Valeant/Bausch + Lomb
Latanoprost hit the U.S. market in 1996, the last new glaucoma agent with a novel MOA. The first novel MOA to reach market since latanoprost could be a related compound, latanoprostene bunod (LBN). The new agent is a nitric oxide-donating prostaglandin F2α receptor agonist that is rapidly metabolized in situ to latanoprost acid and BDMN, an NO-donating moiety.
Latanoprost acid uses the classic latanoprost pathway to enhance uveoscleral outflow, said Baldo Scassellati Sforzolini, MD, vice president of eye care at Valeant. BDMN donates NO, a key signaling molecule that enhances tissue relaxation and improves outflow through the trabecular meshwork. The NO pathway gives LBN a statistically and clinically significant advantage over latanoprost and other IOP-lowering agents.
Animal models showed LBN lowers IOP in animals that are non-responsive to prostaglandins via NO activity. A total of nine clinical trials in Europe, Japan, and the United States have shown uniformly positive results compared to both latanoprost and timolol over a 24-hour period with once-daily topical application.
In what Valeant hopes will be two pivotal phase III studies LBN, which met its primary endpoint, non-inferiority to timolol, and showed superior IOP lowering compared to timolol with no increase in hyperemia or other adverse events. The agent is subject to all the familiar adherence pitfalls associated with eye drops, but is more effective than other drops in lowering IOP.
“We have a drug that is very effective in reducing IOP without the increase in hyperemia that is seen with some of the competitors to latanoprost,” Dr. Sforzolini said. “We believe we have the most effective, IOP-lowering monotherapy to date and we are on track for an NDA submission during the second half of 2015.”