ライフサイエンスコーパス: kinase inhibitor

1 sunitinib, a multitargeted receptor tyrosine kinase inhibitor.

2 roglia by PP2, a Src family protein tyrosine kinase inhibitor.

3 econd-generation, irreversible EGFR tyrosine kinase inhibitor.

4 ho had been pretreated with an EGFR tyrosine kinase inhibitor.

5 PRJ), a known extracellular signal-regulated kinase inhibitor.

6 olitinib) is a highly selective MET tyrosine kinase inhibitor.

7 growth factor receptor (EGFR)/HER2 tyrosine kinase inhibitor.

8 reatment with ibrutinib, a Bruton's tyrosine kinase inhibitor.

9 of oral BGJ398, a selective FGFR1-3 tyrosine kinase inhibitor.

10 r or who had been pretreated with a tyrosine kinase inhibitor.

11 lts justify further investigation of AT with kinase inhibitors.

12 ty and conferred sensitivity to FDA-approved kinase inhibitors.

13 educes the anti-proliferative effect of mTOR kinase inhibitors.

14 erpins the covalent linkage for one class of kinase inhibitors.

15 identified as potent ATP-competitive protein kinase inhibitors.

16 iderations, including new and novel tyrosine kinase inhibitors.

17 were exquisitely sensitive to JAK and Aurora kinase inhibitors.

18 that are amenable to treatment with tyrosine kinase inhibitors.

19 models in the presence and absence of LRRK2 kinase inhibitors.

20 n G2019S-LRRK2 neurons was reversed by LRRK2 kinase inhibitors.

21 the emergence of clinically useful tyrosine kinase inhibitors.

22 ng, persistent state in response to targeted kinase inhibitors.

23 agents and targeted compounds, including PIM kinase inhibitors.

24 phocytic leukaemia who do not have access to kinase inhibitors.

25 ltures that are achieved by use of ROCK (Rho kinase) inhibitors.

26 d we identified the mRNA of cyclin-dependent kinase inhibitor 1A (Cdkn1a, p21) as a direct target of

27 and tensin homolog (PTEN), cyclin dependent kinase inhibitor 2A (CDKN2A), LKB1, and others.

28 insult (e.g. LPSs) induces cyclin-dependent kinase inhibitor 2A (CDKN2A/p16(INK4a)) expression and s

29 on, and thyroxine decreased cyclin-dependent kinase inhibitor 2A (p16(ink4)) expression in organ-cult

30 beta) signaling in cultured cyclin-dependent kinase inhibitor 2B (CDKN2B)-deficient cells, as well as

31 In contrast, the adenosine kinase inhibitor, 5-iodotubericidin, which inhibits the

32 In contrast to catalytic-site ABL1 kinase inhibitors, ABL001 binds to the myristoyl pocket

33 X-82 is an oral tyrosine kinase inhibitor active against vascular endothelial gro

34 us, the sequence of administration of an ATR kinase inhibitor and a DNA damaging agent impacts the DN

35 Combined treatment with an EGFR tyrosine kinase inhibitor and Akt inhibitor causes apoptosis and

36 diverse AML cell lines treated with pan-PIM kinase inhibitor and fms-related tyrosine kinase 3 (FLT3

37 netarsudil 0.02% ophthalmic solution, a rho-kinase inhibitor and norepinephrine transporter inhibito

38 ases who had never received an EGFR tyrosine kinase inhibitor and patients with leptomeningeal metast

39 zing clinical investigation of dual mTORC1/2 kinase inhibitors and developing mTORC2-specific inhibit

40 ed to development of small-molecule tyrosine kinase inhibitors and inhibitors of mammalian target of

41 years, with a number of novel small-molecule kinase inhibitors and monoclonal antibodies now being wi

42 w on the current development of class II PI3 kinase inhibitors and outline the potential use for such

43 ociated therapeutic agents: cyclin-dependent kinase inhibitors and poly(adenosine diphosphate-ribose)

44 Terreic acid (a Bruton's tyrosine kinase inhibitor) and pergolide (a dopamine and serotoni

45 bitors wortmannin, a phosphatidyl inositol 3-kinase inhibitor, and leupeptin plus E64 (inhibitors of

46 nist of the aryl hydrocarbon receptor, Janus kinase inhibitors, and commensal organisms also in trial

47 Vemurafenib, an oncogenic BRAF kinase inhibitor approved for BRAF-positive melanoma, sh

48 Chk1 kinase inhibitors are currently under clinical investiga

49 mors, and common themes regarding the use of kinase inhibitors are developing.

