AMG 420 T-Cell Therapy Induces Responses in Resistant Multiple Myeloma
Posted: Monday, March 9, 2020
The bispecific T-cell engager molecule AMG 420 induced responses in patients with relapsed or refractory multiple myeloma and warrants further investigation, according to a first-in-human-study conducted by Max S. Topp, MD, of the University Hospital Würzburg, Germany, and colleagues. AMG 420 is capable of binding cells that express the B-cell maturation antigen and targeting them for T-cell–mediated lysis—a therapeutic strategy considered complementary to that achieved by the use of chimeric antigen receptor (CAR) T cells. The results from this study were published in the Journal of Clinical Oncology.
In this phase I, dose-escalation study, a total of 42 patients with relapsed or refractory multiple myeloma received intravenous AMG 420 at a dose ranging from 0.2 to 800 µg/day for up to 10 6-week cycles of treatment. Of them, 25 patients discontinued participation in the study due to disease progression; 7, due to adverse events; 4, due to death; and 3 due to completion of 10 cycles; the remaining 2 patients were still being treated at the time of data analysis.
The overall response rate in this study was 31%. At the maximum tolerated dose of 400 µg/day, the response rate was 70% (7 of 10 patient responders); 800 µg/day was not a tolerable dose in this study due to grade 3 cytokine-release syndrome and polyneuropathy (one instance of each; both resolved). Of the seven patient responders receiving 400 µg/day, “five patients experienced [minimal residual disease]-negative complete responses, one had a partial response, and one had a very good partial response; all seven patients responded during the first cycle, and some responses lasted more than 1 year.”
“Results with AMG 420 show comparable response rates and onset and duration of responses as seen with CAR T cells,” the authors concluded, with fewer reported adverse events ≥ grade 3 than seen with CAR T-cell therapy.
Disclosure: For full disclosures of the study authors, visit ascopubs.org.