INTRODUCTION Primary open-angle glaucoma (POAG) is a leading cause for worldwide blindness and is characterized by progressive optic nerve damage. The etiology of POAG is unknown, but elevated intraocular pressure (IOP) and advanced age have been identified as risk factors. IOP reduction is the only known treatment for glaucoma. Recently, drugs that inhibit rho-associated protein kinase (ROCK) have been studied in animals and people for their ability to lower IOP and potentially treat POAG. ROCK inhibitors lower IOP through a trabecular mechanism and may represent a new therapeutic paradigm for the treatment of POAG. AREAS COVERED Exploring the place that ROCK inhibitors may occupy in our treatment of POAG requires a thorough understanding of pathophysiology and treatment. This article summarizes current research on the incidence, proposed etiologies and mechanisms of action for this drug class. ROCK inhibitor research is presented and considered in light of the current standard of pharmacologic care. EXPERT OPINION ROCK inhibitors alter the cell shape and extracellular matrix (ECM) of the trabecular meshwork. Preclinical studies demonstrate that these drugs have the potential to become a new therapy for glaucoma. However, ROCK inhibitors can affect multiple cell types, and their utility can be proven only after clinical studies in patients.