ライフサイエンスコーパス: CETP

1 CETP and ABCG1 may be important mediators of these effec

2 CETP and ABCG1, both of which participate in the HDL-med

3 CETP genotypes did not associate with variation in marke

4 CETP has no apparent preference for high (HDL) or low (L

5 CETP inhibition has been regarded as a promising strateg

6 CETP inhibition increased plasma high-density lipoprotei

7 CETP inhibition increased postprandial insulin and promo

8 CETP inhibitors block the transfer of cholesteryl ester

9 CETP inhibitors form a complex between themselves, CETP,

10 CETP PTV carrier status was associated with reduced risk

11 CETP-D HDL-2 caused a 2- to 3-fold stimulation of net ch

12 CETP-deficient cells had 4-fold more CE but an approxima

13 CETP-mediated CE transfers from [3H]CE VLDL to various l

14 ) or normal coronaries were genotyped for 11 CETP tSNPs.

15 alleles at two loci (LIPC, P = 1.3 x 10(-7); CETP, P = 7.4 x 10(-7)) that were previously associated

16 With the goal of identifying a CETP inhibitor with high in vitro potency and optimal in

17 HDL3 transfer was stimulated, resulting in a CETP preference for HDL3 that was 3-fold greater than th

18 Anacetrapib (MK-0859) is a CETP inhibitor currently under development.

19 The current study assessed the effects of a CETP inhibitor on postprandial insulin, ex vivo insulin

20 e evaluated HDL-C modification from use of a CETP inhibitor.

21 tures of CETP in complex with torcetrapib, a CETP inhibitor that has been tested in phase 3 clinical

22 transport in humans, raising hope of using a CETP inhibitor to elevate HDL levels.

23 ective, but an initial clinical trial with a CETP inhibitor was stopped prematurely because of increa

24 , whereas LPL, TRIB1, ABCA1, APOA1-C3-A4-A5, CETP, and APOE displayed significant strongest associati

25 tiomer 4a represents the most potent acyclic CETP inhibitor reported.

26 tudies provide direct evidence that apoE and CETP are intimately involved in the accumulation of the

27 We have investigated the roles that apoE and CETP may play in this process.

28 in hydrophobic contacts between the CEs and CETP, and a continuous tunnel traversing across the CETP

29 lesterol, LPL, ABCA1, ZNF259/APOA5, LIPC and CETP for HDL cholesterol, CELSR2, APOB and NCAN/MAU2 for

30 elated strongly with that of KC markers, and CETP messenger RNA and protein colocalized specifically

31 0), LIPC (rs10468017), TIMP3 (rs9621532) and CETP (rs3764261) were confirmed with genome-wide signifi

32 of pleiotropy for APOE, TOMM40, TCF7L2, and CETP variants, many with opposing effects (eg, the same

33 SW872 adipocytes stably expressing antisense CETP cDNA and synthesizing 20% of normal CETP were creat

34 ucose and 4 lipids loci (TCF7L2, LPL, APOA5, CETP, and APOC1/APOE/TOMM40) significantly associated wi

35 A4-APOC3-APOA1 and APOE-APOC clusters, APOB, CETP, GCKR, LDLR, LPL, LIPC, LIPG and PCSK9) and also in

36 Several SNPs (e.g. in APOE, CETP, LPL, APOB and LDLR) influenced multiple phenotypes

37 and lipid metabolism (hepatic lipase, APOE, CETP, and PON1).

38 nd replicated for baseline Lp-PLA(2) mass at CETP and for Lp-PLA(2) activity at the APOC1-APOE and PL

39 ompared with noncarriers, carriers of PTV at CETP displayed higher high-density lipoprotein cholester

40 ompared with noncarriers, carriers of PTV at CETP had higher high-density lipoprotein cholesterol (ef

41 as and amides as potent and orally available CETP inhibitors.

