ライフサイエンスコーパス: BMS

1 BMS and DES offer good clinical outcomes in this age gro

2 BMS, Pfizer, Boehringer Ingelheim, Roche Diagnostics.

3 BMS-663068 is an oral prodrug of BMS-626529, an attachme

4 BMS-681 inhibits chemokine binding by occupying the orth

5 BMS-791325 is a novel direct antiviral agent specificall

6 BMS-816336 (6n-2), a hydroxy-substituted adamantyl aceta

7 BMS-911543 is a complex pyrrolopyridine investigated as

8 BMS-936558 was mostly well tolerated.

9 BMS-962212 is a reversible, direct, and highly selective

10 BMS-986001 had similar efficacy to that of tenofovir dis

11 BMS-986001 is a thymidine analogue nucleoside reverse tr

12 BMS-986001 was generally well tolerated through week 48.

13 BMS-986122 is a positive allosteric modulator (PAM) of t

14 BMS-986126 also demonstrated synergy with prednisolone i

15 BMS-986126 demonstrated robust activity in the MRL/lpr a

16 BMS-986126 failed to inhibit assays downstream of MyD88-

17 BMS-986187 is a structurally distinct PAM for the delta-

18 BMS-PCI was associated with worse survival than SA-CABG,

19 t solubility and exposure associated with 1 (BMS-582949), a previously disclosed phase II clinical p3

20 evascularization occurred for 77 DCS and 136 BMS patients (12.0%) (hazard ratio: 0.54; 95% confidence

21 irable tolerability and safety profile, 14f (BMS-986142) was advanced into clinical studies.

22 ety endpoint had occurred in 147 DCS and 180 BMS patients (15.3%) (hazard ratio: 0.80; 95% confidence

23 were acquired in 61 patients (42 DES and 19 BMS) presenting with definite VLST.

24 r, a structurally novel clinical prodrug, 2 (BMS-751324), featuring a carbamoylmethylene linked promo

25 ssel coronary artery disease patients: 2,207 BMS-PCI (age 66.6 +/- 11.9 years); 2,381 DES-PCI (age 65

26 In the basic series, 20c (BMS-884775) was discovered with an improved PK and liabi

27 ers culminating in the identification of 27 (BMS-819881), which entered obesity clinical trials as th

28 Finally, 64 patients (32 EES and 32 BMS) underwent optical coherence tomographic imaging.

29 al trials as the phosphate ester prodrug 35 (BMS-830216).

30 ronary stent implantations (47.6% DES, 52.4% BMS), 28,029 patients (22.5%; 95% CI, 22.2%-22.7%) under

31 hly efficient route for the synthesis of 4a (BMS-986104).

32 ds 1a and 1b led to the identification of 5 (BMS-341) as a dissociated glucocorticoid receptor modula

33 -3-yl)phenyl]- 9H-carbazole-1-carboxamide 6 (BMS-935177) was selected to advance into clinical develo

34 al load of at least 1000 copies per mL and a BMS-626529 half-maximum inhibitory concentration lower t

35 se, number of stents implanted, and use of a BMS rather than a DCS.

36 ts to receive a drug-coated stent (DCS) or a BMS followed by 1-month dual antiplatelet therapy.

37 th a new-generation DES in comparison with a BMS of equal design, in patients who have chronic kidney

38 l molecule inhibitor of Itk kinase activity (BMS-509744) potently blocked wild-type HIV-1 infectivity

39 In addition, BMS-986122 decreased the ability of NaCl to modulate ago

40 , and the appropriate duration of DAPT after BMS is unknown.

41 ne-related AE) was identified 266 days after BMS-936559 infusion; it resolved over time.

42 mic event risk is perceived to be less after BMS, and the appropriate duration of DAPT after BMS is u

43 Generally, for full agonists BMS-986122 enhanced the binding affinity and potency to

44 [bicyclo[2.2.2]octane-2,5'oxazol]-2' -amine (BMS-902483), a potent alpha7 partial agonist, which impr

45 ow and comparable in both groups (2.8% among BMS vs. 2.3% among DES patients; p = 0.54).

