20-5,14-HEDE (WIT003) is an analog of 20-HETE. 20-5,14-HEDE activates PI3K/Akt signaling pathway, thereby exhibiting anti-apoptotic and cell survival promoting effects. 20-5,14-HEDE is the agonist for 20-HETE that increases intracellular Ca 2+ concentrations, thereby enhancing vasoconstriction [1] [2].
In Vivo, 20-5,14-HEDE (1.5 nmol, subarachnoid injection, single dose) exhibits vasoconstrictive effect in rat subarachnoid hemorrhage model[2].
In Vitro, 20-5,14-HEDE (0.1 nM-50 μM, 48 h) promotes the DNA synthesis in bovine pulmonary artery endothelial cells (BPAECs ), enhances the proliferation of BPAECs. 20-5,14-HEDE reduces serum starvation-induced caspase-3 activity and inhibits apoptosis in BPAECs. 20-5,14-HEDE increases ROS production in BPAECs[1].
References:
[1]. Dhanasekaran, et al. "20-HETE increases survival and decreases apoptosis in pulmonary arteries and pulmonary artery endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 296.3 (2009): H777-H786.
[2]. Yu M, et al., Effects of a 20-HETE antagonist and agonists on cerebral vascular tone. Eur J Pharmacol. 2004 Feb 23;486(3):297-306.
In Vivo, 20-5,14-HEDE (1.5 nmol, subarachnoid injection, single dose) exhibits vasoconstrictive effect in rat subarachnoid hemorrhage model[2].
In Vitro, 20-5,14-HEDE (0.1 nM-50 μM, 48 h) promotes the DNA synthesis in bovine pulmonary artery endothelial cells (BPAECs ), enhances the proliferation of BPAECs. 20-5,14-HEDE reduces serum starvation-induced caspase-3 activity and inhibits apoptosis in BPAECs. 20-5,14-HEDE increases ROS production in BPAECs[1].
References:
[1]. Dhanasekaran, et al. "20-HETE increases survival and decreases apoptosis in pulmonary arteries and pulmonary artery endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 296.3 (2009): H777-H786.
[2]. Yu M, et al., Effects of a 20-HETE antagonist and agonists on cerebral vascular tone. Eur J Pharmacol. 2004 Feb 23;486(3):297-306.