Therapeutic cancer vaccine that is a glycoconjugate linking the tumor-associated carbohydrate antigen Globo H to the carrier protein CRM197; designed to induce strong anti–Globo H humoral and cellular immunity against Globo H–expressing tumor cells.
OBI-833 is a glycoconjugate therapeutic cancer vaccine linking the Globo H tumor-associated carbohydrate antigen to the carrier protein CRM197. With adjuvant support (e.g., OBI-821), it induces strong anti–Globo H humoral and helper T-cell responses; elicited antibodies mediate immune effector functions (e.g., complement activation and ADCC) against Globo H–expressing tumor cells, reducing tumor growth.
NO
INDIRECT
The vaccine induces anti–Globo H antibodies that mediate ADCC and complement-dependent cytotoxicity against Globo H–expressing tumor cells; CRM197 is only a carrier protein and is not a killing target.
An investigational CD3 T‑cell engager bispecific antibody (protein immunotherapy) that binds CD3 on T cells and a B‑cell tumor antigen to redirect and activate cytotoxic T cells against malignant B cells in relapsed/refractory B‑cell NHL; administered subcutaneously or intravenously with dose escalation to define RP2R.
Fully human effector-silent Fc IgG1 trispecific antibody that binds CD79b and CD20 on B-cell tumors and CD3 on T cells, redirecting and activating cytotoxic T cells to kill malignant B cells via immune-synapse formation and granzyme/perforin-mediated lysis.
YES
DIRECT
The trispecific T-cell engager binds CD3 on T cells and CD79b on B cells, forming an immune synapse that activates T cells to kill CD79b+ cells via perforin/granzyme-mediated lysis.
An investigational CD3 T‑cell engager bispecific antibody (protein immunotherapy) that binds CD3 on T cells and a B‑cell tumor antigen to redirect and activate cytotoxic T cells against malignant B cells in relapsed/refractory B‑cell NHL; administered subcutaneously or intravenously with dose escalation to define RP2R.
Fully human effector-silent Fc IgG1 trispecific antibody that binds CD79b and CD20 on B-cell tumors and CD3 on T cells, redirecting and activating cytotoxic T cells to kill malignant B cells via immune-synapse formation and granzyme/perforin-mediated lysis.
YES
DIRECT
The trispecific T-cell engager binds CD3 on T cells and CD20 on B cells, creating an immune synapse that activates cytotoxic T cells to kill CD20-expressing cells via perforin/granzyme-mediated lysis.
An investigational CD3 T‑cell engager bispecific antibody (protein immunotherapy) that binds CD3 on T cells and a B‑cell tumor antigen to redirect and activate cytotoxic T cells against malignant B cells in relapsed/refractory B‑cell NHL; administered subcutaneously or intravenously with dose escalation to define RP2R.
Fully human effector-silent Fc IgG1 trispecific antibody that binds CD79b and CD20 on B-cell tumors and CD3 on T cells, redirecting and activating cytotoxic T cells to kill malignant B cells via immune-synapse formation and granzyme/perforin-mediated lysis.
NO
INDIRECT
CD3 serves to engage and activate T cells; the trispecific antibody links CD3+ T cells to CD79b/CD20+ B cells, leading to T cell–mediated granzyme/perforin killing of the B cells, not the CD3-expressing T cells.
Donor-derived antigen-specific CD4+ and CD8+ T lymphocytes selected by IFN-γ capture after brief stimulation with CMV, EBV, and adenovirus peptides; infused as adoptive cellular therapy to restore antiviral immunity in allo-HSCT recipients.
Donor-derived CD4+ and CD8+ T lymphocytes are briefly stimulated with CMV, EBV, and adenovirus peptides and IFN-γ–secreting cells are magnetically captured, enriching for virus-specific TCR specificities. After infusion, these unengineered T cells recognize HLA-presented viral epitopes via their native TCRs, secrete Th1 cytokines (e.g., IFN-γ), and kill infected cells through perforin/granzyme-mediated cytotoxicity, expanding in vivo to restore antiviral immunity in allo-HSCT recipients.
YES
DIRECT
Virus-specific T cells recognize adenoviral peptide–HLA complexes via their native TCRs and kill the presenting infected cells through perforin/granzyme–mediated apoptosis (± Fas–FasL).