Targeting VEGF-C/D pathway in LAM
The “lock and key” system
The Problem: In LAM, excess VEGF-D (and VEGF-C) activates VEGFR-3 on lymphatic vessels, driving abnormal, leaky lymphatics in the lungs and accelerating disease progression.
The Mechanism: By trapping VEGF-C/D with OPT-302 before they activate VEGFR-3, we aim to dampen the lymphatic signaling that fuels LAM, aiming to stabilise lung function and slow disease progression.
VEGF-C and VEGF-D are growth signals that tell lymphatic vessels to grow and become more permeable.
VEGFR-3 is the receptor on lymphatic cells that receives these signals.
When VEGF-C or VEGF-D bind to VEGFR-3, the lymphatic system gets a strong “expand and remodel” message. In LAM, this leads to abnormal, dilated, and leaky lymphatic vessels.