ライフサイエンスコーパス: combination therapy

1 000 mg daily) and prednisolone (5 mg daily) (combination therapy).

2 l patients who received at least one dose of combination therapy.

3 am monotherapy or beta-lactam plus macrolide combination therapy.

4 eated with peginterferon/nucleotide analogue combination therapy.

5 (28.1%) received beta-lactam plus macrolide combination therapy.

6 patients may continue to derive benefit from combination therapy.

7 30294 to anti-TNF monotherapy, and 14229 to combination therapy.

8 will be required if benznidazole is used in combination therapy.

9 in a cohort matched by propensity to receive combination therapy.

10 l days 3 to 7 and within 2 days of receiving combination therapy.

11 schedule to enhance the effectiveness of the combination therapy.

12 improved disease-free survival observed with combination therapy.

13 d IV vancomycin plus piperacillin/tazobactam combination therapy.

14 s simplex virus-1 (oHSV-1) and PD-1 blockade combination therapy.

15 geting multimodal imaging-guided synergistic combination therapy.

16 y, underlining that BB is the key element of combination therapy.

17 umors resistant to single-agent or cisplatin combination therapy.

18 serve as an important therapeutic agent for combination therapy.

19 ring, antithrombotic therapy, and fixed-dose combination therapy.

20 ing anti-cancer drugs, and opportunities for combination therapy.

21 e immune-boosting and therapeutic effects of combination therapy.

22 openem percentage of time above MIC >60%, in combination therapy.

23 effective, well tolerated artemisinin-based combination therapy.

24 intended Kv11.1 blockers via pharmacological combination therapy.

25 rable potential especially in the setting of combination therapy.

26 tumor-associated antigens to T cells in this combination therapy.

27 lly relevant regimens of RBV and IFN alfa as combination therapy.

28 oma, with 1 pneumonitis-related death during combination therapy.

29 and LDR, to explain the cellular response to combination therapy.

30 ported anti-PD-L1 plus olaparib or cediranib combination therapy.

31 ivolumab monotherapy and 40.0% and 54.9% for combination therapy.

32 despread use of small-molecule antimicrobial combination therapy.

33 s of MDB5 leaving a platform for mono and/or combination therapy.

34 KWAR23 represents a promising candidate for combination therapy.

35 ivity are desired as high-value partners for combination therapies.

36 y should be conducted prior to proceeding to combination therapies.

37 , underscoring the need for improvement with combination therapies.

38 measured after exposure to monotherapies and combination therapies.

39 ret trial data and a different way to design combination therapies.

40 eatment with alternative MEK inhibitor-based combination therapies.

41 em of acquired drug resistance is to rely on combination therapies.

42 often predicting nonintuitive strategies for combination therapies.

43 d safety profiles and flexibility for use in combination therapies.

44 biomarkers that may benefit from the use of combination therapies.

45 cancer for the development of more effective combination therapies.

46 e face of emerging resistance to artemisinin combination therapies.

47 een reduced in part due to artemisinin-based combination therapies.

48 polymyxins and the need to explore effective combination therapies.

49 rposing as a cost-effective component of HCV combination therapies.

50 antimalarial agents, either as standalone or combination therapies.

51 ore, there is a need for rationally designed combination therapies.

52 clinically relevant biomarkers and trials of combination therapies.

53 eted drugs and potentially for the design of combination therapies.

54 ate to the introduction of artemisinin-based combination therapies.

55 justed OR 1.42, 95% CI 1.25-1.62; p<0.0001), combination therapy (1.26, 1.08-1.47; p=0.0038), and hav

56 tio [OR] 2.23, 95% CI 1.59-3.12); p<0.0001), combination therapy (1.53, 1.13-2.07; p=0.054), and have

57 lus trametinib at a dose of 2 mg once daily (combination therapy, 438 patients) or two matched placeb

58 We stratified analyses of combination therapy according to INCREMENT-CPE mortality

59 ally limiting the success of allogeneic cell combination therapy (ACCT).

