ライフサイエンスコーパス: drug combination

1 redictive of preclinical sensitivity to this drug combination.

2 evious analyses showing the efficacy of this drug combination.

3 in drug co-prescription or making fixed-dose drug combination.

4 1047R) tumor-bearing mice long term with the drug combination.

5 tory protein short, protected cells from the drug combination.

6 tration is a more important risk factor than drug combination.

7 autophagy and protected tumor cells from the drug combination.

8 s (SRL) is limiting the clinical use of this drug combination.

9 oclax, as well as radiosensitization by this drug combination.

10 type of malfunction to arrive at a suitable drug combination.

11 ry role for ROS in the efficacy of the three drug combination.

12 e metric for assessing the efficacy of novel drug combinations.

13 d to the formidable challenges of optimizing drug combinations.

14 cal trial by assessing potentially hazardous drug combinations.

15 for high-throughput screening of anticancer drug combinations.

16 peed up the entire discovery cycle of potent drug combinations.

17 ion involve inhibition of viral enzymes with drug combinations.

18 to highlight the mechanisms of action of the drug combinations.

19 model for assessing synergy in the action of drug combinations.

20 ficacy of a panel of drugs to select optimal drug combinations.

21 d the drug label to predict 1,508 novel drug-drug combinations.

22 ty about how to optimize scheduling for such drug combinations.

23 ed corresponding synergistic or antagonistic drug combinations.

24 ational design of more potent but less toxic drug combinations.

25 n of synergistic, additive, and antagonistic drug combinations.

26 matologic malignancies against a panel of 48 drug combinations.

27 llel in future trials assessing new drugs or drug combinations.

28 under treatment regimens of single drugs or drug combinations.

29 h complementary informatics tools to examine drug combinations.

30 and identifying well tolerated and effective drug combinations.

31 lity, DEB size tailored to tumor anatomy and drug combinations.

32 HSCT before resistance develops to standard drug combinations.

33 g C(max) and pharmacokinetic coordination of drug combinations.

34 means to explore the large space of possible drug combinations.

35 d prospectively to identify novel or optimal drug combinations.

36 orrect schedule, and (4) nonrecommended drug-drug combinations.

37 trinsic antiviral activity of antiretroviral drug combinations.

38 re sufficient to infer the effects of larger drug combinations.

39 ial advantage was noted with VDCR over the 3-drug combinations.

40 valuable for patient selection or choice of drug combinations.

41 challenges for making more widespread use of drug combinations.

42 olecular signaling mechanisms of synergistic drug combinations.

43 of patient sensitivity to various drugs and drug combinations.

44 n of new RXRalpha-based antitumor agents and drug combinations.

45 lls and translated these hits into effective drug combinations.

46 alog efficacy through prodrug strategies and drug combinations.

47 bination drug therapy, including non-obvious drug combinations.

48 s across seven different clinically relevant drug combinations.

49 ynamic model for both the binary and ternary drug combinations.

50 eatment of preexisting CSCs with a genotoxic drug combination (5-fluorouracil, doxorubicin, and cyclo

51 trate that neither of the major theories for drug combinations accurately predicts the combined effec

52 Drug combinations acting synergistically to kill cancer

53 fadoxine-pyrimethamine or other antimalarial drug combinations adversely affected serological respons

54 sed drugs as compared with oral antidiabetic-drug combinations among patients with a history of heart

55 how that the macaques that had received this drug combination and then stopped antiretroviral therapy

56 The primary endpoint was safety of the drug combination and to identify dose-limiting toxic eff

57 t cell lines after prolonged exposure to the drug combination and was caspase independent.

58 alistic expectations for the efficacy of new drug combinations and inform the design of trials for ne

59 nce of considering heterogeneity in choosing drug combinations and offers a principled approach towar

60 To maximize therapeutic benefit, drug combinations and schedules must be explored to iden

61 evaluating the efficacy of antituberculosis drug combinations and the gaps in the evidence base for

62 elucidates a method to identify synergistic drug combinations and translate them to in vivo by prese

63 l DRUGCOMBORANKER: to prioritize synergistic drug combinations and uncover their mechanisms of action

64 ter than existing best-in-class reactivation drug combinations (and with reduced off-target cytotoxic

65 H2AX activation was maximum with the drug combination, and unscheduled DNA synthesis induced

66 determining the optimal use of PARPi within drug combination approaches has been challenging.

67 egies may help provide rationales for future drug combination approaches with antimetastatic agents t

68 itive breast cancer, and compared with other drug combination approaches.

