kin

26 pair associated (BRCA2) and cyclin-dependent kinase inhibitor 1A (CDKN1A) interacting protein, known

27 K-dependent upregulation of cyclin-dependent kinase inhibitor 1A (Cdkn1a, encoding for p21(Waf1/Cip1)

28 tified as downregulation of cyclin-dependent kinase inhibitor 1B (p27(Kip1)) via upregulation of Akt1

29 nhibitor 1), and p(27KIP1) (cyclin-dependent kinase inhibitor 1B) expression, key cell cycle inhibito

30 those without these mutations after tyrosine kinase inhibitors (2.1 vs 3.7 months, p < 0.001), but no

31 6-OH-BDE-47 is a promiscuous ATP-competitive kinase inhibitor; 2) in vitro in dissociated neurons, wh

32 retinoblastoma) and CDKN2a (cyclin-dependent kinase inhibitor 2a) are critical cell-cycle regulators,

33 tionally, we identified a potent murine RIP1 kinase inhibitor 76 as a valuable in vivo tool molecule

34 ing treatment with multiple classes of LRRK2 kinase inhibitors, a full reversal of mtDNA damage to he

35 high-throughput screen of 42 444 known human kinases inhibitors, a pyrazolo[1,5-b]pyridazine scaffold

36 ety of ripretinib, a switch-control tyrosine kinase inhibitor active against a broad spectrum of KIT

37 or LRRK2 kinase activity and consequently of kinase inhibitor activity.

38 This leptin action was reduced by Janus kinase inhibitor (AG490) or PI3-kinase inhibitor (LY2940

39 DNA topoisomerase I-targeted drugs and mTOR kinase inhibitors against these aggressive nerve sheath

40 Kinase inhibitors aimed at blocking protein kinase C and

41 targeted small-molecule inhibitors, Aurora A kinase inhibitor alisertib (MLN8237) and mTOR inhibitor

42 (2) Tested combinations of approved kinase inhibitors already being individually evaluated f

43 Acutely, a Pyk2 kinase inhibitor also prevents Abetao-induced suppressio

44 ectivity remains a challenge for ATP-mimetic kinase inhibitors, an issue that may be overcome by targ

45 a high target occupancy as its corresponding kinase inhibitor and effectiveness as a dual functional

46 CRs and TLR-MyD88 by using Bruton's tyrosine kinase inhibitor and histone deacetylase inhibitor abrog

47 inases prevents kinase targeting by a single kinase inhibitor and presents a major challenge to the t

48 Using a small kinase inhibitor and RNAi-based gene silencing to disrup

49 ced levels of the p21(Cip1) cyclin-dependent kinase inhibitor and tumor suppressor protein.

50 we used different nonselective and selective kinase inhibitors and activators to test the effect of p

51 ydroxylated PBDE metabolites are promiscuous kinase inhibitors and can cause disruptions of critical

52 nt a fundamental cellular response to Aurora kinase inhibitors and contributes to therapy resistance

53 ght about how cancer cells respond to Aurora kinase inhibitors and identify a new mechanism responsib

54 endothelial growth factor receptor tyrosine kinase inhibitors and may help detect early evidence of

55 e, decreasing expression of cyclin-dependent kinase inhibitors and upregulating pro-apoptotic protein

56 ation of p57Kip2, a Cip/Kip cyclin-dependent kinase inhibitor, and we identified this induction as cr

57 ed through a high-throughput screen of human kinase inhibitors, and the subsequent in vivo experiment

58 tic doses in patients, including the PIKfyve kinase inhibitor apilimod(2-4) and the cysteine protease

59 ity of IFN-gamma and oncostatin M, and Janus kinase inhibitors appear to be an effective treatment.

60 elicited by treatment with imatinib, an ABL kinase inhibitor approved by the FDA for CML treatment.

