Gene-edited autologous T-cell therapy in which CRISPR/Cas9 inserts a CD19-specific STAR receptor at the TRAC locus and ablates the endogenous TCR; the receptor signals via the native TCR–CD3 complex with OX40 costimulation to target CD19+ malignant B cells.
Autologous T cells are CRISPR/Cas9-edited to disrupt the endogenous TRAC and knock in a CD19-specific STAR receptor that grafts an anti-CD19 scFv onto TCR constant regions. This enables HLA-independent recognition of CD19 while signaling through the native TCR–CD3 complex with OX40 costimulation, driving activation, proliferation, and cytotoxic killing of CD19+ malignant B cells; TCR ablation reduces alloreactivity and GVHD risk.
Engineered autologous T cells bearing a CD19-specific STAR receptor recognize CD19 on target cells and, via TCR–CD3 signaling with OX40 costimulation, induce T cell–mediated killing (perforin/granzyme and related cytotoxic pathways).
Anti-EGFR monoclonal antibody that blocks EGFR signaling, suppressing the RAS/RAF/MEK/ERK pathway in RAS/BRAF–wild type tumors.
HLX07 (pimurutamab) is a glycoengineered humanized anti-EGFR monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit EGFR-driven RAS/RAF/MEK/ERK signaling and tumor cell proliferation; glyco-optimization enhances ADCC.
The anti‑EGFR antibody binds EGFR on target cells and its Fc engages FcγRIIIa (CD16) on NK cells to trigger ADCC, killing EGFR+ cells; complement activation and phagocytosis may also contribute, while signaling blockade is mainly cytostatic.
Humanized anti-HER2 monoclonal antibody that inhibits HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody targeting HER2; binds the extracellular domain to block HER2 signaling and receptor dimerization, and mediates antibody‑dependent cellular cytotoxicity (ADCC) against HER2‑overexpressing tumor cells.
Trastuzumab binds HER2 on tumor cells and its Fc engages Fc gamma receptor–bearing immune cells (e.g., NK cells) to mediate ADCC (± complement), killing HER2-positive cells.
Humanized anti-HER2 monoclonal antibody that blocks HER2 dimerization, particularly HER2–HER3.
Humanized anti-HER2 monoclonal antibody that binds the HER2 extracellular dimerization domain (subdomain II), preventing HER2 heterodimerization—especially HER2–HER3—thereby blocking downstream signaling (PI3K/AKT/MAPK), inhibiting tumor cell proliferation and survival; also mediates ADCC.
Pertuzumab binds HER2 on target cells and its Fc engages Fcγ receptors on effector cells to trigger ADCC, leading to lysis of HER2+ cells; it also blocks HER2 dimerization/signaling, promoting apoptosis.
Off-the-shelf allogeneic CAR NK cell therapy with a logic-gated NOT design targeting CD33 and/or FLT3 and an inhibitory CAR to spare healthy cells; includes IL-15 support to enhance NK persistence/function for AML/MDS.
Off-the-shelf allogeneic NK cells engineered with an OR-gated activating CAR targeting CD33 and/or FLT3 and a NOT-gated inhibitory CAR recognizing EMCN to spare healthy hematopoietic stem cells; includes calibrated-release IL-15 to enhance NK persistence and function. Antigen engagement triggers NK activation and cytolytic killing of CD33/FLT3-positive AML/MDS cells while minimizing on-target/off-tumor toxicity.
CAR-engineered NK cells recognize CD33 via the activating CAR and directly lyse target cells through NK degranulation (perforin/granzymes); an EMCN iCAR inhibits killing of EMCN+ healthy cells.