69 This drug combination (AraC+CHK1i+G-CSF) will open the doors

70 functional HR to FdUrd, the effects of this drug combination are more profound in tumors with HR def

71 escribe dose-dependent cellular responses to drug combinations are an essential component of computat

72 In clinical practice, the ideal and feasible drug combinations are combinations of existing Food and

73 gents continues to expand and novel targeted drug combinations are developed.

74 Data from applied drug combinations are input into the differential evolut

75 Rather, drug combinations are largely dictated by empirical or c

76 Our results illustrate how high-order drug combinations are needed to kill drug-resistant canc

77 Many drug combinations are routinely assessed to identify syn

78 onal identification methods of the effective drug combinations are usually associated with significan

79 Drug combinations are valuable tools for studying biolog

80 A total of 89% used 3-drug combination ARV regimens during pregnancy.

81 and tensin homolog were as sensitive to the drug combination as cells expressing the protein.

82 The co-delivery of drug combination at a controlled ratio via the same vehi

83 Identification of synergic drug combinations at their respective effective doses wi

84 eatment for human babesiosis consists of two drug combinations, atovaquone + azithromycin or quinine

85 evelopment while minimizing the risk of late drug combination attrition.

86 It predicts responses to drug combinations based on data for each drug acting as

87 ssion of RCC, we identified the best overall drug combination, being a mixture of four drugs (axitini

88 erapy in monotherapy as well as two to three drug combinations between the two groups.

89 ts, our algorithms not only identified known drug combinations, but also predicted novel drug combina

90 erapeutic successes have renewed interest in drug combinations, but experimental screening approaches

91 We then identify drug combinations by searching drugs whose targets are e

92 g and the question of whether one particular drug combination can be used to treat tuberculosis is le

93 ibitor imatinib mesylate confirmed that this drug combination can impact both mTORC1 and Akt signals

94 e show that the microbial responses to these drug combinations can be predicted using a simple formul

95 Three-drug combinations can control hypertension in about 90%

96 Synergistic drug combinations can lessen potential toxic side effect

97 It is expected that drug combinations can reduce drug resistance and improve

98 Finally, we evaluated the 3-drug combination clarithromycin, cefoxitin, and amikacin

99 t credentialing and validation, implementing drug combinations, clinical trial designs, targeting tum

100 a decreased flux across Caco-2 cells for the drug combinations compared to drug alone.

101 he broad applicability of the method, we use drug combinations comprising protein synthesis inhibitor

102 experimental methods in identifying optimal drug combinations, computational approaches can provide

103 We thus sought to identify drug combinations consisting of one component that would

104 Why only certain drug combinations control viral replication remains uncl

105 Sensitivity to this drug combination correlated with reduced activity of the

106 These drug combinations could directly be used on patients wit

107 istance mechanism through rational design of drug combinations could significantly enhance PI3K-targe

108 biodegradable micelles provide platform for drug combination delivery in a broad range of cancers.

109 Most importantly, the drug combination depletes FLT3/ITD(+) LSCs in a genetic

110 andomly assigned to receive ART (an approved drug combination derived from US Department of Health an

111 s may be envisioned to accelerate successful drug combination development while minimizing the risk o

112 ould be capable of comprehensively assessing drug combinations directly on patients' cellular samples

113 d also allow ready tailoring of a particular drug combination/drug release for the needs of an indivi

114 isualization, analysis and quantification of drug combination effects in terms of synergy and/or anta

115 nd CLL revealed specific patterns of ex vivo drug combination efficacy that were associated with sele

116 Even when drug combinations exhibit additivity or synergy in pre-c

117 Furthermore, cells treated with the drug combination exhibited increased promoter and gene b

118 ssed the reduction in Mcl-1 expression after drug combination exposure, and overexpression of Mcl-1 p

119 isplatin and paclitaxel, the clinically used drug combination for the treatment of advanced ovarian c

120 talk inhibition, to discover new synergistic drug combinations for breast cancer treatment.

121 tional design of nanomedicine of synergistic drug combinations for cancer therapy.

122 l treatment based on curated, individualized drug combinations for each patient (patient-centric appr

123 nce it is impractical to screen all possible drug combinations for every indication, computational me

124 we prioritize approximately 10(5) human TSG-drug combinations for future follow-up.

125 erturbations, enabling derivation of optimal drug combinations for heterogeneous tumors comprising di

126 es not reside within the most broadly useful drug combinations for heterogeneous tumors.

127 a protocol for the discovery of synergistic drug combinations for the treatment of disease.

