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  • Brand : BIOFRON

  • Catalogue Number : BF-H4009

  • Specification : 98%(HPLC)

  • CAS number : 20243-59-8

  • Formula : C16H12O6

  • Molecular Weight : 300.26

  • PUBCHEM ID : 5318214

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow crystalline powder

Botanical Source

Lobelia chinensis,Daphne genkwa,Aquilaria sinensis,Daphne tangutica,Leonurus macranthus

Structure Type



Standards;Natural Pytochemical;API




3',4',5-Trihydroxy-7-methoxyflavone/5,3',4'-trihydroxy-7-methoxyflavanone/7-O-Methylluteolin/4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-5-hydroxy-7-methoxy-/luteolin 7-methyl ester/3',4',5-trihydroxy-7-methoxyflavanone/5,3',4'-Trihydroxy-7-methoxyflavone/2-(3,4-Dihydroxyphenyl)-5-hydroxy-7-methoxy-4H-chromen-4-one/Luteolin 7-methyl ether/luteolin-7-methylether




1.5±0.1 g/cm3



Flash Point

230.6±25.0 °C

Boiling Point

602.7±55.0 °C at 760 mmHg

Melting Point




InChl Key


WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:20243-59-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Epidermal growth factor receptor (EGFR) is frequently overexpressed and mutated in non-small cell lung cancer (NSCLC), which is the major type of lung cancer. The EGFR tyrosine kinase inhibitors (TKIs) are the approved treatment for patients harboring activating mutations in the EGFR kinase. However, most of the patients treated with EGFR-TKIs developed resistance. Therefore, the development of compounds exhibiting unique antitumor activities might help to improve the management of NSCLC patients. The total flavonoids from Daphne genkwa Sieb. et Zucc. have been shown to contain antitumor activity. Here, we have isolated a novel flavonoid hydroxygenkwanin (HGK) that displays selective cytotoxic effects on all of the NSCLC cells tested. In this study, we employed NSCLC cells harboring EGFR mutations and xenograft mouse model to examine the antitumor activity of HGK on TKI-resistant NSCLC cells. The results showed that HGK suppressed cancer cell viability both in vitro and in vivo. Whole-transcriptome analysis suggests that EGFR is a potential upstream regulator that is involved in the gene expression changes affected by HGK. In support of this analysis, we presented evidence that HGK reduced the level of EGFR and inhibited several EGFR-downstream signalings. These results suggest that the antitumor activity of HGK against TKI-resistant NSCLC cells acts by enhancing the degradation of EGFR.


Daphne genkwa; EGFR; NSCLC; apoptosis; hydroxygenkwanin.


Hydroxygenkwanin Suppresses Non-Small Cell Lung Cancer Progression by Enhancing EGFR Degradation


Yann-Lii Leu 1 2 , Tong-Hong Wang 3 4 , Chih-Ching Wu 5 6 , Kuo-Yen Huang 7 , Yu-Wen Jiang 3 , Yi-Chiung Hsu 8 , Chi-Yuan Chen 3 4

Publish date

2020 Feb 19




Hydroxygenkwanin (HYGN) and genkwanin (GN) are major constituents of Genkwa Flos for the treatment of edema, ascites, cough, asthma and cancer. This is a report about the investigation of the metabolic fate of HYGN and GN in human liver microsomes and the recombinant UDP-glucuronosyltransferase (UGT) enzymes by using ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UHPLC-Q-TOF-MS). An on-line data acquisition method multiple mass defect filter (MMDF) combined with dynamic background subtraction (DBS) was developed to trace all probable metabolites. Based on this analytical strategy, three phase I metabolites and seven glucuronide conjugation metabolites of HYGN, seven phase I metabolites and 12 glucuronide conjugation metabolites of GN were identified in the incubation samples of human liver microsomes. The results indicated that demethylation, hydroxylation and o-glucuronidation were main metabolic pathways of HYGN and GN. The specific UGT enzymes responsible for HYGN and GN glucuronidation metabolites were identified using recombinant UGT enzymes. The results indicated that UGT1A1, UGT1A3, UGT1A9, UGT1A10 and UGT2B7 might play major roles in the glucuronidation reactions. Overall, this study may be useful for the investigation of metabolic mechanism of HYGN and GN, and it can provide reference and evidence for further experiments.


