Mechanism-sorted shortcut. Anti-glaucoma drugs split into two camps: those that cut aqueous production and those that boost outflow. The stem hands you the exact mechanism, increased uveoscleral outflow, so only one camp qualifies.
The prostaglandin analogues are the uveoscleral specialists. Latanoprost binds the prostaglandin FP receptor, relaxes and remodels the ciliary muscle, and opens up the uveoscleral drainage route, dropping IOP. It is a first-line agent precisely for this powerful outflow effect.
Sort the rest by their mechanisms: pilocarpine pulls on the trabecular (conventional) outflow, while timolol (beta-blocker) and dorzolamide (carbonic anhydrase inhibitor) both lower IOP by switching down aqueous production. None of them touches the uveoscleral pathway the way the question demands. So the answer is latanoprost. Ref: DrugBank, Latanoprost (DB00654).