作者
Brian Bergmark,Nicholas Marston,Candace Bramson,M. Curto,Vesper Ramos,Alexandra Jevne,Julia Kuder,Jeong‐Gun Park,Sabina A. Murphy,Subodh Verma,Wojciech Wojakowski,Steven G. Terra,Marc S. Sabatine,Stephen D. Wiviott,Diane Carbonneau,Raphael Poulin-Robitaille,Jeffrey D. Wayne,Keung Lee,Samuel Mujica Trenche,Petros Dzongowski,Daniel Gaudet,Joanna Van,Dilawar Ajani,Harold Bays,John O’Mahony,Adam Janas,John Scott,Moustafa Ashraf Moustafa,Thomas Ransom,Sabrina Benjamin,Naresh Aggarwal,Paweł Bogdański,Douglas G Friars,Robert Schlosser,Bogusław Okopień,Madhusudan Budhraja,Lawrence Feld,Leslie J. Klaff,Guy Tellier,Giuseppe Mazza,I Wierzbicka,Ewa Jazwinska-Tarnawska,Fernando Boccalandro,Julio Rosenstock,Elizabeth Marquez,Kim Barbel-Johnson,Katarzyna Madziarska,K W Heaton,Jean‐Claude Tardif,John Rubino,Miguel Á. Treviño,Katie Moriarty,Anil Gupta,Wojciech Wojakowski,James L. Fidelholtz,Dhiraj Gupta,Hani Al‐Asaad,Shane Christensen,Parag K Shah,Stephanie Li,Mark Sherman,Andre Frechette,Cecilia Arango,Alan Egan,Sunny Srivastava,Archna Bajaj,Carlos Ince,Aleksander Żurakowski
摘要
Genetic loss-of-function variants in ANGPTL3 are associated with lower levels of plasma lipids. Vupanorsen is a hepatically targeted antisense oligonucleotide that inhibits Angiopoietin-like 3 (ANGPTL3) protein synthesis.Adults with non-high-density lipoprotein cholesterol (non-HDL-C) ≥100 mg/dL and triglycerides 150 to 500 mg/dL on statin therapy were randomized in a double-blind fashion to placebo or 1 of 7 vupanorsen dose regimens (80, 120, or 160 mg SC every 4 weeks, or 60, 80, 120, or 160 mg SC every 2 weeks). The primary end point was placebo-adjusted percentage change from baseline in non-HDL-C at 24 weeks. Secondary end points included placebo-adjusted percentage changes from baseline in triglycerides, low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (ApoB), and ANGPTL3.Two hundred eighty-six subjects were randomized: 44 to placebo and 242 to vupanorsen. The median age was 64 (interquartile range, 58-69) years, 44% were female, the median non-HDL-C was 132.4 (interquartile range, 118.0-154.1) mg/dL, and the median triglycerides were 216.2 (interquartile range, 181.4-270.4) mg/dL. Vupanorsen resulted in significant decreases from baseline over placebo in non-HDL-C ranging from 22.0% in the 60 mg every 2 weeks arm to 27.7% in the 80 mg every 2 weeks arm (all P<0.001 for all doses). There were dose-dependent reductions in triglycerides that ranged from 41.3% to 56.8% (all P<0.001). The effects on LDL-C and ApoB were more modest (7.9%-16.0% and 6.0%-15.1%, respectively) and without a clear dose-response relationship' and only the higher reductions achieved statistical significance. ANGPTL3 levels were decreased in a dose-dependent manner by 69.9% to 95.2% (all P<0.001). There were no confirmed instances of significant decline in renal function or platelet count with vupanorsen. Injection site reactions and >3× elevations of alanine aminotransferase or aspartate aminotransferase were more common at higher total monthly doses (up to 33.3% and 44.4%, respectively), and there was a dose-dependent increase in hepatic fat fraction (up to 76%).Vupanorsen administered at monthly equivalent doses from 80 to 320 mg significantly reduced non-HDL-C and additional lipid parameters. Injection site reactions and liver enzyme elevations were more frequent at higher doses, and there was a dose-dependent increase in hepatic fat fraction.URL: https://clinicaltrials.gov; Unique identifier: NCT04516291.