Frequently Asked Questions

How do TKIs differ from anti-VEGF therapies?

Currently available anti-VEGF therapies are biologics that bind to VEGF ligands outside the cell, preventing them from binding to VEGF receptors (VEGFRs). In contrast, TKIs are small molecules that are available intracellularly to inhibit VEGFRs and pro-inflammatory IL-6 signaling.

What is the significance of the intracellular mechanism of action of TKIs?

Intracellular VEGFR inhibition allows TKIs to be a potentially complementary treatment strategy with anti-VEGF therapy; offering multimodal VEGF pathway control, both at the ligand and receptor level.

How is vorolanib different from other ophthalmic TKIs?

Unlike other ophthalmic TKIs in development, vorolanib inhibits IL-6 pro-inflammatory signaling in addition to VEGF receptors, potentially offering multiple MOAs.

How is Durasert E™ different from prior Durasert® technologies?

The next-generation Durasert E™ is a bioerodible matrix that delivers a continuous daily dose for at least 6 months.

What clinical data are currently available?

EYP-1901 has been evaluated in over 190 patients with retinal diseases across four phase 1 and phase 2 clinical trials with no EYP-1901 related safety concerns. A recent independent review of the phase 3 LUGANO/LUCIA masked safety data showed that the observed safety profile is consistent with previous EYP-1901 clinical trials. To date, results from two phase 2 trials met their primary endpoints. See phase 2 clinical study results for more information.

MOA, mechanism of action; SAE, serious adverse event; TKI, tyrosine kinase inhibitor; VEGF, vascular endothelial growth factor.

EYP-1901 is an investigational product and the safety and efficacy of EYP-1901 has not been established. FDA has not approved EYP-1901 in the United States. The materials discussed on this site do not predict future FDA approval. Conclusive evidence of efficacy and safety of EYP-1901 will require further investigation in well-controlled Phase 3 clinical trials.

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