Allogeneic, off-the-shelf CD19-targeted CAR-T cell therapy (also referred to as REVO-UWD-19 or UWD-CD19) designed to bind CD19 on B cells and mediate T-cell activation and cytotoxic killing; administered as a single infusion.
Allogeneic T cells engineered with a CD19-directed chimeric antigen receptor bind CD19 on malignant B cells, triggering T‑cell activation, cytokine release, and cytotoxic killing that clears CD19+ cells (with expected on‑target B‑cell aplasia).
CD19-directed CAR-T cells bind CD19 on target B cells, triggering T-cell activation and cytotoxic killing via perforin/granzyme release and death receptor pathways, leading to apoptosis/lysis of CD19+ cells.
An antibody-drug conjugate composed of a humanized anti-HER2 monoclonal antibody (disitamab) linked via a cleavable linker to the microtubule-disrupting payload monomethyl auristatin E (MMAE). After binding HER2 on tumor cells, the ADC is internalized and MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; additional effects may include ADCC and a bystander effect.
Humanized anti-HER2 monoclonal antibody (disitamab) delivers the microtubule toxin MMAE via a cleavable linker. After binding HER2, the ADC is internalized and MMAE is released in lysosomes to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; may also induce Fc-mediated ADCC and a membrane-permeable bystander effect.
Anti-HER2 ADC binds HER2, is internalized, and releases MMAE in lysosomes to inhibit microtubule polymerization, causing G2/M arrest and apoptosis (with possible ADCC and bystander effects).
A TCR-based bispecific T-cell engager that binds the MAGE-A4 peptide presented by HLA-A*02 on tumor cells and CD3 on T cells to redirect and activate cytotoxic T cells.
TCR-based bispecific that binds the MAGE-A4 peptide presented by HLA-A*02 on tumor cells and CD3 on T cells, redirecting and activating polyclonal cytotoxic T cells to induce tumor cell lysis.
TCR-based bispecific bridges CD3 on T cells to the MAGE-A4/HLA-A*02 pHLA on target cells, forming an immune synapse and activating cytotoxic T cells to kill via perforin/granzyme (and Fas–FasL)–mediated apoptosis.
Anti-EGFR IgG1 monoclonal antibody that blocks EGFR signaling (RAS/MAPK, PI3K/AKT) and can mediate ADCC against EGFR-expressing tumor cells.
Humanized IgG1 monoclonal antibody against EGFR that blocks ligand binding and downstream EGFR signaling (RAS/MAPK and PI3K/AKT), inhibiting proliferation and survival of EGFR-overexpressing tumor cells; its Fc region can mediate antibody-dependent cellular cytotoxicity (ADCC).
IgG1 anti-EGFR mAb engages FcγR-bearing effector cells to kill EGFR+ cells via ADCC (and possibly CDC); EGFR signaling blockade is antiproliferative.
Autologous, gene-engineered TCR-T cell therapy expressing an HLA-A*02:01–restricted TCR specific for the TP53 R175H mutant peptide to mediate antigen-specific tumor cell killing.
Autologous T cells are gene-engineered to express an HLA-A*02:01–restricted T-cell receptor that recognizes the TP53 R175H mutant peptide presented on tumor MHC class I. After infusion, these TCR-T cells bind the peptide–MHC complex, become activated, and kill antigen-positive tumor cells via cytotoxic effector functions (perforin/granzymes and cytokines).
Engineered TCR-T cells bind the HLA-A*02:01–presented TP53 R175H peptide on tumor cells and kill them via cytotoxic T-cell effector functions (perforin/granzyme-mediated apoptosis, etc.).