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XL-11 is a novel bispecific antibody (BsAb) engineered to simultaneously target Human Epidermal Growth Factor Receptor 2 (HER2) and C-C Chemokine Receptor Type 4 (CCR4). Developed to address immune evasion in HER2-positive solid tumors, XL-11 employs a dual-action mechanism: it binds to HER2-expressing tumor cells to localize the therapy and targets CCR4-positive regulatory T cells (Tregs) within the tumor microenvironment. By blocking the CCL22/CCR4-mediated recruitment of Tregs and inducing their depletion via antibody-dependent cellular cytotoxicity (ADCC), XL-11 alleviates local immunosuppression and enhances antitumor T-cell activity. This targeted approach is designed to provide superior efficacy over conventional HER2 therapies while avoiding the systemic toxicity associated with non-selective Treg depletion.
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