1421919-75-6
Chemical Structure
KPT-276
- CAS No.: 1421919-75-6
- Formula:C16H10F8N4O
- Molecular Weight:426.26
IUPAC Name: (Z)-3-(3-(3,5-bis(trifluoromethyl)phenyl)-1H-1,2,4-triazol-1-yl)-1-(3,3-difluoroazetidin-1-yl)prop-2-en-1-one
InChIKey: JCHAWRDHMUSLMM-UPHRSURJSA-N
SMILES: O=C(N1CC(F)(F)C1)/C=C\N2N=C(C3=CC(C(F)(F)F)=CC(C(F)(F)F)=C3)N=C2
Biological Activity: KPT-276 is an orally active and blood-brain barrier-penetrant selective XPO1/CRM1 inhibitor. KPT-276 blocks XPO1-mediated nuclear export function and promotes nuclear retention of various tumor suppressor proteins. KPT-276 induces apoptosis and G1 cell cycle arrest in tumor cells, and downregulates c-MYC, CDC25A, and BRD4. KPT-276 reduces immune cell proliferation through nuclear accumulation of cell cycle inhibitors, rescues TDP-43 cytoplasmic mislocalization, and restores axon growth and growth rate in mutant PFN1 motor neurons. KPT-276 maintains axonal cytoskeletal integrity and mitochondrial function, and inhibits tumor growth. KPT-276 can be used for research on glioblastoma, non-Hodgkin lymphoma, amyotrophic lateral sclerosis, multiple myeloma, and non-small cell lung cancer[1][2][3][4][5][6][7].
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KPT-276 | 99.94% | KPT-276 is an orally active and blood-brain barrier-penetrant selective XPO1/CRM1 inhibitor. KPT-276 blocks XPO1-mediated nuclear export function and promotes nuclear retention of various tumor suppressor proteins. KPT-276 induces apoptosis and G1 cell cycle arrest in tumor cells, and downregulates c-MYC, CDC25A, and BRD4. KPT-276 reduces immune cell proliferation through nuclear accumulation of cell cycle inhibitors, rescues TDP-43 cytoplasmic mislocalization, and restores axon growth and growth rate in mutant PFN1 motor neurons. KPT-276 maintains axonal cytoskeletal integrity and mitochondrial function, and inhibits tumor growth. KPT-276 can be used for research on glioblastoma, non-Hodgkin lymphoma, amyotrophic lateral sclerosis, multiple myeloma, and non-small cell lung cancer. | ||||||||||||||||||||
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References
- [1]. Green AL, et al. Preclinical antitumor efficacy of selective exportin 1 inhibitors in glioblastoma. Neuro-oncology. 2015 May;17(5):697-707.
- [2]. Muqbil I, et al. Anti-tumor activity of selective inhibitor of nuclear export (SINE) compounds, is enhanced in non-Hodgkin lymphoma through combination with mTOR inhibitor and dexamethasone. Cancer letters. 2016 Dec 28;383(2):309-317.
- [3]. Han X, et al. CRM1 as a new therapeutic target for non-Hodgkin lymphoma. Leukemia research. 2015 Jan;39(1):38-46.
- [4]. Giampetruzzi A, et al. Modulation of actin polymerization affects nucleocytoplasmic transport in multiple forms of amyotrophic lateral sclerosis. Nature communications. 2019 Aug 23;10(1):3827.
- [5]. Schmidt J, et al. Genome-wide studies in multiple myeloma identify XPO1/CRM1 as a critical target validated using the selective nuclear export inhibitor KPT-276. Leukemia. 2013 Dec;27(12):2357-65. [Content Brief]
- [6]. Haines JD, et al. Nuclear export inhibitors avert progression in preclinical models of inflammatory demyelination. Nature neuroscience. 2015 Apr;18(4):511-20.
- [7]. Parikh K, et al. Selective inhibitors of nuclear export (SINE)--a novel class of anti-cancer agents. Journal of hematology & oncology. 2014 Oct 15;7:78.