46 n allosteric antagonist, that BMS-986187 and BMS-986122 bind to a similar region on all three traditi

47 ree regimen of daclatasvir, asunaprevir, and BMS-791325 was well tolerated and achieved high rates of

48 assigned to biolimus-eluting stent (BES) and BMS at 11 centers, and follow-up rates at 2 years were 9

49 mer-based biolimus-eluting stents (BES), and BMS by means of network meta-analysis.

50 thout significant difference between BRS and BMS groups at 6 months (P=0.68).

51 BRS and BMS have similar 6-month outcomes in porcine coronary ar

52 ily), asunaprevir (200 mg, twice daily), and BMS-791325 (75 or 150 mg, twice daily) for 12 or 24 week

53 l outcomes between second-generation DES and BMS for primary percutaneous coronary intervention using

54 ry late ST was similar between the n-DES and BMS groups (HR: 1.52; 95% CI: 0.78 to 2.98; p = 0.21), w

55 target vessel revascularization for DES and BMS groups was 2.7% (95% confidence interval, 1.1%-5.6%)

56 hy imaging demonstrated that VLST in DES and BMS had a wide variety of abnormal findings, such as neo

57 nt type and surgical timing for both DES and BMS should be reevaluated.

58 e ST is low and comparable between n-DES and BMS up to 3 years of follow-up, whereas o-DES treatment

59 lobal neointimal growth in DES, both DES and BMS+DEB effectively prevented clinically relevant focal

60 2010; 2400 and 845 patients received DES and BMS, respectively.

61 outcomes of between those receiving DES and BMS.

62 ty of treatment weighting to create DES- and BMS-treated groups whose observed baseline characteristi

63 infarction patients differs between EES and BMS at 5 years.

64 findings associated with ST between EES and BMS in patients with ST-segment-elevation myocardial inf

65 fficacy compared with earlier generation and BMS, thus allowing shorter dual antiplatelet therapy dur

66 asunaprevir (an NS3 protease inhibitor), and BMS-791325 (a non-nucleoside NS5B inhibitor), in patient

67 s of everolimus-eluting stent (Xience V) and BMS with an identical design (Multi-Link Vision), both i

68 nth primary patency rates in the Viabahn and BMS groups were: intention-to-treat (ITT) 70.9% (95% con

69 tive and orally bioavailable CCR1 antagonist BMS-817399 (29), which entered clinical trials for the t

70 in gene-related peptide recepotor antagonist BMS-846372 is presented.

71 paration of more than 100 g of the final API BMS-986097 for toxicology studies.

72 emplified by daclatasvir (DCV; also known as BMS-790052 and Daklinza), belong to the most potent clas

73 ET showed the same distribution of uptake as BMS in 13 of 14 patients (1 patient did not undergo BMS)

74 The discovery of asunaprevir (BMS-650032, 24) is described.

75 fficient synthesis of a complex 6-azaindole, BMS-663068, is described.

76 genes were differentially methylated between BMS and AMS siblings, exhibiting a preponderance of gluc

77 Among all 11,648 randomized patients (both BMS and DES), stent thrombosis rates were 0.41% vs 1.32%

78 is achievable from the products generated by BMS, which have valorization potential.

79 the information provided either by PET or by BMS.

80 step in the synthesis of HIV drug candidate BMS-955176.