42 analyses evaluating the association between CETP and HMGCR scores, changes in lipid and lipoprotein

43 We find a strong association between CETP Asp442Gly (rs2303790), an East Asian-specific mutat

44 BPI-CETP chimeras are inhibited by LPS but cannot be inhibit

45 Our study indicates that the APOA5, BUD13, CETP, and LIPA genes may contribute to the risk of MetS

46 sociated with the APOA5, APOC1, BRAP, BUD13, CETP, LIPA, LPL, PLCG1, and ZPR1 genes.

47 cern that large, CE-rich HDL(2) generated by CETP inhibition might impair reverse cholesterol transpo

48 Modification of the lipoprotein profile by CETP inhibitors is promising, but the beneficial effect

49 nnel mechanism for neutral lipid transfer by CETP.

50 the mechanism of CE/triglyceride transfer by CETP.

51 The capacity of cellular CETP to transport CE and TG into storage droplets was di

52 subjects with homozygous deficiency of CETP (CETP-D) to promote cholesterol efflux from macrophages a

53 The consequences of chronic CETP deficiency in lipid-storing cells normally expressi

54 Overall, chronic CETP deficiency disrupts lipid homeostasis and compromis

55 Data relating circulating CETP concentrations to CVD incidence in the community ar

56 we examined whether LTIP might also control CETP-facilitated lipid flux among HDL subfractions.

57 The gene encoding CETP has been shown to be highly variable, with multiple

58 y in lipid-storing cells normally expressing CETP have not been reported.

59 We discuss the two failed CETP inhibitors, torcetrapib and dalcetrapib, and attemp

60 Despite two failures, CETP inhibitors are still in clinical development.

61 RECENT FINDINGS: Torcetrapib, the first CETP inhibitor tested in a phase III clinical trial (ILL

62 sis, demonstrating an intracellular role for CETP as well.

63 ytic cells strongly support a novel role for CETP in intracellular lipid transport and storage.

64 To date, four CETP inhibitors have advanced to phase 3 cardiovascular

65 MIN6N8 beta-cells incubated with plasma from CETP inhibitor-treated individuals (compared with placeb

66 ian-specific coding variants in known genes (CETP p.Asp459Gly, PCSK9 p.Arg93Cys and LDLR p.Arg257Trp)

67 Genetic CETP inhibition associates with reductions in risk of is

68 in CETP Tg mice virtually abolished hepatic CETP expression and largely reduced plasma CETP concentr

69 Hepatic KC content as well as hepatic CETP expression correlated strongly with plasma CETP con

70 Guerin vaccination largely increased hepatic CETP expression and plasma CETP.

71 located in LDLR, PCSK9, APOB, CELSR2, HMGCR, CETP, the TOMM40-APOE-C1-C2-C4 cluster, and the APOA5-A4

72 CETP is known, little is known regarding how CETP binds to HDL.

73 in promoter was used to stably express human CETP in livers of mice and was compared with an AAV8-lac

74 transgenic (Tg) mouse model expressing human CETP.

75 In high-fat fed hamsters, human CETP transgenic mice, and cynomolgus monkeys, the in viv

76 activity at an oral dose of 1 mg/kg in human CETP/apoB-100 dual transgenic mice and increased HDL cho

77 In CETP transgenic mice, CETP expression completely abolish

78 Given ongoing therapeutic development in CETP inhibition and other HDL-raising strategies, furthe

79 zed CE and TG into lipid storage droplets in CETP-deficient cells was just 40% of control, suggesting

80 lective elimination of KCs from the liver in CETP Tg mice virtually abolished hepatic CETP expression

81 However, cholesterol mass in CETP-deficient adipocytes was actually reduced.

82 ETP previously associated with reductions in CETP activity, thus mimicking the effect of pharmacologi

83 In humans, mutations resulting in CETP inhibition have been associated with both reduced a

84 [CI]: 1.19-1.91; P = 0.001) and rs1532624 in CETP (OR = 0.82; CI: 0.69-0.99; P = 0.034); rs4420638 wa

85 The hydrolysis of cellular CE and TG in CETP-deficient cells was reduced by >50%, although hydro

86 reased homozygosity for the I405V variant in CETP.

