丝裂原激活蛋白激酶（MEK）是Ras/Raf/MEK/ERK信号通路的重要组成部分之一，传导细胞生长、分化和发育的信号。 MEK 的失调会导致多种癌症；因此，MEK被认为是治疗癌症的潜在治疗靶点。 MEK1/2抑制剂与其他抑制剂联合使用，在包括耐药性或复发性或难治性癌症在内的各种恶性肿瘤中显示出更好的治疗效果。2016年至2024年5月关于肿瘤学中的MEK抑制剂、其组合产品和结构见解的综合专利文献已经发表通过在 PubMed、Scopus、Espacenet、Web of Science、世界知识产权组织和 Google 专利数据库中检索相关信息进行综述。MEK 的过度表达和突变已被报道可导致多种癌症，特别是耐药癌症。 MEK1/2 抑制剂与其他激酶 (BRaf/KRas/PI3K) 抑制剂组合显示出显着的抗增殖活性。 MEK抑制剂与PD-1、DYRK1、EGFR、BTK和/或VEGF抑制剂等的其他组合在结直肠癌、胰腺癌、胃肠道癌、实体瘤、乳腺癌、黑色素瘤和多发性骨髓瘤等多种癌症中显示出良好的效果。这些组合的双或多靶点方法显示出对耐药癌症患者更好、更精确的治疗。

Mitogen-activated protein kinase (MEK) is one of the important components of Ras/Raf/MEK/ERK signaling pathway, transduces signal for cell growth, differentiation, and development. Deregulation of MEK leads to a wide variety of cancer; hence, MEK is considered as potential therapeutic targets for the treatment of cancer. The MEK1/2 inhibitors in combination with other inhibitors showed better therapeutic outcomes in various malignancies including resistant or relapsed or refractory cancer.A comprehensive patent literature from the year 2016 to May 2024 on MEK inhibitors in oncology, their combination products and structural insights have been reviewed through searching relevant information in PubMed, Scopus, Espacenet, Web of Science, World Intellectual Property Organization and Google Patent databases.Overexpression and mutation of MEK have been reported to cause a wide variety of cancers especially resistant cancers. The MEK1/2 inhibitors in combination with other kinase (BRaf/KRas/PI3K) inhibitors showed significant anti-proliferative activity. Other combination of MEK inhibitor with PD-1, DYRK1, EGFR, BTK and/or VEGF inhibitors, etc. showed promising results in many cancers including colorectal, pancreatic, gastrointestinal, solid tumor, breast cancer, melanoma and multiple myeloma, etc. The dual or multi-targeted approaches of these combinations showed better and precise treatment of patients with resistant cancer.