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Targeting VEGF and the VEGFR2 receptor are promising treatment modalities for wet age-related macular degeneration. This study, published in Investigative Ophthalmology & Visual Science, used the peptide KAI to interfere with VEGFR2 trafficking. The study sought to determine how efficacious this peptide is in the mouse model of choroidal neovascularization.

Surface plasmon resonance was used to test KAI specificity. Then, drug delivery was analyzed using cryosection and the ELISA after treatment with KAI eyedrop to the mice’s eyes. Mice with laser-induced ruptures in Bruch’s membrane received daily treatment with KAI eyedrop or a control peptide. The other groups received treatment with intravitreal injection of anti-VEGF or IgG control.

Ultimately, it was found that after 2 weeks, KAI peptide significantly reduced disease progression in the mice with laser-induced choroidal neovascularization. Moreover, the KAI peptide was found to have specificity and high affinity to VEGFR2 and the potential for successful delivery to mice eyes. The observed mechanism of action of KAI peptide is the genetic deletion of a kinesin KIF13B involved in VEGFR2 trafficking. 

The researchers concluded that their study suggests that KAI eyedrop is as effective as other current treatment methods at preventing choroidal neovascularization in wet age-related macular degeneration [1].

Source:

[1] Waters, S. B., Zhou, C., Nguyen, T., Zelkha, R., Lee, H., Kazlauskas, A., Rosenblatt, M. I., Malik, A. B., & Yamada, K. H. (2021). VEGFR2 trafficking by KIF13B is a novel therapeutic target for wet age-related macular degeneration. Investigative Opthalmology & Visual Science, 62(2), 5. https://doi.org/10.1167/iovs.62.2.5

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