The treatment of glaucoma by reducing intraocular pressure has relied traditionally on inhibiting aqueous humor secretion (inflow). However, recent therapeutic approaches have targeted aqueous humor outflow. Prostanoid FP receptor agonists selectively increase uveoscleral outflow and the prostamide analog bimatoprost alters trabecular and uveoscleral outflow. An emerging therapeutic strategy is direct neuroprotection of retinal ganglion cells, which are selectively lost in glaucoma.