CMC2.24 (TRB-N0224) 是一种口服活性三羰基甲烷制剂，通过抑制 Ras 及其下游效应子 ERK1/2 途径对小鼠胰腺肿瘤有效。CMC2.24 也是一种有效的锌依赖性 MMPs 抑制剂，IC50 范围为 2.0-69 μM。CMC2.24 通过恢复软骨内稳态和通过NF-κB/HIF-2α 轴抑制软骨细胞凋亡来减轻骨关节炎的进展。
货号:ajcx33542
CAS:1255639-43-0
分子式:C26H21NO5
分子量：427.45
溶解度:DMSO :< 1 mg/mL (insoluble or slightly soluble)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

CMC2.24 (TRB-N0224), an orally active tricarbonylmethane agent, is effective against pancreatic tumor in mice by inhibiting Ras activation and its downstream effector ERK1/2 pathway. CMC2.24 is also a potent inhibitor of zinc-dependent MMPs with IC50s ranging from 2.0-69 μM. CMC2.24 alleviates osteoarthritis progression by restoring cartilage homeostasis and inhibiting chondrocyte apoptosis via the NF-κB/HIF-2α axis[1][2][3].

CMC2.24 (0-60 μM; 24 hours) inhibits pancreatic cancer growth in vitro[1].CMC2.24 reduces STAT3Ser727 phosphorylation levels, induces mitochondrial reactive oxygen species and mitochondrial cell death in pancreatic cancer cells. CMC2.24 induces mitochondrial reactive oxygen species and intrinsic apoptosis[1].

CMC2.24 (50 mg/kg; p.o.; five times per week during 17 days) inhibits the growth of pancreatic cancer xenografts[1].CMC2.24 inhibits the growth of human PC through a strong cytokinetic effect. CMC2.24 inhibits ERK signaling pathway in PC cells and xenografts[1].

[1]. Mallangada NA, et al. A novel tricarbonylmethane agent (CMC2.24) reduces human pancreatic tumor growth in mice by targeting Ras. Mol Carcinog. 2018;57(9):1130-1143.
[2]. Zhou Y, et al. Chemically modified curcumin (CMC2.24) alleviates osteoarthritis progression by restoring cartilage homeostasis and inhibiting chondrocyte apoptosis via the NF-κB/HIF-2α axis. J Mol Med (Berl). 2020;98(10):1479-1491.
[3]. Zhang Y, et al. Design, synthesis and biological activity of new polyenolic inhibitors of matrix metalloproteinases: a focus on chemically-modified curcumins. Curr Med Chem. 2012;19(25):4348-4358.