| Bioactivity | VU0071063 is a potent and specific Kir6.2/SUR1 opener (EC50=7.44 μM) and can be used for investigating Kir6.2/SUR1 expressed in the pancreas and brain. VU0071063 inhibits insulin secretion by inducing hyperpolarization of β-cell membrane potential. VU0071063 chemotype has a very steep structure-activity relationships[1][2]. |
| Target | EC50: 7.44 μM (Kir6.2/SUR1) |
| Invitro | VU0071063 (1 nM~1 mM; HEK-293 cells) dose dependently opens Kir6.2/SUR1. VU0071063 (0~20 μM; isolated cells) inhibits β-Cell excitability in mouse Islets. VU0071063 (10 μM; 1 hour; isolated cells) inhibits glucose-stimulated insulin secretion[1].VU0071063 dose dependently and reversibly hyperpolarizes the β-cell membrane potential, which, in turn, inhibits glucose-stimulated Ca2+ entry and insulin secretion. The actions of VU0071063 on the β-cell membrane potential are reversed by tolbutamide, and glucose stimulated insulin secretion is unaffected by the inactive analog 34MT, indicating that the effects are mediated through Kir6.2/SUR1[1]. |
| In Vivo | VU0071063 (50 mg/kg; i.p.; 4 hours) leads to a significant increase in blood glucose at 60 minutes[1]. Animal Model: |
| Name | VU0071063 |
| CAS | 333415-38-6 |
| Formula | C18H22N4O2 |
| Molar Mass | 326.39 |
| Appearance | Solid |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | 4°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light) |
| Reference | [1]. Kharade SV, et al. Structure-Activity Relationships, Pharmacokinetics, and Pharmacodynamics of the Kir6.2/SUR1-Specific Channel Opener VU0071063. J Pharmacol Exp Ther. 2019;370(3):350-359. [2]. Raphemot R, et al. Direct activation of β-cell KATP channels with a novel xanthine derivative. Mol Pharmacol. 2014;85(6):858-865. |