61 atment of Parkinson's disease (PD) and LRRK2 kinase inhibitors are currently being tested in early ph

62 However, many kinase inhibitors are planar and overlap in chemical spa

63 Both multitargeted and highly selective kinase inhibitors are used for the treatment of advanced

64 Tyrosine kinase inhibitors are widely used in the clinic, but lim

65 ining pan-ERBB and mitogen-activated protein kinase inhibitors as a therapeutic approach in subsets o

66 the PKIS library, we identified several ALK5 kinase inhibitors as strong suppressors of the pkd2 tail

67 The Janus kinase/spleen tyrosine kinase inhibitor ASN002 significantly suppressed key AD

68 We confirmed that AT7159 (cyclin-dependent kinase inhibitor), AT9283, (Janus kinase 2/3 inhibitor),

69 The WEE1 kinase inhibitor AZD1775 (WEE1i) overrides cell cycle ch

70 Consistent with this, the IkappaB kinase inhibitor BAY11-7085 and dominant-negative mutant

71 ased proteomics technique called multiplexed kinase inhibitor beads/mass spectrometry (MIB/MS), we pr

72 IF2alpha kinases or treatment with eIF2alpha kinase inhibitors being protective in some animal models

73 ed increased reporting of AF associated with kinase inhibitors blocking Csk versus non-Csk inhibitors

74 tumor-bearing mice were treated with pan-TAM kinase inhibitor (BMS-777607) or anti-PD-1 alone or in c

75 therapeutic administration of either pan-TAM kinase inhibitor (BMS-777607) or anti-PD-1 mAb therapy s

76 serine/threonine-protein kinase B-Raf (BRAF) kinase inhibitor (BRAFi) and anti-PDL1 antibody (aPDL1).

77 follow-up data showing that Bruton tyrosine kinase inhibitors (BTKi's) are effective in chronic lymp

78 -19 diagnosis, most commonly Bruton tyrosine kinase inhibitors (BTKi's; n = 68/90 [76%]).

79 rs are treated using targeted antibodies and kinase inhibitors, but resistance to these therapies lea

80 uding YAP/TAZ signaling and cyclin-dependent kinase inhibitors, by blocking entry into quiescence.

81 Here we show that ERK5 kinase inhibitors cause paradoxical activation of ERK5 t

82 e led to the development of Cyclin-Dependent Kinase inhibitors (CDKi's) as small molecule drugs and c

83 Using a promiscuous covalent kinase inhibitor (CKI) SM1-71 as a starting point, we de

84 Over the past decade, covalent kinase inhibitors (CKI) have seen a resurgence in drug d

85 BRAF inhibitor vemurafenib and the MAPK/ERK kinase inhibitor cobimetinib.

86 t substantially affected by culture with Rho Kinase inhibitor, commonly used in their routine mainten

87 tudy, we discovered a multitargeted tyrosine kinase inhibitor, compound 15a, with potent inhibition a

88 Using the ERK5 kinase inhibitor, Compound 26 (ERK5-IN-1), as a paradigm

89 This repurposing of existing kinase inhibitors could lay the foundation for alternati

90 er baseline measurements, saracatinib, a Fyn kinase inhibitor currently in clinical development for A

91 mTORC1/2 inhibitor AZD2014 and the tyrosine kinase inhibitor dasatinib as monotherapies and in combi

92 ual mTORC1/2 inhibitor AZD2014 and the multi-kinase inhibitor dasatinib.

93 ntiation step with an anti-fibrotic tyrosine kinase inhibitor decreases post-myocardial infarction (p

94 t of EGFR-mutant NSCLC to attenuate tyrosine kinase inhibitor delivery to the tumors by limiting drug

95 alabrutinib, a more specific Bruton tyrosine kinase inhibitor, demonstrating that AF is an off-target

96 antage of a well-characterized multitargeted kinase inhibitor describes a nongenetic approach to teas

97 A typical covalent kinase inhibitor design targets a reactive cysteine; how

98 Ripretinib is a novel switch-control kinase inhibitor designed to inhibit a wide range of KIT

99 with regimens that do not contain a tyrosine-kinase inhibitor, despite the use of high-risk chemother

100 and will serve as a resource for pioneering kinase inhibitor development to address current therapeu

101 sidues provides a new paradigm for selective kinase inhibitor development.