50 Kinase inhibitors are effective cancer therapies, but tu

51 VEGF inhibitors, including receptor tyrosine kinase inhibitors, are used as adjunct therapies in a nu

52 ising in metastatic melanoma to MAPK pathway kinase inhibitors as a strategy to identify candidate st

53 ibiting PI(3)P production, suggesting PI(3)P kinase inhibitors as a therapeutic strategy in Lowe synd

54 h a discussion of current efforts to develop kinase inhibitors as novel antimicrobials.

55 tion vs long-term administration of tyrosine-kinase inhibitors) as well as on MRD testing.

56 n toxicity in patients treated with tyrosine kinase inhibitors at levels not detectable via dermatolo

57 HER2, and HER3 signalling with the tyrosine kinase inhibitor AZD8931 will control growth of all wild

58 o identify the known targets of FDA-approved kinase inhibitors based on templates involving other kin

59 Here, we demonstrate that the selective Axl kinase inhibitor BGB324 targets the tumor-immune interfa

60 F-mediated activation of EGFR blunted fusion kinase inhibitor binding and restored fusion kinase sign

61 Bumped kinase inhibitors (BKIs) of Cryptosporidium parvum calci

62 l drug concentrations for a series of bumped kinase inhibitors (BKIs) that have nearly identical in v

63 Syk kinase inhibitors blocked Syk signaling and exhibited po

64 KDU731, a PI (4) kinase inhibitor, blocks Cryptosporidium infection in vi

65 We demonstrate here that multiple Syk kinase inhibitors both prevent parasite-induced band 3 t

66 The highly specific CDK7 kinase inhibitors, BS-181 and THZ1, each downregulated C

67 mia (CML) is currently treated with tyrosine kinase inhibitors, but these do not effectively eliminat

68 of type II maternal embryonic leucine zipper kinase inhibitors by applying these two complementary ap

69 pression and sensitizes cancer cells to mTOR kinase inhibitors by enhancing 4E-BP1-mediated translati

70 se modifier raloxifene with the c-Met/VEGFR2 kinase inhibitor cabozantinib, dramatically potentiated

71 Although kinase inhibitors can improve outcomes for some patients

72 nib and the epidermal growth factor receptor kinase inhibitor canertinib; these drugs slowed growth o

73 These include the cyclin-dependent kinase inhibitor (CDKI) p18INK4c, the master transcripti

74 stance to a pharmacological cyclin-dependent kinase inhibitor (CDKi), we show that this assumption is

75 ation through repression of cyclin-dependent kinase inhibitor CDKN1A (p21(Cip1)).

76 Checkpoint kinase inhibitors (CHKi) exhibit striking single-agent a

77 discovered a highly selective and potent BTK kinase inhibitor (CHMFL-BTK-11) which exerted its inhibi

78 XO32-mediated ubiquitination of KLF4, as p38 kinase inhibitor coincidently abrogates endogenous KLF4

79 ks and dasatinib (DAS, an oncogenic tyrosine kinases inhibitor) conjugated hydrophobic blocks, were d

80 ety in human clinical trials, we suggest Syk kinase inhibitors constitute a promising class of antima

81 PGE1/misoprostol with conventional tyrosine-kinase inhibitors could provide effective therapy for CM

82 were about 2-fold more sensitive to the FER kinase inhibitor crizotinib and the epidermal growth fac

83 The kinase inhibitor crizotinib was directly conjugated to D

84 Addition of the dual MET/RON tyrosine kinase inhibitor, crizotinib, restored cetuximab sensiti

85 kinase, namely, a commercial drug and type I kinase inhibitor Dasatinib and the type II inhibitor RL4

86 tor genistein, and the more specific Src/Abl kinase inhibitor dasatinib: both reduced ROS-induced deg

87 mplified cells, exposure to an mTORC1/2 dual kinase inhibitor decreased Akt-dependent cell survival,

88 Signaling pathway analysis with protein kinase inhibitors demonstrated that oncogenic regulation

89 s a highly selective, potent Bruton tyrosine kinase inhibitor developed to minimise off-target activi

90 A major goal in kinase-inhibitor development is to selectively engage th

91 Using the cyclin-dependent kinase inhibitor dinaciclib, which downregulates MYC exp

92 screening assays are essential for tyrosine kinase inhibitor discovery.

