Azilsartan medoxomil (AZL-M) is characterized by a high binding potency to the AT1 receptor, with half-maximal inhibitory concentration in the low nanomolar range for inhibiting specific binding of angiotensin II to the receptor. Pharmacodynamic studies showed that AZL-M structure determines its strong binding and slow dissociation to the AT1 receptor, and an inverse agonist activity was also observed. Pharmacokinetic studies revealed that AZL-M’s absolute bioavailability is 60% with peak plasma concentration reached within 3 h. The drug is mainly metabolized via cytochrome CYP2C9. The antihypertensive effect of AZL was demonstrated to be dose-related and long-lasting. Moreover, AZL-M also exerts antiproteinuric effects, with potential benefits in the prevention or delay of renal damage in patients with hypertension and renal impairment. Animal studies have also investigated the role of AZL-M on insulin resistance, demonstrating a protective effect. Thus, AZL-M has very good pharmacodynamic and pharmacokinetic profiles, proven strong antihypertensive efficacy, and may be of benefit in cases of renal damage or metabolic syndrome. However, further long-term clinical trials are needed to deeply investigate the expected organ protective effects.