AK-1

Research use only, not for human use.

A potent, selective and brain-permeable SIRT2 inhibitor with IC50 of 12.5 uM.

A potent, selective and brain-permeable SIRT2 inhibitor with IC50 of 12.5 uM; induces proteasomal degradation of the Snail transcription factor through inactivation of the NF-κB/CSN2 pathway; increases the ubiquitination of HIF-1α in a VHL-dependent manner, leading to the degradation of HIF-1α via a proteasomal pathway.

AK-1 achieves significant neuroprotection in Huntington’s disease flies at 10 μM, improving the number of rhabdomeres from 5.2 to 5.6. AK-1 is a potent, specific and cell-permeable SIRT2 inhibitor, with an IC50 of 12.5 μM. 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. 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.

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DA-42784 | KB-120200 | DA42784 | KB120200 | J018989 | DA 42784 | KB 120200 | J 018989

Chromatin/Epigenetic

Sirtuin

Sirtuin

Metabolic Disease

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330461-64-8

403.45214

C19H21N3O5S

>98% (HPLC)

DMSO

O=C(NC1=CC=CC([N+]([O-])=O)=C1)C2=CC=CC(S(=O)(N3CCCCCC3)=O)=C2

Benzamide, 3-[(hexahydro-1H-azepin-1-yl)sulfonyl]-N-(3-nitrophenyl)-

(-20℃)

With Ice Pack

≥ 2 years