For research use only. Not for therapeutic Use.
HAC-Y6 is a novel and potent microtubule inhitor. HAC-Y60 exhibited potent antitumor activity against human hepatocellular carcinoma (HCC) cells in vitro. Western blot and immunofluorescence experiments showed that HAC-Y6 depolymerized microtubules similarly to the effects of colchicine. HAC-Y6 exhibited its antitumor activity by disrupting microtubule assembly, causing cell cycle arrest and apoptosis through both extrinsic and intrinsic pathways in Hep3B cells. ( Oncol Rep. 2010 Nov;24(5):1169-78. )
| Catalog Number | I007186 |
| CAS Number | 1331959-78-4 |
| Synonyms | HACY6; HAC-Y6; HAC Y6.;1-(9-(3,4,5-trimethoxybenzyl)-9H-pyrido[2,3-b]indol-6-yl)ethanone |
| Molecular Formula | C23H22N2O4 |
| Purity | ≥95% |
| Target | microtubule inhibitor |
| Solubility | Soluble in DMSO, not in water |
| Storage | 0 - 4°C for short term , or -20°C for long term. |
| Reference | 1:Oncol Rep. 2010 Nov;24(5):1169-78. Induction of apoptosis by HAC-Y6, a novel microtubule inhibitor, through activation of the death receptor 4 signaling pathway in human hepatocellular carcinoma cells.Tsai JY,Hung CM,Bai ST,Huang CH,Chen WC,Chung JG,Kuo SC,Way TD,Huang LJ, PMID: 20878107 </br><span>Abstract:</span> The present data showed that a novel synthesized compound, 6-acetyl-9-(3,4,5-trimethoxybenzyl)-9H-pyrido [2,3-b]indole (HAC-Y6), exhibited potent antitumor activity against human hepatocellular carcinoma (HCC) cells in vitro. Western blot and immunofluorescence experiments showed that HAC-Y6 depolymerized microtubules similarly to the effects of colchicine. HAC-Y6-treatment in Hep3B cells resulted in the accumulation of the G2/M phase and induced apoptosis. In addition, HAC-Y6-treatment influenced the expression of cell cycle and apoptosis related proteins in Hep3B cells. HAC-Y6 exposure increased caspases-3, -8, -9 and Bax protein levels, while reducing levels of Bcl-2 family proteins. Moreover, Bid, a substrate of caspase-8, was also activated by HAC-Y6. Treatment of cells caused the up-regulation of the death receptor 4 (DR4) and phosphorylation of p38. Taken together, we show that HAC-Y6 exhibited its antitumor activity by disrupting microtubule assembly, causing cell cycle arrest and apoptosis through both extrinsic and intrinsic pathways in Hep3B cells. Therefore, the novel compound HAC-Y6 is a promising microtubule inhibitor that has great potential for treatment of HCC. |
