Pranlukast hemihydrate is a highly potent, selective and competitive antagonist of peptideleukotrienes. Pranlukast inhibits [³H]LTE₄, [³H]LTD₄, and [³H]LTC₄bindings to lung membranes withK_is of 0.63±0.11, 0.99±0.19, and 5640±680 nM, respectively.

In the radioligand binding assay, Pranlukast (ONO-1078) inhibits [³H]LTE₄, [³H]LTD₄, and [³H]LTC₄bindings to lung membranes with K_is of 0.63±0.11, 0.99±0.19, and 5640±680 nM, respectively. The antagonism of Pranlukast against [³H]LTD₄binding is competitive. In functional experiments, Pranlukast shows competitive antagonism against the LTC₄- and LTD₄-induced contractions of guinea pig trachea and lung parenchymal strips with a pA₂range of 7.70 to 10.71. In the presence of an inhibitor of the bioconversion of LTC₄to LTD₄, Pranlukast also antagonizes the LTC₄-induced contraction of guinea pig trachea (pA₂=7.78). Pranlukast significantly reverses the LTD₄-induced prolonged contraction without effect on the KCl- and BaCl₂-induced contractions of guinea pig trachea^[1]. Oxygen-glucose deprivation (OGD)-induced nuclear translocation of CysLT₁receptors is inhibited by pretreatment with the CysLT₁receptor antagonist Pranlukast (10 μM). Pranlukast protects endothelial cells against ischemia-like injury. The effects of the CysLT₁receptor antagonist Pranlukast and the 5-lipoxygenase inhibitor Zileuton on translocation are also assessed. The results show that Pranlukast, but not Zileuton, inhibits the translocation of the CysLT₁receptor 6 h after OGD^[2].

Carrageenan (CAR, 5 mg per mouse) is injected i.p. 24 h before LPS (50 p,g per mouse) is injected i.v. Various doses of Pranlukast (ONO-1078; 40, 20, and 10 mmol/kg), AA-861 (20, 10, and 5 mmol/kg), Indomethacin (40 mmollkg), and the controls are injected s.c. into mice 30 min before they are challenged with 50 p,g of LPS. The maximum soluble doses are 0.6 mmol/mL in 10% DMSO for AA-861 and 1.2 mmol/mL in 10% ethanol for Pranlukast. These solutions are used as the maximum doses for the treatments. The mortality of mice is significantly decreased in AA-861- Pranlukast-treated mice relative to that in the control mice. Pretreatment with CAR (5 mg i.p.) renders the mice more sensitive to the effect of LPS. Although the survival rate of mice treated with each solvent is 20% at 72 h after LPS (50 p,g per mouse) administration, s.c. treatment with AA-861 (20 mmol/kg) or Pranlukast (40 mmol/kg) significantly increases the survival rate after the LPS administration (AA-861, P<0.001; Pranlukast, P<0.01)^[3].

490.51

Solid

C₂₇H₂₃N₅O₄.1/2H₂O

150821-03-7

普鲁司特半水合物

Room temperature in continental US; may vary elsewhere.

DMSO : 25 mg/mL(50.97 mM;Need ultrasonic)

H₂O : 1 mg/mL(2.04 mM;ultrasonic and warming and heat to 80℃)

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。-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    90% (20%SBE-β-CDin saline)

  Solubility: 2.5 mg/mL (5.10 mM); Suspended solution; Need ultrasonic

  此方案可获得 2.5 mg/mL (5.10 mM) 的均匀悬浊液，悬浊液可用于口服和腹腔注射。

  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