new Trial Shows Promise for Reducing Inflammation After Heart Attack with antibody Therapy
BOSTON, MA - A randomized phase 2 trial has demonstrated that antibody-mediated inhibition of LOX-1 (lectin-like oxidized LDL receptor-1) may reduce residual inflammation in patients following a myocardial infarction (heart attack). The study, detailed in[publicationdetails-[publicationdetails-[publicationdetails-[publicationdetails-not provided in source text], offers a potential new therapeutic avenue for improving outcomes in individuals who continue to experience inflammation despite standard treatment.
Myocardial infarction frequently enough leaves behind lingering inflammation, contributing to adverse cardiac remodeling and increased risk of future events. LOX-1,expressed on various cells including endothelial cells and macrophages,plays a key role in this inflammatory process by mediating the uptake of oxidized LDL cholesterol. Blocking LOX-1 with a monoclonal antibody aims to interrupt this cycle and promote healing.
The trial involved a cohort of researchers with extensive ties to the pharmaceutical industry, as disclosed in accompanying conflict-of-interest statements. J.S. reports research grant support from Biotronik, sanofi, Pfizer and Attralus; consulting fees from BMS, Sanofi and Attralus; and speaker bureau fees from Pfizer, AstraZeneca, Boehringer Ingelheim, Novartis, Bayer, Sanofi, Biotronik, CircleCVi, Takeda, amicus and BMS. E.K. reports lecture fees from Astellas, Abbott, Amgen, astrazeneca, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly Japan KK, Daiichi-Sankyo, Menarini, Ono pharmaceutical, Ootsuka Pharmaceutical, MSD KK, Takeda Pharmaceutical, Tanabe-Mitsubishi, Bayer and Pfizer; and consulting fees or research fund from Boehringer Ingelheim, bayer, Novo Nordisk, Daiichi-Sankyo, Abbott, Ono Pharmaceutical and Tanabe-Mitsubishi. A.Z. has received grant support from Novartis and consulting and/or lecture fees from AstraZeneca, novartis, boehringer Ingelheim, Amarin, Pfizer, Sanofi, Amgen, Eli lilly and Novo Nordisk.A.G.is a former full-time employee of AstraZeneca and current full-time employee and stockholder of Ribocure Pharmaceuticals. M.L.O.D., D.A.M., M.S.S., J.K., J.-G.P. and S.A.M. are members of the TIMI Study Group and have received research grant support thru Brigham and Women’s Hospital from Abbott, Amgen, Anthos Therapeutics, AstraZeneca, Boehringer Ingelheim, Daiichi-Sankyo, Ionis, Marea, Merck, Novartis, Pfizer, Saghmos Therapeutics and Verve Therapeutics and have received consulting fees Amgen, AMPEL BioSolutions, Anthos Therapeutics, AstraZeneca, Beren Therapeutics, Boehringer Ingelheim, Dr. Reddy’s Laboratories, Fibrogen, Merck, Moderna, Novo Nordisk, Precision BioSciences and Silence Therapeutics. B.F. reports grant support from AstraZeneca/Medimmune, MedTrace, Ionis and NIH/NHLBI.J.L.-S. reports research grant from AstraZeneca, Bayer/Johnson & Johnson, pfizer and Amgen, and has received speaker honoraria from Menarini. A.A.D.P.F. reports consulting fees from AstraZeneca, Novartis, Boehringer Ingelheim, Merck Sharp Dohme and Mundipharma. M.T.L. has received research funding through the Massachusetts General Hospital from AstraZeneca, American Heart Association, Ionis, Johnson & Johnson Innovation, MedImmune, National Academy of medicine, National Heart, Lung, and Blood Institute and Risk Management Foundation of the Harvard Medical Institutions. J.A.C.L. reports grant funding from AstraZeneca and Canon Medical Systems. M.S.S. reports research grant support through Brigham and Women’s Hospital from Abbott, Amgen, Anthos Therapeutics, AstraZeneca, Boehringer Ingelheim, Daiichi-Sankyo, ionis, Marea, Merck, Novartis, Pfizer, Saghmos Therapeutics and Verve Therapeutics, and has received consulting fees from Amgen, AMPEL BioSolutions, anthos Therapeutics, AstraZeneca, Beren Therapeutics, Boehringer Ingelheim, Dr. Reddy’s Laboratories, Fibrogen, Merck, Moderna, Novo nordisk, Precision BioSciences and Silence Therapeutics.The othre authors declare no competing interests.
The phase 2 trial’s findings suggest a potential benefit of LOX-1 inhibition,paving the way for larger,phase 3 trials to confirm these results and assess the long-term clinical impact on cardiovascular outcomes. Further research will be crucial to determine the optimal patient populations and treatment strategies for this novel approach.
