CLS-AX is our proprietary suspension of axitinib for suprachoroidal injection. It is an inhibitor of vascular endothelial growth factor (VEGF) receptors-1, -2 and -3 that we believe may benefit patients who respond suboptimally to current anti-VEGF therapies.
Axitinib is a tyrosine kinase inhibitor (TKI) currently approved to treat renal cell cancer, and with its broad VEGF blockade, we believe it may have efficacy advantages over existing retinal therapies, which predominantly focus on VEGF-A blockade and may upregulate other forms of VEGF.
Reduce patient burden from monthly injections to every six months or longer
Offer Pan-VEGF inhibition that is potentially more efficacious than current approaches
Improve long-term, real-world visual outcomes for patients
Provide physicians with ability to titrate dose based on patient need
Protect the anterior chamber from toxic exposure to TKIs
We are developing CLS-AX for administration to the suprachoroidal space as a long-acting therapy for wet age-related macular degeneration (wet AMD).
Current wet AMD therapy has a ceiling of efficacy as increased dosage or more intense regimens yield limited or no additional visual benefit, and is associated with a significant treatment burden. This treatment burden is further highlighted by recent large “real-world” retrospective studies of wet AMD which underscore the difficulty in adhering to regimens. These real-world studies demonstrate that patients are undertreated, receiving only 6 to 7 injections per year on average, resulting in mean improvement of only one to three letters in visual acuity after one year of treatment.
Axitinib achieves pan-VEGF blockade by acting at a different level of the angiogenesis cascade, directly inhibiting VEGF receptors-1, -2, and -3 with high potency and specificity. Based on preclinical data in multiple species, we believe that CLS-AX could benefit patients for several reasons.
Axitinib has intrinsic high potency and can achieve pan-VEGF inhibition through receptor blockade, which may benefit patients who respond suboptimally to current anti-VEGF-A therapy.
Axitinib has been observed to have a pharmacodynamic effect, with reduced growth of experimental neovascularization and decreased fluorescein leakage.
Suprachoroidal administration of axitinib can potentially achieve prolonged duration and targeted delivery to affected tissue layers.