AK-1是一种有效的，特异性的和细胞可渗透的SIRT2抑制剂，其 IC₅₀ 值为 12.5 μM。

AK-1 is a potent, specific and cell-permeable SIRT2 inhibitor, with an IC 50 of 12.5 μM.

Solid

SIRT2 12.5 μM (IC50)

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 g

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. Luthi-Carter R, et al. SIRT2 inhibition achieves neuroprotection by decreasing sterol biosynthesis. Proc Natl Acad Sci U S A. 2010 Apr 27;107(17):7927-32.
[2]. Lee SD, et al. AK-1, a SIRT2 inhibitor, destabilizes HIF-1α and diminishes its transcriptional activity during hypoxia. Cancer Lett. 2016 Apr 1;373(1):138-45.
[3]. David M. Taylor, et al. A Brain

In Vitro: DMSO : ≥ 50 mg/mL (123.93 mM)配制储备液