Cholesterol Synthesis and Absorption Markers
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1 The Yin and Yang of New Lipid-modifying Agents Inhibitors Are They on Life Support? PCSK9 Inhibitors Are They Potential Game Changers? Thomas Dayspring, MD, FACP, FNLA Diplomate of the American Board of Clinical Lipidology Fellow of the National Lipid Association North American Menopause Society Certified Menopause Practitioner Director of Cardiovascular Education The Foundation for Health Improvement and Technology (FHIT) Richmond, VA Disclosures (Last 12 months) Consultant or Advisory Board Abbott Labs Amarin Genetech (The Roche Group) Genzyme Glaxo Smith Kline (GSK) Health Diagnostic Labs Kowa & Eli Lilly Merck Omthera Lecture Bureau Abbott GSK HD Lab Kowa/Lilly Merck Risk Reduction for CHD Events As a Function of Changes in -C, and HDL-C Percent Change CHD Event Rate * -C 1% 1% TC 1% 2% ** HDL-C 1% 3% *4S, CARE, LIPID, WOSCOPS **HELSINKI, VA-HIT,AFCAPS/TexCAPS 1
2 Cholesterol Synthesis and Absorption Markers A line from William Shakespeare's Macbeth, Macbeth's plans are falling apart around him. Life's but a walking shadow, a poor player That struts and frets his hour upon the stage And then is heard no more: it is a tale Told by an idiot, full of sound and fury, Signifying nothing. from Act 5, Scene 5 apoa-i Preβ- HDL α HDL 2 & 1or HDL2a, b α HDL 4 & 3 or HDL3c, b, a Homotypic exchange -rich HDL -rich HDL SR-B1 HL α HDL 4 & 3 or HDL3a,b,c Direct Reverse cholesterol transport Heterotypic exchange Apo A-V Lipoprotein Lipase ( hydrolysis & PL release) apoc-ii apoe (intermediate) apob Liver (large) IDL (small) r Indirect Reverse cholesterol transport Hepatic Lipase To Hepatic ( SmallSinusoid and IDL receptor Lipolysis& HL) Phospholipids apoa-i Preβ- HDL Cholesterol Triglyceride Normal Lipid Trafficking α HDL 2 & 1or HDL2a, b α HDL 4 & 3 or HDL3c, b, a -rich HDL -rich molecule binds to the HDL lipoprotein surface to acquire neutral lipids SR-B1 HL Apo A-V α HDL 4 & 3 or HDL3a,b,c apoc-ii apoe apob Liver (large) (intermediate) r Hepatic Lipase Phospholipids (small) IDL molecule transfers neutral lipids [cholesteryl ester () and triglycerides ()] among both HDL and HDL subparticles as well as changing conformation to accommodate and. Cholesterol Triglyceride Inhibition 2
3 Cholesterol Synthesis and Absorption Markers Inhibitors and Modulators Evacetrapib Barter et al. N Engl J Med. 27;357: Qiu et al. Nat Struct Mol Biol. 27;14: apoa-i Preβ- HDL α HDL 2 & 1or HDL2a, b α HDL 4 & 3 or HDL3c, b, a -rich HDL -rich HDL HL Apo A-V α HDL 4 & 3 or HDL3a,b,c SR-B1 apoc-ii apob Liver apoe (large) (intermediate) r Hepatic Lipase (small) IDL Torcetrapib molecule Torcetrapib increases binding affinity of for lipoproteins, decreasing and exchange between lipoproteins, including among HDL particles Phospholipids Cholesterol Triglyceride Torcetrapib Inhibition MOA Double-blind study involving 15,67 Doublepatients at high cardiovascular risk. Torcetrapib therapy resulted in an increased risk of mortality and morbidity of unknown mechanism. Although there was evidence of an offoff-target effect of torcetrapib, we cannot rule out adverse effects related to inhibition. The Investigation of Lipid Level Management to Understand its IMpact IN ATherosclerotic ATherosclerotic Events (ILLUMINATE (ILLUMINATE)) Barter PJ et al. N Engl J Med 27;357:
4 The Investigation of Lipid Level Management to Understand its IMpact IN ATherosclerotic Events (ILLUMINATE) Death From Any Cause Major Cardiovascular Events Patients without Events (%) Patients without Events (%) Atorvastatin only Torcetrapib plus Atorvastatin Days after Randomization Atorvastatin only Torcetrapib plus Atorvastatin Days after Randomization The hazard ratio for the primary outcome major cardiovascular events was 1.25 in the torcetrapib group, as compared with the atorvastatin-only only group (95% [CI], 1.9 to 1.44; P =.1) Barter PJ et al. N Engl J Med 27;357: The Investigation of Lipid Level Management to Understand its IMpact IN ATherosclerotic Events (ILLUMINATE) Lipids: % Change TC -7. % HDL-C % -C % (median) -9 % p <.1 In the atorvastatin-only only group, all lipid