Receptor-type tyrosine-protein phosphatase beta (PTPRB) (PTPRB)

Receptor-type tyrosine-protein phosphatase beta (PTPRB), also known as Vascular Endothelial Protein Tyrosine Phosphatase (VE-PTP), is a transmembrane enzyme primarily expressed in vascular endothelial cells [1, 2]. It plays a pivotal role in maintaining vascular stability by acting as a negative regulator of the Tie2 (TEK) receptor tyrosine kinase and the adhesion molecule VE-cadherin [2, 4]. By dephosphorylating these targets, PTPRB promotes vascular permeability and destabilization, which are hallmark features of diseases such as diabetic retinopathy and neovascular age-related macular degeneration [4, 5]. Pharmacological inhibition of PTPRB, most notably with the small molecule razuprotafib (AKB-9778), restores Tie2 activity and strengthens endothelial junctions, thereby reducing fluid leakage and edema in the retina [3, 6]. Beyond its role in ocular health, PTPRB is also investigated for its involvement in tumor angiogenesis and the regulation of intraocular pressure in glaucoma [5, 7].

Other names

VE-PTPVascular endothelial protein tyrosine phosphataseHPTP-betaPTPBR-PTP-betaPTP beta

Inhibition of the catalytic activity of PTPRB, which prevents the dephosphorylation of the Tie2 (TEK) receptor and VE-cadherin, thereby promoting vascular stability and reducing endothelial permeability [2, 4].