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mAb2-3 is a human monoclonal antibody targeting the C-C chemokine receptor type 4 (CCR4), primarily developed to modulate regulatory T cells (Tregs) in the tumor microenvironment. Developed at the Dana-Farber Cancer Institute, the antibody exists in two isotypes: an IgG1 version that induces Treg depletion via antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), and an IgG4 version that blocks Treg migration to tumor sites by inhibiting CCL22/CCR4 interactions. Uniquely, mAb2-3 acts as an agonist that triggers CD25 shedding from Tregs through matrix metalloproteinase 9 (MMP-9) activation, thereby disrupting IL-2-mediated Treg survival. It has shown preclinical efficacy in restoring antitumor immunity in ovarian cancer models and is distinct from mogamulizumab in its conformational epitope recognition and agonist properties.
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