V1D

V1D is an experimental **modified netrin-1-derived small peptide** being investigated as a therapeutic for **pulmonary hypertension**. It is derived from the native netrin-1 V1 peptide sequence and was engineered by adding a **D-amino acid at the peptide terminus** to improve stability and resistance to oxidative degradation. In a hypoxia-induced mouse model of pulmonary hypertension, V1D reduced mean pulmonary arterial pressure and right ventricular systolic pressure, reversed right ventricular hypertrophy, decreased pulmonary vascular remodeling, lowered reactive oxygen species and mitochondrial superoxide production, restored nitric oxide bioavailability, and reversed endothelial nitric oxide synthase uncoupling. The reported biology indicates that V1D acts through **binding and activation of the netrin-1 receptor DCC**, promoting **ERK1/2-eNOS-NO signaling** while suppressing oxidative stress pathways relevant to pulmonary vascular disease. It appears to be a preclinical academic-stage peptide program associated with work from the University of California, Los Angeles.

Other names

modified netrin-1-derived peptide V1DV1 peptide with D-amino acid modificationV-1 peptide with D-amino acid modificationV 1 peptide with D-amino acid modification