Lehner Martin D, Marx Degenhard, Boer Rainer, Strub Andreas, Hesslinger Christian, Eltze Manfrid, Ulrich Wolf-Rüdiger, Schwoebel Frank, Schermuly Ralph Theo, Barsig Johannes
Department of Pharmacology, ALTANA Pharma AG, Konstanz, Germany.
J Pharmacol Exp Ther. 2006 Apr;317(1):181-7. doi: 10.1124/jpet.105.098673. Epub 2005 Dec 20.
Excessive release of nitric oxide from inducible nitric-oxide synthase (iNOS) has been postulated to contribute to pathology in a number of inflammatory diseases. We recently identified imidazopyridine derivatives as a novel class of potent nitricoxide synthase inhibitors with high selectivity for the inducible isoform. In the present study, we tested the in vivo potency of BYK191023 [2-[2-(4-methoxy-pyridin-2-yl)-ethyl]-3H-imidazo-[4,5-b]pyridine], a selected member of this inhibitor class, in three different rat models of lipopolysaccharide-induced systemic inflammation. Delayed administration of BYK191023 dose-dependently suppressed the lipopolysaccharide-induced increase in plasma nitrate/nitrite (NO(x)) levels with an ED(50) of 14.9 micromol/kg/h. In a model of systemic hypotension following high-dose lipopolysaccharide challenge, curative administration of BYK191023 at a dose that inhibited 83% of the NO(x) increase completely prevented the gradual decrease in mean arterial blood pressure observed in vehicle-treated control animals. The vasopressor effect was specific for endotoxemic animals since BYK191023 did not affect blood pressure in saline-challenged controls. In addition, in a model of lipopolysaccharide-induced vascular hyporesponsiveness, BYK191023 infusion partially restored normal blood pressure responses to norepinephrine and sodium nitroprusside via an l-arginine competitive mechanism. Taken together, BYK191023 is a member of a novel class of highly isoform-selective iNOS inhibitors with promising in vivo activity suitable for mechanistic studies on the role of selective iNOS inhibition as well as clinical development.
诱导型一氧化氮合酶(iNOS)过度释放一氧化氮被认为与多种炎症性疾病的病理过程有关。我们最近鉴定出咪唑并吡啶衍生物是一类新型的强效一氧化氮合酶抑制剂,对诱导型同工型具有高选择性。在本研究中,我们在三种不同的脂多糖诱导的全身炎症大鼠模型中测试了该抑制剂类别的一个选定成员BYK191023 [2-[2-(4-甲氧基吡啶-2-基)乙基]-3H-咪唑并[4,5-b]吡啶]的体内效力。延迟给予BYK191023剂量依赖性地抑制了脂多糖诱导的血浆硝酸盐/亚硝酸盐(NO(x))水平升高,半数有效剂量(ED(50))为14.9微摩尔/千克/小时。在高剂量脂多糖攻击后的全身低血压模型中,以抑制83%的NO(x)升高的剂量给予BYK191023进行治疗,完全防止了在载体处理的对照动物中观察到的平均动脉血压的逐渐下降。升压作用对内毒素血症动物具有特异性,因为BYK191023不影响盐水攻击的对照动物的血压。此外,在脂多糖诱导的血管反应性低下模型中,BYK191023输注通过L-精氨酸竞争机制部分恢复了对去甲肾上腺素和硝普钠正常的血压反应。综上所述,BYK191023是一类新型的高度同工型选择性iNOS抑制剂的成员,具有有前景的体内活性,适用于关于选择性iNOS抑制作用的机制研究以及临床开发。