93 epresenting gene silencing compounds such as kinase inhibitors, disrupt the encoded cell cycle.

94 By contrast, the multi-targeted tyrosine kinase inhibitors dovitinib and vatalanib, which directl

95 The tyrosine kinase inhibitor erlotinib improves the outcomes of pati

96 he epidermal growth factor receptor tyrosine kinase inhibitor erlotinib in combination with gemcitabi

97 The tyrosine kinase inhibitor erlotinib poorly penetrates the blood-b

98 Treatment with a pan-ErbB kinase inhibitor erlotinib with nanomolar activity again

99 n treated with chloroquine plus the tyrosine kinase inhibitors erlotinib or sunitinib, suggesting tha

100 tance to an IGF-1 receptor (IGF-1R) tyrosine kinase inhibitor exhibited reduced expression of PGC-1be

101 were abrogated by pretreatment with the rho kinase inhibitor fasudil.

102 eRepo-ORP, we discuss the repositioning of a kinase inhibitor for Ras-associated autoimmune leukoprol

103 Tofacitinib is an oral Janus kinase inhibitor for the treatment of rheumatoid arthrit

104 Here we assess 34 host-targeted kinase inhibitors for their capacity to eliminate Plasmo

105 rimary rodent neurons and identified the pan-kinase inhibitor foretinib, which potently rescued sympa

106 TRPM7 kinase inhibitors FTY720 and waixenicin A block the chan

107 ty with that of the reversible EGFR tyrosine kinase inhibitor gefitinib in the first-line treatment o

108 ermal growth factor receptor (EGFR) tyrosine kinase inhibitor gefitinib relative to placebo in patien

109 d after treatment of cells with the tyrosine-kinase inhibitor Gefitinib.

110 Deregulation of ZAP-70 using tyrosine kinase inhibitors, gefitinib or ibrutinib, diminishes HA

111 ntiated by the rescue effect of the tyrosine kinase inhibitor genistein, and the more specific Src/Ab

112 ent-derived LRRK2 G2019S LCLs with the LRRK2 kinase inhibitor GNE-7915, either prevented or restored

113 Small-molecule PIM kinase inhibitors halted the growth of human TN tumors w

114 the fusion oncoprotein BCR-ABL with tyrosine kinase inhibitors has significantly affected chronic mye

115 JAK kinase inhibitors have depressed leukemic T cell line pr

116 ABL1 kinase inhibitors have improved the clinical outcomes fo

117 The novel Bruton's tyrosine kinase inhibitor ibrutinib has demonstrated high respons

118 o combine AZD8835 with the Bruton's tyrosine kinase inhibitor ibrutinib.

119 ory of food-induced anaphylaxis with the ABL kinase inhibitor imatinib protected the mice from severe

120 Imatinib, a selective BCR-ABL1 kinase inhibitor, improved the prognosis for patients wi

121 n combination, and nivolumab plus a tyrosine kinase inhibitor in metastatic renal cell carcinoma (mRC

122 the most important modulators of response to kinase inhibitors in CLL.

123 tivity observed between RAS activity and RAF kinase inhibitors in driving RAF activation.

124 important predictive biomarkers for tyrosine kinase inhibitors in lung cancer.

125 les may hold clues to the ineffectiveness of kinase inhibitors in pathology, which is characteristica

126 Clinical trials testing combinations of kinase inhibitors in Ph-like ALL patients are indicated.

127 nt of effective biologics and small-molecule kinase inhibitors in the past two decades has substantia

128 the sensitivity of glioma cells to tyrosine kinase inhibitors in vivo in preclinical combination tri

129 bosutinib, an oral dual Src/Bcr-Abl tyrosine kinase inhibitor, in patients with ADPKD.

