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-378806 (here called BMS-806) blocks CD4-induced conf

4 BMS-529-complexed gp150 trimers in detergent micelles, w

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

6 BMS-681 inhibits chemokine binding by occupying the orth

7 BMS-806 strengthened the labile, noncovalent interaction

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

9 BMS-911543 is a complex pyrrolopyridine investigated as

10 BMS-919373 is a highly functionalized quinazoline under

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

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

13 BMS-986001 is a thymidine analogue nucleoside reverse tr

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

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

16 BMS-986126 also demonstrated synergy with prednisolone i

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

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

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

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

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

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

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

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

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

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

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

28 han at baseline (mainly between BMS 2 and 3, BMS was >= 4 in only 8.7% of patients).

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

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

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

32 -3-yl)phenyl]- 9H-carbazole-1-carboxamide 6 (BMS-935177) was selected to advance into clinical develo

33 turally diversified Tyk2 JH2 ligands from 6 (BMS-986165), a pyridazine carboxamide-derived Tyk2 JH2 l

34 viral entry inhibitors, such as BMS-626529 (BMS-529), allosterically block CD4 binding to HIV-1 enve

35 y, which directly led to the discovery of 7 (BMS-986202) as a clinical Tyk2 inhibitor that binds to T

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

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

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

39 These long-acting BMS-806 analogues may facilitate enrichment of the metas

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

41 tor occupancy was achieved for 28 days after BMS-936559 (900 mg).

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

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

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

45 Attachment inhibitor (AI) BMS-626529 (fostemsavir) represents a novel class of ant

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

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

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

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

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

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

52 2010; 2400 and 845 patients received DES and BMS, respectively.

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

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

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

56 both uni- and multivariable analysis, FS and BMS < 4 were associated with prolonged progression-free

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

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

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

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

61 all-molecule viral entry inhibitors, such as BMS-626529 (BMS-529), allosterically block CD4 binding t

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

63 antly lower than at baseline (mainly between BMS 2 and 3, BMS was >= 4 in only 8.7% of patients).

64 Remarkable synergy was observed between BMS-626529 and CD4 binding site (CD4bs)-targeting bNAbs

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

66 of monkeys after dosing with branebrutinib (BMS-986195), a covalent BTK inhibitor being evaluated to

67 ble tolerability profile, 5a (branebrutinib, BMS-986195) has advanced into clinical studies.

68 protocol by double N-benzylation followed by BMS-mediated reduction of tertiary amide groups (53-93%)

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

70 the information provided either by PET or by BMS.

71 BMS-378806 (here called BMS-806) blocks CD4-induced conformational changes in En

72 neration synthesis of the clinical candidate BMS-986251, using diester 1 as a critical component.

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

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

75 d from BMS to DES1, then declined with DES2 (BMS: 7.4% versus DES1: 10.2%, DES2: 8.5%, P=0.02).

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

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

78 Participants received single-dose BMS-936559 (10-900 mg; n = 20) or placebo (n = 4) infusi

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

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

81 301 were randomly assigned to receive either BMS-986001 once a day (67 patients to 100 mg, 67 to 200

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

83 o everolimus-eluting DES or to an equivalent BMS platform in the EXAMINATION trial (Clinical Evaluati

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

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

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

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

88 Methods: Data from a study with (18)F-BMS-986192 in patients with advanced-stage non-small cel

89 Conclusion: (18)F-BMS-986192 PET imaging allows detection of membrane-expr

90 We evaluated the usability of (18)F-BMS-986192 PET to detect different PD-L1 expression leve

91 uently, no treatment-induced change in (18)F-BMS-986192 tumor uptake was observed.

92 ion measured immunohistochemically nor (18)F-BMS-986192 tumor uptake.

93 Results: (18)F-BMS-986192 uptake reflected PD-L1 membrane levels in tum

94 Afterward, (18)F-BMS-986192 was administered intravenously, followed by a

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 Methods: In vitro binding assays with (18)F-BMS-986192 were performed on human tumor cell lines with

98 After injection of (18)F-BMS-986192, a 60-min dynamic PET/CT scan was started, fo

99 his work was to quantify the uptake of (18)F-BMS-986192, a programmed cell death ligand 1 (PD-L1) adn

100 (18)F-BMS-986192, an adnectin-based human programmed cell deat

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

102 y tumor uptake of the PD-L1 PET tracer (18)F-BMS-986192.

103 Only nine (15%) fulfilled our criteria for BMS; impaired cognition (57%) and effects on employment

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

105 Population frequency for BMS was estimated at 2.9% (95% CI 2.0 to 4.1).

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

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

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

109 r term, there was no further divergence from BMS after 1 year.

110 E rates between 1 and 5 years increased from BMS to DES1, then declined with DES2 (BMS: 7.4% versus D

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

112 clinical assessment and classified as having BMS according to EDSS score <3, no significant fatigue,

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

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

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

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

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

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

119 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).

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

121 e (Env) trimer have been developed including BMS-626529, also called temsavir, a prodrug version of w

122 panel of small-molecule inhibitors including BMS-818251, which we show to be >10-fold more potent tha

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

124 dy, we report that the viral entry inhibitor BMS-626529 restricts trimer conformational transition an

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

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

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

128 t contained in the NS5B nucleoside inhibitor BMS-986094 was achieved in 23% overall yield on a gram s

129 F, as well as NF-kappaB signalling inhibitor BMS-345541.

130 hese studies indicate that pan-TAM inhibitor BMS-777607 cooperates with anti-PD-1 in a syngeneic mous

131 were treated with pan-TAM kinase inhibitor (BMS-777607) or anti-PD-1 alone or in combination.