87 Genetic variants in CETP associated with increased HDL-C raise the risk of I

88 We selected 2 common genetic variants in CETP previously associated with reductions in CETP activ

89 DL cholesterol and apolipoprotein AI were in CETP, LPL, LIPC, APOA5-A4-C3-A1, and ABCA1; and SNPs ass

90 First, we tested individual CETP variants in a discovery cohort of 1,149 ICH cases a

91 Inefficient CETP-mediated translocation of CE and TG from the endopl

92 RATIONALE: Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to

93 lasma HDL-C; as such, medicines that inhibit CETP and raise HDL-C are in clinical development.

94 Diol (+)-5 inhibited CETP activity with an IC(50) value of 16 microM.

95 which occurs during the HDL cycle, inhibited CETP activity by approximately 2-fold and LTIP activity

96 odels that apolipoprotein (apo) C-I inhibits CETP, and that high mono-unsaturated fat diets prevent t

97 ETP expression in mice (which naturally lack CETP) on macrophage RCT, including in mice that lack the

98 erosclerosis in hyperlipidemic APOE*3-Leiden.CETP mice, a well-established model for human-like lipop

99 d the underlying mechanisms in APOE*3-Leiden.CETP mice, a well-established model for human-like lipop

100 ked to increased HDL levels in APOE*3-Leiden.CETP mice.

101 In subjects with low HDL cholesterol levels, CETP inhibition with torcetrapib markedly increased HDL

102 etected at LPL, TRIB1, APOA1-C3-A4-A5, LIPC, CETP, and LDLR (P range from 4.84x10(-4) to 4.62x10(-18)

103 in ANGPTL3, APOB, ABCA1, NR1H3, APOA1, LIPC, CETP, LDLR, and APOC1) and replicated 14 variants.

104 TRA1 genes/regions and the novel genes LIPC, CETP, and ABCA1 in the high-density lipoprotein (HDL) ch

105 itively differentiate from highly lipophilic CETP inhibitors in its complete elimination from fat tis

106 Variants in the genes LPL, CETP, APOA5 (and its cluster), GCKR (and its cluster), L

107 oprotein receptor/apobec-1 double-null mice, CETP expression reduced high-density lipoprotein cholest

108 cavenger receptor class B, type I-null mice, CETP expression reduced high-density lipoprotein cholest

109 In apobec-1-null mice, CETP expression reduced plasma high-density lipoprotein

110 In CETP transgenic mice, CETP expression completely abolished LXR agonist-mediate

111 PS but cannot be inhibited by small molecule CETP inhibitors as effectively as native CETP.

112 ule CETP inhibitors as effectively as native CETP.

113 teractions that are not observed with native CETP.

114 Evacetrapib, a relatively new CETP inhibitor, exhibited favorable changes in the lipid

115 nse CETP cDNA and synthesizing 20% of normal CETP were created.

116 TA-8995, a novel CETP inhibitor, is well tolerated and has beneficial eff

117 te may provide opportunities to design novel CETP inhibitors possessing more drug-like physical prope

118 erminus of BPI did not retain any observable CETP function.

119 of homozygosity for the 405 valine allele of CETP (VV genotype), respectively, compared with controls

120 We performed 2 candidate-gene analyses of CETP.

121 The inverse association of CETP activity with CVD incidence remained robust in time

122 We tested association of CETP PTV carrier status with both plasma lipids and CHD.

123 opments, and the discovery of new classes of CETP inhibitors.

124 LCAT and apoE contents of CETP-D HDL-2 were markedly increased compared with contr

125 from subjects with homozygous deficiency of CETP (CETP-D) to promote cholesterol efflux from macroph

126 either the metabolic milieu or the degree of CETP inhibition.

