Icatibant，缓激肽B2受体拮抗剂，靶向互连的激肽系统。,Expert Opinion on Pharmacotherapy

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Icatibant，缓激肽B2受体拮抗剂，靶向互连的激肽系统。
Expert Opinion on Pharmacotherapy ( IF 2.5 ) Pub Date : 2012-09-14 , DOI: 10.1517/14656566.2012.723692
Delphine Charignon ₁ , Peter Späth , Ludovic Martin , Christian Drouet

Affiliation

简介HOE-140 /伊卡替班是缓激肽（BK）的选择性竞争性拮抗剂，可抵抗其与激肽B2受体的结合。五个非蛋白原氨基酸类似物的取代使icatibant抵抗激肽分解代谢的金属蛋白酶降解。伊卡替班在由激肽的急性（非控制性）产生及其在内皮B2受体上积累引起的炎症和血管渗漏情况中具有临床应用。血管渗漏的临床表现称为血管性水肿（AE），其特征是皮下和粘膜下组织发生水肿性发作，如果引起喉部感染，可能会引起肠痛，并危及生命。伊卡替班已注册用于治疗遗传性BK介导的AE的急性发作，即由于C1抑制剂缺乏引起的AE。涵盖的领域这篇综述讨论了激肽系统的新兴知识：激肽的药理特性，接触相的生化特性和激肽分解代谢蛋白酶。它强调激肽在AE引发中的责任以及icatibant通过激肽-受体相互作用抑制AE形成的能力。专家意见易激肽拮抗剂的特性可保护BK介导的AE患者免于严重发作，并可开发用于炎性疾病。需要进行更多的研究，以确认长期和频繁使用icatibant是否会导致BK的心脏保护作用受损。接触相的生物化学特征和激肽分解代谢蛋白酶。它强调激肽在AE引发中的责任以及icatibant通过激肽-受体相互作用抑制AE形成的能力。专家意见易激肽拮抗剂特性可保护BK介导的AE患者免于严重发作，并可开发用于炎性疾病。需要进行更多的研究，以确认长期和频繁使用icatibant是否可能导致BK的心脏保护作用受损。接触相的生物化学特征和激肽分解代谢蛋白酶。它强调激肽在AE引发中的责任以及icatibant通过激肽-受体相互作用抑制AE形成的能力。专家意见易激肽拮抗剂特性可保护BK介导的AE患者免于严重发作，并可开发用于炎性疾病。需要进行更多的研究，以确认长期和频繁使用icatibant是否会导致BK的心脏保护作用受损。专家意见易激肽拮抗剂特性可保护BK介导的AE患者免于严重发作，并可开发用于炎性疾病。需要进行更多的研究，以确认长期和频繁使用icatibant是否可能导致BK的心脏保护作用受损。专家意见易激肽拮抗剂特性可保护BK介导的AE患者免于严重发作，并可开发用于炎性疾病。需要进行更多的研究，以确认长期和频繁使用icatibant是否会导致BK的心脏保护作用受损。

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Icatibant , the bradykinin B2 receptor antagonist with target to the interconnected kinin systems.

INTRODUCTION HOE-140/ Icatibant is a selective, competitive antagonist to bradykinin (BK) against its binding to the kinin B2 receptor. Substitution of five non-proteogeneic amino acid analogues makes icatibant resistant to degradation by metalloproteases of kinin catabolism. Icatibant has clinical applications in inflammatory and vascular leakage conditions caused by an acute (non-controlled) production of kinins and their accumulation at the endothelium B2 receptor. The clinical manifestation of vascular leakage, called angioedema (AE), is characterized by edematous attacks of subcutaneous and submucosal tissues, which can cause painful intestinal consequences, and life-threatening complications if affecting the larynx. Icatibant is registered for the treatment of acute attacks of the hereditary BK-mediated AE, i.e., AE due to C1 inhibitor deficiency. AREAS COVERED This review discusses emerging knowledge on the kinin system: kinin pharmacological properties, biochemical characteristics of the contact phase and kinin catabolism proteases. It underlines the responsibility of the kinins in AE initiation and the potency of icatibant to inhibit AE formation by kinin-receptor interactions. EXPERT OPINION Icatibant antagonist properties protect BK-mediated AE patients against severe attacks, and could be developed for use in inflammatory conditions. More studies are required to confirm whether or not prolonged and frequent applications of icatibant could result in the impairment of the cardioprotective effect of BK.

更新日期：2019-11-01

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