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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/advagg_css\/css__ce2QY63WIanKyr8eSq7eavr1XQRRmFD6ZSmwpyJi8lM__zXwFqpqmxrZOXXcd_TpBQpjuELbmIP9wBR5UuTDWAO4__YJWWMMdfCJuAFm5cUEp88OsodhO3ZA-2lzRfoBsSlk4.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EFamilial combined hyperlipidemia is a highly atherogenic disorder that affects 1% to 2% of the Western world [Shoulders CC et al. \u003Cem\u003EHum Mol Genet\u003C\/em\u003E 2004]. It occurs in approximately 20% of patients who develop coronary heart disease before age 60 [Aouizerat BE et al. \u003Cem\u003EAm J Hum Genet\u003C\/em\u003E 1999]. This article discusses the need for continued research of treatments for familial hypercholesterolemia (FH). Emerging therapies include apolipoprotein B (ApoB) inhibitors, microsomal triglyceride transfer protein (MTP) inhibitors, and proprotein convertase subtilism kexin 9 (PCSK9) inhibitors [Alonso R et al. \u003Cem\u003EExpert Rev Cardiovasc Ther\u003C\/em\u003E 2013].\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003ELipid Disorders\u003C\/li\u003E\u003C\/ul\u003E\u003Cul class=\u0022kwd-group clinical-trial\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003ECardiology \u0026amp; Cardiovascular Medicine\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ELipid Disorders\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EFamilial combined hyperlipidemia is a highly atherogenic disorder that affects 1% to 2% of the Western world [Shoulders CC et al. \u003Cem\u003EHum Mol Genet 2004\u003C\/em\u003E]. It occurs in approximately 20% of patients who develop coronary heart disease before age 60 [Aouizerat BE et al. \u003Cem\u003EAm J Hum Genet\u003C\/em\u003E 1999].\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EPatrick M. Moriarty, MD, University of Kansas Medical Center, Lawrence, Kansas, USA, explained that treatment of familial hypercholesterolemia (FH) represents an unmet medical need. Statins have been shown to improve survival and reduce the risk of myocardial infarction (MI) in heterozygous familial hypercholesterolemia (HeFH) [Versmissen J et al. \u003Cem\u003EBMJ\u003C\/em\u003E 2008] and prolong survival in homozygous familial hypercholesterolemia (HoFH) [Raal FJ et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2011]. Emerging therapies include apolipoprotein B (ApoB) inhibitors, microsomal triglyceride transfer protein (MTP) inhibitors, and proprotein convertase subtilism kexin 9 (PCSK9) inhibitors [Alonso R et al. \u003Cem\u003EExpert Rev Cardiovasc Ther\u003C\/em\u003E 2013].\u003C\/p\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EMIPOMERSEN, AN INJECTABLE APOLIPOPROTEIN B-100 INHIBITOR\u003C\/h2\u003E\n         \u003Cp id=\u0022p-4\u0022\u003EJohn J.P. Kastelein, MD, PhD, University of Amsterdam, Amsterdam, The Netherlands, spoke about the benefits of mipomersen, a 20-mer phosphorothioate antisense oligonucleotide that is complementary in sequence to a segment of the human ApoB mRNA [Kastelein JJ et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2006]. Mipomersen is administered as a subcutaneous injection and has been shown to reduce low-density lipoprotein cholesterol (LDL-C), apoB, total cholesterol, and non-high-density lipoprotein cholesterol (non-HDL-C) levels in patients with HoFH, heterozygous FH as well as high-risk hypercholesterolemic patients. It has been developed as an adjunct to standard therapies including a statin; however, its indication was limited by regulatory authorities due to its many side effects, including liver enzyme abnormalities and accumulation of fat in the liver [Raal FJ et al. \u003Cem\u003ELancet\u003C\/em\u003E 2010; Stein EA et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2012].\u003C\/p\u003E\n         \u003Cp id=\u0022p-5\u0022\u003EIn a randomized, double-blind, multicenter, placebo-controlled, Phase 3 study in which 34 HoFH patients who were already receiving the maximum tolerated dose of a lipid-lowering drug were randomly assigned to mipomersen 200 mg subcutaneously every week or placebo for 26 weeks, the mean percent change in LDL-C concentration was significantly greater with the addition of mipomersen (\u221224.7%; 95% CI, \u221231.6 to \u221217.7) compared with placebo (\u22123.3%; 95% CI, \u221212.1 to 5.5; p=0.0003) [Raal FJ et al. \u003Cem\u003ELancet\u003C\/em\u003E 2010].