Dilevalol, the RR-stereoisomer of labetalol, is a non-cardioselective β-adrenoceptor antagonist with substantial partial β2-agonist and negligible α1-blocking activity. Reduction in blood pressure during dilevalol administration is associated with peripheral vasodilatation, and heart rate remains essentially unchanged. Following oral administration, dilevalol is completely absorbed. Once-daily administration is possible, due to a long elimination half-life. In vitro and in vivo animal studies and results obtained in humans reveal that dilevalol is a nonselective blocker of β1- and β2-adrenoceptors, with a similar potency to propranolol, but has negligible antagonistic activity at α1-receptors. Dilevalol, the R,R′ stereoisomer, makes up 25% of racemic labetalol, the drug, approved by FDA for the treatment of hypertension. The relaxing potency of dilevalol was approximately 4.7 times more potent than that of labetalol. Dilevalol markedly reduced the diastolic blood pressure with only a slight increase of heart rate In pithed rats, while isoproterenol and pindolol caused moderate to marked positive chronotropic effects in proportion to their hypotensive effects. These results suggest that dilevalol has more potent ISA than labetalol. In contrast to labetalol, dilevalol possesses little, if any, alpha-adrenergic blocking activity. The compound is 3 to 10 times less potent than labetalol at α1-adrenergic receptors under a variety of experimental conditions. Moreover, it is 300- to 1000-fold less potent at alpha1-adrenergic receptors compared with β1-adrenergic receptors. The pA2 values for dilevalol as an α antagonist range from 5.9 to 6.4. Because maximal plasma concentrations of the drug after administration of a 400-mg dose are approximately 0.5 pmol, it is doubtful that alpha blockade is involved in the antihypertensive response to dilevalol in humans.