128 e computational approach to search effective drug combinations from the enormous number of possibilit

129 odel to recognize the synergistic effects of drug combinations from the molecular response profiles,

130 llow users to iteratively search for optimal drug combinations given a user-defined gene set.

131 on the same IgG framework and small molecule drug combination has shown a very similar distribution o

132 The systematic identification of effective drug combinations has been hindered by the unavailabilit

133 Nanomedicine of synergistic drug combinations has shown increasing significance in c

134 Prediction of synergistic effects of drug combinations has traditionally been relied on pheno

135 RNAi-chemotherapeutic drug combinations have also been found to be effective a

136 In addition, the drug combination (i.e. lapatinib plus YM155) decreased n

137 er-soluble anticancer agents and delivery of drug combinations (i.e. multi-drug delivery) that seeks

138 refocused the interest of scientists toward drug combinations, ie, treating with TKIs and simultaneo

139 e available data support the evaluation of a drug combination in a larger population as a fixed-dose

140 Binary drug combination in cl-micelles exhibited synergistic cy

141 ounds of assaying to identify an optimal tri-drug combination in eight distinct chemoresistant bladde

142 anoid libraries in evaluating inhibitors and drug combinations in a preclinical setting.

143 viability responses of many single drug and drug combinations in agreement with experimental data.

144 rongest signal, we evaluate thousands of TSG-drug combinations in HeLa cells, resulting in networks o

145 an effective strategy to screen synergistic drug combinations in high-throughput and a CRISPR-based

146 , on a much larger drug combination set (245 drug combinations in our dataset compared to 75 in previ

147 he predicted mechanisms, we further screened drug combinations in silico and found that a promising d

148 explain the superiority of many FDA-approved drug combinations in the absence of drug synergy or addi

149 s as either single agents or in 768 pairwise drug combinations in TNBC cell lines to identify synergi

150 omosomal instability and in synthetic lethal drug combinations inspire optimism that CDK inhibitors w

151 and which one is dominant for a given tumor-drug combination is not known.

152 The discovery of anti-resistance drug combinations is challenging as resistance can arise

153 Although the number of possible drug combinations is extensive, a series of principles c

154 ancers, but direct screening of all possible drug combinations is infeasible.

155 However, the search space of drug combinations is large, making the identification of

156 The clinical development of drug combinations is typically achieved through trial-an

157 Drug co-prescription (or drug combination) is a therapeutic strategy widely used

158 vincristine, and dactinomycin (IVA) or a six-drug combination (IVA plus carboplatin, epirubicin, and

159 Synergistic drug combinations lead to the use of drugs at lower dose

160 adenine or knock down of Beclin1 suppressed drug combination lethality by approximately 50%.

161 maH2AX and CHK2 phosphorylation and enhanced drug combination lethality.

162 nd to a lesser extent activated mTOR reduced drug combination lethality.

163 related gene long isoform, protected against drug combination lethality.

164 me 10) function were relatively resistant to drug combination lethality; expression of PTEN in PTEN-n

165 (PTEN) function were relatively resistant to drug combination lethality; expression of PTEN in PTEN-n

166 identify the positive hits among the entire drug combination library in a parallel and rapid manner.

167 ter that can be used to identify problematic drug combinations matrices and prevent further analysis

168 of action." We show that certain synergistic drug combinations may act as a more potent version of a

169 We applied EPN to our generated pairwise drug combination microarray data.

170 drug concentrations and selecting antiviral drug combinations most likely to suppress resistance.

171 therapy and to enable delivery of the unique drug combinations needed for personalized medicine.

172 Twenty (63%) reported at least 1 pathogen-drug combination not recommended for primary or suppleme

173 INTERPRETATION: The two-drug combination of all-injectable, long-acting cabotegr

174 nly highlight the potential of a synergistic drug combination of allosteric PARP inhibitors with DNA-

175 cyclophosphamide) should be offered a three-drug combination of an NK1 receptor antagonist, a 5-HT3

176 The redeployed drug combination of bezafibrate and medroxyprogesterone

177 A redeployed drug combination of bezafibrate and medroxyprogesterone

178 Importantly, our data suggest a novel drug combination of Gli1 and Top1 inhibitors as an effec

179 The three-drug combination of lenalidomide, bortezomib, and dexame

180 ed the outcomes of VEC chemotherapy with a 5-drug combination of vincristine and carboplatin, alterna

181 eatment strategy for ovarian cancer based on drug combinations of cytotoxic agents and molecular targ

182 strategies for ovarian cancer focus on novel drug combinations of cytotoxic agents and molecular targ

183 15 years, large-scale manufacture of 2 or 3 drug combinations of HCV DAAs is feasible, with minimum

184 -1 mRNA and virion production, we compared 2-drug combinations of leading candidate LRAs and identifi

185 k is needed to further delineate the optimal drug, combination of agents, or sequence best suited to

186 iation of current exposure to antiretroviral drug combinations on risk of cardiovascular events inclu

187 aracterize the association of antiretroviral drug combinations on risk of cardiovascular events.