132 stration of either pan-TAM kinase inhibitor (BMS-777607) or anti-PD-1 mAb therapy showed partial anti

133 We found that an HIV-1 entry inhibitor, BMS-806, stabilizes the functional shape of Env.

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

135 an three major clinical stage BET inhibitors BMS-986158, OTX-015, and GSK-525762.

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

137 In rhesus macaques, BMS-529 complexed to CD4 bs-targeting ch.SOSIP immunogen

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

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

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

141 We designed novel BMS-806 analogues that stabilized the Env conformation f

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

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

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

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

146 Here, we show that the binding of BMS-529 to clade C soluble chimeric gp140 SOSIP (ch.SOSI

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

148 o the HIV-1 Env trimer by the combination of BMS-626529 and CD4bs-targeting bNAbs.

149 24 analysis support continued development of BMS-663068, which is being assessed in a phase 3 trial i

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

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

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

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

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

155 cement strategy that led to the discovery of BMS-986165 (11) as a high affinity JH2 ligand and potent

156 These efforts culminated in the discovery of BMS-986166 (14a), which was advanced to human clinical e

157 200 patients received at least one dose of BMS-663068, and 51 patients received at least one dose o

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

159 Here, we evaluated the effects of BMS-806 on the conformation of Env on the surface of cel

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

161 esearch group reported the identification of BMS-986104 (2) as a differentiated S1P(1) receptor modul

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

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

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

165 tient perception and clinician perception of BMS undermines use of the term 'benign' in clinical sett

166 Thus, in the presence of BMS-806, the cleaved Env on the surface of cells and vir

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

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

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

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

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

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

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

174 al antitumor activity, combined treatment of BMS-777607 with anti-PD-1 significantly decreased tumor

175 sults do not support the preferential use of BMS for patients with large coronary vessels.

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

177 We developed new variants of BMS-806 that stabilize Env in its natural state for long

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

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

180 after implantation of new-generation DES or BMS among patients undergoing percutaneous coronary inte

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

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

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

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

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

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

187 acy and safety of second-generation DES over BMS in large coronary culprit ST-segment elevated myocar

188 Pegbelfermin (BMS-986036), a PEGylated human fibroblast growth factor

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

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

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

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

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

194 e JAK2 inhibitor, a complex pyrrolopyridine, BMS-911543, is described.

195 In rabbits, BMS-529-complexed V3 glycan-targeting ch.SOSIP immunogen

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

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

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

199 heart disease, 1550, 2776, and 6661 received BMS, DES1, and DES2, respectively.

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

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

202 ear mortality, compared with those receiving BMS.

203 The improved diffraction reveals BMS-818251 to utilize functional groups that interact wi

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

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

206 and definition of benign multiple sclerosis (BMS) remain controversial.

207 e (DS) was applied to describe BM (BM score [BMS]) and focal lesion (FL; FL score [FS]) uptake and te

208 death-ligand 1 pathway inhibition in sepsis, BMS-936559 was well tolerated, with no evidence of drug-

209 ic ligands such as the Bristol-Myers Squibb (BMS) entry inhibitors.

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

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

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

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

214 oronary intervention with bare-metal stents (BMS) and first-generation and second-generation drug-elu

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

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

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

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

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

220 DES compares with that of bare-metal stents (BMS) is less clear.

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

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

223 and safety compared with bare-metal stents (BMS), and international guidelines recommend their use a

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

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

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

227 nd 5 years after PCI with bare-metal stents (BMS), first-generation drug-eluting stents (DES1) and se

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

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

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

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

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

233 declined with evolution in stent technology (BMS: 24.1% versus DES1: 17.9% versus DES2: 13.4%, P<0.00

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

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

236 with lower risk of the primary outcome than BMS up to 1 year after placement.

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

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

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

240 the first year after implantation means that BMS should no longer be considered the gold standard for

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

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

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

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

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

246 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)

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

248 1.4 months in the DES and 69.9 months in the BMS group (P=0.011).

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

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

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

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

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

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

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

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

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

258 When complexed to BMS-529, ch.SOSIP trimers retained their binding to broa

259 When immunized with gp150 complexed to BMS-529, rhesus macaques showed neutralization against t

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

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

262 harboring mutations conferring resistance to BMS-626529.

263 Our data show that Env mutants resistant to BMS-626529 retained susceptibility to bNAbs.

264 0.042; per protocol P=0.09) and superior to BMS (absolute risk difference, -5.16; -8.32 to -2.01; P=

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

266 13 of 14 patients (1 patient did not undergo BMS).

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

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

269 The impact of DES versus BMS implantation was consistent irrespective of the sten

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

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

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

273 l patients had BM diffuse uptake (35.5% with BMS >= 4).

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

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

276 improve cardiovascular events compared with BMS beyond 1 year.

277 was reduced in DES recipients compared with BMS recipients (HR 0.84, 95% CI 0.78-0.90, p<0.001) owin

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

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

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

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

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

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

284 rate of neoatherosclerosis as compared with BMS.

285 demonstrated superior efficacy compared with BMS.

286 tabilization of Env trimer conformation with BMS-529 improved the immunogenicity of select chimeric S

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

288 whereas spleen uptake was inconclusive with BMS.

289 yields results close to those observed with BMS.

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

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

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

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

294 7%, 11.0%, and 8.3% of patients treated with BMS, DES1, and DES2, respectively (p < 0.0001), linearly

295 , 3,718, 7,934, and 13,380 were treated with BMS, DES1, and DES2, respectively.

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

297 DES, compared with the patients treated with BMS.

298 ere progressively lower after treatment with BMS versus DES1 versus DES2 (17.9% vs.

299 Moreover, combined treatment with BMS-777607 and anti-PD-1 showed increased infiltration o

300 Yet, BMS are still widely used in practice, especially in lar