Defeating MYC with drug combinations or dual-targeting drugs

被引:3
|
作者
Thompson, Philip E. [1 ]
Shortt, Jake [2 ,3 ,4 ]
机构
[1] Monash Univ, Monash Inst Pharmaceut Sci, Fac Pharm & Pharmaceut Sci, Med Chem, Parkville, Vic 3052, Australia
[2] Monash Univ, Fac Med Nursing & Hlth Sci, Sch Clin Sci Monash Hlth, Blood Canc Therapeut Lab, Melbourne, Vic 3168, Australia
[3] Monash Hlth, Monash Hematol, Melbourne, Vic 3168, Australia
[4] Univ Melbourne, Sir Peter MacCallum Dept Oncol, Melbourne, Vic 3000, Australia
关键词
BET BROMODOMAIN INHIBITORS; B-CELL LYMPHOMA; C-MYC; SYNTHETIC LETHALITY; AURORA KINASE; TUMOR-GROWTH; LUNG-CANCER; IN-VITRO; RESISTANCE; THERAPY;
D O I
10.1016/j.tips.2024.04.008
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Members of the MYC family of proteins are a major target for cancer drug discovery, but the development of drugs that block MYC-driven cancers has not yet been successful. Approaches to achieve success may include the development of combination therapies or dual-acting drugs that target MYC at multiple nodes. Such treatments hold the possibility of additive or synergistic activity, potentially reducing side effect profiles and the emergence of resistance. In this review, we examine the prominent MYC-related targets and highlight those that have been targeted in combination and/or dual-target approaches. Finally, we explore the challenges of combination and dual-target approaches from a drug development perspective.
引用
收藏
页码:490 / 502
页数:13
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