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Target binding
T-cell activation
Tumor cell lysis
Binding of ELREXFIO® to BCMA on tumour cells and CD3 on T cells is independent of native T cell receptor (TCR) specificity or reliance on major histocompability (MHC) Class 1 molecules1
Cytotoxic T cells are recruited to tumour cells and form a cytolytic synapse, generating a robust T-cell response that is MHC-independent, which may contribute to the ability to overcome tumour escape mechanisms2-5
Cytolytic enzymes such as granzyme B and perforin are released, leading to tumor cell killing.5
Confer tumour specificity
Promote stability
Dampen immunogenicity
Confer tumour specificity with an affinity for BCMA over CD36,7
Preferential binding to BCMA over CD3 promotes tumour specificity over T-cell activation.
Promote stability using a fully human immunoglobulin G (IgG) backbone8,9
Fully human IgG antibody design promotes stability and can prolong circulating half-life.
Dampen immunogenicity with modifications to inhibit fragment crystallisable receptor (FcR) engagement*8,10
Preclinical studies indicate that reduced FcR binding may minimise activation of immune effector cells.
BCMA is a tumour-associated antigen that is universally present on myeloma cells2,3
BCMA is selectively expressed on plasma cells and overexpressed on myeloma cells, with near ubiquitous expression across the multiple myeloma population. It is minimally expressed on haematopoetic stem cells and non-haematopoetic tissue.2
BCMA expression and activation may contribute to multiple myeloma disease progression, promoting tumour cell survival and proliferation.2,11
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PP-UNP-GBR-7812. January 2024