Glaucoma is a prevalent cause of visual impairment and blindness in the world. It is actually a heterogeneous group of optic neuropathies that have characteristic clinical features. Most current glaucoma therapies are directed at lowering intraocular pressure (IOP), which is commonly elevated in glaucoma and an important risk factor for the development and progression of glaucoma. There are a number of different ocular hypotensive agents being used to treat glaucoma and these agents have very different, class-specific ocular and/or systemic side-effects. At least five new ocular hypotensive drugs have been introduced into the marketplace within the past several years, including topically active carbonic anhydrase inhibitors (CAIs), hypotensive prostaglandins and α2-adrenergic agonists. Although many of these agents are very active ocular hypotensive agents, there is still a need for agents that address the actual disease pathogenic processes. Two ocular hypotensive agents have additional neuroprotective properties which may provide additional protection to the retinal ganglion cells (RGC) that die during the glaucoma disease process. Neuroprotective agents, such as NMDA antagonists, are being considered as potential new glaucoma therapeutic agents. Exciting new discoveries in the molecular pathogenesis of glaucoma and in the molecular genetics of glaucoma are generating potential new therapeutic targets. There are definite needs for earlier diagnostic techniques and better methods to quantify glaucomatous changes in vision. This would enable the efficient and timely testing of new therapeutic agents to treat this important ophthalmic disease.