Department of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Ave, Boston, MA, 02215, USA.
Georgetown-Lombardi Comprehensive Cancer Center, Washington, DC, USA.
Invest New Drugs. 2021 Aug;39(4):1019-1027. doi: 10.1007/s10637-020-01058-2. Epub 2021 Jan 28.
Background The CXCR4 chemokine receptor promotes tumor survival through mechanisms that include suppressing antitumor immune responses. Mavorixafor (X4P-001) is an oral, selective, allosteric CXCR4 inhibitor that decreases the recruitment of immunosuppressive cells into the tumor microenvironment and increases activated cytotoxic Tcell infiltration. Methods Patients with metastatic clear cell renal cell carcinoma (ccRCC) unresponsive to nivolumab monotherapy received oral mavorixafor 400 mg daily plus 240 mg intravenous nivolumab every 2 weeks. Results Nine patients were enrolled, median age 65 years. At baseline 4 had progressive disease (PD) and 5 had stable disease (SD). One of 5 patients with SD at study entry on prior nivolumab monotherapy had a partial response (PR) on combination treatment; all 4 patients with PD at study entry had a best response of SD with the combination treatment (median duration: 6.7 months; range: 3.7-14.7). Four patients discontinued therapy due to treatment-related adverse events (AEs). Grade ≥ 3 drug-related AEs were elevated alanine and aspartate aminotransferase (2 patients each); and autoimmune hepatitis, chronic kidney disease, increased lipase, maculopapular rash, and mucosal inflammation (1 patient each). A robust increase in levels of chemokine (C-X-C motif) ligand 9 CXCL9 on mavorixafor appeared to correlate with clinical benefit. Conclusions The CXCR4 inhibition mediated by mavorixafor, in combination with PD-1 blockade to enhance antitumor immune responses in patients unresponsive to checkpoint inhibitor monotherapy, is worthy of further study. Mavorixafor and nivolumab combination therapy in patients with advanced ccRCC demonstrated potential antitumor activity and a manageable safety profile.Trial registration: ClinicalTrials.gov identifier: NCT02923531. Date of registration: October 04, 2016.
趋化因子受体 CXCR4 通过抑制抗肿瘤免疫反应等机制促进肿瘤存活。马沃里昔芬(X4P-001)是一种口服、选择性、变构的 CXCR4 抑制剂,可减少免疫抑制细胞向肿瘤微环境的募集,并增加激活的细胞毒性 T 细胞浸润。
转移性透明细胞肾细胞癌(ccRCC)患者对纳武单抗单药治疗无反应,接受马沃里昔芬 400mg 每日口服加每 2 周静脉注射 240mg 纳武单抗。
9 名患者入组,中位年龄 65 岁。基线时,4 名患者有进展性疾病(PD),5 名患者有稳定疾病(SD)。在纳武单抗单药治疗前进入研究时有 SD 的 5 名患者之一,联合治疗时出现部分缓解(PR);4 名 PD 患者在进入研究时,联合治疗的最佳反应为 SD(中位持续时间:6.7 个月;范围:3.7-14.7)。由于治疗相关不良反应(AE),4 名患者停止治疗。2 名患者出现药物相关的 3 级以上肝功能异常(AST 和 ALT 升高);1 名患者出现自身免疫性肝炎、慢性肾脏病、脂肪酶升高、斑丘疹皮疹和黏膜炎症。马沃里昔芬引起的趋化因子(C-X-C 基序)配体 9(CXCL9)水平显著升高,似乎与临床获益相关。
马沃里昔芬介导的 CXCR4 抑制作用与 PD-1 阻断联合使用,以增强对单药检查点抑制剂治疗无反应的患者的抗肿瘤免疫反应,值得进一步研究。马沃里昔芬和纳武单抗联合治疗晚期 ccRCC 显示出潜在的抗肿瘤活性和可管理的安全性。
ClinicalTrials.gov 标识符:NCT02923531。注册日期:2016 年 10 月 4 日。