102 upplement or the PDK (pyruvate dehydrogenase kinase) inhibitor dichloroacetate was started 7 days pos

103 A Jak kinase inhibitor did not recapitulate this inhibition in

104 release of multiple therapeutics (including kinase inhibitors, drugs and short interfering RNA) in v

105 al epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that potently and selectivel

106 Although new generations of EGFR-tyrosine kinase inhibitors (EGFR-TKI) have been developed for the

107 ed epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) resistant LA patients.

108 of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs).

109 Known ATP-competitive small-molecule IRE1 kinase inhibitors either allosterically disrupt or stabi

110 demonstrated P-glycoprotein decreases bumped kinase inhibitor enterocyte exposure, resulting in reduc

111 te lymphocytic leukaemia in the pre-tyrosine-kinase inhibitor era.

112 However, selective ERK5 kinase inhibitors fail to recapitulate ERK5 genetic abla

113 The focal adhesion kinases inhibitor (FAKi 14) and cell interactions show e

114 Here, we report screening commercial kinase inhibitors for antibacterial activity and found t

115 activity of small-molecule receptor tyrosine kinase inhibitors for oncogene-addicted subgroups of non

116 mTOR, particularly with new generation mTOR kinase inhibitors, for the effective treatment of cancer

117 protein kinase R-like endoplasmic reticulum kinase inhibitor (GSK2606414) or the translation blocker

118 We show that a specific CSF-1R kinase inhibitor, GW2580, abolishes CSF-1 induced tropho

119 nant PKA, the response to the broad-spectrum kinase inhibitor H89 (N-[2-p-bromocinnamylamino-ethyl]-5

120 3, 2000, and Aug 28, 2018, in which tyrosine-kinase inhibitors had not been given as a first-line tre

121 ng this library of well-annotated, published kinase inhibitors has yielded a plethora of data in dive

122 roxyisoflavone), a tyrosine-specific-protein kinase inhibitor, has been shown to exert an anti-inflam

123 Currently, RIP1 kinase inhibitors have advanced into early clinical tria

124 In addition to sorafenib, other multi-kinase inhibitors have been approved recently for treatm

125 Accordingly, kinase inhibitors have been classified on the basis of d

126 ermal growth factor receptor (EGFR) tyrosine kinase inhibitors have been developed and approved by Fo

127 er and inflammation, and small-molecule ERK5 kinase inhibitors have been developed.

128 Small-molecule kinase inhibitors have the potential for broad efficacy,

129 s using single agent dasatinib, a SRC family kinase inhibitor, have failed in sarcomas.

130 ts with EGFR mutations treated with tyrosine kinase inhibitors, HES1 protein levels increased during

131 VX-680 is an effective pan-Aurora kinase inhibitor; however, its clinical efficacy was not

132 ted by eIF2alpha kinase 1, or heme-regulated kinase inhibitor (HRI).

133 drugs and found three host-directed tyrosine kinase inhibitors (Ibrutinib, Dasatinib and Crizotinib)

134 GF/FGFR blockade by FGF trapping or tyrosine kinase inhibitor impaired the growth and dissemination o

135 Screening of 367 kinase inhibitors in human neutrophils and a zebrafish t

136 e models for predicting different classes of kinase inhibitors including types I, I(1)/(2), and II as

137 Furthermore, an ATM kinase inhibitor increased C-NHEJ-mediated rearrangement

138 in the presence of Ca(2+) Although a general kinase inhibitor increased the current density of BdALMT

139 depletion of Pyk2 and treatment with a Pyk2 kinase inhibitor increased viral DNA content in keratino

140 apoptosis) and staurosporine (STS, a protein kinase inhibitor)-induced apoptosis.

141 rst time, dual assessments of small-molecule kinase inhibitor-induced changes in protein expression a

142 were used to investigate how TP-0903, an AXL kinase inhibitor, influences redundant oncogenic pathway

143 rality within the kinome, a new iteration of kinase inhibitors is being developed to better utilize t

144 dule optimization of treatment with tyrosine kinase inhibitors is of utmost importance.

