Belantamab mafodotin in multiple myeloma

Figures & data

Figure 1. Mechanisms of action of belantamab mafodotin. The interaction between the drug and BCMA promotes the activation of caspase-3 dependent apoptosis after the intracellular release of MMAF. The afucosylation of the antibody permits the linkage with the Fc-bearing NK cells, inducing antibody-dependent cellular cytotoxicity (ADCC). Another mechanism of cell death is mediated by macrophages via antibody-dependent cellular phagocytosis (ADCP) following the release of antigens by apoptotic MM cells.

Table 1. Selected clinical trials of belantamab mafodotin regimens.

Trial	NCT number	Phase	Pts	Intervention	ORR	PFS	Ocular Toxicity
DREAMM-1^4	02064387	I/II	RRMM	Phase 1: Belantamab dose escalation (0.03–4.6 mg/Kg) Q3W Phase 2: Belantamab 3.4 mg/Kg Q3W	Phase 2: 60%	Phase 2: 12 months	Phase 2: 63%
DREAMM-2^5	03525678	II	RRMM	Arm 1: Belantamab 2.5 mg/Kg Q3W Arm 2: Belantamab 3.4 mg/Kg Q3W	Arm 1: 31% Arm 2: 34%	Arm 1: 2.9 monthsArm 2: 4.9 months	Arm 1: 72%
DREAMM-3^12	04162210	III	RRMM	Belantamab vs Pd	41%	11.2 months	NA

Abbreviation: RRMM Relapsed/Refractory Multiple Myeloma, NDMM Newly Diagnosed Multiple Myeloma, ORR Overall Response Rate, PFS Progression-Free Survival, Pd Pomalidomide-dexamethasone.