changes were minimal during the study; In the torcetrapib group, these changes included an increase of 72.1% in the HDL-C, a decrease of 24.9% in -C,, and a decrease of 9% in triglycerides So with that HDL-C rise, why did we not see 72 3 = 216% event reduction? Barter PJ et al. N Engl J Med 27;357: The Investigation of Lipid Level Management to Understand its IMpact IN ATherosclerotic Events (ILLUMINATE): Causes of Death Atorva Atorva/ Torcetrapib Any CV Event Sudden Death Fatal MI 6 8 Hemorrhagic CVA 4 Ischemic CVA 2 CHD 1 2 Other Cardiac 1 4 Cancer Infection 9 Unknown 4 4 At study termination, there were 93 deaths in the torcetrapib group and 59 in the atorvastatin only group, for a hazard ratio of 1.58 in the torcetrapib group (95% CI, 1.14 to 2.19; P =.6). For death from non-cv causes, more patients in the torcetrapib group than in the atorvastatin-only only group died from cancer (24 vs. 14) and infection (9 vs. ). Seven of the nine deaths from infection were in patients with diabetes. Barter PJ et al. N Engl J Med 27;357:
5 Cholesterol Synthesis and Absorption Markers The role of lipoproteins in modulating membrane cholesterol content (HDL in particular) has been extensively investigated and suggests a possible role for these lipoproteins in modulating immune response HDL and ApoAApoA-I-induced cholesterol depletion and consequent disruption of plasma membrane lipid rafts in APCs inhibits their capacity to stimulate T cell activation. This mechanism is highly dependent on the reduction of major histocompatibility complex (MHC class II) molecules present on the cell surface following ABCAABCA-1 activation and on cholesterol efflux. As HDL are a reservoir for several biologically active substances that may impact the immune system, authors ask how the fine tuning of lipid and protein exchange among lipoproteins affect HDLHDL-related immune functions? Atherosclerosis 212;225:34-35 The Investigation of Lipid Level Management to Understand its IMpact IN AT ATherosclerotic herosclerotic Events (ILLUMINATE (ILLUMINATE)) HRs for Major CV Events by Atorvastatin Dose Hazard ratio (95% CI) P=value All doses 464/533 (6.2%) 373/534 (5.%) 1.25 (1.9, 1.44).1 1 mg 22/3218 (6.3%) 147/3274 (4.5%) 1.41 (1.14, 1.74).2 2 mg 118/236 (5.8%) 94/227 (4.6%) 1.26 (.96, 1.65).98 4 mg 87/158 (5.8%) 84/1559 (5.4%) 1.8 (.8, 1.46) mg 57/771 (7.4%) 48/674 (7.1%) 1.4 (.71, 1.53).831 Atorvastatin Dose T/A (Events/n) A (Events/n) T = Torcetrapib A = Atorvastatin Favors A Favors T/A The harm caused by torcetrapib was confined to individuals taking atorvastatin 1 mg. The harm could not be explained by torcetrapibtorcetrapib-induced changes in lipid levels, blood pressure, or electrolytes. It is conceivable that higher doses of atorvastatin protected against the harm caused by torcetrapib Barter PJ et al. J. Lipid Res : apoa-i Preβ- HDL α HDL 2 & 1or HDL2a, b α HDL 4 & 3 or HDL3c, b, a -rich HDL -rich HDL α HDL 4 & 3 or HDL3a,b,c SR-B1 HL Apo A-V apoc-ii apob Liver apoe (large) (intermediate) (small) IDL molecule Dalcetrapib molecule Dalcetrapib prevents the change in conformation required for transfer activity to and, leaving unaffected -mediated exchange among HDL subparticles. Phospholipids Cholesterol Triglyceride Dalcetrapib Modulation MOA 5
6 Role Inhibitors in Generating pre-β-hdl 6 Human plasma Pre-β-HDL (µg/ml) Dalcetrapib Torcetrapib Anacetrapib Human plasma with an endogenous level of 1.25 g/ml was incubated for 21 hours with and without test compounds, dalcetrapib, torcetrapib, and anacetrapib (.1, 1, 3, and 1 µm) Compound Concentration (µm) Dalcetrapib 1, 3, and 1 µm M dose-dependently dependently increased pre-β-hdl, as quantified by ELISA, by 4, 13, and 16% (NS, P <.5, and.1, respectively). Torcetrapib and anacetrapib decreased pre-β-hdl formation by more than 46% ( P <.1) at all concentrations tested. Niesor EJ et al. J. Lipid Res : Assigned 15,871 patients who had had a recent acute coronary syndrome to receive the inhibitor dalcetrapib, at a dose of 6 mg daily, or placebo, in addition to the best available evidence-based care. The primary efficacy end point was a composite of death from coronary heart