145 tant-specific third-generation EGFR tyrosine kinase inhibitor, is emerging as the preferred first-lin

146 i-component explainable framework on protein kinase inhibitors, it can be extended across the proteom

147 ontrol the stability of the CYCLIN-DEPENDENT KINASE inhibitor KIP-RELATED PROTEIN (KRP), which may un

148 Kinase inhibitors (KIs) represent an important class of

149 s to proliferate in the presence of the HER2 kinase inhibitor lapatinib.

150 protein kinase R-like endoplasmic reticulum kinase inhibitor led to expression of late viral protein

151 tary high-throughput screens using a protein kinase inhibitor library in human stem cell-derived reti

152 t screen of PI5P4Kalpha against our in-house kinase inhibitor library.

153 ced by Janus kinase inhibitor (AG490) or PI3-kinase inhibitor (LY294002).

154 ailable, second-line therapy with a tyrosine kinase inhibitor may be recommended for appropriate cand

155 carboplatin chemotherapy to an oral tyrosine kinase inhibitor may improve outcomes.

156 of epigenetic modulators with FGFR-targeted kinase inhibitors may provide improved outcomes for brea

157 o MAPK/extracellular signal-regulated kinase kinase inhibitors (MEKis), which limits their therapeuti

158 ne whether the addition of the multitargeted kinase inhibitor midostaurin to intensive chemotherapy f

159 atment with a VEGF receptor (VEGFR) tyrosine kinase inhibitor might be effective in patients who had

160 The tyrosine kinase inhibitor neratinib is a human epidermal growth f

161 -directed therapy with the irreversible HER2 kinase inhibitor neratinib.

162 Cells that acquired resistance to the ErbB kinase inhibitor, neratinib, displayed increased phospho

163 iated activation of p300 by the FDA-approved kinase inhibitor, nilotinib, ameliorates cancer cachexia

164 ession counteracts the effects of a tyrosine kinase inhibitor, Nilotinib, while USP13 knockdown facil

165 ibitor, sirolimus, and the receptor tyrosine kinase inhibitor, nintedanib, could synergistically full

166 combinatorial treatment with lapatinib [dual kinase inhibitor of EGFR (ERBB1) and ERBB2] and thiostre

167 ro data of treatment with different tyrosine kinase inhibitors of BT-20 triple-negative breast cancer

168 -MLL inhibition with specific small-molecule kinase inhibitors of FLT3 phosphorylation resulted in a

169 Our findings suggest that kinase inhibitors of IRAK4 might be a therapeutic in pat

170 Although the use of ATP-competitive tyrosine kinase inhibitors of oncoprotein BCR-ABL1 has enabled du

171 selective Rho-associated coiled-coil protein kinase inhibitor, on corneal allograft survival.

172 ion immune checkpoint inhibitor and tyrosine-kinase inhibitors or VEGF inhibitors for increasing over

173 gressed on imatinib and one or more tyrosine kinase inhibitor, or only received imatinib previously.

174 discovery of first-in-class dual bromodomain-kinase inhibitors outside the bromodomain and extratermi

175 e tumor protein p53 and the cyclin-dependent kinase inhibitor p21WAF1/CIP1, which are findings consis

176 elevated expression of the cyclin-dependent kinase inhibitor p27, a Siah2 substrate.

177 ions, including repression of the cell-cycle kinase inhibitor p27, whose role is to functionally prom

178 The cyclin-dependent kinase inhibitor p57(kip2) is encoded by an imprinted ge

179 rome, and these patients may be eligible for kinase inhibitors, particularly following resistance or

180 r in their mechanism of action (the tyrosine kinase inhibitor pazopanib in MKN45 gastric carcinoma xe

181 mutation or administration of the selective kinase inhibitor, PF-360, attenuates neurodegeneration i

182 eover, pretreatment of M with a specific Src kinase inhibitor, PP2 completely prevents NE-induced pro

183 gonist, and Wortmannin, a phosphoinositide 3-kinase inhibitor, prevented the LPS-mediated decrease, d

184 Although tyrosine kinase inhibitors provide an effective treatment for the

185 ficient and practical synthesis of the Janus kinase inhibitor (R)-tofacitinib.

