Real-world impact of latanoprostene bunod ophthalmic solution 0.024% in glaucoma therapy: a narrative review

W. Daniel Stamer ¹ Thomas Chiu ² Da-Wen Lu ³ Tsing Hong Wang ⁴ Prin Rojanapongpun ⁵ Ngamkae Ruangvaravate ⁶ Youn Hye Jo ⁷ Marlene R. Moster ⁸ Murray Fingeret ⁹ Nora Lee Cothran ¹⁰ Jessica Steen ¹¹ Ian Benjamin Gaddie ¹² Ömür Uçakhan-Gündüz ¹³ Wesam Shamseldin Shalaby ^14,15 Cindy M. L. Hutnik ^16*

• ¹ Duke University, Durham, North Carolina, United States
• ² The Chinese University of Hong Kong, Shatin, Hong Kong Region, China
• ³ National Defense Medical Center, Taipei, Taiwan
• ⁴ National Taiwan University Hospital, Taipei, Taiwan
• ⁵ Chulalongkorn University & King Chulalongkorn Memorial Hospital, Bangkok, Thailand
• ⁶ Siriraj Hospital, Mahidol University, Bangkok, Thailand
• ⁷ Seoul Konkuk University Hospital, Seoul, Republic of Korea
• ⁸ Sidney Kimmel Medical College, Thomas Jefferson University, and Wills Eye Hospital, Philadelphia, United States
• ⁹ The State University of New York (SUNY), Albany, New York, United States
• ¹⁰ The Eye Institute of West Florda, Largo, United States
• ¹¹ Nova Southeastern University College of Optometry, Fort Lauderdale, United States
• ¹² Gaddie Eye Centers, Louisville, United States
• ¹³ Ankara University School of Medicine, Ankara, Türkiye
• ¹⁴ Wills Eye Hospital, Philadelphia, Pennsylvania, United States
• ¹⁵ Tanta Medical School, Tanta, Gharbia, Egypt
• ¹⁶ Ivey Eye Institute, Western University, London, Canada

Latanoprostene bunod ophthalmic solution (LBN) 0.024% is a topical nitric oxide (NO)-donating prostaglandin F2α (PGF2α) analog first approved in November 2017 for reduction of intraocular pressure (IOP) in patients with ocular hypertension (OHT) or open-angle glaucoma (OAG). This narrative review describes the unique mechanism of action of LBN and summarizes available real-world data. Upon instillation, LBN is metabolized into latanoprost acid and butanediol mononitrate, which is further reduced to NO and an inactive metabolite. Latanoprost acid increases aqueous humor outflow primarily through the uveoscleral (unconventional) pathway, whereas NO increases outflow through the trabecular (conventional) pathway. Eight studies were identified: 2 studies in newly diagnosed, treatment-naïve patients with OHT or OAG, 4 studies of adjunctive therapy in patients with glaucoma receiving other IOP-lowering therapies, and 2 studies in which patients with glaucoma switched to LBN monotherapy or adjunctive therapy. Decreases in IOP after initiating LBN in newly diagnosed patients or adding/switching to LBN were generally consistent with reductions observed in clinical trials and sustained throughout the studies. Rates of discontinuation due to inadequate IOP lowering ranged from 12.2% to 17.1%.LBN was generally well tolerated in real-world studies; the most common adverse events were consistent with the known safety profile of LBN. Data from real-world studies provide important insight regarding the potential effectiveness and tolerability of LBN in the clinical setting and suggest that LBN is well tolerated and associated with significant, clinically meaningful, and durable reductions in IOP.