130 of PDGFRbeta and p57kip2, a cyclin-dependent kinase inhibitor, in these cells.

131 N2 knockout sensitized HCC cells to tyrosine kinase inhibitors, including erlotinib, lapatinib and su

132 Epidermal growth factor receptor tyrosine kinase inhibitors, including gefitinib, erlotinib, and a

133 we show that PI3Kdelta or Bruton's tyrosine kinase inhibitors increase genomic instability in normal

134 Second-generation ABL1 kinase inhibitors induce more potent molecular responses

135 Kinase inhibitors induce response in diverse types of so

136 that identified mechanisms through which ATR kinase inhibitors induce unscheduled origin firing in un

137 Insofar as kinase inhibitors interfere with signaling dynamics, and

138 at the expression of p21, a cyclin-dependent kinase inhibitor involved in cell cycle regulation and m

139 Ibrutinib, a Bruton tyrosine kinase inhibitor, is a new targeted agent approved by th

140 ergy in neuroblastoma cells between the EGFR kinase inhibitor lapatinib and the anticancer compound Y

141 s targeted effectively by the small-molecule kinase inhibitor lapatinib frequently acquire resistance

142 mography (PET) TrkB/C-targeting radiolabeled kinase inhibitor lead.

143 ve response induced upon treatment with EGFR kinase inhibitors, leading to the emergence of resistanc

144 small-molecule p38 mitogen-activated protein kinase inhibitor (Losmapimod; GlaxoSmithKline, Brentford

145 The addition of the multitargeted kinase inhibitor midostaurin to standard chemotherapy si

146 stream, we decided to explore which tyrosine kinase inhibitors might block the kinase-induced membran

147 Tyrosine kinase inhibitors might still have potential in the trea

148 versal and resensitization to other tyrosine kinase inhibitors, mitotic inhibitors, and platinum-base

149 However, similar to other tyrosine kinase inhibitors, most patients achieve disease stabili

150 al strategy combining multitargeted tyrosine kinase inhibitors (MTKIs) and microRNA (miRNA) modulatio

151 d neoadjuvant chemotherapy plus the tyrosine kinase inhibitor neratinib with control.

152 vel targets for two clinically used tyrosine kinase inhibitors, nilotinib and osimertinib.

153 A small molecule kinase inhibitor of EphA2 effectively suppressed tumor c

154 Neratinib, an irreversible tyrosine-kinase inhibitor of HER1, HER2, and HER4, has clinical a

155 Vandetanib is a novel tyrosine kinase inhibitor of VEGFR2, RET, and EGFR, all of which

156 A notable example is kinase inhibitors of EGFR, which display poor clinical e

157 Our approach also predicts host-targeted kinase inhibitors of infection, including compounds alre

158 ons are insensitive to clinically used multi-kinase inhibitors of RAS/RAF/MEK/ERK signaling, includin

159 Effects of 4 multitargeted receptor tyrosine kinase inhibitors on regional hemodynamics in conscious,

160 ses who had either never received a tyrosine kinase inhibitor or who had been pretreated with a tyros

161 alone or in combination with other tyrosine kinase inhibitors or chemotherapeutic agents.

162 s cyclins D, A2, and B2 and cyclin-dependent kinase inhibitor p20 in brain tissue.

163 by increased expression of cyclin-dependent kinase inhibitor p21 and decreased expression of cyclin

164 The cyclin-dependent kinase inhibitor p21 is an important player in stress pa

165 epressing the expression of cyclin-dependent kinase inhibitor, p21(Waf1/Cip1).

166 d that autoantibodies against the cell-cycle kinase inhibitor p27 (KIP1, CDKN1B) were elevated in pla

167 s hyper-accumulation of the cyclin-dependent kinase inhibitor p27, leading to mitotic arrest and subs

168 yc and stabilization of the cyclin-dependent kinase inhibitor p27/KIP1.

169 uitry can be disrupted by the small-molecule kinase inhibitor pacritinib, leading to preferential imp

170 herapy, with or without the cyclin-dependent kinase inhibitor palbociclib.

171 response in ovarian cancer to multityrosine kinase inhibitor pazopanib.