127 The development of CETP (cholesteryl ester transfer protein) inhibitors has

128 ealthy participants received a daily dose of CETP inhibitor (n=10) or placebo (n=15) for 14 days in a

129 r X receptor agonists) and downregulators of CETP (e.g. JTT-705).

130 tudy, we explore the large scale dynamics of CETP by means of multimicrosecond molecular dynamics sim

131 ssay of macrophage RCT to test the effect of CETP expression in mice (which naturally lack CETP) on m

132 However, the beneficial effect of CETP inhibition on cardiovascular outcome remains to be

133 s are that the antiatherosclerotic effect of CETP inhibition varies with either the metabolic milieu

134 tion and atherosclerosis, and the effects of CETP inhibition on cholesterol efflux and reverse choles

135 ene may provide insight into the efficacy of CETP inhibition.

136 Hepatic expression of CETP correlated strongly with that of KC markers, and CE

137 bariatric surgery, showed that expression of CETP is markedly higher in liver than adipose tissue.

138 ies have shown that blocking the function of CETP can increase the level of HDL cholesterol in blood

139 We review the genetics of CETP and coronary disease, preclinical data on CETP inhi

140 Inhibition of CETP has been shown to raise human plasma HDL cholestero

141 sing the level of HDL-C is the inhibition of CETP.

142 ogue was identified as a potent inhibitor of CETP activity in buffer (4a, IC50 0.77 nM, 59 nM in huma

143 Torcetrapib, an inhibitor of CETP, increased risk of death and ischemic cardiovascula

144 ffects of torcetrapib, a potent inhibitor of CETP, on plasma lipoprotein levels in 19 subjects with l

145 We now have pharmacological inhibitors of CETP that are capable of increasing HDL by as much as 50

146 strategy for attenuating the interaction of CETP with HDL.

147 0 amino acids resulted in a complete loss of CETP function even though the chimera was able to retain

148 mation about the lipid transfer mechanism of CETP.

149 the recently proposed "tunnel mechanism" of CETP from cryo-EM studies for the transfer of neutral li

150 s have documented the efficacy and safety of CETP inhibitors in combination with commonly used statin

151 A genetic score of CETP variants found to increase HDL-C by approximately 2

152 fat diets prevent the normal stimulation of CETP activity by dietary cholesterol.

153 that the previously observed stimulation of CETP activity on HDL by LTIP is due solely to its stimul

154 Although the crystal structure of CETP is known, little is known regarding how CETP binds

155 Here, we report the crystal structures of CETP in complex with torcetrapib, a CETP inhibitor that

156 DL in turn became the preferred substrate of CETP.

157 However, short term suppression of CETP biosynthesis in cells alters cellular cholesterol h

158 ants in the genes that encode the targets of CETP inhibitors and statins was associated with discorda

159 Chimeras containing the amino terminus of CETP and the carboxy terminus of BPI did not retain any

160 narrowing neck of the hydrophobic tunnel of CETP and thus block the connection between the N- and C-

161 Examining nine missense variants of CETP, we found some had significant associations with CE

162 TP and coronary disease, preclinical data on CETP inhibition and atherosclerosis, and the effects of

163 However, trials of other CETP inhibitors have shown neutral or adverse effects on

164 Whether pharmacologic CETP inhibition will reduce the risk of cardiovascular d

165 thus mimicking the effect of pharmacological CETP inhibition.

166 Plasma CETP is predominantly derived from KCs, and plasma CETP

167 METHODS AND Plasma CETP activity was measured in 1978 Framingham Heart Stud

168 s predominantly derived from KCs, and plasma CETP level predicts hepatic KC content in humans.

169 increased hepatic CETP expression and plasma CETP.

170 high-density lipoprotein cholesterol, plasma CETP activity was related inversely to the incidence of

171 on of a community-based sample, lower plasma CETP activity was associated with greater CVD risk.

172 c CETP expression and largely reduced plasma CETP concentration, consequently improving the lipoprote

173 er KC content, accompanied by reduced plasma CETP concentration.

