A phase I study of the fully human, fragment crystallizable-engineered, anti-CD-33 monoclonal antibody BI 836858 in patients with previously-treated acute myeloid leukemia

• Type of Material: Article
• Authors: Sumithira Vasu, Ohio State University; Jessica K Altman, Northwestern University; Geoffrey L Uy, Washington University; Martin S Tallman, Memorial Sloan Kettering Cancer Center; Ivana Gojo, The Sidney Kimmel Comprehensive Cancer Center; Gerard Lozanski, Ohio State University; Ute Burkard, Boehringer Ingelheim Pharma GmbH & Co. KG; Annika Osswald, Boehringer Ingelheim Pharma GmbH & Co. KG; Pamela James, Boehringer Ingelheim Pharmaceuticals, Inc; Björn Rüter, Boehringer Ingelheim Pharmaceuticals, Inc; William Blum, Emory University
• Language: English
• Date: 2022-03-01
• Publisher: FERRATA STORTI FOUNDATION
• Publication Version: Final Published Version
• Copyright Statement: © 2022 Ferrata Storti Foundation
• License: Creative Commons Attribution-NonCommercial 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.3324/haematol.2020.274118
• Title of Journal or Parent Work: HAEMATOLOGICA
• Volume: 107
• Issue: 3
• Start Page: 770
• End Page: 773
• Grant/Funding Information: this work was supported by Boehringer Ingelheim.
• Keywords: Science & Technology; CHEMOTHERAPY; ADULT PATIENTS; LINTUZUMAB; Hematology; GEMTUZUMAB OZOGAMICIN; Life Sciences & Biomedicine
• Research Categories: Health Sciences, Pathology; Health Sciences, Oncology

Abstract

In recent years, several research programs in acute myeloid leukemia (AML) have investigated the use of therapeutic monoclonal antibodies, which primarily elicit their effects through direct cell killing (apoptosis), via antibody-dependent cellular cytotoxicity (ADCC) or antibody- dependent cellular phagocytosis (ADCP).1,2 Attention has been particularly focused on the myeloid differentiation antigen CD33,2 which is expressed on the surface of leukemic blast cells of almost all AML patients.1 While the activity of unconjugated anti-CD33 antibodies such as lintuzumab has been generally disappointing to date,3-6 clinical experience with gemtuzumab ozogamicin, a humanized anti-CD33 antibody-drug conjugate, provides proof-of-principle for targeting CD33 in patients with AML.7,8