Autologous, genetically modified TCR-T cell therapy engineered to express an affinity-enhanced T-cell receptor that recognizes MAGE-A4 peptide presented by HLA-A*02; administered as a single weight-based IV infusion to mediate antigen-specific cytotoxicity via TCR/CD3 signaling, perforin/granzyme release, and cytokine secretion.
Autologous T cells genetically modified to express an affinity-enhanced TCR that recognizes MAGE-A4 peptide presented by HLA-A*02 on tumor cells; TCR/CD3 engagement activates the T cells to mediate antigen-specific killing via perforin/granzyme release and cytokine secretion.
Engineered TCR-T cells recognize the MAGE-A4 peptide presented by HLA-A*02 on target cells, activating TCR/CD3 signaling and inducing cytotoxicity via perforin/granzyme release (and Fas/FasL), leading to apoptosis.
Fc-enhanced anti-CTLA-4 monoclonal antibody checkpoint inhibitor designed to enhance T-cell priming and deplete intratumoral Tregs.
Fc-engineered anti-CTLA-4 IgG1 checkpoint inhibitor that binds CTLA-4 on T cells to block inhibitory signaling, enhance T-cell priming and activation, and via enhanced Fc effector function deplete intratumoral regulatory T cells, promoting cytotoxic T-lymphocyte antitumor responses.
Binds CTLA-4 on intratumoral Tregs and, via its Fc-enhanced IgG1, engages Fcγ receptor–bearing effector cells (e.g., NK cells/macrophages) to mediate ADCC/ADCP (±CDC), depleting CTLA-4–expressing cells.
Off-the-shelf, lentiviral gene-modified double-negative T cells expressing an anti-CD19 chimeric antigen receptor to deplete CD19+ B-lineage cells in refractory SLE.
Off-the-shelf, lentiviral-engineered double-negative T cells (CD3+CD4−CD8−) expressing an anti-CD19 chimeric antigen receptor bind CD19 on B-lineage cells and trigger T-cell cytotoxic effector functions (e.g., perforin/granzyme, death receptor pathways), depleting CD19+ B cells and plasmablast precursors to reduce autoantibody production and B cell–driven inflammation in SLE.
Anti-CD19 CAR-expressing double-negative T cells recognize CD19 on target cells and induce cytotoxicity via perforin/granzyme release and death receptor (e.g., Fas/FasL) pathways, causing lysis/apoptosis.
Investigational HER2-directed biologic for HER2-positive tumors; specific type/mechanism not specified in the registry.
HER2-targeted trastuzumab-based monoclonal antibody site-specifically conjugated via a cleavable linker to the microtubule inhibitor MMAE. After binding HER2 on tumor cells and internalization, linker cleavage releases MMAE, which binds tubulin and inhibits microtubule polymerization, causing G2/M arrest and apoptosis in HER2-expressing cells; the antibody may also retain HER2 signaling blockade and ADCC activity.
ADC binds HER2, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; Fc-mediated ADCC may also contribute.
Anti-HER2 monoclonal antibody that blocks ERBB2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody targeting HER2/ERBB2 that blocks receptor signaling and dimerization, downregulates HER2, and induces Fc-mediated antibody-dependent cellular cytotoxicity against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells), triggering antibody-dependent cellular cytotoxicity and lysis of HER2+ cells; signaling blockade also inhibits growth.