Background:

Bevacizumab, a humanized monoclonal antibody, specifically binds to all VEGF-A isoforms with high affinity.

Bevacizumab, a humanized monoclonal antibody, specifically binds to all VEGF-A isoforms with high affinity, and inhibits its interaction with VEGFR-1 and VEGFR-2[1]. Experimental analysis shows that the EC50 of Bevacizumab to bind VEGF analyzed by ELISA is 0.18 μg/mL. Binding kinetics assays show similar results that Bevacizumab inhibits the VEGF-induced proliferation of HUVEC with an IC50 value of 0.047±0.0081 μg/mL[2].

It is demonstrated that the subconjunctival administration of FD006, Bevacizumab and Dexamethasone can all significantly inhibit CoNV in NaOH cauterized rats compared with the control group (p < 0.01)[2]. The combination of NVP-LDE225 and Paclitaxel causes a long-lasting antitumor activity, with a tumor size of 1.64 cm3 at the end of the experiment, whereas Bevacizumab plus Paclitaxel-treated mice reaches the maximum allowed tumor size on day 84[3].

[1]. Tan H, et al. 99mTc-labeled bevacizumab for detecting atherosclerotic plaque linked to plaque neovascularization and monitoring antiangiogenic effects of atorvastatin treatment in ApoE-/-mice. Sci Rep. 2017 Jun 14;7(1):3504. [2]. Wang Q, et al. Pharmacological characteristics and efficacy of a novel anti-angiogenic antibody FD006 in corneal neovascularization. BMC Biotechnol. 2014 Feb 27;14:17. [3]. Di Mauro C, et al. Hedgehog signalling pathway orchestrates angiogenesis in triple-negative breast cancers. Br J Cancer. 2017 May 23;116(11):1425-1435.