disease, nonfatal myocardial infarction, ischemic stroke, unstable angina, or cardiac arrest with resuscitation. Dalcetrapib increased HDL cholesterol levels but did not reduce the risk of recurrent cardiovascular events. N Engl J Med 212;367: dal-outcomes HDL-C mg/dl -C mg/dl HDL-C levels increased from baseline by 4 to 11% in the placebo group and by 31 to 4% in the dalcetrapib group Months Dalcetrapib Placebo Placebo Dalcetrapib With the 25-3 % rise in HDL-C vs. placebo, where is the expected 75-9% reduction in CV events Dalcetrapib had a minimal effect on cholesterol levels. Triglyceride levels increased from baseline by 6 to 17% in the placebo group and by 4 to 1% in the dalcetrapib group Apolipoprotein A-I levels were increased by 1% after 3 months of treatment with dalcetrapib and by 9% at the end of the trial (P<.1), with a minimal effect on levels of apolipoprotein B N Engl J Med 212;367:
7 Eligible patients who were taking a statin and who had an cholesterol level that was consistent with that recommended in guidelines were assigned to receive 1 mg of anacetrapib or placebo daily for 18 months. The primary end points were the percent change from baseline in cholesterol at 24 weeks (HDL cholesterol level was a secondary end point) and the safety and side-effect effect profile of anacetrapib through 76 weeks. Cardiovascular events and deaths were prospectively adjudicated. N Engl J Med 21;363: Determining the EFficacy and Tolerability of INhibition with AnacEtrapib (DEFINE) -C (mg/dl) 11 # 1623 patients 11 Anacetrapib Placebo HDL-C (mg/dl) We can look forward to the x3 (414) and (4) or or 454% event reduction Baseline Week Baseline Week Discontinuation in 14.6% and 17.4% of patients discontinuing anacetrapib and placebo, By 24 weeks, -cholesterol levels had decreased from 81 mg per deciliter to 45 mg,, a 39.8% reduction with anacetrapib beyond that seen with placebo (P<.1) HDL-C increased from 41 mg per deciliter to 11 mg/dl a 138.1% increase with anacetrapib beyond that seen with placebo (P<.1) No appreciable differences between groups in the percentage of patients with adverse events that were thought to be related to the study drug or that led to its discontinuation Cannon CP et al. 21 Dec 16;363(25): Determining the EFficacy and Tolerability of INhibition with AnacEtrapib (DEFINE) Bland-Altman plot over other methods of comparing two different measurement methods: -axis is the mean of your two measurements, which is your best guess as to the "correct" result and the Y-axis is the difference between the two measurement differences. If one method always gives too high a result, then all of the points will be above or all below the zero line. Friedewald BQ -C mg/dl Baseline Bland Altman -C by FF & βq SD Mean SD Friedewald BQ -C mg/dl On Treatment Bland Altman of FF vs βq -C SD Mean SD Mean of Friedewald & β-quant -C Estimation of low-density lipoprotein cholesterol (-C) using the Friedewald (FF) formula and the β-quantification (BQ) reference method Mean of Friedewald & β-quant -C After 24 weeks of treatment with anacetrapib, mean -C values by FF formula, Roche direct method (RDM) and Genzyme direct method (GDM) deviated from that measured by the β-quantification (BQ) reference method by 12.2 ± 7.5, 1.2 ± 6.6, 1.8 ± 8.8 mg/dl, respectively Davidson M et al. J. Lipid Res :
8 Determining the EFficacy and Tolerability of INhibition with AnacEtrapib (DEFINE) Cardiovascular Events During the treatment Phase of Study* Event Anacetrapib (n = 88 Placebo (n = 84 number (percent) Prespecified; adjudicated CV safety endpoint 16 (2.) 21 (2.6) Death from cardiovascular causes Nonfatal myocardial infarction Hospitalization for unstable angina Nonfatal stroke Death from any cause Heart failure Revascularization PCI CABG 4 (2.5) 1 (.1) 6 (.7) 9 (1.1) 1 (.1) 6 (.7) 5 (.6) 5 (.6) 11 (1.4) 8 (1.) 3 (.4) 4 (.5) 8 (1.) 