Remodelin |
| Catalog No.GC11430 |
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. NAT10 is a protein with histone acetylation activity and primarily identified to be involved in regulation of telomerase activity.
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Cas No.: 1622921-15-6
Sample solution is provided at 25 µL, 10mM.
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Remodelin is a small molecule inhibitor of N-acetyltransferase 10 (NAT10).Dysregulation of N-acetyltransferase 10 (NAT10) is associated with the development of many types of tumors[1].
Combined remodelin and doxorubicin treatment reduced cell viability significantly more compared to cells treated with doxorubicin alone. EDU assays confirmed that both doxorubicin and remodelin decreased breast cancer cell proliferation more compared to cells treated with doxorubicin alone, suggesting remodelin attenuates doxorubicin resistance in breast cancer cells (MDA-MB-231)[2]
Remodelin was given daily by intragastric administration for 4 weeks. PDX model tumour volume was recorded and TGI was calculated. As a result, Remodelin significantly inhibited the growth of HNSCC PDXs in vivo[3]
The treatment of Remodelin could suppress the growth of cancer cells but not induce apoptosis, that Remodelin has little cytotoxicity. Remodelin significantly reduced AR-negative prostate cancer tumor growth. The anti-neoplastic effects of Remodelin through NAT10 inhibition should be credited to the slowing down of DNA replication, which could consequently attenuate replication stress-associated genomic instability, and ultimately delay the progression of prostate cancer[4]
References:
[1]. Ma R, Chen J, et al. Up regulation of NAT10 promotes metastasis of hepatocellular carcinoma cells through epithelial-to-mesenchymal transition.
[2]. Wu J, Zhu H, et al. Inhibition of N-acetyltransferase 10 using remodelin attenuates doxorubicin resistance by reversing the epithelial-mesenchymal transition in breast cancer. Am J Transl Res. 2018 Jan 15;10(1):256-264.
[3]. Tao W, Tian G, et al. NAT10 as a potential prognostic biomarker and therapeutic target for HNSCC. Cancer Cell Int. 2021 Aug 6;21(1):413.
[4]. Ma N, Liu H, et al.Inhibition of N-Acetyltransferase 10 Suppresses the Progression of Prostate Cancer through Regulation of DNA Replication. Int J Mol Sci. 2022 Jun 12;23(12):6573.
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