81 DP-DES, or thin-strut silicon-carbide-coated BMS in 8 European centers.

82 icular interest, and from which the compound BMS-791325 (2) was found to have distinguishing antivira

83 Symmetric, dimeric daclatasvir (BMS-790052) is the clinical lead for a class of picomola

84 conjugates (anetumab ravtansine, DMOT4039A, BMS-986148), live attenuated Listeria monocytogenes-expr

85 lthy HIV-1-infected persons, single low-dose BMS-936559 infusions appeared to enhance HIV-1-specific

86 nts were randomly assigned to receive either BMS-663068 (n=52 for the 400 mg twice daily group, n=50

87 domly assigned (1:1:1:1:1) to receive either BMS-663068 at 400 mg twice daily, 800 mg twice daily, 60

88 301 were randomly assigned to receive either BMS-986001 once a day (67 patients to 100 mg, 67 to 200

89 ical revascularization, compared with either BMS-PCI or DES-PCI, resulted in substantially enhanced d

90 Entecavir (BMS-200475) was synthesized from 4-trimethylsilyl-3-buty

91 Clinical studies with (18)F-BMS-986192 are under way to measure PD-L1 expression in

92 Results:(18)F-BMS-986192 bound to human and cynomolgus PD-L1 with a di

93 (18)F-BMS-986192 bound to tumor tissues as a function of PD-L1

94 Conclusion:(18)F-BMS-986192 demonstrated the feasibility of noninvasively

95 (18)F-BMS-986192 was evaluated for distribution, binding, and

96 (18)F-BMS-986192 was evaluated in tumors using in vitro autora

97 ion to a modified adnectin to generate (18)F-BMS-986192.

98 ess did not differ between groups (97.7% for BMS vs. 95.4% for DES; p = 0.07).

99 to clinical development discontinuation for BMS-986094, an HCV nucleotide polymerase (nonstructural

100 ticipants, and investigators were masked for BMS-663068 dose but not for allocation.

101 e mortality and unplanned reintervention for BMS-PCI and DES-PCI to respective propensity-matched SA-

102 Thirty-four patients received IFN-free BMS-986094 regimens.

103 Two patients had BMS-986001-related serious adverse events (atypical drug

104 We have identified BMS-986126, a potent, highly selective inhibitor of IRAK

105 netic and pharmacodynamic studies identified BMS-814580 (compound 10) as a highly efficacious antiobe

106 to 12.0 +/- 7.2 in BES- and 39.6 +/- 25.2 in BMS-treated lesions (P < 0.001).

107 y observed in BMS (40.5% in DES and 68.4% in BMS; P=0.056).

108 (percentage uncovered struts 5.64+/-9.65% in BMS+DEB versus 4.93+/-9.29% in DES; P=0.366) were found.

109 erved and had more longitudinal extension in BMS compared with DES.

110 eoatherosclerosis was frequently observed in BMS (40.5% in DES and 68.4% in BMS; P=0.056).

111 neoatherosclerosis was lower in DES than in BMS (15.56% [12.24-28.57] versus, 56.41% [40.74-70.00],

112 neointima length was shorter in DES than in BMS (2.4 [1.2-3.6] and 5.3 [3.0-7.0] mm; P=0.011).

113 more frequently demonstrated in DES than in BMS patients, whereas neoatherosclerosis was frequently

114 that of the most potent attachment inhibitor BMS-626529, a prodrug of which is currently undergoing p

115 The small molecule attachment inhibitor BMS-663068 has shown potent antiviral activity in early

116 We report that the IGF1R/IR inhibitor BMS-754807 cooperated with the CDK4/6 inhibitor PD-03329

117 ration synthesis of HIV maturation inhibitor BMS-955176 is described.

118 HPDE cells using a small molecule inhibitor BMS-777607 blocked constitutive activation and decreased

119 ultimate precursor to the HCV NS5A inhibitor BMS-986097, along with the final API step are described.

120 pression of IGFBP3 with the IGF1R inhibitor, BMS 536924, restoring EGFR inhibitor sensitivity.

121 cholic acid, whereas an NF-kappaB inhibitor, BMS-345541 (25 muM), inhibited DCA-induced HbetaD2, but

122 Lastly, BMS-986126 inhibited TLR7- and TLR9-dependent responses

123 systemic circulating glucuronide metabolite, BMS-801576, concentrations in human plasma.

124 m to provide reasons as to why we still need BMS in our cardiac catheterization laboratory.

