CMC2.24 (Synonyms: TRB-N0224) |
| Katalog-Nr.GC62347 |
CMC2.24 (TRB-N0224), ein oral aktiver Tricarbonylmethan-Wirkstoff, ist bei MÄusen wirksam gegen BauchspeicheldrÜsentumoren, indem er die Ras-Aktivierung und den nachgeschalteten Effektor-ERK1/2-Weg hemmt.
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Cas No.: 1255639-43-0
Sample solution is provided at 25 µL, 10mM.
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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.
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