\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ELOMITAPIDE, AN ORAL MICROSOMALTRANSFER PROTEIN INHIBITOR\u003C\/h2\u003E\n         \u003Cp id=\u0022p-6\u0022\u003EMichael Davidson, MD, University of Chicago, Chicago, Illinois, USA, discussed the oral MTP inhibitor, lomitapide. MTP, an intracellular lipid-transfer protein found in the lumen of the endoplasmic reticulum, is responsible for binding and shuttling individual lipid molecules between membranes [Hussain MM et al. \u003Cem\u003EJ Lipid Res\u003C\/em\u003E 2003]. Normal concentrations and function of MTP are necessary for the proper assembly and secretion of apoB-containing lipoproteins in the liver and intestines [Liao W et al. \u003Cem\u003EJ Lipid Res\u003C\/em\u003E 2003].\u003C\/p\u003E\n         \u003Cp id=\u0022p-7\u0022\u003EA dose-escalation study to examine the safety, tolerability, and effects on lipid levels of lomitapide (BMS-201038), an inhibitor of the miscrosomal triglyceride transfer protein, showed that all patients tolerated titration to the highest dose of 1.0 mg\/kg\/day. Treatment at this dose decreased LDL-C levels by 51% and apoB levels by 56% from baseline (p\u0026lt;0.001 for both comparisons) [Cuchel M et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2007]. Serious adverse effects associated with lomitapide included hepatic fat accumulation and elevated liver aminotransferase levels. Thus as with mipomersen, lomitapide has received FDA approval for use only in patients with HoFH due to adverse events which include elevations in serum transaminase and hepatic steatosis and gastrointestinal side effects [Robinson JG. \u003Cem\u003EJ Manag Care Pharm\u003C\/em\u003E 2013].\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-3\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ECHOLESTERYL ESTER TRANSFER PROTEIN INHIBITORS\u003C\/h2\u003E\n         \u003Cp id=\u0022p-8\u0022\u003EChristopher Cannon, MD, Harvard Medical School, Boston, Massachusetts, USA, discussed the oral CETP inhibitors. The ILLUMINATE trial studied torcetrapib, and, in spite of favorable effects on lipids including a 72% increase in HDL and a 25% reduction in LDL-C, was stopped early due to increased major cardiovascular (CV) events and higher blood pressure [ILLUMINATE; Barter PJ et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2007]. Later studies suggested that the adverse effects of torcetrapib came from molecule-specific off-target effects on the adrenal gland, and were not related to the direct effect of CETP inhibition [Krishna R et al. \u003Cem\u003ELancet\u003C\/em\u003E 2007].\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EDalcetrapib, the second CETP inhibitor developed, was evaluated in the dal-OUTCOMES trial in patients (n=15,871) with a recent acute coronary syndrome. A substantial increase in HDL levels was seen with dalcetrapib compared with placebo (31% to 40% vs 4% to 11%), and no off-target effects on the adrenal gland or hypertension were observed. However, dalcetrapib did not reduce the primary composite outcome of death from coronary heart disease, a major nonfatal coronary event or ischemic stroke (8.3% with dalcetrapib vs 8.0% with placebo; HR, 1.04; 95% CI, 0.93 to 1.16; p=0.52) [Schwartz GG et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2012].\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EAnacetrapib is the third CETP inhibitor. It increases HDL-C by over 100% and lowers LDL-C by 30% to 40% as monotherapy and when coadministered with statins [Cannon CP et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2010]. In a recent 1.5-year safety study in \u223c1600 patients with CV disease [Cannon CP et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2010], anacetrapib treatment had no effect on blood pressure, electrolytes, or aldosterone, and the distribution of CV events suggested that anacetrapib treatment would not be associated with an increase of CV risk as was seen with torcetrapib.\u003C\/p\u003E\n         \u003Cp id=\u0022p-11\u0022\u003EA randomized controlled trial in 398 patients with elevated LDL-C or low HDL-C of a fourth CETP inhibitor, evacetrapib, showed that evacetrapib monotherapy produced dose-dependent increases in HDL-C of 54% to 129% and decreases in LDL-C of \u221214% to \u221236% (both p\u0026lt; 0.001 compared with placebo) [Nicholls SJ et al. \u003Cem\u003EJAMA\u003C\/em\u003E 2011].