172 Side effects of this protein kinase inhibitor (PKI) include arthralgia, rash, and fat

173 ormoxic (Nx), HI and HI pre-treated with Src kinase inhibitor PP2 (PP2 + HI).

174 inase (ERK1/2) was blocked by the Src family kinase inhibitor PP2, indicating that the action of pilo

175 f neuroendocrine prostate cancer as Aurora A kinase inhibitors promoting N-Myc destabilization progre

176 Recently the endogenous Raf kinase inhibitor protein (RKIP) was found to activate be

177 ic GRK2 and ERK cascade inhibitor, RKIP (Raf kinase inhibitor protein), triggered dysfunctional cardi

178 olymersomes can deliver the cyclin-dependent kinase inhibitor (R)-roscovitine into human neutrophils

179 ressed after treatment with an EGFR tyrosine kinase inhibitor received AZD3759 at 50 mg, 100 mg, 200

180 ersity and unpredictability of EGFR tyrosine kinase inhibitor resistance mechanisms presents a challe

181 ly combat the heterogeneity of EGFR tyrosine kinase inhibitor resistance mechanisms.EGFR-mutant non-s

182 trategy to circumvent multiple mechanisms of kinase inhibitor resistance that could be rapidly tested

183 l patients succumb to acquired EGFR tyrosine kinase inhibitor resistance that occurs via diverse mech

184 chronic myeloid leukemia (CML) and tyrosine kinase inhibitor resistance through poorly understood me

185 convergent feature of acquired EGFR tyrosine kinase inhibitor resistance, across a spectrum of divers

186 suggesting autophagy inhibition overcame the kinase inhibitor resistance.

187 cancer patients with acquired EGFR tyrosine kinase inhibitor resistance.

188 otential therapeutic opportunity to overcome kinase inhibitor resistance.

189 ing new treatments to overcome EGFR tyrosine kinase inhibitor resistance.

190 growth inhibition in multiple EGFR tyrosine kinase inhibitor-resistant non-small-cell lung cancer mo

191 Querying the Kinase Inhibitor Resource database revealed that dasatin

192 k has been dedicated to the discovery of JAK kinase inhibitors resulting in several compounds enterin

193 hyaluronic acid (HA) in combination with Rho-kinase inhibitor (ROCK) Y-27632 for the cultivation of H

194 nd intrinsic resistance to receptor tyrosine kinase inhibitors (RTKi) represents a major hurdle in im

195 rospinal fluid penetration of the Src family kinase inhibitor saracatinib in patients with AD.

196 The TGFbetarI kinase inhibitor (SB431542) was used in palatal organ cu

197 rotein kinase/extracellular signal-regulated kinase inhibitor selumetinib.

198 a thorough characterization of the Published Kinase Inhibitor Set (PKIS), a set of 367 small-molecule

199 gether, our data suggest that JAK and Aurora kinase inhibitors should be further explored as potentia

200 neratinib, an irreversible pan-HER tyrosine kinase inhibitor, significantly improves 2-year invasive

201 ioxidant and an EGFR-specific small molecule kinase inhibitor (SMKI) could be an effective, novel the

202 ting the efficacy of the clinically approved kinase inhibitor, sorafenib.

203 Conversely, the c-Jun N-terminal kinase inhibitor SP600125 and the peroxisome proliferato

204 me dependent neuroregenerative effect of the kinase inhibitor SRN-003-556 could be quantitatively mon

205 Treatment with the KDR tyrosine kinase inhibitor SU1498 or the KDR ligand VEGFA revealed

206 in polystyrene microspheres (PE) + tyrosine kinase inhibitor SU5416 (SU) group.

207 odies, e.g., trastuzumab, and small molecule kinase inhibitors, such as lapatinib, have been develope

208 a prediction supported by the ability of the kinase inhibitor sunitinib alone and in combination with

209 respond to treatment with the multi-tyrosine kinase inhibitor sunitinib eventually relapse.

210 FR3 deletion, administration of the tyrosine kinase inhibitor sunitinib, or expression of VEGF-C/D tr

211 ) and the clinically approved antiangiogenic kinase inhibitor sunitinib, three novel dual conjugates

212 which can be amplified by the multitargeted kinase inhibitor sunitinib.