28 (3.5) 6 (.7) 25 (3.1) 2 (.2) 3 (.4) * The duration of the treatment phase of the study was 76 weeks. CABG = coronary artery bypass grafting and PCI is percutaneous coronary intervention Cannon CP et al. 21 Dec 16;363(25): Activity % Women Men %tile 1 th percentile 4 Mass and Activity A 9 th percentile Women Percentiles Percentiles Distribution of individuals (men and women) as a function of endogenous plasma activity (Panel A) or as a function of plasma concentration (Panel B). Panel A arrows indicate endogenous plasma activity corresponding to the 1th and 9th percentile. Panel B: arrows indicate median value for plasma concentration in both men and women. Concentration (ug/ml) Men Median Values There is an optimal activity range comprised between 22% and 34% thus representing the future clinical therapeutic goal for endogenous activity in patients with metabolic disorders and high cardiovascular risk. These observations are particularly useful in the context of pharmacological modulation of plasma activity in patients with high cardiovascular risk. 2 Villard EF et al. Atherosclerosis 213;227: B Unanswered Questions is an essential part of normal lipoprotein catabolism and lipid trafficking and plays crucial roles in direct and indirect reverse cholesterol transport Will i only be of benefit in those with increased i activity? Is there a danger in over suppressing? Does i create partially dysfunctional HDL particles? They do not seem to hinder macrophage delipidation But what does the induced size and core lipid changes do to HDL proteomics, lipidomics and metabolomics Is HDLs role in innate immunity affected adversely? Will anaceptrapib and evacetrapib work because of their apob lowering potential? 8
9 Proprotein Convertase Subtilisin Kexin Type 9 The family of the secretory proprotein convertases (PCs) comprises seven basic amino acid-specific subtilisin-like serine proteinases known as PC1/3, PC2, furin, PC4, PC5/6, PA4 and PC7, and two other PCs, SKI-1 (subtilisin-kexin isozyme-1)/s1p (site-1 protease) and PCSK9 (proprotein convertase subtilisin kexin 9) that cleave at nonbasic residues. PCSK9 acts as a chaperone that binds the receptor, thereby targeting it for lysosomal degradation. The enzymatic activity of PCSK9 is not involved in that process, but rather permits proper intramolecular processing of PCSK9. Gilles Lambert et al. Atherosclerosis 23 (29) 1 7 Participants with several genetic variants of PCSK9 (loss of function) have persistently lower serum -C levels than noncarriers from ages 18 to 5. Such long-term reduction in -C levels is associated with reduced subclinical atherosclerosis burden in black men. Huang,C. et al Circ Cardiovasc Genet.29 Aug;2(4): Atherosclerosis Risk In the Community (ARIC) Study Frequency (%) Frequency (%) No nonsense mutation (n = th percentile PCSK9 124 or PCSK9 679 (n = 85) % The data used in this study included that from black participants (predominantly, those living in Jackson) and white participants C in Black Subjects (mg/dl) Cholesterol Levels among Black Subjects, According to the Presence or Absence of a PCSK9 142 or PCSK9 679 Allele. Top: The distribution of plasma cholesterol levels at baseline among 3278 black subjects who did not have a PCSK9142 or PCSK9679 allele Bottom: The distribution of levels among the 85 black subjects who had one of these two alleles. Cohen JC et al. N Engl J Med 26;354:
10 Atherosclerosis Risk In the Community (ARIC) Study 12 Coronary Heart Disease (%) 8 4 P =.8 Graph shows the percentage of participants from these two groups who had no evidence of coronary heart disease at baseline and in whom coronary heart disease developed during the 15-year follow-up period. No Yes PCSK9 142x or PCSK9 679x Cohen JC et al. N Engl J Med 26;354: Proprotein Convertase Subtilisin Kexin type 9 Cellular trafficking of PCSK9. r ARH ARH (I) Recycling Degradation ARH = autosomal recessive hypercholesterolemia adaptor protein Endosome (II) r Endoplasmic Reticulum Golgi PCSK9 PCSK9 is synthesized as a proprotein that undergoes autocatalytic cleavage in the ER, becoming a self-inhibited enzyme with the prodomain non-covalently attached to the catalytic site. (i) As a secreted factor PCSK9 is internalized in the endosome by the r, thereby directing the receptor for degradation rather than recycling to the plasma membrane. r endocytosis in clathrin-coatedcoated pits requires the expression of the ARH adaptor protein. (ii) In the secretory