Gossamer Bio, Inc., San Diego, CA, USA.
A. Galkin and R. Sitapara contributed equally as first authors.
Eur Respir J. 2022 Dec 1;60(6). doi: 10.1183/13993003.02356-2021. Print 2022 Dec.
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.
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.
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.
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.
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。
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。
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。
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。