186 Fostamatinib is a spleen tyrosine kinase inhibitor recently approved for the treatment of

187 tes how the paradoxical activation of Raf by kinase inhibitors reflects an innate mechanism, with 14-

188 and clinical applications of small-molecule kinase inhibitors require comprehensive characterization

189 red BRAF/MAPK/extracellular signal-regulated kinase inhibitor resistance in melanoma results in a new

190 e conducted gene expression analyses of HER2 kinase inhibitor-resistant cell lines as compared to the

191 en in mice injected with de novo or tyrosine kinase inhibitor-resistant primary Ph+ ALL cells, and th

192 Importantly, we showed that tyrosine kinase inhibitor-resistant tumors, with EGFRT790M and EG

193 Treatment with BCR-ABL1 kinase inhibitors results in elevated expression of IL7R

194 ted C57BL/6 mice with doramapimod, a p38 MAP-kinase inhibitor, results in reduced inflammation, granu

195 inally, functional assays in the presence of kinase inhibitors reveal that binding of MED12 remodels

196 Here, a chemical genetics screen of kinase inhibitors revealed phosphoinositide 3-kinase (PI

197 lcium channel blocker nifedipine and the Rho-kinase inhibitor ROCKi significantly relax human uretera

198 er layer, rho-associated coiled coil protein kinase inhibitor (ROCKi), and low oxygen (2%), normal hu

199 ike adenosine 5'-triphosphate-site PI3K/mTOR kinase inhibitor: (S)-4-(difluoromethyl)-5-(4-(3-methylm

200 Small-molecule tyrosine kinase inhibitors seem well suited to be tailor-made the

201 or with the mitogen-activated protein kinase kinase inhibitor selumetinib by oral gavage for 24 h.

202 ut mutation and six patients with a tyrosine kinase inhibitor-sensitive mutation, p=0.0031).

203 The Published Kinase Inhibitor Set (PKIS) is a publicly-available chem

204 In contrast, treatments with an LRRK2 kinase inhibitor significantly reduced the dopaminergic

205 ected mainly in spinal neurons, and MAPK/ERK kinase inhibitors significantly inhibited chronic itch i

206 24 months either the multitargeted and FLT3-kinase inhibitor sorafenib (n = 43) or placebo (n = 40 p

207 hibitors, such as the multitargeted tyrosine kinase inhibitor sorafenib, improves outcome after HCT.

208 to atezolizumab and/or bevacizumab, tyrosine kinase inhibitors sorafenib or lenvatinib may be offered

209 highly selective dihydropyrazole (DHP) RIP1 kinase inhibitors starting from a high-throughput screen

210 The long-term effectiveness of tyrosine kinase inhibitors such as the EGFR inhibitor (EGFRi), os

211 Allosteric kinase inhibitors, such as cGMP analogs, offer enhanced

212 harbors the common BRAF(V600E) mutation with kinase inhibitors, such as vemurafenib, reduces tumor bu

213 Aurora kinase inhibitors suppress this adaptive survival progra

214 on of SHP2 in combination with FGFR-targeted kinase inhibitors synergistically blocked the growth of

215 Using a panel of kinase inhibitors targeting signaling pathways of the os

216 Here, we tested the effect of tyrosine kinase inhibitors targeting the ErbB receptors for their

217 ificantly better with crizotinib (a tyrosine kinase inhibitor) than with the combination of pemetrexe

218 eport incorporation of sunitinib, a tyrosine kinase inhibitor that blocks VEGF receptors, into a non-

219 Ripretinib is a "switch-control" kinase inhibitor that forces the activation loop (or act

220 ll molecule screening results in a cytotoxic kinase inhibitor that impairs growth of cells with slow

221 In addition, nilotinib, an FDA-approved kinase inhibitor that preferentially binds p38beta MAPK,

222 lly bioavailable, and well tolerated pan-Pim kinase inhibitor that proved efficacious in RPMI8226 and

223 ble method that exploits the large number of kinase inhibitors that have been profiled on near-kinome

224 We identified several tyrosine kinase inhibitors that inhibit CAR T-cell cytotoxicity b

225 tion of the amidobenzimidazoles (AB) protein kinase inhibitors that show nanomolar potency against T.