213 he main target of drugs such as the tyrosine kinase inhibitor sunitinib.

214 BC resistance to the antiangiogenic tyrosine kinase inhibitor sunitinib.

215 sive tumor, a multi-target receptor tyrosine kinase inhibitor, sunitinib base, was efficiently encaps

216 We also show that the same Syk kinase inhibitors suppress merozoite egress near the end

217 Kinase inhibitors targeting the B-cell receptor (BCR) ar

218 ll or endothelial-derived therapies-eg, with kinase inhibitors targeting tumour-associated macrophage

219 Erlotinib is an EGFR tyrosine kinase inhibitor that has shown a significant but only m

220 690693, an imidazopyridine aminofurazan-type kinase inhibitor that increases the sensitivity of the i

221 ition of midostaurin - an oral multitargeted kinase inhibitor that is active in patients with a FLT3

222 Tofacitinib is an oral Janus kinase inhibitor that is under investigation for the tre

223 Tofacitinib, an oral Janus kinase inhibitor that targets Jak1/Jak3 dependent Stat a

224 The list of kinase inhibitors that have been approved by the US Food

225 ne aminofurazans represent a family of PASTA kinase inhibitors that have the potential to be optimize

226 s of cytokine-receptor interactions, and JAK kinase inhibitors that may revolutionize therapy for T c

227 As such, small-molecule kinase inhibitors that target PASTA kinases may prove be

228 a set of 367 small-molecule ATP-competitive kinase inhibitors that was recently made freely availabl

229 Janus kinase inhibitor therapy could represent an effective ta

230 Studies of resistance to tyrosine kinase inhibitor therapy have not fully reflected this h

231 diagnosis on molecular response to tyrosine kinase inhibitor therapy in early chronic-phase CML.

232 CLC who progressed on previous EGFR tyrosine-kinase inhibitor therapy received osimertinib 80 mg oral

233 ne epidermal growth factor receptor tyrosine kinase inhibitor therapy, and T790M mutation, osimertini

234 (ALL) who progress after failure of tyrosine kinase inhibitor (TKI) -based therapy.

235 STOP second generation (2G)-tyrosine kinase inhibitor (TKI) is a multicenter observational st

236 myeloid leukemia (CML) patients on tyrosine kinase inhibitor (TKI) therapy and may promote treatment

237 Tyrosine-kinase inhibitor (TKI) therapy for human cancers is not

238 Although tyrosine kinase inhibitor (TKI) therapy has improved clinical out

239 Tyrosine kinase inhibitor (TKI) therapy has led to substantial im

240 Discontinuation of tyrosine kinase inhibitor (TKI) therapy is feasible for some pati

241 ung cancer (NSCLC) are sensitive to tyrosine kinase inhibitor (TKI) therapy, but resistance invariabl

242 e a central role in the response to tyrosine kinase inhibitor (TKI) therapy, we analyzed if IFNgamma

243 Tyrosine kinase inhibitor (TKI) treatment of chronic myeloid leuk

244 iagnosis and following conventional tyrosine kinase inhibitor (TKI) treatment.

245 bled monitoring cell sensitivity to tyrosine kinase inhibitors (TKI) - a common drug used for restori

246 The BCR-ABL specific tyrosine kinase inhibitors (TKI) changed the outcome of chronic m

247 FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibitors (TKI) have been tested extensively to

248 is currently treated with BCR-ABL1 tyrosine kinase inhibitors (TKI) in combination with chemotherapy

249 Antiangiogenic tyrosine kinase inhibitors (TKI) that target VEGF receptor-2 (VEG

250 Mutant-selective EGFR tyrosine kinase inhibitors (TKI), such as osimertinib, are active

251 e antiproliferative effects of EGFR tyrosine kinase inhibitors (TKI).

252 ls sensitive to treatment with EGFR tyrosine kinase inhibitors (TKI).

253 l pathway of acquired resistance to tyrosine kinase inhibitors (TKIs) and cytotoxic drugs in AML.

