Intravenous type II anti-CD20 monoclonal antibody used in a pre-phase to deplete B cells and mitigate cytokine release syndrome risk.
Glycoengineered humanized type II anti‑CD20 IgG1 monoclonal antibody that binds CD20 on B cells and enhances FcγRIIIa engagement (via reduced fucosylation) to drive potent antibody‑dependent cellular cytotoxicity and phagocytosis, and induces caspase‑independent direct cell death, resulting in efficient B‑cell depletion.
YES
DIRECT
Binds CD20 on B cells and triggers FcγRIIIa-mediated ADCC and antibody-dependent phagocytosis (ADCP), and also induces caspase-independent direct cell death (type II anti-CD20).
Anti-CD38 immunocytokine/fusion protein (TAK-573) that targets CD38 and delivers attenuated interferon-α to CD38+ cells, activating type I IFN signaling (IFNAR1/2 → JAK–STAT) to drive antiproliferative/apoptotic effects and immune stimulation.
Anti-CD38 IgG4–interferon-alpha immunocytokine that targets CD38+ cells and delivers attenuated IFN-alpha to engage IFNAR1/2, activating JAK–STAT type I interferon signaling to drive antiproliferative/apoptotic effects and immune stimulation against CD38-expressing tumor cells.
YES
DIRECT
Binds CD38 on target cells and delivers IFN-alpha to engage IFNAR1/2 on the same cell, activating JAK-STAT type I interferon signaling that drives antiproliferative and apoptotic effects (IgG4 minimizes Fc-mediated killing).
Anti-CD38 immunocytokine/fusion protein (TAK-573) that targets CD38 and delivers attenuated interferon-α to CD38+ cells, activating type I IFN signaling (IFNAR1/2 → JAK–STAT) to drive antiproliferative/apoptotic effects and immune stimulation.
Anti-CD38 IgG4–interferon-alpha immunocytokine that targets CD38+ cells and delivers attenuated IFN-alpha to engage IFNAR1/2, activating JAK–STAT type I interferon signaling to drive antiproliferative/apoptotic effects and immune stimulation against CD38-expressing tumor cells.
YES
INDIRECT
Modakafusp alfa binds CD38 on target cells and delivers attenuated IFN-α that engages IFNAR1/2 on those same cells, activating JAK–STAT type I IFN signaling to induce antiproliferative/apoptotic effects. IFNAR1 is the executing receptor for the payload, not the antibody’s binding target.
Antigen-specific T cells expanded ex vivo and reinfused to recognize tumor peptides on MHC class I via the TCR, mediating cytotoxicity through perforin/granzyme release and IFN-gamma-mediated effects.
Autologous antigen-specific CTLs expanded ex vivo are reinfused to recognize tumor peptides presented on MHC class I via their endogenous TCR, inducing tumor-cell killing via perforin/granzyme release and death-receptor pathways (FasL/TRAIL), along with IFN-γ secretion to enhance antitumor immune responses.
YES
DIRECT
Adoptively transferred CTLs recognize the tumor peptide–HLA-B complex via their TCR and kill targets by perforin/granzyme-mediated apoptosis and death-receptor signaling (FasL/TRAIL).
Anti-CD38 immunocytokine/fusion protein (TAK-573) that targets CD38 and delivers attenuated interferon-α to CD38+ cells, activating type I IFN signaling (IFNAR1/2 → JAK–STAT) to drive antiproliferative/apoptotic effects and immune stimulation.
Anti-CD38 IgG4–interferon-alpha immunocytokine that targets CD38+ cells and delivers attenuated IFN-alpha to engage IFNAR1/2, activating JAK–STAT type I interferon signaling to drive antiproliferative/apoptotic effects and immune stimulation against CD38-expressing tumor cells.
NO
INDIRECT
The drug targets CD38, not IFNAR2. After binding CD38, its IFN-α payload engages IFNAR1/2 to activate JAK–STAT and induce antiproliferative/apoptotic effects in CD38+ cells; IFNAR2-only cells are not specifically targeted and may only be affected via bystander IFN signaling.