Amiloride hydrochloride (MK-870 hydrochloride) is an inhibitor of both epithelialsodium channel(ENaC^[1]) and urokinase-type plasminogen activator receptor (uTPA^[2]). Amiloride hydrochloride is a blocker ofpolycystin-2(PC2;TRPP2^[3]) channel.

ENaC^[1]; uTPA^[2]; polycystin-2(TRPP2)^[3]

Amiloride blocks δβγ channels with an IC₅₀of 2.6 μM. The K_iof amiloride for δβγ ENaC is 26-fold that of αβγ channels (0.1 μM for αβγ ENaC). Amiloride blockade of δβγ ENaC is much more voltage dependent compared with the αβγ channel. The K_iof amiloride for δαβγ channels is 920 and 13.7 μM at –120 and⁺80 mV, respectively, which significantly differs from that of both αβγ and δβγ channels^[1]. Amiloride is a relatively selective inhibitor of the epithelial sodium channel (ENaC) with an IC₅₀(the concentration required to reach 50% inhibition of an ion channel) in the concentration range of 0.1 to 0.5 μM. Amiloride is a relatively poor inhibitor of the the Na⁺/H⁺exchanger (NHE) with an IC₅₀as low as 3 μM in the presence of a low external [Na⁺] but as high as 1 mM in the presence of a high [Na⁺]. Amiloride is an even weaker inhibitor of the Na⁺/Ca²⁺exchanger (NCX), with an IC₅₀of 1 mM. Amiloride (1 μM) and submicromolar doses of Benzamil (30 nM), doses known to inhibit the ENaC, inhibit the myogenic vasoconstriction response to increasing perfusion pressure by blocking the activity of ENaC proteins. Amiloride completely inhibits Na⁺influx in doses known to be relatively specific for ENaC (1.5 μM) in vascular smooth muscle cells (VSMC)^[2].

Amiloride (1 mg/kg/day) subcutaneously is found to reverse the initial increases in collagen deposition and prevent any further increases in the DOCA-salt hypertensive rat. Amiloride delays the onset of proteinuria and improved brain and kidney histologic scores in the saline-drinking, stroke-prone spontaneously hypertensive rats (SHRSP) compared with controls. Amiloride antagonizes or prevents actions of aldosterone in these cells and in cardiovascular and renal tissues in animals with salt-dependent forms of hypertension^[2].

266.09

Solid

C₆H₉Cl₂N₇O

2016-88-8

盐酸阿米洛利

Room temperature in continental US; may vary elsewhere.

4°C, sealed storage, away from moisture

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

DMSO : ≥ 100 mg/mL(375.81 mM)

H₂O : 7.14 mg/mL(26.83 mM;Need ultrasonic)

*"≥" means soluble, but saturation unknown.

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80℃, 6 months; -20℃, 1 month (sealed storage, away from moisture)。-80℃ 储存时，请在 6 个月内使用，-20℃ 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% DMSO    40%PEG300   5%Tween-80   45% saline

  Solubility: ≥ 2.5 mg/mL (9.40 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (9.40 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH2O 中，得到澄清透明的生理盐水溶液
• 2.

  请依序添加每种溶剂： 10% DMSO    90% (20%SBE-β-CDin saline)

  Solubility: ≥ 2.5 mg/mL (9.40 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (9.40 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 3.

  请依序添加每种溶剂： 10% DMSO    90%corn oil

  Solubility: ≥ 2.5 mg/mL (9.40 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (9.40 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。