174 on the role of KCs in determining the plasma CETP concentration were performed in a transgenic (Tg) m

175 P expression correlated strongly with plasma CETP concentration.

176 on led to the potent and comparatively polar CETP inhibitor 26 showing robust high density lipoprotei

177 Compound 10g is a potent CETP inhibitor that maximally inhibited cholesteryl este

178 Anacetrapib, another potent CETP inhibitor, raises HDL-C levels by approximately 138

179 derivatives was identified exhibiting potent CETP inhibition.

180 rease blood pressure, suggesting that potent CETP inhibition by itself might not lead to increased bl

181 Anacetrapib and evacetrapib, two potent CETP inhibitors, are now being tested in large clinical

182 The mechanisms by which potent CETP inhibition increases ABCA1-specific CEC and pre-bet

183 re could help in devising methods to prevent CETP function as a cardiovascular disease therapeutic.

184 nhibited cholesteryl ester transfer protein (CETP) activity and L1210 leukemic cell viability with IC

185 hibiting cholesteryl ester transfer protein (CETP) activity raises high-density lipoprotein cholester

186 odulates cholesteryl ester transfer protein (CETP) activity to raise high-density lipoprotein cholest

187 contains cholesteryl ester transfer protein (CETP) and phospholipid transfer protein (PLTP).

188 s5882 in cholesteryl ester transfer protein (CETP) and rs4148217 in ATP-binding cassette subfamily G

189 ition of cholesteryl ester transfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and

190 Cholesteryl ester transfer protein (CETP) catalyzes the transfer of cholesteryl ester from h

191 n (apo)B/cholesteryl ester transfer protein (CETP) double transgenic mice-were treated with either ve

192 Cholesteryl ester transfer protein (CETP) facilitates the transfer of cholesteryl ester and

193 decrease cholesteryl ester transfer protein (CETP) gene activity increase plasma HDL-C; as such, medi

194 s in the cholesteryl ester transfer protein (CETP) gene have been associated with exceptional longevi

195 s of the cholesteryl ester transfer protein (CETP) gene with coronary artery disease (CAD) with taggi

196 n in the cholesteryl ester transfer protein (CETP) gene, which is involved in regulation of lipoprote

197 ition of cholesteryl ester transfer protein (CETP) has been proposed as a strategy to raise HDL chole

198 lations, Cholesteryl Ester Transfer Protein (CETP) inhibition and ATP-binding cassette transporter me

199 g potent cholesteryl ester transfer protein (CETP) inhibition at reduced lipophilicity was identified

200 ffect of cholesteryl ester transfer protein (CETP) inhibition on risk of ischemic events and on total

201 with the cholesteryl ester transfer protein (CETP) inhibitor anacetrapib exhibit a reduction in both

202 novel cholesterol esterase transfer protein (CETP) inhibitor TA-8995 in patients with mild dyslipidae

203 rapib, a cholesteryl ester transfer protein (CETP) inhibitor, in subjects with low high-density lipop

204 rapib, a cholesteryl ester transfer protein (CETP) inhibitor, increases HDL cholesterol levels, but t

205 Cholesteryl ester transfer protein (CETP) inhibitors (JTT-705 and torcetrapib) are currently

206 high in cholesteryl ester transfer protein (CETP) inhibitors as cardioprotective agents.

207 Potent cholesteryl ester transfer protein (CETP) inhibitors have been shown to substantially increa

208 Some cholesteryl ester transfer protein (CETP) inhibitors lower low-density lipoprotein cholester

209 Cholesteryl ester transfer protein (CETP) inhibitors raise HDL-C in animals and humans and m

210 the new cholesteryl ester transfer protein (CETP) inhibitors torcetrapib, dalcetrapib, anacetrapib a

211 ledge of cholesteryl ester transfer protein (CETP) inhibitors, heart disease risk reduction, and huma