60 The synergistic combination therapy achieved effective local and distant

61 Despite the widespread adoption of combination therapy across diseases, drug resistance rat

62 nin (ART) and its partner drugs in ART-based combination therapies (ACT) is threatening the efficacy

63 Artemisinin-based combination therapy (ACT) is the first-line treatment of

64 Administration of artemisinin-based combination therapy (ACT) to infant and young children c

65 a treatment, the so-called Artemisinin-based Combination Therapy (ACT).

66 Artemisinin-based combination therapies (ACTs) are the mainstay of the cur

67 Artemisinin-based combination therapies (ACTs) are the most effective trea

68 Artemisinin-based combination therapies (ACTs) have been widely adopted as

69 lies almost exclusively on artemisinin (ART) combination therapies (ACTs) in endemic regions.

70 its efficacy with that of artemisinin-based combination therapies (ACTs) in Latin America.

71 The global adoption of artemisinin-based combination therapies (ACTs) in the early 2000s heralded

72 ere randomized to receive 1 of 3 artemisinin combination therapies (ACTs) with or without primaquine

73 erapy, globally reliant on artemisinin-based combination therapies (ACTs), is threatened by the sprea

74 nd spread of resistance to artemisinin-based combination therapies (ACTs).

75 semisynthetic analogs), known as artemisinin combination therapies (ACTs).

76 oor residual spraying (IRS), and artemisinin combination therapies (ACTs).

77 uction for first 12 weeks, re-intensified to combination therapy after week 96; protease inhibitor mo

78 udy anti-HBV immune responses and screen for combination therapies against hepatotropic viruses.

79 eagues propose deploying multiple first-line combination therapies against malaria within a community

80 for preclinical development of innovative AG combination therapies against resistant TB.

81 (aHR, 2.41; 95% CI, 1.60-3.64; P < .001), or combination therapy (aHR, 6.11; 95% CI, 3.46-10.8; P < .

82 am monotherapy vs beta-lactam plus macrolide combination therapy among a cohort of children hospitali

83 By using combination therapies and correlating response to gene e

84 ving appropriate therapy, 135 (39%) received combination therapy and 208 (61%) received monotherapy.

85 We used a propensity score for receiving combination therapy and a validated mortality score (INC

86 an the individual cytokines or IL4 plus IL10 combination therapy and also inhibited allodynia in a mo

87 ically model the dynamics of CML response to combination therapy and analyze the impact of combinatio

88 influence the use of anti-VISTA antibody in combination therapy and how genomic analysis may assist

89 the feasibility of triazole dose escalation, combination therapy, and prophylaxis were explored as st

90 or patients are eligible for immuno-targeted combination therapy, and they suggest prioritizing speci

91 This combination therapy approach might provide a new treatme

92 Artemisinin-based combination therapies are the first line of treatment fo

93 Artemisinin (ART)-based combination therapies are the most efficacious treatment

94 m monotherapy and beta-lactam plus macrolide combination therapy are both common empirical treatment

95 died, but the processes governing successful combination therapy are poorly understood.

96 markers that predict failure of artemisinin combination therapy are urgently needed to monitor the s

97 cin plus 1 other antipseudomonal beta-lactam combination therapy at 1 of 6 large children's hospitals

98 age ICS plus long-acting beta2 agonist fixed-combination therapy at screening, had a morning prebronc

99 rly case management with quality artemisinin combination therapies (avoiding artesunate monotherapies

100 e genes are attractive candidate targets for combination therapy because they are essential in breast

101 c antibodies show great promise as intrinsic combination therapies, but often suffer from poor physio

102 This local, triple-combination therapy can be adapted to other cancer cell

103 g new approaches to treating ARDS, including combination therapies, cell-based therapies, and generic

104 antimalarial therapy, including artemisinin combination therapy, chloroquine, and sulfadoxine-pyrime

105 n able to swallow received artemisinin-based combination therapy (Coartem).

