Oral tyrosine kinase inhibitor active against NTRK1/2/3, ROS1, and ALK fusion kinases.
Oral tyrosine kinase inhibitor that selectively targets TRKA/B/C (NTRK1/2/3), ROS1, and ALK fusion kinases, blocking their signaling (e.g., MAPK and PI3K pathways) to inhibit tumor proliferation and induce apoptosis in fusion-positive cancers.
Entrectinib directly inhibits the ROS1 tyrosine kinase in ROS1-driven tumor cells, blocking MAPK/PI3K signaling and inducing apoptosis.
Oral tyrosine kinase inhibitor active against NTRK1/2/3, ROS1, and ALK fusion kinases.
Oral tyrosine kinase inhibitor that selectively targets TRKA/B/C (NTRK1/2/3), ROS1, and ALK fusion kinases, blocking their signaling (e.g., MAPK and PI3K pathways) to inhibit tumor proliferation and induce apoptosis in fusion-positive cancers.
Entrectinib is a small‑molecule ALK kinase inhibitor that blocks ALK-driven signaling (e.g., MAPK/PI3K), leading to tumor cell growth arrest and apoptosis in ALK fusion–positive cells without immune engagement.
An antibody–drug conjugate (brand name BESPONSA) composed of a humanized anti‑CD22 IgG4 monoclonal antibody linked to the cytotoxic antibiotic calicheamicin; binds CD22 on B‑lineage lymphoblasts, is internalized, and releases calicheamicin to induce DNA double‑strand breaks leading to apoptosis.
CD22-directed antibody-drug conjugate; the anti-CD22 IgG4 binds CD22 on B-lineage cells, is internalized, and releases the calicheamicin payload, which binds DNA and induces double-strand breaks leading to apoptosis.
Anti-CD22 ADC binds CD22 on B cells, is internalized, and releases calicheamicin intracellularly, which binds DNA and causes double‑strand breaks leading to apoptosis.
Gene-modified autologous T cells engineered to express a chimeric antigen receptor targeting CD19 for cellular immunotherapy.
Autologous T cells genetically engineered to express an anti-CD19 chimeric antigen receptor; binding to CD19 on B-cell malignancies triggers MHC-independent activation, cytokine release, proliferation, and perforin/granzyme-mediated cytotoxicity, eliminating CD19-positive cells and causing B-cell aplasia.
Anti‑CD19 CAR T cells bind CD19 and, upon activation, directly lyse CD19+ cells via perforin/granzyme release (and Fas/FasL apoptosis), eliminating the target cells.
Subcutaneous bispecific IgG1 T-cell engager (CD3×CD20) that redirects cytotoxic T cells to kill CD20+ B cells.
Bispecific IgG1 antibody that binds CD3 on T cells and CD20 on B cells, cross-linking them to activate cytotoxic T cells and induce perforin/granzyme-mediated killing of CD20-positive B-cell tumor cells.
Epcoritamab binds CD3 on T cells and CD20 on target B cells, crosslinking them to activate cytotoxic T cells that kill CD20+ cells via perforin/granzyme-mediated lysis.