Raymond K. Tong

TL;DR: It is proposed that blocking NRP1 function inhibits vascular remodeling, rendering vessels more susceptible to anti-VEGF therapy, and generated two monoclonal antibodies that bind to the Sema- and VEGF-binding domains of N RP1.

TL;DR: The results demonstrate that Nrp2, which was originally identified as an axon-guidance receptor, is an attractive target for modulating metastasis and reduces tumoral lymphangiogenesis and, importantly, functional lymphatics associated with tumors.

TL;DR: It is shown that bispecific antibodies with optimized binding to the transferrin receptor (TfR) that target β-secretase (BACE1) can cross the BBB and reduce brain amyloid-β (Aβ) in mice.

TL;DR: It is reported that when mice were dosed with therapeutic TfR antibodies, the animals showed acute clinical reactions and a reduction in immature red blood cells, known as reticulocytes, which suggest that the blood-brain barrier is not the only obstacle to surmount on the way to the brain, at least when using TFR as a molecular lift.

TL;DR: It is reported that blocking NRP1 function, using a recently described antibody that inhibits VEGF165 binding to N RP1, surprisingly reduces V EGF121-induced migration and sprout formation of endothelial cells.