PYC Therapeutics released a comprehensive summary of preclinical findings supporting the potential of PYC's VP-002 program as the first disease modifying therapy for patients suffering from Autosomal Dominant Optic Atrophy (ADOA). PYC's PPMO technology used in the VP-002 program significantly increases levels of OPA1 protein and corrects major functional deficits that underly ADOA. Building on recent announcements relating to the VP-002 program, further optimized lead candidates have shown an even more potent ability to increase the OPA1 protein to greater than 1.5-fold. These data support continued development of the program toward clinical trials, which are estimated to initiate in the first half of 2023. Together with VP-001, PYC's development program for Retinitis Pigmentosa type 11, the Company is now progressing two lead programs towards clinical trials, both of which could be the first disease modifying therapies for two important inherited retinal diseases. This approach also underscores the breadth of potential application of the Company's PPMO technology which PYC will continue to apply towards additional programs within and outside of ocular diseases. ADOA is a genetic disease that causes progressive blindness affecting approximately 1 in 30,000 people globally. The majority of ADOA cases are caused by loss of function mutations in the OPA1 gene, leading to haploinsufficiency of the OPA1 protein. The VP-002 program aims to treat ADOA through the upregulation of the target OPA1 protein. Highlights from PYC's preclinical research, which includes both in vivo assessments together with assessments in cells derived from four different patients with OPA1 ADOA, underscore the potential of the VP-002 program as the first disease modifying approach for the treatment of OPA1 ADOA. To-date, the Company has demonstrated the ability of PYC's PPMOs to: Increase the target OPA1 protein by greater than 1.5-fold in a dose-dependent and mutation agnostic manner; Increase mitochondrial bioenergetics and adenosine triphosphate (ATP) production in a dose-dependent and mutation agnostic manner; Protect cells from apoptosis in a dose-dependent and mutation agnostic manner, rescuing the critical functional deficit observed in ADOA patients to near healthy levels; and Effectively reach target retinal ganglion cells in vivo, compared to alternative antisense oligonucleotide (ASO) approaches that have demonstrated limited ability to reach these cells at much higher doses.