Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
YES
DIRECT
Vγ9Vδ2 T cells engage ULBP2 via their NKG2D receptor, triggering immune synapse formation and perforin/granzyme-mediated cytotoxic killing of the target cell.
A fully humanized IgG1 antibody-drug conjugate (ADC) targeting B7-H3 (CD276); it binds B7-H3 on tumor cells, is internalized, and releases a cytotoxic payload to induce targeted tumor cell death. Administered intravenously every 3 weeks.
B7-H3–targeted IgG1 antibody-drug conjugate that binds CD276 on tumor cells, is internalized, and releases a topoisomerase inhibitor payload to inhibit DNA topoisomerase activity, causing replication arrest and apoptosis in B7-H3–expressing tumor cells.
YES
DIRECT
The anti–B7-H3 ADC binds CD276 on target cells, is internalized, and releases a topoisomerase inhibitor payload that blocks DNA topoisomerase activity, causing replication arrest, DNA damage, and apoptosis of B7-H3–expressing cells.
A fully humanized IgG1 antibody-drug conjugate (ADC) targeting B7-H3 (CD276); it binds B7-H3 on tumor cells, is internalized, and releases a cytotoxic payload to induce targeted tumor cell death. Administered intravenously every 3 weeks.
B7-H3–targeted IgG1 antibody-drug conjugate that binds CD276 on tumor cells, is internalized, and releases a topoisomerase inhibitor payload to inhibit DNA topoisomerase activity, causing replication arrest and apoptosis in B7-H3–expressing tumor cells.
NO
INDIRECT
HS-20093 targets B7-H3 (CD276) on tumor cells, is internalized, and releases a topoisomerase-inhibitor payload that blocks DNA topoisomerase activity to induce apoptosis. DNA topoisomerase I expression alone is not the binding target and does not make cells directly killed by the drug.
Personalized therapeutic mRNA cancer vaccine (V940/mRNA-4157) delivered in lipid nanoparticles encoding patient-specific tumor neoantigens to drive MHC I/II presentation and expand neoantigen-specific CD8+ and CD4+ T cells.
Lipid nanoparticle–encapsulated mRNA encoding patient-specific tumor neoantigens is taken up by antigen-presenting cells, translated, and processed, with peptides presented on MHC I and II to prime and expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, inducing antitumor immunity against neoantigen-expressing cancer cells.
YES
INDIRECT
The mRNA vaccine primes neoantigen-specific CD8+ T cells that recognize the MHC I–presented neoantigen peptides on tumor cells and kill them via perforin/granzyme release and Fas–FasL pathways, with CD4+ T-cell help.
Personalized therapeutic mRNA cancer vaccine (V940/mRNA-4157) delivered in lipid nanoparticles encoding patient-specific tumor neoantigens to drive MHC I/II presentation and expand neoantigen-specific CD8+ and CD4+ T cells.
Lipid nanoparticle–encapsulated mRNA encoding patient-specific tumor neoantigens is taken up by antigen-presenting cells, translated, and processed, with peptides presented on MHC I and II to prime and expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, inducing antitumor immunity against neoantigen-expressing cancer cells.
YES
INDIRECT
The mRNA vaccine primes neoantigen-specific T cells; CD8+ CTLs (and CD4+ CTLs if tumors present the peptide on MHC II) recognize the neoantigen–MHC complexes on cancer cells and kill them via perforin/granzyme-mediated cytolysis.