VU0071063 是一种有效且特异的 Kir6.2/SUR1 开启剂 (EC₅₀=7.44 μM)，可用于研究 Kir6.2 /SUR1 在胰腺和大脑中的表达。VU0071063 通过诱导 β 细胞膜电位的超极化来抑制胰岛素分泌。VU0071063 化学型具有非常陡峭的构效关系。

VU0071063 is a potent and specific Kir6.2/SUR1 opener (EC 50 =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.

Solid

EC50: 7.44 μM (Kir6.2/SUR1)

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.
VU0071063 dose dependently and reversibly hyperpolarizes the β-cell membrane potential, which, in turn, inhibits glucose-stimulated Ca 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. has not independently confirmed the accuracy of these methods. They are for reference only.

VU0071063 (50 mg/kg; i.p.; 4 hours) leads to a significant increase in blood glucose at 60 minutes. has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Male C57BL/6 mice (10-12 weeks age)

Room temperature in continental US; may vary elsewhere.

4°C, protect from light In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

[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.

In Vitro: DMSO : 100 mg/mL (306.38 mM; Need ultrasonic)配制储备液