An intravenously administered biparatopic anti-5T4 (TPBG) antibody-drug conjugate that binds two epitopes on 5T4 to enhance binding/internalization and delivers an intracellular cytotoxic payload to kill 5T4-expressing tumor cells.
JK06 is a biparatopic anti‑5T4 (TPBG) antibody–drug conjugate that binds two distinct epitopes on 5T4 to enhance binding and internalization, then releases an intracellular cytotoxic payload to kill 5T4‑expressing tumor cells.
YES
DIRECT
Anti-5T4 antibody-drug conjugate binds 5T4, is internalized, and releases an intracellular cytotoxic payload that kills 5T4-expressing cells.
Intravenous antibody–drug conjugate (ado-trastuzumab emtansine, T-DM1) linking trastuzumab to the maytansinoid DM1 via a non-cleavable linker; binds HER2, inhibits signaling, mediates ADCC, and delivers DM1 to disrupt microtubules causing mitotic arrest and apoptosis, including activity in brain metastases.
HER2-targeted monoclonal antibody (trastuzumab) linked via a non-cleavable linker to the maytansinoid DM1. Binds HER2 to inhibit signaling and mediate ADCC; after internalization, DM1 binds tubulin to disrupt microtubules, causing mitotic arrest and apoptosis in HER2-overexpressing tumor cells.
YES
DIRECT
Binds HER2, is internalized, and releases the DM1 payload that disrupts microtubules causing mitotic arrest and apoptosis; Fc engagement can also mediate ADCC against HER2-positive cells.
Intravenous antibody–drug conjugate (ado-trastuzumab emtansine, T-DM1) linking trastuzumab to the maytansinoid DM1 via a non-cleavable linker; binds HER2, inhibits signaling, mediates ADCC, and delivers DM1 to disrupt microtubules causing mitotic arrest and apoptosis, including activity in brain metastases.
HER2-targeted monoclonal antibody (trastuzumab) linked via a non-cleavable linker to the maytansinoid DM1. Binds HER2 to inhibit signaling and mediate ADCC; after internalization, DM1 binds tubulin to disrupt microtubules, causing mitotic arrest and apoptosis in HER2-overexpressing tumor cells.
NO
INDIRECT
T-DM1 targets HER2 on the cell surface; after HER2-mediated internalization, the DM1 payload binds tubulin beta and disrupts microtubules, causing mitotic arrest and apoptosis in HER2-overexpressing cells. Tubulin itself is not the targeted antigen.
Oral small-molecule, highly selective HER2 (ERBB2) tyrosine kinase inhibitor with CNS penetration that suppresses downstream PI3K/AKT and MAPK signaling in HER2-driven tumors.
Highly selective HER2 (ERBB2) tyrosine kinase inhibitor that blocks HER2 autophosphorylation and downstream PI3K/AKT and MAPK signaling, inhibiting proliferation and promoting death of HER2-driven tumor cells; has CNS penetration.
YES
DIRECT
Inhibits HER2 kinase activity, blocking autophosphorylation and downstream PI3K/AKT and MAPK signaling, leading to growth arrest and apoptosis of HER2-dependent tumor cells.
An autologous anti-GPRC5D chimeric antigen receptor (CAR) T-cell therapy in which a patient’s T cells are engineered to express a CAR targeting GPRC5D, leading to antigen-dependent T-cell activation and cytolytic killing of GPRC5D-positive myeloma cells.
Autologous T cells are gene-modified to express a chimeric antigen receptor targeting GPRC5D. Antigen engagement activates CAR signaling (CD3z with costimulatory domains), leading to T-cell activation, proliferation, cytokine release, and antigen-dependent cytolytic killing of GPRC5D-positive myeloma cells.
YES
DIRECT
Anti-GPRC5D CAR T cells bind GPRC5D on target cells and, upon CAR activation, kill them via T-cell cytolysis (perforin/granzyme and Fas–FasL–mediated apoptosis).