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多选择性RAS ((ON) 抑制针对瘤性RAS,并克服RAS介导的AML中FLT3i和BCL2i的耐药性.

Bogdan Popescu1, Matthew F Jones1, Madison Piao1

  • 1University of California San Francisco, San Francisco, California, United States.

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概括
此摘要是机器生成的。

一种名为RMC-7977的新药通过向RAS信号来治疗急性髓性白血病 (AML) 是有前途的. 这种多选择性RAS抑制剂在临床前AML模型中有效克服对FLT3抑制剂和venetoclax等现有疗法的耐药性.

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科学领域:

  • 在瘤学瘤学.
  • 分子生物学分子生物学
  • 药理学 药理学是指药理学的学科.

背景情况:

  • 异常RAS/MAPK信号传递是限制向治疗在急性髓性白血病 (AML) 疗效的关键机制.
  • 在AML中,RAS突变驱动对FLT3抑制剂 (FLT3i) 和venetoclax的耐药性,这代表了重要的未满足的临床需求.
  • 目前,没有专门针对RAS驱动的AML的向疗法显示出临床益处.

研究的目的:

  • 为了研究RMC-7977的临床前活性,RMC-7977是一种新的多选择性抑制剂,GTP结合的活性[RAS(ON]异型.
  • 评估RMC-7977在AML模型中克服对FLT3抑制剂和venetoclax耐药性的潜力.
  • 在临床前模型中评估RMC-7977与现有AML疗法的联合疗效.

主要方法:

  • 选RMC-7977跨AML细胞系与各种MAPK激活信号突变.
  • 评估RMC-7977在由于RAS突变而获得抗性细胞系中恢复对FLT3i的敏感性的能力.
  • 评估RMC-7977对RAS成的AML细胞系模型中的venetoclax耐药性的影响.
  • 测试RMC-7977与吉尔特利尼布或威尼托克拉克斯结合使用,用于小鼠患者衍生的RAS突变AML异种移植模型.

主要成果:

  • RMC-7977在具有MAPK激活突变的AML细胞系中表现出强烈的抗增殖和亲亡活性.
  • 在AML模型中,RMC-7977恢复了对FLT3抑制剂的敏感性,AML模型中获得了由二次RAS突变介导的耐药性.
  • 在RAS野生型和突变AML细胞系模型中,RMC-7977逆转了venetoclax耐药性.
  • 在体内,RMC-7977被耐受性良好,并且在组合疗法中显著抑制了白血病负担.

结论:

  • 用RMC-7977进行广谱RAS (ON) 抑制是AML的一种有前途的治疗策略.
  • 在AML中,RMC-7977有效地克服了与RAS激活相关的抵抗机制.
  • 强烈支持对RMC-7977进行临床研究,以治疗和预防RAS驱动的AML中的耐药性.