Chemical Properties
Pale yellow crystalline powder, soluble in organic solvents such as methanol, ethanol, and DMSO, derived from Selaginella tamariscina (P.Beauv.) Spring.
Uses
Hinokiflavone is a novel modulator of pre-mRNA splicing activity extracted from plants with anti-inflammatory, anti-tumor and antiviral activities. Hinokiflavone is also a potent inhibitor for matrix metalloproteinases (MMPs). Hinokiflavone attenuates the virulence of Methicillin (HY-121544)-resistant staphylococcus aureus by inhibiting caseinolytic protease P (ClpP) with an IC50 value of 34.36 mg/mL. Hinokiflavone induces apoptosis via the reactive oxygen species-mitochondria-mediated apoptotic pathway and inhibits tumor cell migration and invasion. Hinokiflavone is a SUMO protease inhibitor against sentrin-specific protease 1 (SENP1) activity[1][2][3].
Definition
ChEBI: A biflavonoid that is apigenin substituted by a 4-(5,7-dihydroxy-4-oxo-4H-chromen-2-yl)phenoxy group at position 6. A diflavonyl ether, it is isolated from Rhus succedanea and has been found to possess significant cytotoxic
otential.
Biological Activity
Hinokiflavone is a plant biflavone th at exhibit potent anticancer, hepatoprotective, antibacterial, antiviral, and anti-inflammatory activities. Hinokiflavone induces apoptosis and cell cycle arrest, and blocks migration and invasion of melanoma cells. It is a potent inhibitor of dengue 2 virus RNA-dependent RNA polymerase (DV-NS5 RdRp). Hinokiflavone is a modulator of pre-mRNA splicing in cells. It increases SUMOylation of a subset of spliceosome proteins by inhibiting SENP1 protease activity. It induces apoptosis in esophageal squamous cell carcinoma (ESCC) through regulation of PI3K/AKT/mTOR pathway.
in vivo
Hinokiflavone (25 or 50 mg/kg, i.p., daily for 24 days) has antitumor activity via suppressing tumor proliferation, metastasis and inducing Apoptosis in CT26 tumor-bearing mice[2].
Hinokiflavone (100 mg/kg, s.c., every 12 h for 96 h) shows a protective effect on pneumonia infection by Improving survival rate in mice[3].
| Animal Model: | CT26 tumor-bearing mice model[2] |
| Dosage: | 25 or 50 mg/kg |
| Administration: | i.p., daily for 24 days |
| Result: | Resulted in retarded tumor progression and reduction of tumor weight without affecting body weight of mice, suppressed tumor proliferation and invasion ability by staining nuclear Ki-67 and MMP9, induced the apoptosis by staining cleaved caspase-3. |
References
[1] Pawellek A, et al. Characterisation of the biflavonoid hinokiflavone as a pre-mRNA splicing modulator that inhibits SENP. Elife. 2017 Sep 8;6. pii: e27402. DOI:
10.7554/eLife.27402[2] Zhou J, et al. Antitumor activity in colorectal cancer induced by hinokiflavone. J Gastroenterol Hepatol. 2019 Sep;34(9):1571-1580. DOI:
10.1111/jgh.14581[3] Kong X, et al. Hinokiflavone Attenuates the Virulence of Methicillin-Resistant Staphylococcus aureus by Targeting Caseinolytic Protease P. Antimicrob Agents Chemother. 2022 Aug 16;66(8):e0024022. DOI:
10.1128/aac.00240-22
