BACKGROUND: Idecabtagene vicleucel (ide-cel, ABECMA) is an autologous, B-cell maturation antigen (BCMA)-directed, chimeric antigen receptor (CAR) T-cell therapy. The current modeling analyses aim to characterize the cellular kinetics (CK) of ide-cel and to assess the covariate effects impacting ide-cel cellular kinetics in patients with relapsed/refractory multiple myeloma. METHODS: A modified piecewise model was developed to characterize ide-cel CK through the nonlinear mixed effects method. The model parameterization was conducted using the ide-cel whole-blood transgene data in CK-evaluable subjects (N = 225) from the ide-cel arm of the study KarMMa-3 (NCT03651128). The structural model consists of an initial lag phase and then saturable cell expansion, followed by conversion from effector cells to memory cells and their elimination. Model simulations were performed to evaluate covariate effects on ide-cel exposure parameters. RESULTS: The piecewise CK model with saturable expansion sufficiently captured the clinically observed ide-cel transgene data. The simulations using the final population CK model suggested that the magnitude of covariate effects on ide-cel exposure parameters was considerably smaller than the intersubject variability in the population. Additional analyses revealed a negative effect of treatment-emergent immunogenicity on the ide-cel persistence. Apparent associations were identified between cellular kinetic parameters and clinical responses. CONCLUSIONS: The cellular kinetics of ide-cel can be adequately described by the modified piecewise model. No clinically meaningful covariate effects on cellular kinetics were identified from this modeling study. The population CK model suggests that higher cell expansion rate and lower elimination rates of effector and memory cells were observed in patients with longer progression-free survival.