Cheryl Guttman Krader
Published: Sunday, September 1, 2019
An investigational intracameral sustained-release bimatoprost implant (Bimatoprost SR, Allergan) appears to provide very durable IOP control, premarketing clinical trials suggest.
The research, which was presented at the 2019 annual meeting of the American Society of Cataract and Refractive Surgery, showed that in a large percentage of patients, the IOP-lowering benefit persisted far longer than the anticipated four-to-six months and was maintained even when the biodegradable pellet was no longer visible in the eye.
E Randy Craven MD is Associate Professor of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University, Baltimore, USA, and a Bimatoprost SR study investigator. He told EuroTimes: “BimSR is potentially a very long-term solution to the problem of adherence to glaucoma medications that could be moving us toward drop-free therapy.”
The longevity of the IOP-lowering effect of the Bimatoprost SR implant was analysed using data from the phase I/II APOLLO study and the phase III ARTEMIS program. APOLLO was a 24-month, paired-eye comparison study that included 75 patients with open-angle glaucoma who received one of four dose strengths of bimatoprost SR in the study eye – 6, 10, 15 and 20μg. Its results showed that IOP control was maintained without need for retreatment with the implant or rescue with a topical IOP-lowering medication in 68% of patients at six months, 40% of patients at 12 months and 28% of patients at 24 months.
Patients randomised to Bimatoprost SR treatment in ARTEMIS received implants containing 10μg or 15μg at day one, week 16 and week 32. By Kaplan-Meier analysis, the Bimatoprost SR-treated patients had an 83% probability of surviving 360 days without need for rescue treatment. Among patients in APOLLO who received a Bimatoprost SR 10 or 15µg implant as a one-time procedure, the probability of surviving 360 days without need for rescue or retreatment was 36%.
The researchers postulated that the sustained benefit of IOP lowering after the implant was no longer visible may be explained by bimatoprost-induced remodelling of aqueous outflow pathways that is mediated by its ability to increase matrix metalloproteinase release from ciliary smooth muscle cells.
E Randy Craven: erandycraven@gmail.com
Tags: iop control
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