Remodelin | Acetyltransferase NAT10 inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $65.00 | ||
| 25 mg | $280.00 |
Remodelin (949912-58-7) is a potent and selective inhibitor of N-acetyltransferase 10 (NAT10) which is capable of acetylating microtubules and histones.1 Improves nuclear architecture, chromatin organization and fitness of both human lamin A/C-depleted cells and Hutchinson-Gilford progeria syndrome patient cells1, normalizing progeric and aging cells2. Enhances health span in a mouse model of human accelerated aging syndrome.3 Significantly reduces many of the defects associated with accumulation of the lamin A precursor, prelamin A.4 Inhibits NAT10-promoted metastasis which may be mediated by endothelial-to-mesenchymal transition in hepatocellular carcinoma.5
References/Citations:
1) Larrieu et al. (2014), Chemical Inhibition of NAT10 Corrects Defects of Laminopathic Cells; Science, 344 527
2) Larrieu et al. (2018), Inhibition of the Acetyltransferase NAT10 Normalizes Progeric and Aging Cells by Rebalancing the Transportin-1 Nuclear Import Pathway; Sci. Signal., 11 eaar5401
3) Balmus et al. (2018), Targeting of NAT10 Enhances Healthspan in a Mouse Model of Human Accelerated Aging Syndrome; Nat. Commun., 9 1700
4) Cobb et al. (2016), Prelamin A impairs 53BP1 nuclear entry by mislocalizing NUP153 and disrupting the Ran gradient; Aging Cell, 15 1039
5) Ma et al. (2016), Up regulation of NAT10 promotes metastasis of hepatocellular carcinoma cells through epithelial-to-mesenchymal transition; Am. J. Transl. Res., 8 4215
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
Remodelin (949912-58-7) is a potent and selective inhibitor of N-acetyltransferase 10 (NAT10) which is capable of acetylating microtubules and histones.1 Improves nuclear architecture, chromatin organization and fitness of both human lamin A/C-depleted cells and Hutchinson-Gilford progeria syndrome patient cells1, normalizing progeric and aging cells2. Enhances health span in a mouse model of human accelerated aging syndrome.3 Significantly reduces many of the defects associated with accumulation of the lamin A precursor, prelamin A.4 Inhibits NAT10-promoted metastasis which may be mediated by endothelial-to-mesenchymal transition in hepatocellular carcinoma.5
References/Citations:
1) Larrieu et al. (2014), Chemical Inhibition of NAT10 Corrects Defects of Laminopathic Cells; Science, 344 527
2) Larrieu et al. (2018), Inhibition of the Acetyltransferase NAT10 Normalizes Progeric and Aging Cells by Rebalancing the Transportin-1 Nuclear Import Pathway; Sci. Signal., 11 eaar5401
3) Balmus et al. (2018), Targeting of NAT10 Enhances Healthspan in a Mouse Model of Human Accelerated Aging Syndrome; Nat. Commun., 9 1700
4) Cobb et al. (2016), Prelamin A impairs 53BP1 nuclear entry by mislocalizing NUP153 and disrupting the Ran gradient; Aging Cell, 15 1039
5) Ma et al. (2016), Up regulation of NAT10 promotes metastasis of hepatocellular carcinoma cells through epithelial-to-mesenchymal transition; Am. J. Transl. Res., 8 4215
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