Eprosartan: A Comprehensive Pharmacological and Clinical Review

1. Introduction

Eprosartan is an antihypertensive medication belonging to the Angiotensin II Receptor Blocker (ARB) class of drugs.[1] It functions primarily as a selective antagonist of the Angiotensin II Type 1 (AT1) receptor subtype.[3] Its main therapeutic application is in the management of essential hypertension.[6]

Chemically, eprosartan possesses a unique structure that distinguishes it from many other ARBs. It is characterized as a non-biphenyl, non-tetrazole compound, belonging to the chemical classes of imidazoles and thiophenes.[1] This structural distinction may contribute to some of its specific pharmacological properties.

The mechanism of action involves more than simple receptor blockade. Eprosartan inhibits the physiological effects mediated by angiotensin II binding to the AT1 receptor, leading to vasodilation and reduced aldosterone secretion.[1] Furthermore, some evidence suggests a dual mechanism involving the inhibition of norepinephrine release from sympathetic nerve endings, potentially via presynaptic AT1 receptor blockade, which may contribute further to its blood pressure-lowering effect.[1]

Eprosartan was originally developed by SmithKline Beecham (now part of GSK) [10] and received initial FDA approval in the United States in 1997 under the brand name Teveten.[11] However, it is important to note that both the brand name (Teveten, Teveten HCT) and generic formulations of eprosartan have been discontinued in the United States market.[13] This discontinuation was reportedly due to business reasons and not related to concerns about the drug's safety or efficacy.[15] This significantly impacts its current clinical availability and utility for practitioners in the US, rendering its study more relevant for understanding ARB pharmacology, historical context, or for potential use in regions where it might still be available.