212 Cholesteryl ester transfer protein (CETP) is a serum component responsible for both choleste

213 Cholesteryl ester transfer protein (CETP) is an important modulator of high density lipoprot

214 ition of cholesteryl ester transfer protein (CETP) is considered a potential new mechanism for treatm

215 sis that cholesteryl ester transfer protein (CETP) is mainly derived from KCs and may predict KC cont

216 ition of cholesteryl ester transfer protein (CETP) leads to a marked increase in plasma levels of lar

217 Cholesteryl ester transfer protein (CETP) mediates the transfer of cholesterol esters (CE) f

218 Cholesteryl ester transfer protein (CETP) mediates the transfer of cholesteryl esters (CEs)

219 Cholesterol ester transfer protein (CETP) moves triglyceride (TG) and cholesteryl ester (CE)

220 Cholesterol ester transfer protein (CETP) plays an important role in the regulation of HDL m

221 The cholesteryl ester transfer protein (CETP) plays an integral role in the metabolism of plasma

222 ition of cholesteryl ester transfer protein (CETP) raises HDL cholesterol levels and might therefore

223 levels, cholesterol ester transfer protein (CETP) rs3764261 and hepatic lipase (LIPC) rs8034802, wer

224 Cholesteryl ester transfer protein (CETP) transfers cholesteryl ester (CE) and triglyceride

225 Cholesteryl ester transfer protein (CETP) transfers cholesteryl esters from high-density lip

226 n plasma cholesteryl ester transfer protein (CETP) transports cholesteryl ester from the antiatheroge

227 nsfer by cholesteryl ester transfer protein (CETP) were measured using (3)H-cholesterol-labeled cell

228 ition of cholesteryl ester transfer protein (CETP), a molecule that plays a central role in HDL metab

229 Cholesteryl ester transfer protein (CETP), bactericidal/permeability inducing protein (BPI),

230 n of the cholesteryl ester transfer protein (CETP), which mediates the transfer of cholesteryl esters

231 DL levels by inhibiting CE transfer protein (CETP), which transfers CE from HDL to lower-density lipo

232 bitor of cholesteryl ester transfer protein (CETP).

233 inhibit cholesteryl ester transfer protein (CETP).

234 inhibit cholesteryl ester transfer protein (CETP).

235 icient, cholesterol ester transport protein (CETP) transgenic, and wild type mice with various doses

236 rs662799, BUD13 rs11216129, BUD13 rs623908, CETP rs820299, and LIPA rs1412444 single nucleotide poly

237 rs662799, BUD13 rs11216129, BUD13 rs623908, CETP rs820299, LIPA rs1412444, alcohol consumption, smok

238 increased lipoprotein sizes and lower serum CETP concentrations.

239 Strikingly, CETP-deficient adipocytes stored <50% of normal TG, prin

240 ficiency has led to the search for synthetic CETP inhibitors over the past 15 years.

241 verall, these results show that LTIP tailors CETP-mediated remodeling of HDL3 and HDL2 particles in s

242 e low-density lipoprotein receptor, and that CETP expression restores to normal the impaired RCT in m

243 ns, if confirmed, challenge the concept that CETP inhibition may lower CVD risk.

244 The present results demonstrate that CETP expression promotes macrophage RCT in mice, that th

245 Here, we test the hypothesis that CETP DNA sequence variants associated with higher HDL-C

246 However, the role that CETP plays in mediation of reverse cholesterol transport

247 Results showed that CETP binds to HDL via hydrophobic interactions rather th

248 Available data would suggest that CETP inhibitors will fail as lipid-altering medications

249 This preliminary report suggests that CETP V405 valine homozygosity is associated with slower

250 The CETP gene plays a critical role in lipoprotein metabolis

251 The CETP inhibitor torcetrapib was associated with a substan

252 The CETP modulator dalcetrapib raises HDL-C levels by approx

253 nd a continuous tunnel traversing across the CETP long axis appeared spontaneously.

