The final patient has completed their last clinical visit in Opthea's (ASX:OPT) Phase 2b trial of OPT-302 for wet age-related macular degeneration (AMD).
“The final patient's last visit is an important milestone in the clinical development pathway for OPT302, as it paves the way for the company to finalise data cleaning activities, with top-line results expected to be reported within the coming months,” said Dr Megan Baldwin, CEO and managing director of Opthea.
Patients enrolled in Opthea’s double-masked Phase 2b trial received intravitreal injections of OPT302, a selective VEGF-C/D ‘trap’ therapy, administered in combination with Novartis' PBS-listed VEGF-A inhibitor ranibizumab (LUCENTIS) or ranibizumab alone, on a monthly basis for 6 months.
The final clinical visit was scheduled at week 24, one month after the final dose administration.
Of the 366 patients randomised in the trial, 348 (95.1 per cent) patients completed the week 24 visit, therefore meeting the prospectively defined statistical assumptions for the study.
Opthea’s Phase 2b trial enrolled patients who have not received prior therapy and is designed to investigate whether the addition of OPT-302 to ranibizumab therapy over a 6 month dosing period improves visual acuity and anatomical parameters including reductions in retinal thickness, as assessed by a central independent imaging reading centre.
“This milestone brings us closer to assessing the potential of OPT-302 combination treatment to improve vision and ocular anatomical outcomes in wet AMD patients receiving standard of care anti-VEGF-A monotherapy,” said Dr Baldwin.
“We are very pleased with the trial’s progress, which completed patient recruitment several months ahead of schedule, and has continued to demonstrate a favourable safety profile for OPT-302. We now look forward to reporting outcomes from the Phase 2b trial given encouraging previously reported Phase 1/2a study data as well as the scientific rationale for targeted inhibition of VEGF-C/D, two important regulators of aberrant retinal vessel growth and vascular leakage, which are implicated in mediating resistance to selective VEGF-A inhibitors.”