Autologous, ex vivo–expanded, multi–tumor-associated antigen (TAA)–specific CD4+ and CD8+ T cells used as adoptive T-cell therapy for relapsed/refractory lymphomas; mediates TCR/HLA-dependent recognition of multiple TAAs to induce cytotoxic killing and helper cytokine support.
Autologous, ex vivo–expanded CD4+ and CD8+ T cells specific for multiple tumor-associated antigens recognize HLA-presented TAAs via their native TCRs, leading to cytotoxic killing (perforin/granzyme) and helper cytokine support; multi-antigen targeting aims to reduce antigen escape.
Native TCRs on the infused autologous T cells recognize HLA-presented SSX2 peptides and kill the target cells via perforin/granzyme-mediated cytolysis.
An intratumoral, engineered oncolytic adenovirus (also known as suratadenoturev/Telomelysin) that uses the hTERT promoter for selective replication in telomerase-positive cancer cells, inducing oncolysis and immunogenic tumor antigen release.
Replication-competent adenovirus (Ad5) engineered with the hTERT promoter driving E1A/E1B expression (via IRES) to enable selective replication in telomerase-positive tumor cells. Intratumoral infection leads to tumor-selective oncolysis, releasing tumor antigens and danger signals that can prime antitumor immunity, with minimal replication in normal cells.
Oncolytic adenovirus uses the hTERT promoter to drive E1A/E1B, enabling selective viral replication in telomerase-positive cells, causing lytic cell death (oncolysis).
A first-in-human, intravenous bispecific antibody–drug conjugate that co-engages TROP2 and EGFR on tumor cells to enable receptor-mediated internalization and targeted delivery of a cytotoxic payload; administered every 3 weeks for advanced solid tumors.
Bispecific antibody–drug conjugate that co-binds TROP2 and EGFR on tumor cells, undergoes receptor-mediated internalization, and releases the cytotoxic payload MMAE via a protease-cleavable linker; MMAE binds tubulin, inhibits microtubule polymerization, and induces G2/M arrest and apoptosis in TROP2/EGFR-expressing tumors.
Bispecific ADC binds TROP2 (and EGFR) on tumor cells, is internalized, and releases MMAE via protease cleavage; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis in TROP2/EGFR–coexpressing cells.
HER2‑directed antibody–drug conjugate that binds HER2 via trastuzumab, mediates ADCC, is internalized, and releases a topoisomerase I inhibitor payload (deruxtecan) causing DNA damage and cell death, including a bystander effect.
HER2-directed antibody–drug conjugate: trastuzumab binds HER2 and mediates ADCC, is internalized, and releases the deruxtecan (DXd) topoisomerase I inhibitor payload, causing DNA damage and tumor cell death with a bystander killing effect.
The ADC binds HER2, is internalized, and releases deruxtecan (DXd), a topoisomerase I inhibitor that induces DNA damage and apoptosis; Fc engagement can also trigger ADCC, with some bystander killing.
A first-in-human, intravenous bispecific antibody–drug conjugate that co-engages TROP2 and EGFR on tumor cells to enable receptor-mediated internalization and targeted delivery of a cytotoxic payload; administered every 3 weeks for advanced solid tumors.
Bispecific antibody–drug conjugate that co-binds TROP2 and EGFR on tumor cells, undergoes receptor-mediated internalization, and releases the cytotoxic payload MMAE via a protease-cleavable linker; MMAE binds tubulin, inhibits microtubule polymerization, and induces G2/M arrest and apoptosis in TROP2/EGFR-expressing tumors.
The bispecific ADC binds EGFR (with TROP2) on tumor cells, is internalized, and releases MMAE via linker cleavage; MMAE disrupts microtubules, causing G2/M arrest and apoptosis.