An autologous, gene-modified CAR T-cell therapy (BMS-986393; CC-95266; “Arlo-cel”) targeting GPRC5D for relapsed/refractory multiple myeloma. Patient T cells are engineered to express a CAR that binds GPRC5D on myeloma cells, activating T cells and inducing cytokine release and perforin/granzyme-mediated cytotoxic killing.
Autologous T cells are gene-modified to express a chimeric antigen receptor targeting GPRC5D on myeloma cells. CAR engagement activates the T cells, triggering cytokine release, proliferation, and perforin/granzyme-mediated cytotoxic lysis of GPRC5D-expressing tumor cells.
YES
DIRECT
CAR T cells recognize GPRC5D on target cells and, upon engagement, kill them via T‑cell cytotoxic mechanisms, primarily perforin/granzyme-mediated lysis (with possible Fas–FasL signaling).
Chimeric type I IgG1 monoclonal antibody targeting CD20 on B cells; depletes CD20+ pre-B and mature B cells via ADCC, CDC, and apoptosis to reduce autoantibody production and inflammatory signaling. Includes MabThera brand and biosimilar comparator.
Chimeric type I IgG1 monoclonal antibody against CD20 on pre‑B and mature B cells; binds CD20 and depletes CD20+ B cells via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and induction of apoptosis, thereby reducing autoantibody production and inflammatory signaling.
YES
DIRECT
Anti‑CD20 IgG1 binds CD20 on B cells and induces killing via FcγR-mediated ADCC by effector cells, complement-dependent cytotoxicity (CDC), and direct apoptosis signaling.
A masked immunocytokine comprising an anti‑CD138 human IgG1 antibody fused to human interferon‑α2a, administered IV every 2 weeks to target CD138+ tumor cells and concentrate IFN‑α signaling (IFNAR–JAK/STAT), enhancing antiproliferative/apoptotic effects and immune activation; Fc may mediate ADCC/CDC.
Masked immunocytokine: an anti‑CD138 IgG1 fused to IFN‑α2a via a protease‑cleavable, peptide mask. After binding CD138 on tumor cells, tumor proteases unmask IFN‑α, enabling local IFNAR engagement and JAK/STAT signaling to induce antiproliferative/apoptotic effects and enhance innate/adaptive immunity; the IgG1 Fc may also mediate ADCC/CDC against CD138+ cells.
YES
DIRECT
The anti-CD138 IgG1 binds CD138 on tumor cells; tumor proteases unmask the fused IFN-alpha, enabling local IFNAR engagement and JAK/STAT signaling that induces antiproliferative/apoptotic death. The IgG1 Fc can also recruit immune effectors to mediate ADCC/CDC against CD138+ cells.
A masked immunocytokine comprising an anti‑CD138 human IgG1 antibody fused to human interferon‑α2a, administered IV every 2 weeks to target CD138+ tumor cells and concentrate IFN‑α signaling (IFNAR–JAK/STAT), enhancing antiproliferative/apoptotic effects and immune activation; Fc may mediate ADCC/CDC.
Masked immunocytokine: an anti‑CD138 IgG1 fused to IFN‑α2a via a protease‑cleavable, peptide mask. After binding CD138 on tumor cells, tumor proteases unmask IFN‑α, enabling local IFNAR engagement and JAK/STAT signaling to induce antiproliferative/apoptotic effects and enhance innate/adaptive immunity; the IgG1 Fc may also mediate ADCC/CDC against CD138+ cells.
YES
DIRECT
After anti‑CD138 binding and protease unmasking at the tumor site, the released IFN‑α binds IFNAR1/2 on nearby cells, activating IFNAR–JAK/STAT signaling that induces antiproliferative/apoptotic programs leading to cell death (independent of T‑cell engagement).
Lentiviral CAR T cells targeting CD2; dose-escalated IV infusion; mediates MHC-independent killing of CD2+ T-cell malignancies via perforin/granzyme release and cytokine-driven clearance.
Lentivirally engineered T cells expressing a CD2-specific chimeric antigen receptor bind CD2 on malignant T cells in an MHC-independent manner, triggering T‑cell activation and cytotoxicity with perforin/granzyme release and cytokine-driven tumor clearance after IV infusion.
YES
DIRECT
CD2-specific CAR T cells bind CD2 on target cells, activate, and kill via perforin/granzyme-mediated cytolysis (apoptosis).