125 There were no BMS-936559-related grade 3 or greater AEs.

126 bleeding occurred in 8.9% of DCS and 9.2% of BMS patients (p = 0.95), and a coronary thrombotic event

127 mbosis) occurred in 8.2% of DCS and 10.6% of BMS patients (p = 0.045).

128 The affinity of BMS-986187 for delta-ORs and kappa-ORs is approximately

129 sed on this new approach for the analysis of BMS-C in monkey serum.

130 d for an in-depth resource use assessment of BMS where two full-scale BMS and seven system variations

131 +) spleen was reduced by coadministration of BMS-986192.

132 at and dog supported clinical development of BMS-650032 (24).

133 24 analysis support continued development of BMS-663068, which is being assessed in a phase 3 trial i

134 tinued its involvement in the development of BMS-986001, and future decisions on development will be

135 ties that resulted in the discontinuation of BMS-605339 (1) from clinical trials.

136 The discovery of BMS-605339 (35), a tripeptidic inhibitor of the NS3/4A e

137 these combined SARs led to the discovery of BMS-890068 (29).

138 These efforts led to the discovery of BMS-929075 (37), which maintained ligand efficiency rela

139 200 patients received at least one dose of BMS-663068, and 51 patients received at least one dose o

140 with the combination of suboptimal doses of BMS-986126 and prednisolone, suggesting the potential fo

141 re unresponsive to the modulatory effects of BMS-986122.

142 ized 5ratio1 to receive a single infusion of BMS-936558 (0.03, 0.1, 0.3, 1.0, 3.0 mg/kg [n = 5 each]

143 Data on single infusions of BMS-936559 (0.3 mg/kg) versus placebo are described.

144 Eight men enrolled: 6 received 0.3 mg/kg of BMS-936559, and 2 received placebo infusions.

145 e inhibition profile and binding kinetics of BMS-791325 provides experimental evidence for the dynami

146 ther investigate the potential mechanisms of BMS-986094 toxicity.

147 BMS-663068 is an oral prodrug of BMS-626529, an attachment inhibitor that binds to HIV-1

148 g the efficacy, safety, and dose-response of BMS-663068 in treatment-experienced, HIV-1-infected pati

149 r-boosted atazanavir, efficacy and safety of BMS-663068 up to the week 24 analysis support continued

150 We assessed the efficacy and safety of BMS-986001 versus tenofovir disoproxil fumarate in treat

151 placebo-controlled, dose-escalating study of BMS-936559, including HIV-1-infected adults aged >18 to

152 Described herein is the synthesis of BMS-986001 by employing two novel organocatalytic transf

153 ective, and chromatography-free synthesis of BMS-986001.

154 ion revascularization associated with use of BMS have led to the development of drug-eluting stents,

155 ed with the randomly assigned DES (n=257) or BMS (n=255).

156 ith n-DES (n = 4,811), o-DES (n = 4,271), or BMS (n = 25,065).

157 e treated with either XIENCE V DES (n=51) or BMS postdilated with the SeQuent Please DEB (n=54).

158 ly assigned to receive either EES (n=751) or BMS (n=747).

159 BP-BES versus currently U.S.-approved DES or BMS were searched through MEDLINE, EMBASE, and Cochrane

160 rst-generation DES, second-generation DES or BMS) were considered for inclusion.

161 ly assigned in a 1:1 ratio to receive EES or BMS.

162 contrast, the SIRT1 activator resveratrol or BMS-345541 (inhibitor of IKK) inhibited IL-1beta- and NA

163 ertain candidates for DES, to receive ZES or BMS.

164 R2 in a ternary complex with an orthosteric (BMS-681) and allosteric (CCR2-RA-[R]) antagonist.

165 Safety and efficacy benefits of DCS over BMS were maintained for 2 years in high bleeding risk pa

166 Overall, BMS-986122 displayed marked probe dependence that was ba

167 s we examined the interaction of the mu-PAM, BMS-986122, with a chemically diverse range of MOPr orth

168 rates were 48.0% for DES and 35.1% for PTA+/-BMS (P=0.096) in the modified-intention-to-treat and 51.