188 2 tumor spheroids, whereas single drugs or 2-drug combinations only slowed growth of ES-2 tumor spher

189 The development of drug combinations or novel antifungal drugs to address e

190 ts, identifying well tolerated and effective drug combinations or sequences, and determining the role

191 The ability to assess drug combinations other than tofacitinib plus methotrexa

192 A multi-drug combination, particularly including a thiazide diur

193 ng one of these associations, we validated a drug combination predicted to overcome resistance to MEK

194 there is a great need of new algorithms for drug combination prediction.

195 Our drug combination preserves the structure of the existing

196 ffective approach to examine novel drugs and drug combinations prior to animal testing.

197 Eight weeks of the drug combination produced an SVR12 in 17 of 17 (100%) pa

198 This triple-drug combination prolonged the median overall survival f

199 neity essentially homogenizes the benefit of drug combinations, reducing the special advantage of a p

200 oposed program led to the development of a 3-drug combination regimen for children from scratch, inde

201 , but a metric for the antiviral activity of drug combinations relative to a target value needed for

202 two macaques that had received the complete drug combination remained healthy and did not develop AI

203 The best drug combination remains to be determined.

204 Currently approved drug combinations result largely from empirical clinical

205 The removal of AZD4547 from the optimized drug combination resulted in 80% of cell viability inhib

206 ced when, on the basis of a matrix screen of drug combinations, ruxolitinib was combined with the Bcl

207 ld be given to the identification of optimal drug combination(s) for the treatment of all forms of tu

208 s biology approaches to identify synergistic drug combination(s) that can mimic RAS inhibition.

209 ma and BRAFi-resistant melanoma models, this drug combination safely and significantly extended host

210 Applying a systematic pairwise drug combination screen we observed a highly potent syne

211 ppropriate determination of the quality of a drug combination screen.

212 cer cells, and they also show how systematic drug combination screening together with a molecular und

213 ogy approach to studying drug resistance and drug combination selection.

214 The time has now come to define the optimal drug combinations, sequence of treatment, and drug regim

215 0.69 in a previous method, on a much larger drug combination set (245 drug combinations in our datas

216 The drug combination significantly delayed the onset of epil

217 Most 2-drug combinations similarly reduce hemoglobin A(1c) leve

218 valuate and cross-compare multiple drugs and drug combinations simultaneously in living tumors and ac

219 In drug combination studies, compound 15 showed good effica

220 plore pharmacokinetic optimization, rational drug combinations, synthetic lethality strategies, novel

221 nations in silico and found that a promising drug combination targeting ERK1/2 and NFkappaB might red

222 1 :aa3 , as well as for the development of a drug combination targeting oxidative phosphorylation in

223 om GABAergic drugs enables, at least for the drug combinations tested, a straightforward method to ac

224 understanding of drug function, and limited drug combination testing.

225 nel, we evaluated RAS pathway inhibitors and drug combinations that are currently in clinical trial f

226 drug combinations, but also predicted novel drug combinations that are worth further testing.

227 platform that facilitates rapid discovery of drug combinations that can overcome resistance.

228 First, the use of drug combinations that include bedaquiline might prevent

229 oing in our laboratory to identify effective drug combinations that include JQ1.

230 ombinations and their translation into novel drug combinations that modulate complex human disease ph

231 es, yet the systematic discovery of gene and drug combinations that modulate these phenotypes in huma

232 plus paclitaxel represent highly synergistic drug combinations that should be explored further in the

233 an enrichment of anti-inflammatory drugs in drug combinations that synergize against HIV.

234 Such results might be expected if drug combinations that synergize in sensitive tumor cell

235 ate environment-mediated drug resistance and drug combinations that target it.

236 , it may be possible to rationally construct drug combinations that yield more penetrant and lasting

237 After 72 h of incubation with the drug combinations, the resulting overconsumption of ATP

238 ombination therapy (NECT) and other anti-HAT drug combination therapies (CTs) on radiolabelled-nifurt

239 has implications on the choice and timing of drug combination therapies.

240 vely evaluated the induction of apoptosis by drug combination therapies.

241 to BETi and 2) inform the rational design of drug combination therapies.

242 ate the desired therapeutic effects of other drugs (combination therapies).

