Replicating arenavirus-based therapeutic cancer vaccine (viral vector) encoding HPV16 E6/E7 designed to elicit HPV16-specific CD8+ T-cell responses; heterologous partner to HB-201 in an alternating prime-boost regimen.
Replicating arenavirus vector delivering genes encoding an inactivated HPV16 E6/E7 fusion protein to antigen-presenting cells, driving strong MHC I presentation and expansion of HPV16-specific CD8+ cytotoxic T cells that recognize and kill HPV16 E6/E7–expressing tumor cells; used in a heterologous prime–boost with HB-201 to mitigate anti-vector immunity.
YES
INDIRECT
Therapeutic vaccine primes and expands HPV16 E7-specific CD8+ T cells; these CTLs recognize E7 peptides on MHC I of tumor cells and kill them via perforin/granzyme-mediated cytolysis.
Autologous T cells engineered to express a tri-specific chimeric antigen receptor targeting CD19, CD20, and CD22; CAR engagement triggers CD3ζ signaling, T-cell activation, cytokine release, and cytotoxic killing to eliminate malignant B cells and reduce antigen escape.
Autologous T cells engineered with a tri-specific CAR targeting CD19, CD20, and CD22; antigen binding triggers CD3zeta and costimulatory signaling to activate the T cell, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of malignant B cells, with multi-antigen targeting designed to reduce antigen escape.
YES
DIRECT
CAR T cells recognize CD19 on target cells; CAR signaling activates T-cell cytotoxicity, causing perforin/granzyme-mediated apoptosis (and death-receptor killing) of CD19+ cells.
Autologous T cells engineered to express a tri-specific chimeric antigen receptor targeting CD19, CD20, and CD22; CAR engagement triggers CD3ζ signaling, T-cell activation, cytokine release, and cytotoxic killing to eliminate malignant B cells and reduce antigen escape.
Autologous T cells engineered with a tri-specific CAR targeting CD19, CD20, and CD22; antigen binding triggers CD3zeta and costimulatory signaling to activate the T cell, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of malignant B cells, with multi-antigen targeting designed to reduce antigen escape.
YES
DIRECT
CAR T cells bind CD20 via the CAR, triggering CD3ζ/co-stimulatory signaling and T‑cell cytotoxicity (perforin/granzyme-mediated killing) of CD20+ cells.
Autologous T cells engineered to express a tri-specific chimeric antigen receptor targeting CD19, CD20, and CD22; CAR engagement triggers CD3ζ signaling, T-cell activation, cytokine release, and cytotoxic killing to eliminate malignant B cells and reduce antigen escape.
Autologous T cells engineered with a tri-specific CAR targeting CD19, CD20, and CD22; antigen binding triggers CD3zeta and costimulatory signaling to activate the T cell, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of malignant B cells, with multi-antigen targeting designed to reduce antigen escape.
YES
DIRECT
CAR T cells bind CD22 on target cells, activating CD3zeta/costimulatory signaling and inducing cytotoxic degranulation (perforin/granzyme-mediated apoptosis; also death-receptor pathways) to kill the cells.
HER2-targeted antibody–drug conjugate composed of a humanized anti-HER2 IgG1 (disitamab) linked via a cleavable linker to the cytotoxic payload MMAE. After binding ERBB2 (HER2) on tumor cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the Fc region may mediate ADCC and bystander killing.
Disitamab vedotin targets HER2 (ERBB2) on tumor cells; after binding and internalization, its cleavable linker releases the microtubule poison MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis. The IgG1 Fc may also mediate ADCC and enable bystander killing.
YES
DIRECT
The ADC binds HER2, is internalized, and releases MMAE that inhibits tubulin polymerization, causing G2/M arrest and apoptosis; its IgG1 Fc can also recruit ADCC, with potential bystander killing from released MMAE.