ar-9281 and Hypertension

ar-9281 has been researched along with Hypertension* in 2 studies

Other Studies

2 other study(ies) available for ar-9281 and Hypertension

Article	Year
Design, synthesis and evaluation of non-urea inhibitors of soluble epoxide hydrolase. Bioorganic & medicinal chemistry letters, 2012, Jan-01, Volume: 22, Issue:1 Inhibition of soluble epoxide hydrolase (sEH) has been proposed as a new pharmaceutical approach for treating hypertension and vascular inflammation. The most potent sEH inhibitors reported in literature to date are urea derivatives. However, these compounds have limited pharmacokinetic profiles. We investigated non-urea amide derivatives as sEH inhibitors and identified a potent human sEH inhibitor 14-34 having potency comparable to urea-based inhibitors. Topics: Amides; Chemistry, Pharmaceutical; Drug Design; Enzyme Inhibitors; Epoxide Hydrolases; Fluorescent Dyes; Humans; Hydrogen Bonding; Hypertension; Inflammation; Inhibitory Concentration 50; Microscopy, Fluorescence; Models, Chemical; Solubility; Structure-Activity Relationship	2012
1-(1-acetyl-piperidin-4-yl)-3-adamantan-1-yl-urea (AR9281) as a potent, selective, and orally available soluble epoxide hydrolase inhibitor with efficacy in rodent models of hypertension and dysglycemia. Bioorganic & medicinal chemistry letters, 2011, Feb-01, Volume: 21, Issue:3 1-(1-Acetyl-piperidin-4-yl)-3-adamantan-1-yl-urea 14a (AR9281), a potent and selective soluble epoxide hydrolase inhibitor, was recently tested in a phase 2a clinical setting for its effectiveness in reducing blood pressure and improving insulin resistance in pre-diabetic patients. In a mouse model of diet induced obesity, AR9281 attenuated the enhanced glucose excursion following an intraperitoneal glucose tolerance test. AR9281 also attenuated the increase in blood pressure in angiotensin-II-induced hypertension in rats. These effects were dose-dependent and well correlated with inhibition of the sEH activity in whole blood, consistent with a role of sEH in the observed pharmacology in rodents. Topics: Adamantane; Administration, Oral; Angiotensin II; Animals; Antihypertensive Agents; Blood Glucose; Disease Models, Animal; Enzyme Inhibitors; Epoxide Hydrolases; Hypertension; Insulin Resistance; Mice; Obesity; Rats; Urea	2011

Article

Year

Design, synthesis and evaluation of non-urea inhibitors of soluble epoxide hydrolase.

Bioorganic & medicinal chemistry letters, 2012, Jan-01, Volume: 22, Issue:1

Inhibition of soluble epoxide hydrolase (sEH) has been proposed as a new pharmaceutical approach for treating hypertension and vascular inflammation. The most potent sEH inhibitors reported in literature to date are urea derivatives. However, these compounds have limited pharmacokinetic profiles. We investigated non-urea amide derivatives as sEH inhibitors and identified a potent human sEH inhibitor 14-34 having potency comparable to urea-based inhibitors.

Topics: Amides; Chemistry, Pharmaceutical; Drug Design; Enzyme Inhibitors; Epoxide Hydrolases; Fluorescent Dyes; Humans; Hydrogen Bonding; Hypertension; Inflammation; Inhibitory Concentration 50; Microscopy, Fluorescence; Models, Chemical; Solubility; Structure-Activity Relationship

2012

1-(1-acetyl-piperidin-4-yl)-3-adamantan-1-yl-urea (AR9281) as a potent, selective, and orally available soluble epoxide hydrolase inhibitor with efficacy in rodent models of hypertension and dysglycemia.

Bioorganic & medicinal chemistry letters, 2011, Feb-01, Volume: 21, Issue:3

1-(1-Acetyl-piperidin-4-yl)-3-adamantan-1-yl-urea 14a (AR9281), a potent and selective soluble epoxide hydrolase inhibitor, was recently tested in a phase 2a clinical setting for its effectiveness in reducing blood pressure and improving insulin resistance in pre-diabetic patients. In a mouse model of diet induced obesity, AR9281 attenuated the enhanced glucose excursion following an intraperitoneal glucose tolerance test. AR9281 also attenuated the increase in blood pressure in angiotensin-II-induced hypertension in rats. These effects were dose-dependent and well correlated with inhibition of the sEH activity in whole blood, consistent with a role of sEH in the observed pharmacology in rodents.

Topics: Adamantane; Administration, Oral; Angiotensin II; Animals; Antihypertensive Agents; Blood Glucose; Disease Models, Animal; Enzyme Inhibitors; Epoxide Hydrolases; Hypertension; Insulin Resistance; Mice; Obesity; Rats; Urea

2011