254 ermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are standard treatments for adv

255 ermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are treatment options for brain

256 Tyrosine kinase inhibitors (TKIs) are used in the clinical manage

257 insic resistance to small molecular tyrosine kinase inhibitors (TKIs) by concurrently stimulating EGF

258 /or third-generation c-Abl-specific tyrosine kinase inhibitors (TKIs) has substantially extended pati

259 CML therapy based on tyrosine kinase inhibitors (TKIs) is highly effective in inducing

260 Tyrosine kinase inhibitors (TKIs) of the EGF receptor (EGFR) have

261 Although tyrosine kinase inhibitors (TKIs) that target the kinase activity

262 plified cell lines resistant to ALK tyrosine kinase inhibitors (TKIs) underwent apoptosis upon drug w

263 ction between drug transporters and tyrosine kinase inhibitors (TKIs), which has uncovered widespread

264 is enriched following therapy with tyrosine kinase inhibitors (TKIs).

265 attenuation of sensitivity to EGFR tyrosine kinase inhibitors (TKIs).

266 f resistance against promising EGFR tyrosine kinase inhibitors (TKIs).

267 ermal growth factor receptor (EGFR) tyrosine-kinase inhibitors (TKIs).

268 leukemia (CP-CML) are treated with tyrosine kinase inhibitors (TKIs).

269 eukemia/lymphoma 2 (BCL2), and many tyrosine kinase inhibitors (TKIs).

270 dicated that targeted delivery of a tyrosine kinase inhibitor to tumors can be used in a novel synerg

271 Trials comparing the addition of tyrosine kinase inhibitors to conventional therapy are required t

272 -based design and synthesis of novel type II kinase inhibitors to overcome these mutations in KIT.

273 incompletely block mTORC1 compared with mTOR kinase inhibitors (TORKi).

274 xtending the inhibition profile of a p38 MAP kinase inhibitor toward mutant EGFR inhibition.

275 ctivated extracellular signal-related kinase kinase inhibitor trametinib.

276 (Ph(+) ALL) undergoing maintenance tyrosine-kinase inhibitor treatment, little is known about the po

277 rotein kinase/extracellular signal-regulated kinase inhibitor treatment, the overwhelming majority of

278 tations typically benefit from EGFR tyrosine kinase inhibitor treatment.

279 cancer are often resistant to EGFR tyrosine kinase inhibitor treatment.

280 opy to predict skin toxicity due to tyrosine kinase inhibitors treatment.

281 (MAPK/extracellular signal-regulated kinase kinase) inhibitor treatment, and consequently, inhibitin

282 gence of mutant clones arising from tyrosine kinase inhibitor treatments.

283 We show that the known tyrosine kinase inhibitor tyrphostinA23, which is routinely used

284 res are used as biomarkers of sensitivity to kinase inhibitors used widely to treat human cancer, but

285 Finally, oral administration of the VEGFR2 kinase inhibitor Vandetanib attenuates OA progression.

286 asatinib, a potent and specific Src tyrosine kinase inhibitor, was found to decrease the levels of be

287 Tofacitinib, an oral, small-molecule Janus kinase inhibitor, was shown to have potential efficacy a

288 Bruton tyrosine kinase inhibitors were active in progressive CLL, but ou

289 ing, small interfering RNA interference, and kinase inhibitors were used to study the molecular mecha

290 and erlotinib (EGFR small-molecule tyrosine kinase inhibitor) were marginal.

291 Midostaurin is a small-molecule kinase inhibitor with activity against the receptor tyro

292 AZD3759 is a novel EGFR tyrosine kinase inhibitor with high capability to penetrate the b

293 ed 1a (skepinone-L) as a type I p38alpha MAP kinase inhibitor with high potency and excellent selecti

294 stigation of multimodality therapy combining kinase inhibitors with additional systemic and local the

295 eted screens can successfully identify PASTA kinase inhibitors with both biochemical and antimicrobia

296 mouse model, we assessed a panel of tyrosine kinase inhibitors with different selectivity profiles.

297 yrazolo[3,4-d]pyrimidines are potent protein kinase inhibitors with promising antitumor activity but

298 emical optimization of a novel series of COT kinase inhibitors, with unprecedented nanomolar potency

299 n, was not effective, treatment with the Rho-kinase inhibitor Y-27632 reduced vessel constriction and

300 an epithelial cells in the presence of a Rho kinase inhibitor (Y-27632).