SIRPα–Fc fusion protein that binds CD47 to inhibit the "don’t‑eat‑me" signal and promote macrophage-mediated phagocytosis.
Recombinant SIRPα–Fc fusion protein that binds and blocks CD47 on tumor cells, interrupting the CD47–SIRPα inhibitory checkpoint (“don’t‑eat‑me” signal) to promote macrophage/monocyte-mediated phagocytosis, aided by Fc engagement of Fcγ receptors.
NO
INDIRECT
TTI-621 binds CD47 on tumor cells; its Fc engages FcγRI (CD64) on macrophages/monocytes to activate antibody-dependent cellular phagocytosis of CD47+ targets. CD64+ cells are effectors, not killed.
SIRPα–Fc fusion protein that binds CD47 to inhibit the "don’t‑eat‑me" signal and promote macrophage-mediated phagocytosis.
Recombinant SIRPα–Fc fusion protein that binds and blocks CD47 on tumor cells, interrupting the CD47–SIRPα inhibitory checkpoint (“don’t‑eat‑me” signal) to promote macrophage/monocyte-mediated phagocytosis, aided by Fc engagement of Fcγ receptors.
NO
INDIRECT
TTI-621 binds CD47 on tumor cells and, via its IgG1 Fc, engages Fc gamma receptor IIa on macrophages/monocytes to trigger antibody-dependent cellular phagocytosis of CD47+ tumor cells; Fc gamma receptor IIa–expressing cells act as effectors, not targets.
SIRPα–Fc fusion protein that binds CD47 to inhibit the "don’t‑eat‑me" signal and promote macrophage-mediated phagocytosis.
Recombinant SIRPα–Fc fusion protein that binds and blocks CD47 on tumor cells, interrupting the CD47–SIRPα inhibitory checkpoint (“don’t‑eat‑me” signal) to promote macrophage/monocyte-mediated phagocytosis, aided by Fc engagement of Fcγ receptors.
NO
INDIRECT
TTI-621 binds CD47 on tumor cells and, via its Fc, engages Fc gamma receptors on macrophages to promote antibody-dependent phagocytosis of CD47+ tumor cells. Cells expressing Fc gamma receptor IIb act as effectors, not targets, and are not directly killed by the drug.
SIRPα–Fc fusion protein that binds CD47 to inhibit the "don’t‑eat‑me" signal and promote macrophage-mediated phagocytosis.
Recombinant SIRPα–Fc fusion protein that binds and blocks CD47 on tumor cells, interrupting the CD47–SIRPα inhibitory checkpoint (“don’t‑eat‑me” signal) to promote macrophage/monocyte-mediated phagocytosis, aided by Fc engagement of Fcγ receptors.
NO
INDIRECT
CD16A is on effector cells (NK cells/macrophages). TTI-621 binds CD47 on tumor cells and its Fc engages CD16A to activate phagocytosis/ADCC against CD47+ tumor cells; CD16A+ cells are not killed.
Autologous second-generation anti-CD19 chimeric antigen receptor T-cell therapy using an HI19α-derived scFv with 4-1BB and CD3ζ signaling domains to target and eliminate CD19+ B cells/plasmablasts, aiming to reduce pathogenic autoantibody production in AIHA/Evans syndrome.
Autologous T cells are genetically engineered to express an anti‑CD19 chimeric antigen receptor (HI19a-derived scFv with 4-1BB costimulatory and CD3zeta signaling domains). Binding to CD19 on B cells and plasmablasts activates the CAR T cells, leading to expansion and cytotoxic elimination of CD19+ cells, thereby depleting pathogenic B-cell populations and reducing autoantibody production in AIHA/Evans syndrome.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on B cells, become activated, and kill targets via T cell cytotoxic mechanisms (immune synapse formation, perforin/granzyme release and Fas–FasL–mediated apoptosis).