226 Kinase inhibitors that stabilize an open conformation re

227 oma following prior failed Bruton's tyrosine kinase inhibitor therapy, with an overall response rate

228 ss, and received no previous Bruton tyrosine-kinase inhibitor therapy.

229 The irreversible ErbB family tyrosine kinase inhibitor (TKI) afatinib plus the EGFR monoclonal

230 The development of the tyrosine kinase inhibitor (TKI) imatinib allows patients with CML

231 ore be effectively treated with the tyrosine kinase inhibitor (TKI) imatinib mesylate.

232 brogated by treatment with the FGFR tyrosine kinase inhibitor (TKI) lucitanib.

233 int mutation-mediated resistance to tyrosine kinase inhibitor (TKI) therapy in Philadelphia chromosom

234 ermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment of EGFR-mutant non-smal

235 molecular recurrence after stopping tyrosine kinase inhibitor (TKI) treatment substantially depends o

236 etion of alpha6 in combination with tyrosine kinase inhibitor (TKI) treatment was more effective in e

237 d that exhibited potent activity in tyrosine kinase inhibitor (TKI)-sensitive and TKI-resistant NSCLC

238 Evolved resistance to tyrosine kinase inhibitor (TKI)-targeted therapies remains a majo

239 of ctDNA with clinical responses to tyrosine kinase inhibitors (TKI) and immune checkpoint inhibitors

240 are proven therapeutic targets for tyrosine kinase inhibitors (TKI) in lung adenocarcinoma, but acqu

241 elanoma using immune checkpoint and tyrosine kinase inhibitors (TKI), the majority of stage IV melano

242 cularly targeted therapies, such as tyrosine kinase inhibitors (TKI), with concurrent chemotherapy an

243 le to the clinical efficacy of EGFR tyrosine kinase inhibitors (TKI).

244 ptor, including small-molecule FLT3 tyrosine kinase inhibitors (TKIs) and anti-FLT3 antibodies, have

245 e highly effective CML therapeutics tyrosine kinase inhibitors (TKIs) and interferon-alpha (IFNalpha)

246 While tumor responses to tyrosine kinase inhibitors (TKIs) are accompanied by marked tumor

247 Accordingly, FGFR targeted tyrosine kinase inhibitors (TKIs) are currently under development

248 onse rate of those patients to EGFR tyrosine kinase inhibitors (TKIs) are not well understood.

249 ROS1-directed tyrosine kinase inhibitors (TKIs) are therapeutically active agai

250 e development of resistance to EGFR Tyrosine kinase inhibitors (TKIs) in NSCLC with activating EGFR m

251 Tyrosine kinase inhibitors (TKIs) induce molecular remission in t

252 ic myeloid leukemia (CML) patients, tyrosine kinase inhibitors (TKIs) may select for drug-resistant B

253 Preclinical data suggest that EGFR tyrosine kinase inhibitors (TKIs) plus MET TKIs are a possible tr

254 ng the potential of the addition of tyrosine kinase inhibitors (TKIs) to chemotherapy to improve clin

255 most patients with CML treated with tyrosine kinase inhibitors (TKIs), a greater number of comorbidit

256 ) mutations spurred the use of EGFR tyrosine kinase inhibitors (TKIs), such as erlotinib, as the firs

257 Tyrosine kinase inhibitors (TKIs), the treatment of choice for ch

258 g resistance when treated with EGFR tyrosine kinase inhibitors (TKIs).

