Name | 3-(azepane-1-sulfonyl)-N-(3-nitro-phenyl)-benzamide |
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Synonyms |
3-(1-Azepanylsulfonyl)-N-(3-nitrophenyl)benzamide
Benzamide, 3-[(hexahydro-1H-azepin-1-yl)sulfonyl]-N-(3-nitrophenyl)- sirt2 inhibitor ii, ak-1 AK-1 |
Description | AK-1 is a potent, specific and cell-permeable SIRT2 inhibitor. |
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Related Catalog | |
Target |
SIRT2 |
In Vitro | AK-1 achieves significant neuroprotection in Huntington’s disease flies at 10 μM, improving the number of rhabdomeres from 5.2 to 5.6[1]. AK-1 treatment induces proteasomal degradation of the Snail transcription factor through inactivation of the NF-κB/CSN2 pathway. Reduction in the level of Snail results in upregulation of p21, leading to G1 arrest, slow proliferation, and slow wound-healing activity. The regulation of Snail-p21 axis by AK-1 also occurs in HT-29 colon cancer cells[2]. Under hypoxic conditions, AK-1 increases the ubiquitination of HIF-1α in a VHL-dependent manner, leading to the degradation of HIF-1α via a proteasomal pathway. Downregulation of HIF-1α expression reduces its transcriptional activity and, eventually, reduces the expression of BNIP3, one of HIF-1 target genes, in AK-1-treated cells[3]. |
Cell Assay | HEK293 cells are co-transfected with 3 μg of pGL2-PGK1-HRE-Luc and 1 μg of pCMV-β-galactosidase plasmids. Twenty-four hours later, the cells are incubated under hypoxic conditions for 24 hr in the presence of 10 μM AK-1 and then lysed with luciferase cell lysis buffer. Luciferase and β-galactosidase activities are measured using luciferin and ο-nitrophenyl-β-d-galactopyranoside, respectively, as substrates. Transfection efficiency is normalized according to β-galactosidase activity[3]. |
References |
Density | 1.4±0.1 g/cm3 |
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Molecular Formula | C19H21N3O5S |
Molecular Weight | 403.452 |
Exact Mass | 403.120178 |
PSA | 120.68000 |
LogP | 4.11 |
Index of Refraction | 1.630 |
Storage condition | 2-8℃ |
RIDADR | NONH for all modes of transport |
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