169 nificantly worse treatment failure for PTA+/-BMS versus DES (P=0.041).

170 eal lesions were randomized to receive PTA+/-BMS or DES with paclitaxel.

171 ES and 66 limbs (64 patients) received PTA+/-BMS.

172 ns after 6 and 12 months compared with PTA+/-BMS.

173 were randomly assigned (2:2:2:3) to receive BMS-986001 100 mg, 200 mg, or 400 mg once a day or to re

174 treated with aspirin, of whom 1687 received BMS and 9961 DES.

175 Of these, 38% received BMS, 15% received first-generation DES, and 47% received

176 Patients who received BMS had shorter stent implants (24.0 +/- 13.4 mm vs. 26.

177 Five patients who received BMS-936558 (0.1 [n = 1] or 10 mg/kg) and one placebo pat

178 ial increases in 2 participants who received BMS-936559.

179 tations in 17 (9%) of 198 patients receiving BMS-986001 versus none of 99 and one (1%) of 99 patients

180 ear mortality, compared with those receiving BMS.

181 video-based monitoring using high-resolution BMS in accurately representing activity patterns in an i

182 e use assessment of BMS where two full-scale BMS and seven system variations were analyzed.

183 rrow histology and bone marrow scintigraphy (BMS), the gold standard techniques in this clinical situ

184 The potent and selective BMS-903452 (42) was efficacious in both acute and chroni

185 f an earlier lead from this chemical series, BMS-605339 (1), from clinical trials.

186 and more effective than a bare-metal stent (BMS) for patients with high risk of bleeding.

187 aling in comparison with a bare metal stent (BMS).

188 asty (PTA) and bail-out bare metal stenting (BMS) is hampered by restenosis.

189 pare the findings between bare-metal stents (BMS) and drug-eluting stents (DES).

190 nts (n-DES) compared with bare-metal stents (BMS) and old-generation drug-eluting stents (o-DES) enro

191 -eluting stents (DES) and bare-metal stents (BMS) by means of a network meta-analysis.

192 vious generation DES, and bare-metal stents (BMS) for percutaneous coronary intervention in saphenous

193 uting stents (DES) versus bare metal stents (BMS) has not been studied in the kidney transplant popul

194 The introduction of bare-metal stents (BMS) has represented a major advancement over plain old

195 eluting stents (EES) with bare-metal stents (BMS) in an all-comer population with ST-segment elevatio

196 nts (DES) are superior to bare-metal stents (BMS) in octogenarian patients with angina.

197 zation in comparison with bare-metal stents (BMS) in patients with chronic kidney disease.

198 uting stents (DES) versus bare-metal stents (BMS) in SVG-PCI are unclear.

199 ts (EES) in patients with bare-metal stents (BMS) in-stent restenosis (ISR).

200 with EES in patients with bare-metal stents (BMS) in-stent restenosis (ISR).

201 ention (PCI) using either bare-metal stents (BMS) or drug-eluting stents (DES).

202 st-release profile versus bare-metal stents (BMS) under similar durations of dual-antiplatelet therap

203 larizations compared with bare-metal stents (BMS), but their effects on death and myocardial infarcti

204 of late ST compared with bare-metal stents (BMS), especially in patients with ST-segment-elevation m

205 SVG in patients receiving bare-metal stents (BMS), first-generation DES, and newer generation DES in

206 Compared with bare metal stents (BMS), first-generation drug-eluting stents (DES) have si

207 tents (DES) compared with bare metal stents (BMS), the relative risk of stent thrombosis and adverse

208 S) and as safe >1 year as bare-metal stents (BMS).

209 ES) and for 6 weeks after bare metal stents (BMS).

210 -eluting stents (DES) and bare-metal stents (BMS); however, most prior trials in these meta-analyses

211 biodegradable polymer and bare-metal stents (BMSs) in the COMFORTABLE trial (Comparison of Biolimus E

212 iferation of a therapy of bare metal stents (BMSs) postdilated with the paclitaxel drug-eluting ballo

213 eluting stents (DESs) and bare-metal stents (BMSs) with respect to stent thrombosis (ST) continues to

214 th DP-DES and more effective than thin-strut BMS, but without evidence for better safety nor lower VL

215 evaluation of biosolids management systems (BMS) from a natural resource consumption point of view.

