3301-49-3
Chemical Structure
Kumatakenin
- CAS No.: 3301-49-3
- Formula:C17H14O6
- Molecular Weight:314.29
IUPAC Name: 5-hydroxy-2-(4-hydroxyphenyl)-3,7-dimethoxy-4H-chromen-4-one
InChIKey: BJBUTJQYZDYRMJ-UHFFFAOYSA-N
SMILES: O=C1C2=C(O)C=C(OC)C=C2OC(C3=CC=C(O)C=C3)=C1OC
Biological Activity: Kumatakenin is an orally active apoptosis inducer and autophagy inhibitor, with a Kd value of 2.94 μM for mouse ATG5. Kumatakenin increases the activities of caspase-3, caspase-8 and caspase-9, thereby inducing caspase-dependent apoptosis in ovarian cancer cells. Kumatakenin reduces the expression of chemokines and pro-oncogenic factors in ovarian cancer cells, and inhibits M2 macrophage polarization. Kumatakenin inactivates TRIM65 function, reduces the expression and stability of FASN, and thus inhibits the proliferation, migration, invasion and tumor progression of esophageal cancer cells. Kumatakenin interacts with ATG5 to reduce its protein level, decrease LC3 level, and reduce the number of autophagosomes in the hippocampus. Kumatakenin binds to Eno3 to upregulate its expression, reduce the stability and expression level of IRP1 mRNA, inhibit ferroptosis, alleviate intestinal inflammation, and restore epithelial barrier function. Kumatakenin enhances the efficacy of antibiotics against pathogenic bacteria, inhibits SARS-CoV-2 replication, and reduces cytokine production. Kumatakenin is applicable to research related to ovarian cancer, esophageal cancer, depression and colitis[1][2][3][4][5].
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Kumatakenin | 99.31% | Kumatakenin is an orally active apoptosis inducer and autophagy inhibitor, with a Kd value of 2.94 μM for mouse ATG5. Kumatakenin increases the activities of caspase-3, caspase-8 and caspase-9, thereby inducing caspase-dependent apoptosis in ovarian cancer cells. Kumatakenin reduces the expression of chemokines and pro-oncogenic factors in ovarian cancer cells, and inhibits M2 macrophage polarization. Kumatakenin inactivates TRIM65 function, reduces the expression and stability of FASN, and thus inhibits the proliferation, migration, invasion and tumor progression of esophageal cancer cells. Kumatakenin interacts with ATG5 to reduce its protein level, decrease LC3 level, and reduce the number of autophagosomes in the hippocampus. Kumatakenin binds to Eno3 to upregulate its expression, reduce the stability and expression level of IRP1 mRNA, inhibit ferroptosis, alleviate intestinal inflammation, and restore epithelial barrier function. Kumatakenin enhances the efficacy of antibiotics against pathogenic bacteria, inhibits SARS-CoV-2 replication, and reduces cytokine production. Kumatakenin is applicable to research related to ovarian cancer, esophageal cancer, depression and colitis. | ||||||||||||||||||||
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- [1]. Woo JH, et al. Effect of Kumatakenin Isolated From Cloves on the Apoptosis of Cancer Cells and the Alternative Activation of Tumor-Associated Macrophages. J Agric Food Chem. 2017 Sep 13;65(36):7893-7899. [Content Brief]
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[2]. Tingting Zhang, et al. Supplementary kumatakenin prevents esophagus cancer progression by
blocking TRIM65-FASN axis-mediated metabolic reprogramming. Journal of Functional Foods
Volume 117, June 2024, 106223. - [3]. Li L, et al. Kumatakenin alleviates depressive-like behaviors by suppressing excessive autophagy in hippocampus via ATG5. Eur J Pharmacol. 2025;999:177688. [Content Brief]
- [4]. Ripperger H, et al. Steroidal alkaloid glycosides from Solanum suaveolens. Phytochemistry. 1997;46(7):1279-1282. [Content Brief]
- [5]. Arenbaoligao, et al. Kumatakenin inhibited iron-ferroptosis in epithelial cells from colitis mice by regulating the Eno3-IRP1-axis. Front Pharmacol. 2023;14:1127931. Published 2023 Mar 17. [Content Brief]
Keywords