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福司可匹罗抑制高级别尿路上皮癌的生长,作用靶点是γ-分泌酶复合物。

Fosciclopirox suppresses growth of high-grade urothelial cancer by targeting the γ-secretase complex.

机构信息

Department of Cancer Biology, University of Kansas Medical Center, Kansas City, KS, USA.

Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, USA.

出版信息

Cell Death Dis. 2021 May 31;12(6):562. doi: 10.1038/s41419-021-03836-z.

Abstract

Ciclopirox (CPX) is an FDA-approved topical antifungal agent that has demonstrated preclinical anticancer activity in a number of solid and hematologic malignancies. Its clinical utility as an oral anticancer agent, however, is limited by poor oral bioavailability and gastrointestinal toxicity. Fosciclopirox, the phosphoryloxymethyl ester of CPX (Ciclopirox Prodrug, CPX-POM), selectively delivers the active metabolite, CPX, to the entire urinary tract following parenteral administration. We characterized the activity of CPX-POM and its major metabolites in in vitro and in vivo preclinical models of high-grade urothelial cancer. CPX inhibited cell proliferation, clonogenicity and spheroid formation, and increased cell cycle arrest at S and G0/G1 phases. Mechanistically, CPX suppressed activation of Notch signaling. Molecular modeling and cellular thermal shift assays demonstrated CPX binding to γ-secretase complex proteins Presenilin 1 and Nicastrin, which are essential for Notch activation. To establish in vivo preclinical proof of principle, we tested fosciclopirox in the validated N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) mouse bladder cancer model. Once-daily intraperitoneal administration of CPX-POM for four weeks at doses of 235 mg/kg and 470 mg/kg significantly decreased bladder weight, a surrogate for tumor volume, and resulted in a migration to lower stage tumors in CPX-POM treated animals. This was coupled with a reduction in the proliferation index. Additionally, there was a reduction in Presenilin 1 and Hes-1 expression in the bladder tissues of CPX-POM treated animals. Following the completion of the first-in-human Phase 1 trial (NCT03348514), the pharmacologic activity of fosciclopirox is currently being characterized in a Phase 1 expansion cohort study of muscle-invasive bladder cancer patients scheduled for cystectomy (NCT04608045) as well as a Phase 2 trial of newly diagnosed and recurrent urothelial cancer patients scheduled for transurethral resection of bladder tumors (NCT04525131).

摘要

环吡酮胺(CPX)是一种获得美国食品药品监督管理局批准的局部抗真菌药物,已在多种实体瘤和血液系统恶性肿瘤的临床前研究中显示出抗肿瘤活性。然而,由于其口服生物利用度差和胃肠道毒性,其作为口服抗癌药物的临床应用受到限制。环吡酮胺的磷酰氧甲基酯(CPX 前药,CPX-POM),经静脉给药后可将活性代谢物 CPX 选择性递送至整个泌尿道。我们在高分级尿路上皮癌的体外和体内临床前模型中对 CPX-POM 及其主要代谢物的活性进行了表征。CPX 抑制细胞增殖、集落形成和球体形成,并增加细胞周期在 S 和 G0/G1 期的阻滞。机制上,CPX 抑制了 Notch 信号的激活。分子建模和细胞热转移分析表明 CPX 与 Notch 激活所必需的 γ-分泌酶复合物蛋白早老素 1 和 Nicastrin 结合。为了在体内建立临床前原理验证,我们在已验证的 N-丁基-N-(4-羟丁基)亚硝胺(BBN)小鼠膀胱癌模型中测试了福司匹酯。CPX-POM 每周腹腔注射一次,连续四周,剂量分别为 235mg/kg 和 470mg/kg,可显著降低膀胱重量(肿瘤体积的替代指标),并导致 CPX-POM 治疗动物的肿瘤向较低分期迁移。这与增殖指数的降低有关。此外,CPX-POM 治疗动物的膀胱组织中早老素 1 和 Hes-1 的表达也减少了。在首例人体 I 期临床试验(NCT03348514)完成后,福司匹酯的药理活性目前正在接受肌层浸润性膀胱癌患者行膀胱切除术的 I 期扩展队列研究(NCT04608045)以及新诊断和复发性尿路上皮癌患者行经尿道膀胱肿瘤切除术的 II 期试验(NCT04525131)进行评估。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d54/8166826/73764279d510/41419_2021_3836_Fig1_HTML.jpg

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