KRAS-targeted adenoviral vector vaccine used as a prime to induce and expand KRAS-mutant–specific T cells.
A non-replicating adenoviral vector delivers genes encoding shared KRAS-mutant neoantigens to antigen-presenting cells, leading to intracellular expression and MHC I/II presentation of the neoantigen peptides. This primes and expands KRAS-mutant–specific CD8+ and CD4+ T cells, promoting cytotoxic T‑cell responses against KRAS‑mutant tumor cells (used as a prime prior to an mRNA boost).
YES
INDIRECT
Vaccine primes and expands KRAS G12V–specific CD8+ T cells, which recognize KRAS G12V peptides on MHC I of tumor cells and kill them via perforin/granzyme-mediated cytotoxicity (with CD4+ T-cell help).
KRAS-targeted mRNA vaccine used as a boost to expand KRAS-mutant–specific T cells and support infused cells.
An mRNA cancer vaccine encoding shared KRAS neoantigens. After administration (as a boost following a priming vaccine), antigen-presenting cells translate the mRNA and present the neoantigen peptides on MHC I/II, expanding KRAS-mutant–specific CD8+ and CD4+ T cells and enhancing cytotoxic killing of tumor cells expressing KRAS mutations, including support of infused KRAS-specific TCR T cells.
YES
INDIRECT
The vaccine expands KRAS G12D–specific T cells; these CTLs recognize the KRAS G12D peptide on MHC of tumor cells and kill them via perforin/granzyme (and related) cytotoxic pathways.
KRAS-targeted mRNA vaccine used as a boost to expand KRAS-mutant–specific T cells and support infused cells.
An mRNA cancer vaccine encoding shared KRAS neoantigens. After administration (as a boost following a priming vaccine), antigen-presenting cells translate the mRNA and present the neoantigen peptides on MHC I/II, expanding KRAS-mutant–specific CD8+ and CD4+ T cells and enhancing cytotoxic killing of tumor cells expressing KRAS mutations, including support of infused KRAS-specific TCR T cells.
YES
INDIRECT
The mRNA vaccine primes/boosts KRAS G12V–specific CD8+ T cells (and supports infused KRAS-specific TCR T cells). These CTLs recognize KRAS G12V peptide–MHC on tumor cells and kill them via perforin/granzyme-mediated cytotoxicity.
Fully humanized IgG1 antibody-drug conjugate targeting B7-H3 (CD276); binding triggers internalization and delivery of a cytotoxic payload with potential Fc-mediated effector activity.
Fully humanized IgG1 antibody-drug conjugate targeting B7-H3 (CD276). Upon binding to B7-H3 on tumor cells, the ADC is internalized and releases a topoisomerase inhibitor payload that inhibits topoisomerase activity (primarily Topo I), blocking DNA replication and inducing cell-cycle arrest and apoptosis; the IgG1 Fc may also engage immune effector functions (e.g., ADCC/ADCP).
YES
DIRECT
HS-20093 ADC binds B7-H3 on target cells, is internalized, and releases a topoisomerase I inhibitor that blocks DNA replication causing cell-cycle arrest and apoptosis; its IgG1 Fc can also trigger ADCC/ADCP against B7-H3–positive cells.
Fully humanized IgG1 antibody-drug conjugate targeting B7-H3 (CD276); binding triggers internalization and delivery of a cytotoxic payload with potential Fc-mediated effector activity.
Fully humanized IgG1 antibody-drug conjugate targeting B7-H3 (CD276). Upon binding to B7-H3 on tumor cells, the ADC is internalized and releases a topoisomerase inhibitor payload that inhibits topoisomerase activity (primarily Topo I), blocking DNA replication and inducing cell-cycle arrest and apoptosis; the IgG1 Fc may also engage immune effector functions (e.g., ADCC/ADCP).
NO
INDIRECT
HS-20093 targets B7-H3 on tumor cells; after internalization it releases a topoisomerase I inhibitor that blocks DNA replication and induces apoptosis (with possible Fc-mediated ADCC/ADCP). Killing is determined by B7-H3 binding, not by topoisomerase I expression itself.