Acrizanib hydrochloride

Hydrochloride of Acrizanib (1% suspension; 3.5 μL/eye; topical ocular administration; tid) (LHA510 hydrochloride) inhibits neovascular area by 99% in the laser-induced CNV model of C57BL/6 mice^[1].
Hydrochloride of Acrizanib (3% suspension; 4 μL/eye; topical ocular administration; bid) inhibits neovascular area by 94% in the laser-induced CNV model of Brown Norway rats^[1].
Hydrochloride of Acrizanib (1% suspension; 4 μL/eye; topical ocular administration; tid) inhibits neovascular area by 90% in laser-induced CNV models of Brown Norway rats^[1].
Dose-response experiments of Acrizanib hydrochloride in a laser-induced CNV model of Brown Norway rats show that the ED₅₀ values for qd, bid and tid administration are 1.4%, 1.0% and 0.5%, respectively; the ED₉₀ values for bid and tid administration are 2.6% and 1.2%, respectively, while the ED₉₀ for qd administration is not determined^[1].
Hydrochloride of Acrizanib (2% suspension; 30 μL; unilateral topical ocular administration; tid; 7 days) achieves sustained exposure in the retina and retinal pigment epithelium/choroid of pigmented New Zealand White × New Zealand Red F1 rabbits; based on an analysis of exposure differences between dosed and undosed eyes, the paper reports that 37% and 57% of the total AUC in the RPE/choroid and retina, respectively, are attributable to direct local delivery of the eye drops^[1].