Multi-antigen DNA vaccine (nucleic acid immunotherapy) encoding CMV antigens IE-1+pp65 (fusion) and gB, each fused to LAMP1 to enhance MHC II presentation and cross-presentation to MHC I, intended to elicit CMV-specific CD4+ and CD8+ T-cell responses against CMV-expressing GBM cells.
Off‑the‑shelf plasmid DNA vaccine encoding CMV IE‑1/pp65 (fusion) and gB, each fused to LAMP1. Following intramuscular delivery with electroporation, plasmids are taken up by antigen‑presenting cells; LAMP1 targets antigens to lysosomes to enhance MHC II presentation with cross‑presentation on MHC I, inducing CMV‑specific CD4+ and CD8+ T‑cell responses to recognize and kill CMV‑expressing GBM cells.
YES
INDIRECT
The DNA vaccine primes APCs to present pp65, inducing pp65-specific CD8+ T cells that recognize pp65 peptides on MHC I of tumor cells and kill them via perforin/granzyme CTL mechanisms (with CD4+ T-cell help).
Multi-antigen DNA vaccine (nucleic acid immunotherapy) encoding CMV antigens IE-1+pp65 (fusion) and gB, each fused to LAMP1 to enhance MHC II presentation and cross-presentation to MHC I, intended to elicit CMV-specific CD4+ and CD8+ T-cell responses against CMV-expressing GBM cells.
Off‑the‑shelf plasmid DNA vaccine encoding CMV IE‑1/pp65 (fusion) and gB, each fused to LAMP1. Following intramuscular delivery with electroporation, plasmids are taken up by antigen‑presenting cells; LAMP1 targets antigens to lysosomes to enhance MHC II presentation with cross‑presentation on MHC I, inducing CMV‑specific CD4+ and CD8+ T‑cell responses to recognize and kill CMV‑expressing GBM cells.
YES
INDIRECT
DNA vaccine primes CMV gB–specific T cells; activated CD8+ T cells recognize gB peptides on MHC and kill CMV-expressing cells via perforin/granzyme-mediated cytolysis.
Subcutaneous T-cell–engaging trispecific antibody that binds BCMA and GPRC5D on myeloma cells and CD3 on T cells, redirecting T-cell cytotoxicity.
Subcutaneous trispecific antibody that binds BCMA and GPRC5D on myeloma cells and CD3 on T cells, bridging them to activate CD3 signaling and redirect T-cell cytotoxicity for targeted lysis of malignant plasma cells.
NO
INDIRECT
The trispecific antibody engages CD3 on T cells to activate them and simultaneously binds BCMA/GPRC5D on myeloma cells, redirecting T‑cell killing to BCMA/GPRC5D+ tumor cells; CD3+ T cells are not targeted for lysis.
A humanized IgG1 monoclonal antibody given subcutaneously that binds c-Kit (CD117) and blocks stem cell factor (SCF) signaling, leading to inhibition/depletion of c-Kit–positive cells, particularly airway mast cells, to reduce early and late allergic bronchoconstriction and airway hyperresponsiveness; may also impact c-Kit+ hematopoietic progenitors.
Humanized IgG1 monoclonal antibody targeting c‑Kit (CD117) that blocks stem cell factor (SCF) signaling, leading to functional inhibition and depletion of c‑Kit–positive cells—particularly airway mast cells—thereby reducing allergic activation/bronchoconstriction and airway hyperresponsiveness; may also affect c‑Kit+ hematopoietic progenitors.
YES
DIRECT
Humanized IgG1 anti–c-Kit binds CD117 on target cells, blocks SCF survival signaling, and via its Fc engages immune effectors (NK cells/macrophages, complement) to mediate ADCC/ADCP/CDC, leading to depletion/apoptosis of c‑Kit–positive cells.
Autologous gene-modified T-cell therapy engineered to express a chimeric antigen receptor targeting mesothelin (MSLN) on ovarian cancer cells. CAR engagement activates CD3ζ/costimulatory signaling, inducing cytokine release and perforin/granzyme-mediated cytotoxicity. Administered as a single IV infusion in dose-escalation cohorts (1×10^6, 3×10^6, 1×10^7, 2×10^7 cells/kg) for advanced, platinum-resistant, MSLN-positive ovarian cancer.
Autologous T cells are engineered to express a chimeric antigen receptor that recognizes mesothelin on tumor cells. CAR engagement activates CD3ζ and costimulatory signaling, inducing T‑cell activation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of mesothelin‑positive ovarian cancer cells.
YES
DIRECT
CAR-T cells bind mesothelin on target cells, triggering CD3ζ/costimulatory signaling and killing via perforin–granzyme–mediated cytolysis (and Fas/FasL apoptosis).