Fisetin
Chemical Name: 2-(3,4-Dihydroxyphenyl)-3,7-dihydroxy-4H-1-benzopyran-4-one
Purity: ≥97%
Biological Activity
Fisetin is a naturally occuring flavonoid and antioxidant. Inhibits PI 3-K, Akt, mTOR and Cdk6. Displays antiproliferative activity in prostate cancer cells. Shown to activate ERK; exhibits neuroprotective activity in Huntington's disease models. Also a DNMT1 inhibitor.Technical Data
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Background References
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ERK activation by the polyphenols fisetin and resveratrol provides neuroprotection in multiple models of Huntington's disease.
Maher et al.
Hum.Mol.Genet., 2011;20:261 -
Antiproliferative mechanisms of the flavonoids 2,2'-dihydroxychalcone and fisetin in human prostate cancer cells.
Haddad et al.
Nutr.Cancer, 2010;62:668 -
Dietary flavonoid fisetin: a novel dual inhibitor of PI3K/Akt and mTOR for prostate cancer management.
Adhami et al.
Biochem.Pharmacol., 2012;84:1277 -
Crystal structure of a human cyclin-dependent kinase 6 complex with a flavonol inhibitor, fisetin.
Lu et al.
J.Med.Chem., 2005;48:737 -
Mechanisms for the inhibition of DNA methyltransferases by tea catechins and bioflavonoids.
Lee et al.
Mol.Pharmacol., 2005;68:1018
Product Datasheets
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Citations for Fisetin
The citations listed below are publications that use Tocris products. Selected citations for Fisetin include:
4 Citations: Showing 1 - 4
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How CD40L reverse signaling regulates axon and dendrite growth.
Authors: Alun M Et al.
Cell Mol Life Sci 2021;78:1065-1083
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A splicing variant of TFEB negatively regulates the TFEB-autophagy pathway.
Authors: Young Ho Et al.
Sci Rep 2021;11:21119
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Signalling Pathways Mediating the Effects of CD40-Activated CD40L Reverse Signalling on Inhibitory Medium Spiny Neuron Neurite Growth.
Authors: Alun M Et al.
Cells 2021;10
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Fisetin stimulates autophagic degradation of phosphorylated tau via the activation of TFEB and Nrf2 transcription factors.
Authors: Kim Et al.
PLoS Pathog 2016;6:24933
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