Remodelin, a specific inhibitor of N-acetyltransferase NAT10, can ameliorate Hutchinson-Gilford Progeria Syndrom (HGPS) cellular phenotypes. Remodelin acts in a progerin- and FTI-independent pathway, by targeting and inhibiting NAT10[1]. NAT10 is a protein with histone acetylation activity and primarily identified to be involved in regulation of telomerase activity[2].
体外研究 (In Vivo)
Remodelin blocks invasion and migration of HCC cells in hypoxic conditions[3] We has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Remodelin (100 mg/kg; p.o) significantly reduces the loss of subcutaneous adipose tissue that is seen in the HGPS mouse model[1]. We has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model: LmnaG609G/G609G mice (HGPS mice)[1]
Dosage:100 mg/kg
Administration: P.o; daily schedule from 3 weeks of age onward, until the end-point (individual weight maxima)
Result: Well-tolerated by both genotypes, with no weight loss.
分子量
363.28
Formula
C₁₅H₁₅BrN₄S
CAS 号
1622921-15-6
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
参考文献
[1]. Balmus G, et al. Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome. Nat Commun. 2018;9(1):1700. Published 2018 Apr 27.
[2]. Liu H, et al. DNA damage induces N-acetyltransferase NAT10 gene expression through transcriptional activation. Mol Cell Biochem. 2007;300(1-2):249-258.
[3]. Ma R, et al. Up regulation of NAT10 promotes metastasis of hepatocellular carcinoma cells through epithelial-to-mesenchymal transition. Am J Transl Res. 2016;8(10):4215-4223. Published 2016 Oct 15.