Aumolertinib (HS-10296; almonertinib) is an oral, third-generation, irreversible EGFR tyrosine kinase inhibitor selective for activating EGFR mutations, inhibiting downstream MAPK and PI3K/AKT signaling.
Third-generation, irreversible EGFR tyrosine kinase inhibitor selective for mutant EGFR (e.g., Ex19del, L858R, T790M). Covalently inhibits EGFR kinase activity, blocking autophosphorylation and downstream MAPK and PI3K/AKT signaling, resulting in growth inhibition and apoptosis of EGFR-mutant tumor cells.
Aumolertinib covalently inhibits mutant EGFR (L858R), blocking autophosphorylation and downstream MAPK/PI3K-AKT signaling, which triggers growth arrest and apoptosis of the EGFR-mutant tumor cells.
A HER2-targeted antibody–drug conjugate composed of trastuzumab linked via a cleavable linker to the topoisomerase I inhibitor payload deruxtecan (DXd); binds HER2 (ERBB2), is internalized, and releases DXd to inhibit topo I and induce DNA damage/apoptosis, with potential bystander effect and Fc-mediated ADCC.
HER2-targeted ADC: trastuzumab binds HER2 (ERBB2), is internalized, and via a cleavable linker releases the topoisomerase I inhibitor deruxtecan (DXd) in lysosomes, causing DNA damage and apoptosis; the membrane-permeable payload enables a bystander effect, and the antibody Fc can mediate ADCC.
The ADC binds HER2 on target cells, is internalized, and releases the deruxtecan topoisomerase I inhibitor via a cleavable linker, causing DNA damage and apoptosis; the antibody Fc can also mediate ADCC, with potential bystander killing from the membrane-permeable payload.
Autologous engineered T-cell therapy with a logic-gate circuit to recognize PSMA and CA9; CAR-like activation enabling targeted cytotoxicity against clear-cell renal cell carcinoma. Administered as a single IV infusion; designed to enhance tumor specificity and reduce off-tumor toxicity.
Autologous T cells engineered with a PSMA-inducible anti-CA9 CAR (logic-gate circuit). Engagement of PSMA triggers expression of an anti-CA9 CAR, enabling CAR-like activation and cytotoxic killing of PSMA/CA9-expressing tumor cells. Embedded shRNA-miR modules downregulate Fas and TGFβRII to resist apoptosis and TGF-β–mediated immunosuppression, and a constitutive activator enhances STAT3 signaling to promote T-cell expansion and function, improving specificity and reducing off-tumor toxicity.
PSMA engagement induces anti-CA9 CAR expression; the CAR T cells then recognize CA9 on tumor cells and directly lyse them via T-cell cytotoxic pathways (perforin/granzyme, death-receptor signaling).
Anti-CD20 monoclonal antibody that depletes malignant B cells via complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and induces cell death via complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis, leading to depletion of CD20+ malignant B cells.
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity, Fc-mediated ADCC by effector cells (e.g., NK cells), and can induce apoptosis, leading to direct killing of CD20+ cells.