Pranlukast hemihydrate (ONO-1078 hemihydrate) is a selective and potent leukotriene (LT) antagonist with anti-asthmatic activity that inhibits [3H]LTD4 and [3H]LTE4 binding to lung membranes and antagonizes LTC4-induced constriction of guinea-pig airways.Pranlukast hemihydrate is used in the study of asthma. Pranlukast hemihydrate is used in the study of asthma.

3H-LTC4 to lung membranes:5640 nM (Ki), 3H-LTE4 to lung membranes:0.63 nM (Ki)

In radioligand binding assays, Pranlukast hemihydrate inhibited the binding of [3H]LTE4, [3H]LTD4, and [3H]LTC4 to lung membranes with Ki values of 0.63 nM, 0.99 nM, and 5640 nM, respectively.Pranlukast hemihydrate inhibited [3H]LTC4 binding competitively. The inhibition of [3H]LTC4 binding by Pranlukast hemihydrate was characterized by competitive antagonism.
In functional assays, Pranlukast hemihydrate competitively antagonized LTC4- and LTD4-induced constriction of tracheal and parenchymal bands in guinea pigs, with pA2 values ranging from 7.70 to 10.71. Pranlukast hemihydrate antagonized LTC4-induced constriction of guinea pig tracheal and lung parenchymal bands, even in the presence of an inhibitor of the transition from LTC4 to LTD4. Pranlukast hemihydrate antagonized LTC4-induced tracheal constriction in guinea pigs even in the presence of an inhibitor of the conversion of LTC4 to LTD4 (pA2=7.78). In addition, Pranlukast hemihydrate significantly reversed the long-term contraction induced by LTD4, but had no significant effect on KCl and BaCl2-induced tracheal contraction in guinea pigs. [1]
As a CysLT1 receptor antagonist, Pranlukast hemihydrate (10 μM) inhibits oxygen-glucose deprivation (OGD)-induced nuclear translocation of CysLT1 receptors. The effects of Pranlukast hemihydrate on receptor translocation were evaluated in the study with the 5-lipoxygenase inhibitor Zileuton. The results showed that Pranlukast hemihydrate effectively inhibited the nuclear translocation of CysLT1 receptor after 6 hours of OGD, whereas Zileuton did not show such an effect. [2]

Mice were injected subcutaneously with different doses of Pranlukast hemihydrate (40, 20, and 10 mmol/kg), AA-861 (20, 10, and 5 mmol/kg), indomethacin (40 mmol/kg), and a control group 30 minutes before LPS injection. Mice treated with AA-861 and Pranlukast hemihydrate showed significantly lower mortality compared to controls. Pretreatment with carrageenan (CAR, 5 mg per mouse, intraperitoneally) sensitized mice to the effects of LPS. Although the survival rate of solvent-only treated mice was only 20% at 72 hours after LPS (50 μg per mouse, i.v.) injection, subcutaneous injection of AA-861 (20 mmol/kg) or Pranlukast hemihydrate (40 mmol/kg) significantly increased the survival rate of mice. [3]