Effect of Switching to Azilsartan From Fixed-Dose Combination of an Angiotensin II Receptor Blocker and Calcium Channel Blocker or a Thiazide in Patients With Hypertension

Abstract

Background Despite the availability of antihypertensive treatments, fewer than half of patients who receive treatment successfully achieve blood pressure (BP) goals. The purpose of this study was to evaluate the effect of switching to azilsartan 40 mg from a fixed-dose combination tablet of an angiotensin II receptor blocker (ARB) and amlodipine at 5 mg or azelnidipine at 16 mg (ARB/CCB) or an ARB and hydrochlorothiazide (HCT) at 6.25 mg or 12.5 mg (ARB/HCT) on BP. Methods This prospective, multicenter, open-labeled, single-arm study included 40 patients treated with a fixed-dose combination tablet of an ARB/CCB or an ARB/HCT, which was switched to azilsartan 40 mg after enrollment. The primary outcome was the change in BP from baseline to the 24-week follow-up. Results Of the 40 patients who completed this study, 33 did not require changes in their antihypertensive medications after switching to azilsartan, and their BP did not change from baseline to follow-up. However, the systolic BP in seven patients was elevated at 12 weeks, and amlodipine at 5 mg was therefore added; these patients’ baseline medications were an ARB/CCB (n = 6) and an ARB/HCT (n = 1). In all patients, the serum potassium level was slightly increased after switching to azilsartan at 6 months, while the serum creatinine, hemoblobinA1c, and lipid profile did not change. Conclusions Azilsartan at 40 mg did not result in a greater decrease in BP than a fixed-dose combination tablet of an ARB/CCB or an ARB/HCT. However, our findings suggest a substantial BP-lowering effect of azilsartan at 40 mg in patients with hypertension.

Azelnidipine inhibits esophageal squamous cell carcinoma proliferation in vivo and in vitro by targeting MEK1/2

“… 46 The low dose (2 mg/kg) of azelnidipine was calculated according to the clinical dose. 47 Then our studies showed that azelnidipine inhibited the growth of the PDX model of ESCC in vivo ( Figure 5 ). Furthermore, the azelnidipine group had a similar inhibitory effect in PDX mice compared with the trametinib group in LEG110, another ESCC PDX model.…”

Drug-Targeted Genomes: Mutability of Ion Channels and GPCRs

“…The publicly open NIH program announcement (PA-19-034) detailing the classification and identification of 390 understudied druggable genomes was utilized to acquire the list of 261 candidate genes encoding GPCRs and ion channels. The associated literature survey was performed until 9 December 2021, with emphasis on published title words with (1) ion channels since 2017 [4,5,[9][10][11][12][13][14]16,26,27,30,33,[39][40][41][42]44,[46][47][48]53,54,59,61,[69][70][71][72][73][74][75][76][77][78][79][80], (2) ion channel blockers since 2017 [41,[81][82][83][84][85][86][87][88][89][90]…”

“…When designing a new drug, some would rather avoid interactions with ion channel proteins, particularly due to cardiovascular safety concerns. Although several attempts have been made to target ion channels, such as K + channel blockers for autoimmune disease [34,35] and antiseizure medications [36][37][38][39][40], and antiarrhythmic treatments [41][42][43][44][45][46], targeting ion channels has resulted in a limited commercialization, as evidenced in the development of Ca 2+ channel blockers for hypertension [47,48]. Nevertheless, a pathway for therapeutic success [49] and significant progress have been achieved with drugs that target Cl − channels, such as cystic fibrosis transmembrane conductance regulator (CFTR) [50].…”