3059333-98-8
Chemical Structure
SZU-B6
- CAS No.: 3059333-98-8
- Formula:C29H32FN7O6
- Molecular Weight:593.61
InChIKey: LYSCIXOLYLBNGF-UHFFFAOYSA-N
SMILES: NC1=C([N+]([O-])=O)C=CC(N2CCN(CC3CCN(C4=CC5=C(C(N(C6C(NC(CC6)=O)=O)C5=O)=O)C=C4F)CC3)CC2)=C1
Biological Activity: SZU-B6 is an orally active SIRT6 PROTAC degrader with DC50 values of 45 nM in SK-HEP-1 cells and 154 nM in Huh-7 cells, respectively. SZU-B6 mediates proteasome-dependent degradation of SIRT6 by recruiting the CRBN E3 ubiquitin ligase. SZU-B6 impairs DNA damage repair and promotes radiosensitization of cancer cells. SZU-B6 induces cell cycle arrest and apoptosis in cancer cells. SZU-B6 inhibits the proliferation of liver cancer cells. SZU-B6 suppresses the tumor growth of hepatocellular carcinoma and intrahepatic cholangiocarcinoma in mice. SZU-B6 can be used in research related to hepatocellular carcinoma and intrahepatic cholangiocarcinoma[1][2].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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SZU-B6 | 98.78% | SZU-B6 is an orally active SIRT6 PROTAC degrader with DC50 values of 45 nM in SK-HEP-1 cells and 154 nM in Huh-7 cells, respectively. SZU-B6 mediates proteasome-dependent degradation of SIRT6 by recruiting the CRBN E3 ubiquitin ligase. SZU-B6 impairs DNA damage repair and promotes radiosensitization of cancer cells. SZU-B6 induces cell cycle arrest and apoptosis in cancer cells. SZU-B6 inhibits the proliferation of liver cancer cells. SZU-B6 suppresses the tumor growth of hepatocellular carcinoma and intrahepatic cholangiocarcinoma in mice. SZU-B6 can be used in research related to hepatocellular carcinoma and intrahepatic cholangiocarcinoma. | ||||||||||||||||||||
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- [1]. Huang J, et al. Discovery of Novel PROTAC SIRT6 Degraders with Potent Efficacy against Hepatocellular Carcinoma. Journal of medicinal chemistry. 2024 Oct 10;67(19):17319-17349. [Content Brief]
- [2]. Zhang M, et al. SIRT6 promotes intrahepatic cholangiocarcinoma development by reprogramming glutamine metabolism via enhanced GLUL. Gut. 2026 Jun 09;75(7):1383-1396. [Content Brief]
Keywords