MEK Inhibitors

기타 MAPK 억제제

아이소폼 선택적 제품

• 주요 억제제
• 억제제 (35)
• 길항제 (1)

Cat.No.	제품명	정보	제품 사용 인용	제품 검증
S2673	Trametinib (GSK1120212)	Trametinib (GSK1120212, JTP-74057)은 세포 무함유 분석에서 0.92 nM/1.8 nM의 IC50을 보이는 매우 특이적이고 강력한 MEK1/2 억제제이며, c-Raf, B-Raf, ERK1/2의 키나아제 활성은 억제하지 않습니다. 이 화합물은 Autophagy를 활성화하고 Apoptosis related를 유도합니다.	Nat Genet, 2026, 58(5):1112-1125. Nat Commun, 2026, 10.1038/s41467-026-70862-w Cell Rep Med, 2026, 7(1):102546
S1036	PD0325901 (Mirdametinib)	PD0325901 (Mirdametinib)은 무세포 분석에서 0.33 nM의 IC50을 갖는 선택적이고 비 ATP 경쟁적인 MEK 억제제로, ERK1 및 ERK2의 인산화에 있어 CI-1040보다 대략 500배 더 강력합니다. 임상 2상.	Cancer Research Communications, October 2021, 17-29 American Journal of Cancer Research, June 1, 2019, 1282-1292 Reproduction, February 2021, 183-193
S1008	AZD6244 (Selumetinib)	Selumetinib(AZD6244, ARRY-142886)은 강력하고 매우 선택적인 MEK 억제제로, MEK1에 대해 14 nM의 IC50과 MEK2에 대해 530 nM의 Kd 값을 가집니다. 또한 10 nM의 IC50으로 ERK1/2 인산화를 억제하며, p38α, MKK6, EGFR, ErbB2, ERK2, B-Raf 등에는 억제 효과가 없습니다. Selumetinib은 세포 증식과 이동을 억제하고 Apoptosis related 반응을 유도합니다. 임상 3상 단계입니다.	Cancer Res, 2026, 10.1158/0008-5472.CAN-25-4114. Cell Death Dis, 2026, 17(1)389 Cells, 2026, 15(5)434
S8041	Cobimetinib (GDC-0973)	Cobimetinib (GDC-0973, RG7420)은 4.2 nM의 IC50 값을 가지는 강력하고 매우 선택적인 MEK1 억제제이며, 100개 이상의 세린-트레오닌 및 티로신 키나아제 패널을 대상으로 한 테스트에서 유의미한 억제 효과를 보이지 않았습니다. 이 화합물은 Apoptosis related를 유도합니다. 임상 3상 단계입니다.	Cancer Res, 2026, 86(10):2508-2521 iScience, 2026, 29(3):114954 iScience, 2026, 29(4):115493
S7170	Avutometinib (Ro5126766, CH5126766)	Avutometinib(RO5126766,CH5126766,VS 6766, CKI-27, R-7304, RG-7304)은 BRAF V600E, BRAF, CRAF 및 MEK1에 대해 각각 8.2 nM, 19 nM, 56 nM 및 160 nM의 IC50을 가진 이중 Raf/MEK 억제제입니다. 임상 1상.	Genome Med, 2026, 18(1)43 Cancer Res, 2026, 86(10):2508-2521 Cancer Chemother Pharmacol, 2025, 95(1):78
S1102	U0126-EtOH	U0126-EtOH은 세포 없는 분석에서 0.07 μM/0.06 μM의 IC50을 가지며, PD98059보다 ΔN3-S218E/S222D MEK에 대해 100배 더 높은 친화력을 보이는 MEK1/2의 매우 선택적인 억제제입니다. U0126은 항바이러스 활성을 나타내며 Autophagy 및 Mitophagy를 억제합니다.	Cell Death Dis, 2026, 17(1)400 Oncogene, 2026, 45(11):1013-1025 Allergol Int, 2026, S1323-8930(26)00013-4
S1177	PD 98059	PD98059은 무세포 분석에서 2 μM의 IC50을 갖는 비-ATP 경쟁적 MEK 억제제로, MEK-1 매개 MAPK 활성화를 특이적으로 억제하며 ERK1 또는 ERK2를 직접적으로 억제하지는 않습니다. PD98059는 aryl hydrocarbon receptor (AhR)의 리간드이며 AhR 길항제로 작용합니다.	Anticancer Research, September 2017, 4911-4918 Cancer Research, September 15, 2019, 4650-4664 Journal of Clinical Medicine, June 24, 2019, 900
S1020	CI-1040 (PD184352)	PD184352 (CI-1040)은 세포 기반 분석에서 17 nM의 IC50을 갖는 ATP 비경쟁적 MEK1/2 억제제로, MEK5보다 MEK1/2에 대해 100배 더 선택적입니다. PD184352 (CI-1040)는 선택적으로 Apoptosis related를 유도합니다.	Cell Host Microbe, 2025, 33(4):512-528.e7 Int J Mol Sci, 2025, 26(8)3536 Front Cell Dev Biol, 2025, 13:1601887
S7007	MEK162 (Binimetinib, ARRY-162)	Binimetinib (MEK162, ARRY-162, ARRY-438162)은 무세포 분석에서 12 nM의 IC50을 가지는 강력한 MEK1/2 억제제입니다. Binimetinib은 인간 NSCLC 세포주에서 G1 세포 주기 정지 및 apoptosis를 유도하며 Autophagy를 유도합니다. 임상 3상.	Cancer Discovery, September 2019, 1182-1191 Proceedings of the National Academy of Sciences, December 6, 2022, e2208900119 Cell Rep Med, 2025, 6(2):101943
S1531	(E/Z)-BIX02189	(E/Z)-BIX02189는 MEK5의 선택적 억제제로 IC50가 1.5 nM이며, 세포 유리 분석에서 ERK5 촉매 활성을 IC50 59 nM으로 억제하며, 밀접하게 관련된 키나아제인 MEK1, MEK2, ERK2, JNK2는 억제하지 않습니다.	Anticancer Research, June 2024, 2511-2515 Biochimica et Biophysica Acta (BBA) - General Subjects, July 2015, 1415-1425 Experimental Cell Research, January 1, 2015, 199-211
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In the mitogen-activated protein kinase (MAPK) pathway, receptor tyrosine kinase activation results in adaptor proteins phosphorylating RAS. This results in the activation of the RAF-MEK-ERK kinase signalling pathway, and consequently leads to the activation of several downstream substrates that affect a number of transcription factors. The knock-on effect is that a myriad of cellular processes such as cell proliferation, survival, transformation, translational control and cytoskeletal rearrangement. In oncology, the MAPK pathway is a key contributor to tumor progression, angiogenesis, and metastasis.