\u003C\/p\u003E\n         \u003Cp id=\u0022p-12\u0022\u003EBoth anacetrapib and evacetrapib are currently involved in ongoing Phase 3 trials (\u003Ca id=\u0022xref-table-wrap-1-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T1\u0022\u003ETable 1\u003C\/a\u003E).\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-4\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EPROPROTEIN CONVERTASE SUBTILISM KEXIN 9 INHIBITORS\u003C\/h2\u003E\n         \u003Cp id=\u0022p-13\u0022\u003EJames M. McKenney, PharmD, Virginia Commonwealth University, Richmond, Virginia, USA, discussed PCSK9 inhibitors, a novel therapy for lowering LDL-C. PCSK9 regulates cholesterol and\/or lipid homeostasis via cleavage at nonbasic residues or through induced degeneration of receptors. Reduction in LDL-C levels with PCSK9 is associated with a substantial reduction in the incidence of coronary events, even in populations with a high prevalence of non\u2013lipid-related CV risk factors [Cohen JC et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2006].\u003C\/p\u003E\n         \u003Cp id=\u0022p-14\u0022\u003EIn the LAPLACE-TIMI 57 Phase 2, multicenter, dose-ranging study, 631 stable patients with hypercholesterolemia on a statin, were randomly assigned to AMG 145, a fully human monoclonal IgG2 antibody against PCSK9, administered subcutaneously every 2 (70, 105, or 150 mg) or 4 weeks (280, 350, or 420 mg) or matching placebo injections [Giugliano RP et al. \u003Cem\u003ELancet\u003C\/em\u003E 2012]. At the end of the 12-week period, largely dose-dependent reductions in the mean LDL-C concentrations for the every 2-week regimens ranged from 42% to 66% and from 42% to 50% for the every 4-week regimens (p\u0026lt;0.0001 for each dose vs placebo). These results suggest that PCSK9 inhibition could be a new model in lipid management and is being evaluated in ongoing Phase 3 clinical trials.\u003C\/p\u003E\n         \u003Cp id=\u0022p-15\u0022\u003ESAR236553\/REGN727, another injectable monoclonal antibody to PCSK9, also showed promising results in a multicenter, randomized, placebo-controlled Phase 2 trial in adults with HeFH and LDL-C concentrations of 100 mg\/dL or higher on stable diet and statin dose, with or without ezetimibe. Patients were randomized to receive subcutaneous REGN727 150, 200, or 300 mg every 4 weeks, or 150 mg every 2 weeks, or matching placebo every 2 weeks (ratio 1:1:1:1:1). The primary endpoint of LDL-C reduction from baseline to Week 12 was 29% for 150 mg every 4 weeks (p=0.0113), 32% for 200 g every 4 weeks (p=0.0035), 43% for 300 mg every 4 weeks (p\u0026lt;0.0001), and 68% for 150 mg every 2 weeks (p\u0026lt;0.0001), compared with 11% with placebo. [Stein EA et al. \u003Cem\u003ELancet\u003C\/em\u003E 2012]. A Phase 3 trial is underway to evaluate the CV effects and long-term safety of this compound on a background of statin therapy.\u003C\/p\u003E\n         \u003Cp id=\u0022p-16\u0022\u003EUntil recently, many patients with HeFH and HoFH had difficultly achieving adequate reduction in LDL-C. Mipomersen and lomitapide have recently received FDA approval for the treatment of HoFH and offer new options as adjuncts to high-dose statins and second-line treatments. As emerging therapies such as CETP inhibitors and PCSK9 inhibitors continue development, options will increase for patients with HoFH, HeFH, and other patients with severe dyslipidemia.\u003C\/p\u003E\n         \u003Cdiv id=\u0022T1\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/13147\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/13147\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/13147\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-17\u0022 class=\u0022first-child\u0022\u003EOngoing Phase 3 Trials of Anacetrapib and Evacetrapib\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2013 MD Conference Express\u00ae\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/13\/2\/30.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzo1w1\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_tables.js?nzo1w1\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}