Mechanism of Action
- The VEGF/VEGFR pathway is recognised as the most important pathway driving angiogenesis and vessel leakage.
- Existing therapies for wet AMD target VEGF-A but not VEGF-C or VEGF-D.
- VEGF-C and VEGF-D stimulate blood vessel growth via overlapping & distinct pathways to VEGF-A.
- Combined VEGF-A/VEGF-C/VEGF-D inhibition has the potential to improve patient response by more complete blockade of vessel growth and vascular leakage.
Existing Therapies for wet AMD
Existing therapies for wet AMD include Lucentis® and Eylea® which block the activity of VEGF-A, but not VEGF-C or VEGF-D which belong to the same family of molecules.
Blockade of VEGF-C and VEGF-D can be achieved by administration of OPT-302. Used in combination with VEGF-A inhibitors, a more complete blockade of the VEGF/VEGFR pathway can be achieved.
A Complementary Treatment
Although OPT-302 safety and activity will be investigated as a monotherapy in the Phase 1/2A clinical trial, OPT-302 is primarily being developed as a complementary medicine to be used in conjunction with existing drugs such as Eylea™ and Lucentis™.
By using OPT-302 in combination with these agents, more complete blockade of the pathways involved in the progression of wet AMD can be achieved.
This is a multi-billion dollar market opportunity, estimated to be in excess of US$10 billion per annum worldwide. Sales of the drug Lucentis™ (Roche/Novartis), which targets VEGF-A but not VEGF-C, were over $US4billion in 2014. Sales of Eylea™ (Regeneron/Bayer), which also targets VEGF-A but not VEGF-C, first marketed in November 2011 for the treatment of wet AMD, were over $US1.8billion in 2014.