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V1T is an experimental **modified netrin-1-derived small peptide** being studied as a potential therapy for **pulmonary hypertension**. It is a variant of the native V1 netrin-1 peptide in which the N-terminal cysteine of the original V1 sequence is replaced with **threonine** to improve **stability and resistance to oxidative stress**. Based on the provided preclinical study, V1T is intended to bind and activate the netrin-1 receptor **Deleted in Colorectal Carcinoma**, promoting restoration of endothelial nitric oxide synthase coupling, increasing nitric oxide bioavailability, and reducing reactive oxygen species and mitochondrial superoxide generation. In hypoxia-exposed mice, V1T reduced mean pulmonary arterial pressure, normalized right ventricular systolic pressure, reversed right ventricular hypertrophy, and attenuated pulmonary vascular remodeling. The program appears to be at the **preclinical** stage and is associated with academic research led at **University of California, Los Angeles** rather than a commercial branded drug program.
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