106 benefits of beta lactam plus aminoglycoside combination therapy compared to beta lactam monotherapy

107 ble tumor in bone was significantly less for combination therapy compared with control (P = .02), SPI

108 fatal stroke, the relative risk reduction of combination therapy compared with monotherapy differed b

109 Empirical macrolide combination therapy conferred no benefit over beta-lacta

110 We aimed to assess whether ultra-low-dose combination therapy could meet these needs.

111 tor pathways, particularly in the setting of combination therapies, could become a valuable immunosup

112 Combination therapy coupling autophagy inhibition and TA

113 with a modest increase in artemisinin-based combination therapy coverage (3.56 percentage point incr

114 Combination therapies deemed immediately tractable to tr

115 issue of Cancer Cell, Pan et al. show that a combination therapy designed to reactivate the p53 tumor

116 lecular basis for patient stratification and combination therapy development.

117 Response to combination therapy did not appear to be associated with

118 ith 329 overall survival events (75.3%), the combination therapy did not provide a survival advantage

119 Mechanistically, combination therapy efficacy stemmed from the upregulati

120 ma treatment and provide a rationale to test combination therapies employing CXCR4 and BCL-2 inhibito

121 atients, but some patients treated with this combination therapy experience early relapse.

122 to disrupt oncogenic NF-kappaB signaling in combination therapies for malignant brain tumors.

123 evidence of the safety of artemisinin-based combination therapies for the treatment of malaria durin

124 Patients were eligible if they received combination therapy for >/=48 hours.

125 x holds promise as a novel, exclusively oral combination therapy for a subset of high-risk DLBCL pati

126 treatment option and suggests advantages of combination therapy for CCM disease.

127 e clinical translation of PDT and irinotecan combination therapy for effective pancreatic cancer trea

128 in the future to tailor the L. lactis-based combination therapy for individual patients.

129 These findings might be useful in developing combination therapy for MDR cancer treatment.

130 orable safety and efficacy profile of E10030 combination therapy for nAMD was evident across multiple

131 y of ceftazidime/avibactam plus aztreonam as combination therapy for S. maltophilia infections and co

132 of aspirin and PI3K pathway inhibitors as a combination therapy for targeting breast cancer.

133 These studies identify an effective combination therapy for the most aggressive form of MB.

134 his strategy using molecularly targeted oral combination therapy for the treatment of chemotherapy-re

135 re clinical evaluation of ELQ and atovaquone combination therapy for treatment of human babesiosis.

136 therapy regimens (one or more platinum based combination therapies) for stage IIIB or IV non-small-ce

137 ed treatment, fewer patients had died in the combination therapy group (3 [1%] of 302 patients) compa

138 from baseline was noted in the E10030 1.5 mg combination therapy group compared with the anti-VEGF mo

139 al acuity outcomes favored the E10030 1.5 mg combination therapy group regardless of baseline VA, les

140 rate of relapse-free survival was 58% in the combination-therapy group and 39% in the placebo group (

141 3-year overall survival rate was 86% in the combination-therapy group and 77% in the placebo group (

142 freedom from relapse were also higher in the combination-therapy group than in the placebo group.

143 Patients who responded to combination therapy had increased CD8(+) T cells, elevat

144 The administration of antifungal combination therapy had no apparent impact on outcome.

145 enhancing CAR T-cell responses and that this combination therapy has high translational potential, gi

146 Multimodal imaging-guided synergistic combination therapy has shown great potential for cancer

147 However, this combination therapy has significant limitations due to r

148 ric mouse model of mCRPC to efficiently test combination therapies in an autochthonous setting.

149 translate clinically and that the results of combination therapies in mouse models or human clinical

150 perative genes and provide novel insights to combination therapies in personalized cancer medicine.

151 e, causing high failure rates of artemisinin combination therapies in some areas.

152 c denervation alone in 18 (3%) patients, and combination therapy in 166 (27%) patients.

153 treatment failures with an oral artemisinin combination therapy in a pre-artemisinin resistant P. fa

154 follow-up to date with BRAF + MEK inhibitor combination therapy in BRAF V600-mutant MM.