In the RAS-RAF-MEK-ERK pathway, MEK has been the target of oncology research. The MEK kinase is expressed from MEK1 and MEK2 – two genes that share ~80% structural homology – that display slightly different isoforms of MEK to produce potentially different functions. Both MEK1 and MEK2 kinases are implicated in ~30% of all human cancers where MAPK signalling pathway is involved.^[1] These dual-specificity kinases phosphorylate both tyrosine and threonine residues; MEK1 and MEK2 sequentially phosphorylate ERK1 at ¹⁸⁵Tyr and then at ¹⁸³Thr. MEK exists just downstream of RAF in the classical MAPK pathway known as RAS-RAF-MEK-ERK pathway. Phosphorylation of MEK by RAF results in the phosphorylation of ERK1 and ERK2. MEK kinases show very high specificity for ERK, in fact it is the only known substrate for MEK. Therefore, constitutive phosphorylation of MEK in the RAF-MEK-ERK kinase pathway occurs by either the overexpression or mutation of receptor tyrosine kinases, and/or mutations of RAS and RAF (A-RAF and B-RAF).^[2]

The MEK enzyme itself consists of hydrophobic allosteric pockets adjacent to the ATP-binding site that facilitates the design of highly selective allosteric inhibitors. This is in contRASt to the many kinases for which there is no allosteric-binding site. Consequently, this feature is recognized by many pharmaceutical companies as a characteristic that facilitates more selective inhibitor design since the more conserved ATP-binding site is not directly targeted. MEK1 and MEK2 are positioned at the focal point of many mitogenic signaling pathways that integrates into the ERK pathway. Characteristics such as unusually restricted and unique substrate specificities, plus the integrating role of mitogenic signaling pathways demonstrates the benefits of developing a MEK inhibitor against the ERK pathway.^[3]

The utility of targeting MEK inhibition is likely to be best realized among tumors where the MEK pathway is constitutively activated. Such a scenario includes activating mutations of BRAF that results in tumors that are dependent to MEK signaling, and consequently very sensitive to MEK inhibition.^[4] This is likely to be the case among a sub-population of BRAF mutations observed in melanoma and thyroid cancers. Currently, MEK inhibition is likely to prove most effective when used in a combination strategy. This is because there is cross-talk involved between RAS-RAF-MEK-ERK and the PI3K-AKT pathway. As a consequence, inhibition of one pathway leads to constitutive signalling in the other. This is a reflection of the complexity of the kinase signalling pathways implicated in cancer.^[2]

Aside from anti-tumor potential, MEK inhibition may play a role where inflammation is concerned. Several key protein downstream of MEK are involved in inflammatory responses including TNF, IL-1, and other cytokines. MEK signaling directly impacts both the expression of cytokines and subsequent activation pathways. Therefore, MEK inhibitors –particularly orally bioavailable compounds – may be suitable agents for the treatment of inflammatory disease. In addition, it should be noted that anaphylatoxins utilize the MEK kinase cascade to initiate disease processes such as arthritis.^[2]