5,3',4'-Trihydroxy-6,7-dimethoxyflavone/2-(3,4-dihydroxyphenyl)-5-hydroxy-6,7-dimethoxychromen-4-one/6,7-dimethoxy-5,3',4'-trihydroxyflavone/4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-5-hydroxy-6,7-dimethoxy-/3',4',5-Trihydoxy-6,7-dimethoxyflavone/2-(3,4-Dihydroxyphenyl)-5-hydroxy-6,7-dimethoxy-4H-chromen-4-one/6-Hydroxyluteolin-6,7-dimethyl ether/3',4',5-Trihydroxy-6,7-dimethoxyflavone/Cirsiliol
Cirsiliol is a potent and selective 5-lipoxygenase inhibitor and a competitive low affinity benzodiazepine receptor ligand.
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
616.1±55.0 °C at 760 mmHg
280-281.5℃ (methanol )
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:34334-69-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Malignant melanoma is a highly aggressive form of skin cancer which has a propensity for metastasis. Epithelial mesenchymal transition (EMT) plays a primordial role in the progression of metastatic disease. Metastatic melanoma is resistant to conventional therapies. Hence, researchers have been exploring alternative approaches, including the utility of bioactive phytochemicals to manage metastatic disease. In the present study, we investigated the potential of cirsiliol, a flavonoid isolated from Centaurea jacea L., in modulating the aggressive behavior of B16F10 metastatic melanoma cells, including EMT, and associated molecular mechanisms of action. Cirsiliol was found to be effective in restraining the colony formation and migration of fibronectin-induced B16F10 metastatic melanoma cells. Cirsiliol inhibited the activity and expression of matrix metalloproteinase-9 (MMP-9). Cirsiliol also suppressed the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (also known as Akt)/nuclear factor-κB (NF-κB) signaling pathway which, in turn, caused upregulation of E-cadherin and downregulation of N-cadherin, Snail and Twist. Based on these results, cirsiliol may be considered a promising compound against EMT in the therapeutic management of malignant melanoma.
Akt; Centaurea jacea; EMT; MMP-9; NF-κB; PI3K; cadherin; cirsiliol; melanoma
Cirsiliol Suppressed Epithelial to Mesenchymal Transition in B16F10 Malignant Melanoma Cells through Alteration of the PI3K/Akt/NF-κB Signaling Pathway.
Prasad P1, Vasas A2, Hohmann J3,4, Bishayee A5, Sinha D6.
2019 Jan 31
Growth inhibition of the pathogen Staphylococcus aureus with currently available antibiotics is problematic in part due to bacterial biofilm protection. Although recently characterized natural products, including 3′,4′,5-trihydroxy-6,7-dimethoxy-flavone , 3′,4′,5,6,7-pentahydroxy-flavone , and 5-hydroxy-4′,7-dimethoxy-flavone , exhibit both antibiotic and biofilm inhibitory activities, the mode of action of such hydroxylated flavonoids with respect to S. aureus inhibition is yet to be characterized. Enzymatic digestion and high-resolution MS analysis of differentially expressed proteins from S. aureus with and without exposure to antibiotic flavonoids (1-3) allowed for the characterization of global protein alterations induced by metabolite treatment. A total of 56, 92, and 110 proteins were differentially expressed with bacterial exposure to 1, 2, or 3, respectively. The connectivity of the identified proteins was characterized using a search tool for the retrieval of interacting genes/proteins (STRING) with multitargeted S. aureus inhibition of energy metabolism and biosynthesis by the assayed flavonoids. Identifying the mode of action of natural products as antibacterial agents is expected to provide insight into the potential use of flavonoids alone or in combination with known therapeutic agents to effectively control S. aureus infection.
LC−MS/MS proteomics; Staphylococcus aureus; antibacterial flavonoids; multitargeted bacterial inhibition
Multitargeted Flavonoid Inhibition of the Pathogenic Bacterium Staphylococcus aureus: A Proteomic Characterization.
Elmasri WA1, Zhu R1, Peng W1, Al-Hariri M2, Kobeissy F2, Tran P, Hamood AN, Hegazy MF3, Pare PW1, Mechref Y1.
2017 Jul 7;
Radioresistance is a major cause of decreasing the efficiency of radiotherapy for non-small cell lung cancer (NSCLC). To understand the radioresistance mechanisms in NSCLC, we focused on the radiation-induced Notch-1 signaling pathway involved in critical cell fate decisions by modulating cell proliferation. In this study, we investigated the use of Notch-1-regulating flavonoid compounds as novel therapeutic drugs to regulate radiosensitivity in NSCLC cells, NCI-H1299 and NCI-H460, with different levels of radioresistance. Rhamnetin and cirsiliol were selected as candidate Notch-1-regulating radiosensitizers based on the results of assay screening for activity and pharmacological properties. Treatment with rhamnetin or cirsiliol reduced the proliferation of NSCLC cells through the suppression of radiation-induced Notch-1 expression. Indeed, rhamnetin and cirsiliol increased the expression of tumor-suppressive microRNA, miR-34a, in a p53-dependent manner, leading to inhibition of Notch-1 expression. Consequently, reduced Notch-1 expression promoted apoptosis through significant down-regulation of the nuclear factor-κB pathway, resulting in a radiosensitizing effect on NSCLC cells. Irradiation-induced epithelial-mesenchymal transition was also notably attenuated in the presence of rhamnetin and cirsiliol. Moreover, an in vivo xenograft mouse model confirmed the radiosensitizing and epithelial-mesenchymal transition inhibition effects of rhamnetin and cirsiliol we observed in vitro. In these mice, tumor volume was significantly reduced by combinational treatment with irradiation and rhamnetin or cirsiliol compared with irradiation alone. Taken together, our findings provided evidence that rhamnetin and cirsiliol can act as promising radiosensitizers that enhance the radiotherapeutic efficacy by inhibiting radiation-induced Notch-1 signaling associated with radioresistance possibly via miR-34a-mediated pathways.
Cancer Therapy; Cirsiliol; EMT; Lung Cancer; Natural Products; Notch-1; Radiation Biology; Radiosensitization; Rhamnetin; miR-34a
Rhamnetin and cirsiliol induce radiosensitization and inhibition of epithelial-mesenchymal transition (EMT) by miR-34a-mediated suppression of Notch-1 expression in non-small cell lung cancer cell lines.
Kang J1, Kim E, Kim W, Seong KM, Youn H, Kim JW, Kim J, Youn B.
2013 Sep 20;