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7ND gene therapy is an experimental anti-inflammatory gene therapy that utilizes a dominant-negative mutant of the human monocyte chemoattractant protein-1 (MCP-1/CCL2). The 7ND protein is characterized by the deletion of amino acids 2 through 8 at the N-terminus, which allows it to bind to the C-C chemokine receptor type 2 (CCR2) with high affinity while lacking the ability to induce signal transduction or monocyte chemotaxis. By competing with endogenous MCP-1, 7ND effectively blocks the recruitment of monocytes and macrophages to sites of vascular injury or inflammation. This therapy is typically delivered using adenoviral vectors, either through local catheter-based administration or systemic skeletal muscle transfection. Preclinical studies in various animal models, including non-human primates, have demonstrated its efficacy in reducing neointimal hyperplasia (restenosis), stabilizing atherosclerotic plaques, and preventing vein graft failure.
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