pathway PCSK9 may also target the r for lysosomal degradation. Gilles Lambert et al. Atherosclerosis 29:23:1 7 This study provides new insights into the action of PCSK9 in regulating apob metabolism. A new role for PCSK9 is proposed that involves shuttling between apob and the receptor. Endogenous interacted with apob in By inhibiting PCSK9, apob hepatocytes. would be driven down the The PCSK9/apoB interaction resulted in increased production of apob, possibly through degradation the inhibition of intracellular pathway apob degradation? via the autophagosome/lysosome pathway. The physical interaction of PCSK9 with apob acts to shunt apob away from autophagosomes and degradation.. In turn, most of the apob would be destined for assembly and secretion as from hepatocytes. ATVB 212;32:
11 Assessed the effects of AMG 145, a human monoclonal antibody against PCSK9 (prevents binding to r), in patients with hypercholesterolemia in the absence of concurrent lipid-lowering lowering treatment. AMG 145 significantly reduced free PCSK9 and serum -C concentrations compared with placebo in patients with hypercholesterolemia not given statins. AMG 145 reduced -C concentrations rapidly and consistently during repeated dosing in both the every 2 weeks and every 4 weeks groups. The -C-lowering effect of AMG 145 and its duration seem to be dose dependent. AMG 145 administered every 2 or 4 weeks significantly reduced concentrations of -C and other apolipoprotein B containing lipoproteins compared with every 2 weeks and every 4 weeks placebo injections or open-label ezetimibe. AMG 145 was well tolerated during this 12 week study. Lancet 212; 38: Monoclonal Antibody Against PCSK9 to Reduce Elevated -C in Patients Currently Not Receiving Drug Therapy For Easing Lipid Levels (MENDEL) Mean Change From Baseline -C (%) Mean Change From Baseline -C (%) A Placebo q 2 wks Ezetimibe once daily AMG mg q 2 wks 2 AMG mg q 2 wks AMG mg q 2 wks Placebo B AMG mg q 4 wks Baseline Week 2 Week 4 Week 6 Week 8 Week 1 Week 12 Placebo q 4 wks AMG mg q 4 wks Ezetimibe AMG Ezetimibe once daily AMG mg q 4 wks AMG Ezetimibe AMG mg q 4 wks Placebo Data are mean. -8 Baseline Week 2 Week 4 Week 6 Week 8 Week 1 Week 12 -C is Friedewald calculated Koren MJ et al. Lancet 212; 38: Lancet 212; 38: Enrolled adults with heterozygous familial hypercholesterolemia and -C concentrations of 2 6 mmol/l or higher on stable diet and statin dose, with or without ezetimibe. Patients were randomly assigned to receive REGN mg, 2 mg, or 3 mg every 4 weeks, or 15 mg every 2 weeks, or placebo every 2 REGN727, weeks (ratio 1:1:1:1:1). a fully Randomization human was monoclonal stratified by concomitant use of ezetimibe at baseline. antibody targeted to PCSK9, inhibits Blinding was maintained by administration of placebo alternating with REGN727 for the groups of binding 4 week dosing. to the The primary receptor endpoint was mean percent reduction in -C from baseline at week 12 REGN727 was well tolerated and achieved substantial further -C reduction in patients with heterozygous FH and elevated -C treated with high-dose statins, with or without ezetimibe. 11
12 Mean Change (%) Mean Change (%) Placebo q 2 wks Regn727 2 mg q 4 wks Regn mg q 2 wks Regn mg q 4 wks Regn727 3 mg q 4 wks Baseline Week 2 Week 4 Week 6 Week 8 Week 1 Week 12 Week 16 Week 2 LOCF ApoB -C Effect of a monoclonal antibody to PCSK9, REGN727/SAR236553, to reduce -C in patients with heterozygous FH on stable statin with or without ezetimibe therapy Mean percent change in baseline -C (A) and ApoB (B) versus week during treatment and follow-up period for the mitt population -6-8 Baseline Week 2 Week 4 Week 6 Week 8 Week 1 Week 12 Week 16 Week 2 LOCF Visit Evan A Stein et al. Lancet 212; 38: Will the lipid/lipoprotein efficacy persist long term? Will there be compliance issues? (SQ injection q 2 wks) What will the cost be? What are the long term safety issues? Immune response to the human antibody? Very low -C Monotherapy? FH patients only? Statin intolerant patient? Remnants? Unanswered Questions Two Hearts Peter Max Thank You For Your Attention 12
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