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  • Brand : BIOFRON

  • Catalogue Number : BF-D1012

  • Specification : 98%

  • CAS number : 484-29-7

  • Formula : C12H9NO2

  • Molecular Weight : 199.21

  • PUBCHEM ID : 68085

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow needle-shaped crystal

Botanical Source

Dictamnus dasycarpus

Structure Type



Standards;Natural Pytochemical;API




4-methoxyfuro[2,3-b]quinoline/Dictamine/Dictamnine/Furo[2,3-b]quinoline, 4-methoxy-/4-Methoxy-furo[2,3-b]quinoline




1.3±0.1 g/cm3


Methanol; Chloroform; Acetone

Flash Point

161.4±22.3 °C

Boiling Point

343.2±22.0 °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#:484-29-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Dictamnine (DTM) is a natural alkaloid isolated from the root of Dictamnus dasycarpus Turcz and has been shown to exhibit multiple biological functions, including anti-inflammatory, antifungal, anti-angiogenic and anticancer activity. However, the mechanisms by which dictamnine inhibits tumor growth are not fully understood. In this study, we investigated the effectiveness of dictamnine as a treatment for cancer and to identify the underlying mechanisms of its anticancer activity. Here, dictamnine showed the potent inhibitory activity against HIF-1α and Slug activation induced by hypoxia in various human cancer cell lines. This compound markedly decreased the hypoxia-induced accumulation of HIF-1α and Slug protein in a dose-dependent manner. Further analysis revealed that dictamnine inhibited HIF-1α protein synthesis, without affecting its degradation. Our results demonstrated that dictamnine reduced HIF-1α protein synthesis by downregulating the mTOR/p70S6K/eIF4E and MAPK pathways, and reduced the expression of Slug by inhibiting the GSK-3β/Slug signaling pathway. Moreover, epithelial-mesenchymal transition (EMT) was inhibited in dictamnine-treated tumors by downregulation of HIF-1α and Slug, as reflected by the upregulation of E-cadherin and Occludin, and the downregulation of N-cadherin and Vimentin. Phenomenological experiments showed that dictamnine reduced migration and invasion, inhibited HCT116 cell proliferation and promoted HCT116 cell apoptosis by downregulating HIF-1α and Slug. In vivo studies further confirmed that dictamnine treatment caused significant inhibition of tumor growth in a xenograft tumor model. These findings suggest that dictamnine is a potent cancer inhibitor, providing a rationale for anticancer pathway-targeted therapy.
Copyright © 2018 Elsevier B.V. All rights reserved.


Antitumor activity; Dictamnine; Epithelial-mesenchymal transition; HIF-1α; Slug


Dictamnine promotes apoptosis and inhibits epithelial-mesenchymal transition, migration, invasion and proliferation by downregulating the HIF-1α and Slug signaling pathways.


Wang JY1, Wang Z1, Li MY1, Zhang Z1, Mi C1, Zuo HX1, Xing Y1, Wu YL1, Lian LH1, Xu GH1, Piao LX1, Ma J2, Jin X3.

Publish date

2018 Dec 25




Dictamnine, a furoquinoline alkaloid isolated from the root bark of Dictamnus dasycarpus Turcz. (Rutaceae), is reported to have a wide range of pharmacological activities. In this study, the in vitro metabolic profiles of dictamnine in mouse, rat, dog, monkey, and human liver microsomes were investigated and compared. Dictamnine was incubated with liver microsomes in the presence of an NADPH-regenerating system, resulting in the formation of eight metabolites (M1-M8). M1 is an O-desmethyl metabolite. M5 and M6 are formed by a mono-hydroxylation of the benzene ring of dictamnine. M8 was tentatively identified as an N-oxide metabolite. The predominant metabolic pathway of dictamnine occurs through the epoxidation of the 2,3-olefinic to yield a 2,3-epoxide metabolite (M7), followed by the ring of the epoxide opening to give M4. Likewise, cleavage of the furan ring forms M2 and M3. Slight differences were observed in the in vitro metabolic profiles of dictamnine among the five species tested. A chemical inhibition study with a broad and five specific CYP450 inhibitors revealed that most of the dictamnine metabolites in liver microsomes are mediated by CYP450, with CYP3A4 as the predominant enzyme involved in the formation of M7, the major metabolite. These findings provide vital information to better understand the metabolic processes of dictamnine among various species.
Copyright © 2015 Elsevier B.V. All rights reserved.


CYP450; Dictamnine; Liver microsomes; Mass spectrometry; Metabolism


Metabolism of dictamnine in liver microsomes from mouse, rat, dog, monkey, and human.


Wang P1, Zhao Y2, Zhu Y3, Sun J4, Yerke A3, Sang S3, Yu Z5.

Publish date

2016 Feb 5




Cortex Dictamni is extensively used as an herbal medicine worldwide, but is believed to induce hepatotoxicity and even causes mortality in many Asian and European countries. As the most abundant furoquinoline alkaloid ingredient of Cortex Dictamni, dictamnine (DIC) can be metabolically activated by CYP3A to an epoxide metabolite, which possesses the potential to induce hepatotoxicity by covalent binding with proteins. As yet, the hepatotoxicity of DIC and the role played by metabolic activation remain unknown. Here, we found that DIC caused acute liver injury in a time- and dose-dependent manner in mice. The hepatic and urinary DIC epoxide intermediates were observed in DIC-treated mice. Ketoconazole, a CYP3A inhibitor, significantly reduced the hepatotoxicity of DIC and inhibited the formation of reactive metabolites of DIC. Moreover, treatment with 2,3-dihydro-DIC, a DIC analog synthesized by selective reduction of the furan moiety, produced no hepatotoxicity in mice, and no reactive metabolite was formed, suggesting a structural necessity of furan moiety in DIC hepatotoxicity. A time course of gradual hepatic glutathione consumption was observed in DIC-treated mice, while depletion of hepatic glutathione by L-buthionine-S,R-sulfoximine enhanced the hepatotoxicity of DIC. Collectively, this study demonstrates that DIC induces acute hepatocellular injury in mice, and that metabolic activation of furan plays a crucial role in DIC-induced hepatotoxicity.


Cortex dictamni; Dictamnine; Furan moiety; Hepatotoxicity; Metabolic activation


Dictamnine-induced hepatotoxicity in mice: the role of metabolic activation of furan.


Shi F1, Pan H2, Cui B3, Li Y4, Huang L2, Lu Y5.

Publish date

2019 Feb 1

Description :

Dictamnine (Dictamine) has the ability to exert cytotoxicity in human cervix, colon, and oral carcinoma cells; A natural plant product has been reported to have antimicrobial activity against bacteria and fungi.IC50 value:Target: Dictamnine has antimicrobial activities against the model fungus Saccharomyces cerevisiae, with a minimum inhibitory concentration (MIC) value of 64 microg/ml [1]. Dic induced S phase cell cycle arrest at low concentration and cell apoptosis at high concentration in which loss of mitochondrial membrane potential (Δψmm) was not involved. In addition, inhibition of caspase-3 using the specific inhibitor, z-DQMD-fmk, did not attenuate Dic-induced apoptosis, implying that Dic-induced caspase-3-independent apoptosis [2].