We Offer Worldwide Shipping
Login Wishlist



  • Brand : BIOFRON

  • Catalogue Number : BF-D3014

  • Specification : 98%

  • CAS number : 520-34-3

  • Formula : C16H12O6

  • Molecular Weight : 300.26

  • PUBCHEM ID : 5281612

  • Volume : 200mg

In stock

Checkout Bulk Order?

Catalogue Number


Analysis Method






Molecular Weight



Yellow needle crystal

Botanical Source

Blumea balsamifera,Lobelia chinensis,Notopterygium franchetii,Trichosanthes kirilowii,Cirsium japonicum

Structure Type



Standards;Natural Pytochemical;API




Vitamin P/3',5,7-dihydroxy-4'-methoxyflavone/Cyanidenon-4'-methyl Ether 1479/3,3',5,7-tetrahydroxy-4'-methoxyflavone/4'-Methylluteolin/5,7-Dihydroxy-2-(3-hydroxy-4-methoxyphenyl)-4H-1-benzopyran-4-one/5,7,3'-Trihydroxy-4'-methoxyflavone/3',5,7-trihydroxy-4'-methoxy-2-phenylchromone/5,7-Dihydroxy-2-(3-hydroxy-4-methoxyphenyl)-4H-chromen-4-one/Luteolin 4'-methyl ether/3',5,7-TRIHYDROXY-4'METHOXYFLAVONE/Diosmetin/4H-1-Benzopyran-4-one, 5,7-dihydroxy-2-(3-hydroxy-4-methoxyphenyl)-/Luteolin-4'-methyl Ether/5,7-dihydroxy-2-(3-hydroxy-4-methoxyphenyl)chromen-4-one/Salinigricoflavonol




1.5±0.1 g/cm3



Flash Point

220.3±23.6 °C

Boiling Point

576.7±50.0 °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#:520-34-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Renal ischemia/reperfusion (I/R)-induced acute kidney injury remains to be a troublesome condition in clinical practice. Although the exact molecular mechanisms underlying renal I/R injury are incompletely understood, the deleterious progress of renal I/R injury involves inflammation, apoptosis, and oxidative stress. Diosmetin is a member of the flavonoid glycosides family, which suppresses the inflammatory response and cellular apoptosis and enhances antioxidant activity. The purpose of this study was to investigate the protective effect of diosmetin on I/R-induced renal injury in mice.

Thirty BALB/c mice were randomly divided into five groups. Four groups of mice received diosmetin (0.25, 0.5, and 1 mg/kg) or vehicle (I/R group) before ischemia. Another group received vehicle without ischemia to serve as a negative control (sham-operated group). Twenty-four hours after reperfusion, serum and renal tissues were harvested to evaluate renal function and histopathologic features. In addition, the expression of inflammation-related proteins, apoptotic molecules, and antioxidant enzymes was analyzed.

Compared with sham mice, the I/R group significantly exacerbated renal function and renal tube architecture and increased the inflammatory response and renal tubule apoptosis. Nevertheless, pretreatment with diosmetin reversed these changes. In addition, diosmetin treatment resulted in a marked increase in antioxidant protein expression compared with I/R mice.

The renoprotective effects of diosmetin involved suppression of the nuclear factor-κB and mitochondrial apoptosis pathways, as well as activation of the nuclear factor erythroid 2-related factor 2/heme oxygenase-1 pathway. Diosmetin has significant potential as a therapeutic intervention to ameliorate renal injury after renal I/R.

Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.


Apoptosis; Diosmetin; Inflammation; Oxidative stress; Renal I/R injury


Diosmetin protects against ischemia/reperfusion-induced acute kidney injury in mice.


Yang K1, Li WF2, Yu JF3, Yi C3, Huang WF4.

Publish date

2017 Jun 15




Diosmetin, a plant flavonoid, has been shown to exert promising effects on prostate cancer cells as an anti‑proliferative and anticancer agent. In this study, using western blot analysis for protein expression and flow cytometry for cell cycle analysis, we determined that the treatment of the LNCaP and PC‑3 prostate cancer cells with diosmetin resulted in a marked decrease in cyclin D1, Cdk2 and Cdk4 expression levels (these proteins remain active in the G0‑G1 phases of the cell cycle). These changes were accompanied by a decrease in c-Myc and Bcl-2 expression, and by an increase in Bax, p27Kip1 and FOXO3a protein expression, which suggests the potential modulatory effects of diosmetin on protein transcription. The treatment of prostate cancer cells with diosmetin set in motion an apoptotic machinery by inhibiting X-linked inhibitor of apoptosis (XIAP) and increasing cleaved PARP and cleaved caspase-3 expression levels. On the whole, the findings of this study provide an in-depth analysis of the molecular mechanisms responsible for the regulatory effects of diosmetin on key molecules that perturb the cell cycle to inhibit cell growth, and suggest that diosmetin may prove to be an effective anticancer agent for use in the treatment of prostate cancer in the future.


Diosmetin suppresses human prostate cancer cell proliferation through the induction of apoptosis and cell cycle arrest.


Oak C1, Khalifa AO1, Isali I1, Bhaskaran N1, Walker E2, Shukla S1.

Publish date

2018 Aug




Diosmetin is a natural flavonoid obtained from citrus fruits and some medicinal herbs. Previous studies have reported the anti-cancer activity of diosmetin in some types of tumors. However, it is still unclear whether diosmetin exerts anti-cancer effects, particularly anti-angiogenic effects, in skin cancer. In this study, we used B16F10 melanoma cells and human umbilical vein endothelial cells to investigate the inhibitory effect of diosmetin on cell proliferation, migration and tube formation in vitro. Rat aorta ring assays were performed to determine the effect of diosmetin on ECs sprouting ex vivo. Furthermore, a B16F10 mouse melanoma model was used to observe the effect of diosmetin on tumor growth, angiogenesis, and metastasis in vivo. Our results showed that diosmetin not only suppressed tumor cell proliferation and migration but also induced cell apoptosis via the caspase pathway in B16F10 cells, and potently inhibited tube formation and cell migration in HUVECs. Rat aorta ring assays showed that diosmetin attenuated the ECs sprouting. Moreover, the mouse melanoma model showed that diosmetin significantly delayed tumor growth by inhibiting tumor vessels sprouting and expansion during tumor progression. Notably, diosmetin induced the normalization of tumor vasculature through the downregulation of angiopoietin-2 and the improvement of pericyte coverage, leading to suppression of metastasis formation in lungs and lymph nodes. In conclusion, our results demonstrate that diosmetin suppresses tumor progression and metastasis by inducing tumor cell death and inhibiting tumor angiogenesis as well as normalizing the defective tumor vasculature, suggesting that diosmetin is a potential adjuvant chemotherapy agent.

Copyright © 2019 The Authors. Published by Elsevier Masson SAS.. All rights reserved.


Diosmetin; Melanoma; Metastasis; Tumor angiogenesis; angiopoietin-2


Diosmetin inhibits tumor development and block tumor angiogenesis in skin cancer.


Choi J1, Lee DH1, Park SY1, Seol JW2.

Publish date

2019 Sep

Description :

Diosmetin is a natural flavonoid which inhibits human CYP1A enzyme activity with an IC50 of 40 μM in HepG2 cell.