Daphne genkwa; EGFR; NSCLC; apoptosis; hydroxygenkwanin.


Metabolism Studies on Hydroxygenkwanin and Genkwanin in Human Liver Microsomes by UHPLC-Q-TOF-MS


Lin Yuan 1 , Caijuan Liang 1 , Xinpeng Diao 1 , Xiaoye Cheng 1 , Man Liao 1 , Lantong Zhang 1

Publish date

2018 Apr




The incidence and mortality of oral squamous cell carcinoma (OSCC) are high, and the number of oral cancers had risen in the world. However, chemotherapy drugs have numerous side effects. There is an urgent requirement to develop a novel drug that can be used to treat oral cancer. Hydroxygenkwanin (HGK) is a nature flavonoid extracted from Daphne genkwa Sieb. et Zucc. (Thymelaeaceae). Previous studies had demonstrated that HGK exhibits anticancer effect, but the effect is still unclear in oral cancer. HGK inhibited cell growth dose-dependently in SAS and OCEM1 cells. The functional enrichment analysis showed the significant pathway in cellular movement, cell cycle and cellular growth and proliferation. We further demonstrated the HGK induced the cell cycle arrest by flow cytometry and inhibited colony formation ability and cell movement. The western blot showed that HGK induced cell cycle arrest through p21 activation and caused intrinsic cell apoptosis pathway. HGK inhibited the cell invasion and migration through down-regulation vimentin. HGK might be an effective natural product for oral cancer therapy.


RNA sequencing; apoptosis; cell cycle; invasion; migration; oral cancer.


Anticancer Effect and Mechanism of Hydroxygenkwanin in Oral Squamous Cell Carcinoma


Yi-Chao Huang 1 2 , Po-Chuan Lee 1 , Jane Jen Wang 3 , Yi-Chiung Hsu 1 Affiliations Expand

Publish date

2019 Sep 18

Description :

Synergistic anti-glioma effect of Hydroxygenkwanin and Apigenin in vitro. PUMID/DOI:24144774 Chem Biol Interact. 2013 Nov 25;206(2):346-55. Apigenin (AP) and Hydroxygenkwanin (HGK) are two natural flavonoid compounds. Previous studies have already demonstrated the anti-tumor capability of AP. However, it is not clear whether Hydroxygenkwanin has such property. In the current study, the anti-glioma activities of Hydroxygenkwanin and its synergistic anti-glioma effects with AP on C6 glioma cells were investigated. In addition, the possible mechanisms were also studied. MTT assay and morphologic analysis including acridine orange/ethidium bromide (AO/EB) and 4',6-diamidino-2-phenylindole (DAPI) staining were used in the research, and the results indicated that the treatment with AP or Hydroxygenkwanin could inhibit C6 glioma cell proliferation respectively. Moreover, when AP was administrated simultaneously, the anti-glioma effect of Hydroxygenkwanin was dramatically enhanced in a dose-dependent manner, which is obviously better than that of carmustine (BCNU) at the concentration 25μM for treating of 24h. Compared with control, mitochondrial membrane potential (MPP) loss and mitochondrion damage were detected by JC-1 fluorescence probes (JC-1) and transmission electron microscopy (TEM) after treatment. Obvious DNA damage and cell cycle S phase arrest were detected by alkaline comet assay and flow cytometric analysis (FCM). Additionally, up regulation of TNF-α level, activations of caspase-3, -8, over expressions of BID and BAK protein and BCL-XL protein down expression were also observed after treatment by the combination of AP and Hydroxygenkwanin . The results indicate that Hydroxygenkwanin may be an effective natural product to treat glioma, and the combination of AP and Hydroxygenkwanin may be a promising method for glioma chemotherapy.