Anderson Elizabeth, Mehta Priyanka, Heywood Jonathan, Rees Barbara, Bone Heather, Robinson Gareth, Reynolds Darren, Salisbury Vyv, Mayer Lawrence
University of the West of England, Bristol, United Kingdom.
Bristol Haematology and Oncology Centre, University Hospital Bristol NHS Foundation Trust, Bristol, United Kingdom.
Leuk Res. 2018 Nov;74:121-129. doi: 10.1016/j.leukres.2018.08.007. Epub 2018 Aug 11.
CPX-351, a liposomal formulation co-encapsulating cytarabine and daunorubicin (DNR) in a synergistic 5:1 M ratio, has shown favourable response in newly diagnosed elderly high-risk AML. This study assessed intracellular ara-CTP levels following in vitro exposure of human immortalised leukaemic cell lines and primary AML blasts to CPX-351, and investigated fludarabine potentiation of intracellular ara-CTP formation from CPX-351. Comparison of intracellular handling of CPX-351 to cytarabine in HL-60 cells indicated slower conversion to ara-CTP for CPX-351, but equivalent cytotoxicity to cytarabine and combined DNR/cytarabine (DA) at 48 h, mostly likely reflecting the need for intracellular liposome processing to release encapsulated drugs. Further assessment demonstrated cytotoxicity of CPX-351 to be superior to DA at 48 and 72 h in cytarabine-resistant THP-1 cells (p < 0.001), and this effect could not be inhibited upon blockade of human equilibrative nucleoside transporter (hENT) function with dipyridamole. Assessment of Flu-CPX in primary blasts from presentation AML patients (n = 5) demonstrated a more rapid and pronounced potentiation of ara-CTP from CPX-351 than in immortalised cell lines, with 4/5 patients showing significant increases in ara-CTP, notably for those that went on to fail induction and relapse treatment in vivo (n = 3). This suggests a favourable impact on patient outcome from Flu-CPX.
CPX-351是一种脂质体制剂,以5:1的协同摩尔比共封装阿糖胞苷和柔红霉素(DNR),在新诊断的老年高危急性髓系白血病(AML)中显示出良好的反应。本研究评估了人永生化白血病细胞系和原发性AML原始细胞在体外暴露于CPX-351后细胞内阿糖胞苷三磷酸(ara-CTP)的水平,并研究了氟达拉滨对CPX-351形成细胞内ara-CTP的增强作用。在HL-60细胞中比较CPX-351和阿糖胞苷的细胞内处理情况表明,CPX-351转化为ara-CTP的速度较慢,但在48小时时对阿糖胞苷以及联合使用柔红霉素/阿糖胞苷(DA)的细胞毒性相当,这很可能反映了需要细胞内脂质体加工来释放封装的药物。进一步评估表明,在阿糖胞苷耐药的THP-1细胞中,CPX-351在48小时和72小时时的细胞毒性优于DA(p<0.001),并且用双嘧达莫阻断人平衡核苷转运体(hENT)功能后,这种作用无法被抑制。对初治AML患者(n = 5)的原始细胞进行氟达拉滨-CPX(Flu-CPX)评估表明,与永生化细胞系相比,CPX-351形成ara-CTP的增强作用更快、更明显,5名患者中有4名显示ara-CTP显著增加,尤其是那些在体内诱导和复发治疗失败的患者(n = 3)。这表明Flu-CPX对患者预后有有利影响。