Glaucoma is characterized by an increase in intra ocular pressure (IOP) which leads to damage of the optic nerve resulting in vision loss and ultimately blindness. Glaucoma is expected to affect seven million patients in the seven major markets with 50% of the patients estimated to be undiagnosed. Despite being ineffective in up to 40% of patients, the leading glaucoma treatment, Latanoprost, had global sales of more than $1.5bn in 2010.

Current glaucoma drugs include Timolol (a non-selective beta-adrenergic receptor blocker) and the carbonic anhydrase inhibitors (eg Brinzolamide) which reduce the production of aqueous humor to reduce IOP. These drugs have moderate efficacy but, in the case of Timolol, can cause substantial side effects. More recent drugs, the prostaglandins (eg Xalatan or Latanoprost and Lumigan), reduce IOP by increasing the outflow of aqueous humor, predominantly through the uveoscleral pathway. Up to 40% of glaucoma patients may not benefit from Latanoprost.

In contrast to the prostaglandins, AMA0076 and other ROCK inhibitors target outflow of aqueous humor through the trabecular meshwork. This accounts for 60% of outflow in young adults and up to 98% in older people and therefore represents a highly attractive target for effective glaucoma treatment. The ROCK inhibitors work by increasing flow through the relaxation of smooth muscle cells and have been shown to be effective in clinical trials. However, all ROCK inhibitors cause hyperemia, an unwanted side effect that limits effective dosing. AMA0076 is designed to exploit Amakem’s ‘Localized Drug Action’ technology to avoid or reduce hyperemia and other systemic side effects.