Ocugen (Nasdaq: OCGN) has signed a binding term sheet to license OCU400, its Phase III modifier gene therapy for retinitis pigmentosa, to Kuwait-based Roots Pharmaceutical and its strategic partner Al-Dhow International Holding for exclusive commercialization rights across the Middle East and North Africa. The deal is the second regional sub-license Ocugen has executed for OCU400, following a completed agreement with South Korea's Kwangdong Pharmaceutical in 2025, and arrives four months after Phase III enrollment closed for the liMeliGhT trial, with topline data expected in Q1 2027.
Deal structure
Under the term sheet, Ocugen is expected to receive upfront license fees and near-term development milestones totaling up to USD 4 million alongside cumulative sales milestones of up to USD 255 million and a 22% royalty on net sales generated by the MENA partners. Ocugen will retain manufacturing and commercial supply responsibilities under a related supply agreement, meaning the company captures both the milestone and royalty stream and the manufacturing margin, while bearing the associated production risk.
The arrangement is a binding term sheet, not a signed license. The definitive agreement is expected within 90 days. This mirrors the structure of the Korea deal, where Ocugen announced a term sheet in June 2025 and completed the agreement in September 2025 — a roughly three-month gap.
Deal context
OCU400 delivers the NR2E3 nuclear receptor gene, which functions as a transcriptional regulator of multiple retinal pathways. Unlike mutation-specific approaches such as voretigene neparvovec (Luxturna, Spark Therapeutics/Roche) — approved only for patients carrying biallelic RPE65 mutations, a narrow genotype subset — OCU400 is described by the company as designed to work across diverse RP genotypes. The only currently approved RP gene therapy addresses approximately 2% of RP patients; OCU400's mutation-agnostic design is commercially significant in MENA, where consanguinity rates are among the highest globally, producing elevated prevalence of rare recessive mutations that would not be addressable by RPE65-specific therapies.