155 p53, which may potentially be exploited for combination therapy in GBM and possibly other malignanci

156 namics, and efficacy of lumacaftor/ivacaftor combination therapy in patients aged 6-11 years with cys

157 s is the longest follow-up for NIVO plus IPI combination therapy in patients with advanced melanoma.

158 s warrant the clinical investigation of this combination therapy in patients with NF1 mutant melanoma

159 non-inferior to adalimumab and methotrexate combination therapy in the treatment of rheumatoid arthr

160 about the routine empirical use of macrolide combination therapy in this population.

161 onstrated the critical importance of initial combination therapy in treatment-naive patients.

162 y examines the potency of neoadjuvant TSL HT combination therapy in two orthotopic mouse models of hu

163 Mycophenolate mofetil (MMF) and combination therapies including MMF, at serum trough lev

164 Combination therapy, including inhaled corticosteroids a

165 Combination therapy induced CD8(+) T lymphocyte-dependen

166 Paclitaxel and rubone combination therapy inhibited tumor cell growth, migrati

167 geting, desirable drug release kinetics, and combination therapies into LbL nanomaterials.

168 with PI3K inhibitors and nominate potential combination therapies involving PI3K inhibition.

169 suggesting that either single-agent ATRi or combination therapy involving ATRi might be further asse

170 Combination therapy involving strategies to expand myelo

171 I, 0.27-0.55), and 14 in patients exposed to combination therapy (IR, 0.95; 95% CI, 0.45-1.45).

172 Identification of effective combination therapies is critical to address the emergen

173 rtant determinants of cancer evolution under combination therapies is therefore crucial for correctly

174 Combination therapy is deployed for the treatment of mul

175 In conclusion, bendamustine-rituximab combination therapy is highly efficient, sufficiently sa

176 The number of studies on combination therapy is limited.

177 Combination therapy is one of the most effective tools f

178 defined, based on which a broadly applicable combination therapy is proposed to combat the pathologic

179 nts with preserved liver function (Child A), combination therapy is recommended because it is more ef

180 bility of highly effective artemisinin-based combination therapies, it is time to reconsider first-tr

181 Combination therapy likely represents the best approach

182 provers, suggesting that immunomodulatory or combination therapy may have benefitted these patients.

183 ildren receiving beta-lactam monotherapy and combination therapy (median, 55 vs 59 hours; adjusted ha

184 These data indicate that initial combination therapy might be associated with a survival

185 active monotherapy (only one active drug) or combination therapy (more than one).

186 rapy (n = 506) vs beta-lactam plus macrolide combination therapy (n = 566), with an absolute adjusted

187 sion who were randomly assigned and received combination therapy (n=302) or monotherapy (n=303; 152 p

188 These data provide a rationale to explore combination therapy of adoptive HSPC-NK cells and DAC in

189 in decreased tumor growth kinetics, whereas combination therapy of aspirin and a PI3K inhibitor furt

190 Combination therapy of ceftriaxone and lansoprazole is a

191 results provide a mechanistic rationale for combination therapy of CXCR4 and BCL-2 inhibitors to tre

192 Recent clinical studies on combination therapy of decitabine (DAC) and arsenic trio

193 favorable short-term safety profile for the combination therapy of E10030 and ranibizumab.

194 Combination therapy of ISF35 with systemic anti-PD-1 gen

195 Here we show that a combination therapy of low-dose anti-CD3 with a clinical

196 six animals per group were treated with (a) combination therapy of magnetic resonance imaging heatin

197 x regression models revealed that TACE and a combination therapy of TACE and sorafenib were significa

198 ct of appropriate therapy and of appropriate combination therapy on mortality of patients with bloods

199 apy consisting of beta-lactam plus macrolide combination therapy or fluoroquinolone monotherapy initi

200 ty was not different between those receiving combination therapy or monotherapy (47 [35%] of 135 vs 8

201 amantadine (100 mg), and ribavirin (600 mg) combination therapy or oseltamivir monotherapy twice dai

202 However, whether combination therapy or statin alone resulted in cardiova

203 purine monotherapy, anti-TNF monotherapy, or combination therapy, or being unexposed.