243 superior therapeutic benefits to the current drug combination therapy used in clinical practice.

244 A two-drug combination therapy where one drug targets an offen

245 applying nanocarriers to improve anticancer drug combination therapy, review the use of nanocarriers

246 For patients who start triple-drug combination therapy, we find that drug resistance e

247 improved efficacy in clinical trials of new drug combinations, thereby increasing the survival of pa

248 was consistent with the ability of the same drug combination to abolish acantholysis in mouse skin.

249 es provide evidence of the potential of this drug combination to eliminate FLT3/ITD(+) LSCs and reduc

250 ciency) mice also revealed the ATRA plus TCP drug combination to have a potent anti-leukemic effect t

251 in the clinic, the quickest way to move the drug combination to patients would be to combine these a

252 This approach will likely require effective drug combinations to achieve high levels of latency reve

253 us opening a promising approach to translate drug combinations to clinically viable treatment regimen

254 d tested 10 drugs in all permutations of two-drug combinations to define synergistic combinations by

255 apeutic antibody in vivo and suggest various drug combinations to enhance antibody activity and to ov

256 pathways, with implications on how to tailor drug combinations to improve therapeutic efficacy.

257 Furthermore, they can suggest drug combinations to increase efficacy and combat acquir

258 nd explore how they may relate to successful drug combinations to overcome acquired resistance to can

259 m for preclinical testing of novel drugs and drug combinations to treat ALL.

260 tic and comprehensive method to find optimal drug combinations to use in children, ideal exposures, a

261 e case studies discovered a set of effective drug combinations top ranked in our prediction list, and

262 s-associated death domain protein suppressed drug combination toxicity.

263 This drug combination transiently administered for 2 weeks du

264 By immunohistochemical analysis, in drug combination-treated cells, microtubule-associated p

265 protein/78-kDa glucose-regulated protein, in drug combination-treated cells.

266 iotic dosages so low that the equivalent two-drug combination treatments are ineffective.

267 mirrored the patterns of response to several drug combination treatments, suggesting that the activit

268 and neck, and discuss directions for future drug combination trials and biomarkers to use with drugs

269 son of the inhibitory potential of different drug combinations under clinical concentrations, reconci

270 Triple drug combinations using colistin, tigecycline, and imipe

271 chronized co-delivery of the platinum-taxane drug combination via single carrier to the same targeted

272 nd disappeared when the otherwise successful drug combination was applied to the same NSCLC cancer im

273 un NH(2)-terminal kinase 1/2 (JNK1/2) by the drug combination was enhanced by radiation, and signalin

274 The triple-drug combination was not more active than cefoxitin alon

275 This drug combination was recently approved by the U.S. Food

276 ohort, exposure to both individual drugs and drug combinations was associated with modestly increased

277 To develop novel drug combinations, we conducted a synthetic lethal siRNA

278 teps in this circuit with rationally applied drug combinations, we demonstrate the potential of combi

279 To identify novel and effective drug combinations, we performed ex vivo sensitivity prof

280 evels at the end of 2-minute applications of drug combinations were >10% of the peak response to satu

281 Only 9 drug combinations were assessed on >1 phase 2A endpoint

282 Second, 2-drug combinations were examined for zones of synergy, an

283 Multiple effective drug combinations were identified.

284 The associations for some tissue-drug combinations were remarkably strong, with genetic l

285 These optimized drug combinations were significantly more potent than mo

286 The organism-drug combinations were Staphylococcus epidermidis and va

287 Drug combinations were tested in various therapy-resista

288 Ten novel drug combinations were validated experimentally, and sev

289 pared with those receiving oral antidiabetic-drug combinations, were estimated by means of conditiona

290 m two patients exhibited unique responses to drug combinations when cultured on the drug-eluting micr

291 These complexities mandate the study of drug combinations, which will also become necessary to r

292 Ultimately, the hope is that drug combinations will be selected based on biomarkers,

293 and anticoagulant therapy evolves, potential drug combinations will multiply, introducing variability

294 ent subpopulations, for both monotherapy and drug combinations, will be important.

295 dy identifies a rapid approach to assess the drug combinations with a mechanistic basis for selection

296 We find that it is often better to use drug combinations with matched penetration profiles, alt

297 rable challenges for the design of effective drug combinations with predictable outcomes.

298 by using an in vitro system may define novel drug combinations with significant in vivo activity.

299 ignificant increase in the use of ezetimibe, drug combinations with statins, and maximal LLT.

300 Guidelines suggest avoiding certain drug combinations, yet little is known about the magnitu