Since the introduction of belladonna alkaloids, drugs blocking the cholinergic nervous system have dominated therapeutics for peptic ulcer. Until recently, the only modification of this therapy has been the use of synthetic anticholinergic agents. Recent developments in neurohormonal relations to stomach secretions have suggested that other pharmacologic approaches may be practical: (1) A number of chemical entities are devoid of anticholinergic action but can decrease gastric secretions and protect animals against experimentally induced gastric lesions—eg, 2-phenyl-2-(2-pyridyl)-thioacetamide (SC-15,396); 2,2′-Bipyridine (CI-588); 3-(methylamino)-2,1-benzisothiazole (CI-624); and benzyltris-(2-propoxyethyl) ammonium iodide (U 247–51); (2) substances have been found that inactivate pepsin—ie, a sulfated polysaccharide (SN-263) or degraded carrageenin; (3) chemicals have been tested that demonstrate enhanced ulcer healing—eg, carbenoxolone sodium and geranyl farnesyl acetate; (4) antral mucosal local anesthetics are also available—eg, oxethazaine; (5) many agents that possess other pharmacologic actions also inhibit gastric secretion as an additional property; major tranquilizers (chlorpromazine), carbonic anhydrase inhibitors (acetazolamide),α-blocking agents (phenoxybenzamine), ganglionic blocking agents (hexamethonium), catecholamines, and others.