254 Considered alone, the CETP score was associated with higher levels of HDL-C, l

255 er protein-truncating variants (PTVs) at the CETP gene were associated with plasma lipid levels and C

256 ; 1 in 975 participants carried a PTV at the CETP gene.

257 e comprised of 7 independent variants at the CETP locus and tested this score for association with HD

258 uggested a potential interaction between the CETP TaqIB polymorphism and intake of dietary fat on pla

259 We examined the association between the CETP TaqIB polymorphism and plasma HDL concentrations an

260 ary artery disease (CAD); (ii) excluding the CETP locus, there was not a predictable relationship bet

261 between bent and linear conformations in the CETP core tunnel as a consequence of the high degree of

262 f the existence of strongly bound CEs in the CETP core, very little is known about the mechanism of C

263 tudy tested whether genetic variation in the CETP gene is consistent with a protective effect of chol

264 Variants in the CETP gene region associated with increased circulating H

265 iovascular events related to variants in the CETP gene, both alone and in combination with variants i

266 etabolism, and the TaqIB polymorphism of the CETP gene has been associated with elevated HDL concentr

267 METHODS AND We sequenced the exons of the CETP gene in 58 469 participants from 12 case-control st

268 e data confirmed a significant effect of the CETP Taq1 gene on HDL concentrations and suggested a pot

269 the relative activity for inhibition of the CETP-mediated transfer of [3H]-cholesteryl ester from HD

270 ecent acute coronary syndrome to receive the CETP inhibitor dalcetrapib, at a dose of 600 mg daily, o

271 When combined with the HMGCR score, the CETP score was associated with the same reduction in LDL

272 Lipid modification) trial has shown that the CETP inhibitor anacetrapib decreased coronary heart dise

273 uman DNA sequence variants that truncate the CETP gene may provide insight into the efficacy of CETP

274 nhibitors form a complex between themselves, CETP, and HDL particles, which may interfere with the ma

275 Thus, CETP might not be essential for reverse cholesterol tran

276 Thus, CETP-D HDL has enhanced ability to promote cholesterol e

277 showed that increased cholesterol efflux to CETP-D HDL was ABCG1 dependent.

278 erates a hydrophobic environment, leading to CETP hydrophobic distal end interaction.

279 We have extended those observations to CETP.

280 Two CETP inhibitors, anacetrapib and evacetrapib, are in pha

281 Two CETP inhibitors, dalcetrapib and torcetrapib, have been

282 common SNPs and haplotype variants underlie CETP-related CAD risk, for which the common TaqIB varian

283 Various CETP inhibitors are currently being evaluated in phase I

284 increasing HDL-cholesterol (particularly via CETP inhibition) will increase AMD risk.

285 In our view, CETP inhibitors in combination with statins will be prof

286 reduction, but there is debate about whether CETP inhibition will reduce coronary heart disease risk.

287 structure, dynamics, and mechanism by which CETP transfers the neutral lipids has received tremendou

288 eed to identify the patient subsets in which CETP inhibition may be more or less effective.

289 It predicts that while CETP inhibition would not result in an increased RCT rat

290 oprotein cholesterol (LDL-C) associated with CETP deficiency has led to the search for synthetic CETP

291 found some had significant associations with CETP mass and high density lipoprotein cholesterol level

292 ng cardiovascular risk by raising HDL-C with CETP inhibition.

293 how various HDL-like particles interact with CETP by electron microscopy and molecular dynamics simul

294 unknown if HDL produced by interaction with CETP had pro-atherogenic or pro-inflammatory properties.

295 Among 58 469 participants with CETP gene-sequencing data available, average age was 51.

296 protein B (apoB) levels in participants with CETP scores at or above vs below the median.

297 or older from the Einstein Aging Study with CETP genotype available.

298 inical populations that will be treated with CETP inhibitors, all commonly occurring haplotypes were

299 Treatment with CETP inhibitors, either alone or in combination with sta

300 Twelve variants within CETP demonstrated nominal association with ICH, with the