Diprotin A (TFA) is an inhibitor of dipeptidyl peptidase IV (DPP-IV).

Diprotin A increases the phosphorylation of Src and vascular endothelial-cadherin (VE-cadherin) in human endothelial cells and disrupts endothelial cell-to-cell junctions, which are attenuated by CXCR4 (receptor of SDF-1α)-blocker or Src-inhibitor[1].

In the model of retinopathy of prematurity, Diprotin A increases not only retinal vascularity but also leakage. Additionally, in the murine diabetic retinopathy model, Diprotin A increases the phosphorylation of Src and VE-cadherin and aggravates vascular leakage in the retinas. Collectively, Diprotin A induces vascular leakage by augmenting the SDF-1α/CXCR4/Src/VE-cadherin signaling pathway[1].

[1]. Lee CS, et al. Dipeptidyl Peptidase-4 Inhibitor Increases Vascular Leakage in Retina through VE-cadherin Phosphorylation. Sci Rep. 2016 Jul 6;6:29393.

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