259 ls anticipate their response to ABL tyrosine kinase inhibitors (TKIs).

260 ma (ALCL) resistant to ALK-specific tyrosine kinase inhibitors (TKIs).

261 ntly benefited from the use of EGFR tyrosine kinase inhibitors (TKIs).

262 lial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs).

263 -small cell lung cancer, NSCLC, are tyrosine kinase inhibitors, TKIs, and immune checkpoint inhibitor

264 umvented by liver-specific delivery of a rho kinase inhibitor to effector cells.

265 hat is centered on the use of small molecule kinase inhibitor to modulate the immune response against

266 the first Plasmodium phosphatidylinositol 4-kinase inhibitor to reach clinical development as a new

267 Upadacitinib is an oral selective Janus kinase inhibitor to treat rheumatoid arthritis.

268 , it was necessary to use the combination of kinase inhibitors to block desensitization of the somato

269 ions of transcription factor inhibitors with kinase inhibitors to block the development of resistance

270 chemotherapeutics and the potency of mitotic kinase inhibitors to generate a class of high-precision

271 emonstrate a potential for the ErbB tyrosine kinase inhibitors to induce neuromuscular toxicity in a

272 e development, and suggest the potential for kinase inhibitors to therapeutically restrict ANDV repli

273 ease platform for local delivery of tyrosine kinase inhibitors to treat corneal NV.

274 Rapalogs and mTOR kinase inhibitors (TORKi) have recently been applied to

275 -NeoBOMB1 in patients with advanced tyrosine-kinase inhibitors-treated GIST using PET/CT.

276 the potential benefit of first-line tyrosine-kinase inhibitor treatment in patients with ABL-class fu

277 and EMT that could be attenuated by Aurora B kinase inhibitor treatment.

278 Tyrosine kinase inhibitors (TyKIs) approach disease gene through

279 xperiments correctly predicted that selected kinase inhibitors used for cancer therapy shifted subset

280 Treatment with a combination of kinase inhibitors (vandetanib and dasatinib) showed enha

281 Additionally, using CATNIP, we predicted the kinase inhibitor, vandetanib, as a possible treatment fo

282 The activity of MET tyrosine kinase inhibitors varies by MET alteration category.

283 A three-step synthesis of 20 kinase inhibitors was achieved by employing this oxidati

284 Lenvatinib, another tyrosine-kinase inhibitor, was found to be non-inferior to sorafe

285 phenotypic screens, signaling analyses, and kinase inhibitors, we found that dual inhibition of MEK1

286 After screening a library of 627 kinase inhibitors, we found that targeting the pro-survi

287 that 6-OH-BDE-47 is structurally similar to kinase inhibitors, we hypothesized that certain hydroxyl

288 ated by the addition of a phosphoinositide 3-kinase inhibitor, which has previously been shown to rea

289 2-degradation target p27, a cyclin-dependent kinase inhibitor, which was confirmed as the mechanism o

290 d osimertinib is a third-generation tyrosine kinase inhibitor, which was granted full FDA approval in

291 FOXO1 nuclear efflux, phosphatidylinositol 3-kinase inhibitors, which we show to be effective in thes

292 nib is a selective, covalent Bruton tyrosine-kinase inhibitor with activity in chronic lymphocytic le

293 Ibrutinib is a Bruton tyrosine kinase inhibitor with remarkable efficacy against B-cell

294 w will address the latest discoveries around kinase inhibitors with an emphasis on clinically validat

295 immense progress has been made in advancing kinase inhibitors with desirable drug-like properties in

296 the discovery of a series of JAK1-selective kinase inhibitors with high potency and excellent JAK fa

297 However, designing kinase inhibitors with target selectivity and minimal of

298 tructure-based design of next-generation RAF kinase inhibitors with unique mechanisms of action is pr

299 wever, treatment with the phosphoinositide 3-kinase inhibitor wortmannin did not disrupt localization

300 Chronic treatment with Rho-kinase inhibitor Y-27632 after chronic social defeat str