216 nd lower rates of myocardial infarction than BMS and PES.

217 ombosis (ST), and myocardial infarction than BMS, paclitaxel-eluting stents (PES), and sirolimus-elut

218 DES was associated with lower mortality than BMS (hazard ratio [HR]: 0.72; 95% confidence interval [C

219 from the notion that DES are less safe than BMS to the converse.

220 enged the notion that DES are less safe than BMS.

221 EES) have shown similar rate of late ST than BMS.

222 farction (MI) and stent thrombosis (ST) than BMS.

223 d target vessel revascularization (TVR) than BMS and lower rates of TVR than fast-release zotarolimus

224 modulator as an allosteric antagonist, that BMS-986187 and BMS-986122 bind to a similar region on al

225 emical and biophysical studies revealed that BMS-791325 is a time-dependent, non-competitive inhibito

226 ing and second-messenger assays to show that BMS-986187 is an effective PAM at the mu-OR and at the k

227 curred in 17 (9%) of 200 patients across the BMS-663068 groups and 14 (27%) of 51 patients in the rit

228 s low and comparable between the BRS and the BMS groups (4.6+/-6.7 versus 4.6+/-5.1%; P=0.98).

229 For the BMS-663068 groups these events were mostly single instan

230 However, the BMS subset may have been underpowered to identify such d

231 nts in the EES group versus 192 (26%) in the BMS group (hazard ratio 0.80, 95% CI 0.65-0.98; p=0.033)

232 t, compared with 178 patients (22.1%) in the BMS group (hazard ratio: 0.76; 95% confidence interval:

233 1.4 months in the DES and 69.9 months in the BMS group (P=0.011).

234 apy at 1 year were 32.2% for patients in the BMS group and 94.0% for patients in the DES group.

235 ndpoint occurred in 18.7% of patients in the BMS group versus 14.3% of patients in the DES group (p =

236 .001) occurred more often in patients in the BMS group.

237 more global neointimal proliferation in the BMS+DEB group (15.7+/-7.8 versus 11.0+/-5.2 mm(3) prolif

238 At week 24, 40 (80%) of 50 patients in the BMS-663068 400 mg twice daily group, 34 (69%) of 49 pati

239 were noted in 13 (7%) of 200 patients in the BMS-663068 groups and five (10%) of the 51 patients in t

240 Four (2%) of the 200 patients in the BMS-663068 groups and two (4%) of the 51 patients in the

241 ovir disoproxil fumarate, individuals in the BMS-986001 groups showed a smaller decrease in lumbar sp

242 I: 0.41 to 0.89; p = 0.01) compared with the BMS group.

243 Twenty-three BMS (3.0x12 mm) and 36 lactic acid-based bioresorbable s

244 Thus, BMS+DEB achieved the prespecified noninferiority margin

245 FLT PET may be foreseen as an alternative to BMS.

246 M5 shows a dramatic decrease in binding to BMS-986010 (which contains the 7B7 Fab, where Fab is fra

247 rect (comparison of second-generation DES to BMS) and indirect evidence (first-generation DES with BM

248 ety and efficacy of second-generation DES to BMS.