204 Taken together, we conclude that combination therapy potently reverses immunosuppression

205 ither cell line was observed suggesting this combination therapy primarily targets lipid biosynthesis

206 Combination therapy programs are the hallmark of the suc

207 Combination therapy protected 100% of mice, even when de

208 recent studies highlighting the potential of combination therapies recruiting both innate and adaptiv

209 The E10030 (1.5 mg) combination therapy regimen met the prespecified primary

210 The benefits of 3-d artemisinin combination therapy regimens to treat malaria in early p

211 Mechanistically, combination therapy relies on the interdependence betwee

212 Gemcitabine, as a single agent or in combination therapy, remains the frontline chemotherapy

213 This combination therapy represents an important advance in t

214 s within 10 days of acute coronary syndrome, combination therapy seemed to be more effective than mon

215 g resistance to partner drugs in artemisinin combination therapies seriously threatens global efforts

216 hway such as Raf and SphK1, we conclude that combination therapy should be much more effective in blo

217 nt longitudinal data from patients receiving combination therapy show that the 3-year survival rate i

218 Eyes that received combination therapy showed a trend toward thickening of

219 Sequential monotherapy (strategy 1), step-up combination therapy (strategy 2), or initial combination

220 ) + monthly sham intraocular injections; (2) combination therapy: subcutaneous AKB-9778 15 mg BID + m

221 Further refinements in combination therapies such as algorithms consisting of l

222 Preliminary studies of DAA combination therapies suggest improved response rates, a

223 d MEK inhibitors aligned to standard-of-care combination therapy, suggesting these reprogramming even

224 Combination therapies targeting multiple pathways can au

225 Combination therapies targeting multiple recovery mechan

226 amplification might benefit from epigenetic combination therapy targeting both the KDM5A demethylase

227 Our results indicate that combination therapy targeting the ETC can be exploited t

228 Pneumonitis was more frequent during combination therapy than monotherapy for all-grade (6.6%

229 er medication, and this risk was higher with combination therapy than with each of these treatments u

230 These findings highlight the potential of combination therapies that enhance PP2A and inhibit prot

231 al cells and utilize them to design targeted combination therapies that maximize sensitivity over tum

232 pave the way for identifying new targets for combination therapies that overcome resistance to curren

233 algorithms provide a framework for design of combination therapy that tackles tumor heterogeneity whi

234 CL6 is a new therapeutic target in NSCLC and combination therapy that targets multiple vulnerabilitie

235 e antimalarial treatments, ACTs (artemisinin combination therapies), the discovery of novel chemical

236 g-term clinical utility of artemisinin-based combination therapies, the cornerstone of modern day mal

237 ore, using cell-specific models, we tailored combination therapies to individual cell lines and succe

238 xic effects of PARP inhibition, and point at combination therapies to potentiate PARP inhibitor treat

239 Additional investigations including combination therapy to augment response rates and durabi

240 uation of anti-TNF therapy or switching from combination therapy to monotherapy may be considered in

241 tients with lymphoma and are being tested in combination therapy trials with other immunomodulatory a

242 d risk of rebleeding and death compared with combination therapy, underlining that BB is the key elem

243 ions uniformly treated with current standard combination therapies used in colon cancer (CC).

244 ors and proved safer and more effective than combination therapy using unmodified myxoma and systemic

245 ess, intensive care unit status, duration of combination therapy, vancomycin dose, and number of conc

246 rafenib (D) and MEK inhibitor trametinib (T) combination therapy versus D monotherapy in the randomiz

247 The risk was higher in patients exposed to combination therapy vs those exposed to thiopurine monot

248 Combination therapy was additive for the total replicon

249 , IV vancomycin plus piperacillin/tazobactam combination therapy was associated with higher odds of A

250 Combination therapy was associated with improved surviva

251 Combination therapy was associated with low-grade toxic

252 However, combination therapy was associated with lower mortality

253 -term safety profile of lumacaftor/ivacaftor combination therapy was consistent with previous RCTs.

