YM-244769 是一种有效的、选择性的、具有口服活性的 Na⁺/Ca²⁺ 交换体 (NCX) 抑制剂。YM-244769 优先抑制 NCX3，抑制 NCX 单向向外电流 (Ca²⁺ 进入模式)，IC₅₀ 值分别为 18 nM 和 50 nM。YM-244769 可有效预防缺氧/复氧诱导的 SH-SY5Y 神经元细胞损伤。YM-244769 还能增加小鼠的尿量和尿液中电解质的排泄。

YM-244769 is a potent, selective and orally active Na/Ca exchanger (NCX) inhibitor. YM-244769 preferentially inhibits NCX3 and suppresses the unidirectional outward NCX current (Ca entry mode), with IC 50 s of 18 nM and 50 nM, respectively. YM-244769 efficiently protects against hypoxia/reoxygenation-induced SH-SY5Y neuronal cell damage. YM-244769 can also increase urine volume and urinary excretion of electrolytes in mice.

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IC50: 18 nM (NCX3), 68 nM (NCX1), 96 nM (NCX2)

YM-244769 (0.003-1 μM) inhibits dose dependently the initial rates of Ca uptake into NCX1, NCX2, and NCX3 transfectants with IC50 values of 68 ± 2.9, 96 ± 3.5, and 18 ± 1.0 nM, respectively.
YM-244769 (0.3 or 1 μM) efficiently protects against the hypoxia/reoxygenation-induced lactate dehydrogenase (LDH) release in SH-SY5Y cells and in LLC-PK1 cells (1 μM).
YM-244769 possesses reverse mode-selectivity.
YM-244769 (1 and 10 μM) inhibits NCX current (INCX) in a concentration- and [Na]i-dependent manner, the IC50 against the unidirectional outward INCX (Ca entry mode) is 0.05 μM. The IC50 values against the bidirectional outward and inward INCX are similar and approximately 100 nM with a Hill coefficient of about 1.
YM-244769 is trypsin-insensitive.

YM-244769 (0.1-1 mg/kg; p.o.; once) exhibits dose-dependently natriuretic action in mice and significantly increases urinary excretion of Ca as well as Ca/Cr ratio. has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model:

Room temperature in continental US; may vary elsewhere.

4°C, sealed storage, away from moistur In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

[1]. Iwamoto T, Kita S. YM-244769, a novel Na+/Ca2+ exchange inhibitor that preferentially inhibits NCX3, efficiently protects against hypoxia/reoxygenation-induced SH-SY5Y neuronal cell damage. Mol Pharmacol. 2006 Dec;70(6):2075-83.
[2]. Gotoh Y, et al. Genetic knockout and pharmacologic inhibition of NCX2 cause natriuresis and hypercalciuria. Biochem Biophys Res Commun. 2015 Jan 9;456(2):670-5.

In Vitro: DMSO : 120 mg/mL (270.59 mM; Need ultrasonic)配制储备液