249 The sensitivity of an orthosteric ligand to BMS-986122 was strongly correlated with its sensitivity

250 th patients and investigators were masked to BMS-986001 dose (achieved with similar looking placebo t

251 led trials comparing DES to each other or to BMS were searched through MEDLINE, EMBASE, and Cochrane

252 3.5 +/- 3.2 years of age) were randomized to BMS (n = 401) or DES (n = 399) for treatment of stable a

253 0.042; per protocol P=0.09) and superior to BMS (absolute risk difference, -5.16; -8.32 to -2.01; P=

254 The surgery-to-BMS-PCI hazard ratios (HR) were as follows: versus SA-CA

255 13 of 14 patients (1 patient did not undergo BMS).

256 ivided into 3 groups according to stent use: BMS, first-generation DES, and newer generation DES grou

257 Using BMS-833923, a uniquely effective Smo inhibitor, and high

258 Using BMS-C as a probe compound, the incorporation of the albu

259 o examine the association between DES versus BMS used during SVG PCI and clinical outcomes in the nat

260 , and examined the association of DES versus BMS with 1-year outcomes: death; death or MI; and death,

261 with the use of second-generation DES versus BMS.

262 rt, no significant association among DES (vs BMS) use and outcomes was observed at 1 and 2 years of f

263 verse events leading to discontinuation were BMS-663068-related.

264 -driven target vessel revascularization were BMS implantation (odds ratio, 4.95; 95% confidence inter

265 tive scaffold remodeling (P<0.0001), whereas BMS diameter remained constant (P=0.159).

266 ith BP-DES, 6.8% with DP-DES, and 12.7% with BMS.

267 eous coronary intervention with DES and with BMS in dialysis patients.

268 ate ST was observed with o-DES compared with BMS (HR: 2.88; 95% CI: 1.70 to 4.89; p < 0.01).

269 ith superior clinical outcomes compared with BMS and first-generation DES and similar rates of cardia

270 ed with improved late outcomes compared with BMS and paclitaxel-eluting stents, considering the lates

271 improve cardiovascular events compared with BMS beyond 1 year.

272 Compared with BMS, DES implantation using a stent with a biocompatible

273 In long-term follow-up, compared with BMS, DES use was safe and effective in SVG-PCI patients.

274 DES, compared with BMS, were associated with a significant 18% lower risk o

275 tion were reduced with all DES compared with BMS, with cobalt-chromium EES, platinum chromium-EES, SE

276 of BES-treated patients (5.8%) compared with BMS-treated patients (11.9%; hazard ratio = 0.48; 95% co

277 ent among BES-treated patients compared with BMS-treated patients.

278 not with first-generation DES, compared with BMS-treated patients.

279 demonstrated superior efficacy compared with BMS.

280 iated with adverse events when compared with BMS.

281 0.54; 95% CI, 0.80-0.98) when compared with BMS.

282 ith second-generation DES when compared with BMS.

283 0.49; 95% CI, 0.30-0.79) when compared with BMS.

284 econd-generation DES, but also compared with BMS.

285 stent thrombosis with any DES compared with BMS.

286 rate of neoatherosclerosis as compared with BMS.

287 indirect evidence (first-generation DES with BMS and second-generation DES) from the randomized trial

288 P=0.02) were numerically more frequent with BMS.

289 whereas spleen uptake was inconclusive with BMS.

290 that pharmacological inhibition of LIMK with BMS-5 decreased the viability of Nf2(DeltaEx2) MSCs in a

291 yields results close to those observed with BMS.

292 A total of 189 patients with BMS-ISR from 25 Spanish sites were included (95 were all

293 In patients with BMS-ISR, both DEB and EES provided excellent clinical re

294 nts undergoing coronary stent placement with BMS and who tolerated 12 months of thienopyridine, conti

295 P=0.02) were larger with EES than that with BMS.

296 tients treated with EES and 727 treated with BMS (97% of both groups).

297 Among 1687 patients treated with BMS who were randomized to continued thienopyridine vs p

298 s observed in infected patients treated with BMS-791325 in combination with other anti-HCV agents in

299 DES, compared with the patients treated with BMS.

300 of early/late ST than patients treated with BMS.