Small-molecule tyrosine kinase inhibitor targeting ROS1 (also active against NTRK).
Orally bioavailable tyrosine kinase inhibitor that binds the ATP sites of TRK A/B/C (NTRK1/2/3), ROS1, and ALK, blocking kinase phosphorylation and downstream signaling (e.g., MAPK/PI3K pathways), leading to growth inhibition and apoptosis in tumors driven by these fusions/activations.
Entrectinib directly inhibits ROS1 kinase in ROS1-driven cells, shutting down MAPK/PI3K survival signaling and inducing growth arrest and apoptosis.
Engineered T cells (autologous or allogeneic) expressing a CD22-specific CAR via lentiviral transduction; IV dosing 2×10^6–1×10^7 CAR-T/kg; targets CD22+ B-cell malignancies through CAR-mediated activation and cytotoxicity.
Autologous or allogeneic T cells engineered to express a CD22-specific chimeric antigen receptor bind CD22 on B‑cell malignancies and, via CAR signaling (CD3ζ ± co‑stimulation), activate, proliferate, secrete cytotoxic granules (perforin/granzymes) and cytokines, mediating MHC‑independent lysis of CD22‑positive tumor cells.
CD22-specific CAR T cells bind CD22 and, upon CAR signaling, degranulate to deliver perforin/granzymes (and Fas/FasL), inducing MHC-independent apoptosis/lysis of CD22+ cells.
Small-molecule tyrosine kinase inhibitor targeting ROS1 (also active against NTRK).
Orally bioavailable tyrosine kinase inhibitor that binds the ATP sites of TRK A/B/C (NTRK1/2/3), ROS1, and ALK, blocking kinase phosphorylation and downstream signaling (e.g., MAPK/PI3K pathways), leading to growth inhibition and apoptosis in tumors driven by these fusions/activations.
Entrectinib directly inhibits ALK kinase activity by binding the ATP site, shutting down downstream survival pathways (e.g., MAPK/PI3K) and inducing growth arrest and apoptosis in ALK-driven cells.
Subcutaneous bispecific T‑cell engager antibody (CD3×BCMA) that redirects T cells to lyse BCMA‑positive myeloma cells; used pre‑collection for in‑vivo purging and as MRD‑guided maintenance.
Bispecific antibody that binds CD3 on T cells and BCMA on malignant plasma cells, crosslinking them to activate cytotoxic T cells and induce lysis of BCMA-expressing myeloma cells.
CD3×BCMA bispecific antibody crosslinks T cells to BCMA+ cells, triggering T-cell activation and perforin/granzyme-mediated lysis/apoptosis of the target cells.
A subcutaneous bispecific monoclonal antibody (CD20xCD3) T-cell engager that binds CD20 on malignant B cells and CD3 on endogenous T cells to form an immune synapse, activate TCR/CD3 signaling, and induce T-cell mediated cytotoxicity, resulting in depletion of CD20-positive lymphoma cells.
Bispecific CD20xCD3 monoclonal antibody that simultaneously binds CD20 on malignant B cells and CD3 on endogenous T cells to create an immune synapse, activate TCR/CD3 signaling, and drive T cell–mediated cytotoxic killing and depletion of CD20-positive lymphoma cells.
Bispecific CD20xCD3 antibody bridges CD20+ cells to T cells, activating CD3 signaling to form an immune synapse and trigger perforin/granzyme-mediated killing of the CD20-expressing cells.