160431-85-6Relevant articles and documents
Preparation and evaluation of soluble epoxide hydrolase inhibitors with improved physical properties and potencies for treating diabetic neuropathic pain
Hammock, Bruce D.,Hwang, Sung-Hee,Lee, Kin Sing Stephen,Morisseau, Christophe,Ng, Jen C.,Wagner, Karen,Yang, Jun
, (2020/09/16)
Soluble epoxide hydrolase (sEH), a novel therapeutic target for neuropathic pain, is a largely cytosolic enzyme that degrades epoxy-fatty acids (EpFAs), an important class of lipid signaling molecules. Many inhibitors of sEH have been reported, and to dat
Optimized inhibitors of soluble epoxide hydrolase improve in vitro target residence time and in vivo efficacy
Lee, Kin Sing Stephen,Liu, Jun-Yan,Wagner, Karen M.,Pakhomova, Svetlana,Dong, Hua,Morisseau, Christophe,Fu, Samuel H.,Yang, Jun,Wang, Peng,Ulu, Arzu,Mate, Christina A.,Nguyen, Long V.,Hwang, Sung Hee,Edin, Matthew L.,Mara, Alexandria A.,Wulff, Heike,Newcomer, Marcia E.,Zeldin, Darryl C.,Hammock, Bruce D.
, p. 7016 - 7030 (2014/11/07)
Diabetes is affecting the life of millions of people. A large proportion of diabetic patients suffer from severe complications such as neuropathic pain, and current treatments for these complications have deleterious side effects. Thus, alternate therapeu
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
Anandan, Sampath-Kumar,Webb, Heather Kay,Chen, Dawn,Wang, Yi-Xin,Aavula, Basker R.,Cases, Sylvaine,Cheng, Ying,Do, Zung N.,Mehra, Upasana,Tran, Vinh,Vincelette, Jon,Waszczuk, Joanna,White, Kathy,Wong, Kenneth R.,Zhang, Le-Ning,Jones, Paul D.,Hammock, Bruce D.,Patel, Dinesh V.,Whitcomb, Randall,MacIntyre, D. Euan,Sabry, James,Gless, Richard
, p. 983 - 988 (2011/03/20)
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.