254 INTERPRETATION: Tofacitinib and methotrexate combination therapy was non-inferior to adalimumab and m

255 safety and efficacy of lumacaftor/ivacaftor combination therapy was shown in two randomised controll

256 Combination therapy was superior to placebo in MADRS res

257 of cancer cases that might benefit from such combination therapy, we conducted an exploratory study o

258 To understand the rationale of combination therapy, we investigated Sini Decoction, a w

259 oral agents, insulin monotherapy and insulin combination therapy were 2.9%, 60.5%, 11.5%, and 25.1%,

260 rtraline monotherapy, and lithium/sertraline combination therapy were associated with similar switch

261 l of 1915 hospitalized children who received combination therapy were identified.

262 ognizant of the potential added risk of this combination therapy when making empirical antibiotic cho

263 A two-drug combination therapy where one drug targets an offending

264 s displayed profiles that could benefit from combination therapy, which corresponded to approximately

265 ty of malignancies and argue that customized combination therapies will be essential to optimize canc

266 zid monotherapy, rifampicin monotherapy, and combination therapies with 3 to 4 months of isoniazid an

267 al therapeutic strategy to be implemented in combination therapies with anti-CD20 monoclonal antibodi

268 gies to be used either as single-agent or in combination therapies with chemotherapeutics or radiothe

269 ntial predictors of response to short-course combination therapies with direct-acting antiviral drugs

270 dulated other signaling pathways, suggesting combination therapies with inhibitors of these pathways.

271 useful in developing new rationally designed combination therapies with sorafenib.

272 receiving monotherapy, individuals receiving combination therapy with a baseline eGFR of 60 ml/min pe

273 ent strategies against each other, including combination therapy with a biologic and immunomodulator

274 domly assigned in a 2:1:1 ratio and received combination therapy with ambrisentan and tadalafil, ambr

275 Combination therapy with amphotericin and flucytosine is

276 Conversely, nonbiologic combination therapy with azathioprine exhibited the high

277 Effects of combination therapy with benznidazole and posaconazole h

278 e introduction of early immunosuppression or combination therapy with biologicals in high-risk patien

279 uration NUC therapy and which should receive combination therapy with both NUC and pegylated interfer

280 In preclinical studies, combination therapy with compound 7 and gammadelta T cel

281 Adjuvant use of combination therapy with dabrafenib plus trametinib resu

282 elalisib monotherapy followed by 6 months of combination therapy with idelalisib and the anti-CD20 an

283 Combination therapy with IFN-beta-1a (Avonex) and mycoph

284 Combination therapy with intranasal corticosteroid plus

285 However, promising data on the use of combination therapy with lenalidomide, bortezomib, and d

286 cantly longer overall survival occurred with combination therapy with nivolumab plus ipilimumab or wi

287 ed with talimogene laherparepvec followed by combination therapy with pembrolizumab.

288 S-mTOR signaling and is prevented by upfront combination therapy with PLX8394 and either an EGFR or m

289 combination therapy (strategy 2), or initial combination therapy with prednisone (strategy 3) or with

290 es, multiple fractionated administration and combination therapy with radiation sensitizers, chemothe

291 hermia alone, and phosphate-buffered saline, combination therapy with RF hyperthermia and chemotherap

292 drug isoniazid, both as a monotherapy and in combination therapy with rifampicin.

293 Combination therapy with rituximab enhanced activity in

294 drug, photosensitizer and light irradiation, combination therapy with SN-38-encapsulated nanoporphyri

295 providing a potential therapeutic target for combination therapy with TAE.

296 ntrolled, parallel-group trial, we evaluated combination therapy with tezacaftor and ivacaftor in pat

297 Combination therapy with the BRAF inhibitor dabrafenib p

298 istered patients with leprosy should receive combination therapy with three antibiotics: rifampicin,

299 he incidence of AKI among patients receiving combination therapy with VPT to a matched group receivin

300 Further, our data suggest combination therapy with WNT and SHH inhibitors as a the