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吸入型塞拉替尼在肺动脉高压模型中表现出强大的疗效。

Inhaled seralutinib exhibits potent efficacy in models of pulmonary arterial hypertension.

机构信息

Gossamer Bio, Inc., San Diego, CA, USA.

A. Galkin and R. Sitapara contributed equally as first authors.

出版信息

Eur Respir J. 2022 Dec 1;60(6). doi: 10.1183/13993003.02356-2021. Print 2022 Dec.

Abstract

BACKGROUND

Signalling through platelet-derived growth factor receptor (PDGFR), colony-stimulating factor 1 receptor (CSF1R) and mast/stem cell growth factor receptor kit (c-KIT) plays a critical role in pulmonary arterial hypertension (PAH). We examined the preclinical efficacy of inhaled seralutinib, a unique small-molecule PDGFR/CSF1R/c-KIT kinase inhibitor in clinical development for PAH, in comparison to a proof-of-concept kinase inhibitor, imatinib.

METHODS

Seralutinib and imatinib potency and selectivity were compared. Inhaled seralutinib pharmacokinetics/pharmacodynamics were studied in healthy rats. Efficacy was evaluated in two rat models of PAH: SU5416/Hypoxia (SU5416/H) and monocrotaline pneumonectomy (MCTPN). Effects on inflammatory/cytokine signalling were examined. PDGFR, CSF1R and c-KIT immunohistochemistry in rat and human PAH lung samples and microRNA (miRNA) analysis in the SU5416/H model were performed.

RESULTS

Seralutinib potently inhibited PDGFRα/β, CSF1R and c-KIT. Inhaled seralutinib demonstrated dose-dependent inhibition of lung PDGFR and c-KIT signalling and increased bone morphogenetic protein receptor type 2 (BMPR2). Seralutinib improved cardiopulmonary haemodynamic parameters and reduced small pulmonary artery muscularisation and right ventricle hypertrophy in both models. In the SU5416/H model, seralutinib improved cardiopulmonary haemodynamic parameters, restored lung BMPR2 protein levels and decreased N-terminal pro-brain natriuretic peptide (NT-proBNP), more than imatinib. Quantitative immunohistochemistry in human lung PAH samples demonstrated increased PDGFR, CSF1R and c-KIT. miRNA analysis revealed candidates that could mediate seralutinib effects on BMPR2.

CONCLUSIONS

Inhaled seralutinib was an effective treatment of severe PAH in two animal models, with improved cardiopulmonary haemodynamic parameters, a reduction in NT-proBNP, reverse remodelling of pulmonary vascular pathology and improvement in inflammatory biomarkers. Seralutinib showed greater efficacy compared to imatinib in a preclinical study.

摘要

背景

血小板衍生生长因子受体(PDGFR)、集落刺激因子 1 受体(CSF1R)和 mast/stem cell growth factor receptor kit(c-KIT)的信号传导在肺动脉高压(PAH)中起着关键作用。我们研究了临床开发用于 PAH 的吸入性 seralutinib(一种独特的小分子 PDGFR/CSF1R/c-KIT 激酶抑制剂)与概念验证激酶抑制剂伊马替尼相比的临床前疗效。

方法

比较了 seralutinib 和伊马替尼的效力和选择性。在健康大鼠中研究了吸入性 seralutinib 的药代动力学/药效学。在两种 PAH 大鼠模型中评估了疗效:SU5416/缺氧(SU5416/H)和单克隆抗体环磷酰胺肺切除术(MCTPN)。检查了炎症/细胞因子信号的影响。在大鼠和人 PAH 肺样本中进行了 PDGFR、CSF1R 和 c-KIT 免疫组织化学检查,并在 SU5416/H 模型中进行了 microRNA(miRNA)分析。

结果

Seralutinib 能强烈抑制 PDGFRα/β、CSF1R 和 c-KIT。吸入性 seralutinib 可剂量依赖性抑制肺 PDGFR 和 c-KIT 信号传导并增加骨形态发生蛋白受体 2(BMPR2)。Seralutinib 改善心肺血流动力学参数,并减少两种模型中小肺动脉肌化和右心室肥厚。在 SU5416/H 模型中,seralutinib 改善心肺血流动力学参数,恢复肺 BMPR2 蛋白水平,降低 N 端脑利钠肽前体(NT-proBNP),优于伊马替尼。人肺 PAH 样本的定量免疫组织化学显示 PDGFR、CSF1R 和 c-KIT 增加。miRNA 分析显示了可能介导 seralutinib 对 BMPR2 作用的候选物。

结论

吸入性 seralutinib 是两种动物模型中严重 PAH 的有效治疗方法,可改善心肺血流动力学参数,降低 NT-proBNP,逆转肺血管病理重塑,改善炎症生物标志物。在一项临床前研究中,seralutinib 比伊马替尼更有效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/838e/9724289/d9ee9a2e515b/ERJ-02356-2021.01.jpg

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