Product Name Evodiamine
CAS No.: 518-17-2
Catalog No.: CFN99993
Molecular Formula: C19H17N3O
Molecular Weight: 303.36 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Yellow powder
Targets: PARP | Caspase | Bcl-2/Bax | Akt | PI3K | NF-kB | ERK | IL Receptor | CGRP Receptor | Autophagy
Source: The fruits of Evodia rutaecarpa (Juss.) Benth.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $40/20mg
Evodiamine, a novel non-pungent vanilloid receptor agonist, which has the effects of anti-obese, analgesic, vasodilator, anti-oxidation, anti-inflammatory and anti-cancer. It prevents the accumulation of perivisceral fat and the body weight increase, blocks of the Ca2+ influx through receptor-mediated Ca2+ channels, inhibits NF-kB activation through suppression of IkB kinase activity.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Phytother Res. 2015 Apr 22.
    In Vitro Assessment of the Anticancer Potential of Evodiamine in Human Oral Cancer Cell Lines.[Pubmed: 25903972]
    Evodiamine, a bioactive alkaloid, has been regarded as having antioxidant, antiinflammatory, and anticancer properties.
    In the present study, we explored the effects of Evodiamine on cell growth and apoptosis in human oral cancer cell lines. Our data revealed that Evodiamine significantly inhibited the proliferation of human oral cancer cells and resulted in the cleavages of PARP (poly (ADP-ribose) polymerase) and caspase-3, in addition to causing the typical characteristics of apoptosis. Evodiamine also increased Bax protein levels and caused translocation of Bax into mitochondria and Bax oligomerization. In addition, Evodiamine decreased expression of myeloid cell leukemia (Mcl-1) at the transcriptional modification, and knockdown of Mcl-1 clearly resulted in an increase in expression of Bax and active Bax, resulting in induction of apoptosis. Evodiamine reduced expression of phosphorylated AKT, and LY294002 potentiated Evodiamine-induced apoptosis by regulating Mcl-1 protein.
    Our results suggest that Evodiamine induces apoptosis in human oral cancer cells through the AKT pathway. These findings provide a rationale for its clinical application in the treatment of oral cancer.
    Planta Med. 2001 Apr;67(3):244-8.
    The positive inotropic and chronotropic effects of evodiamine and rutaecarpine, indoloquinazoline alkaloids isolated from the fruits of Evodia rutaecarpa, on the guinea-pig isolated right atria: possible involvement of vanilloid receptors.[Pubmed: 11345696]
    Cardiotonic effects of Evodiamine and rutaecarpine, constituents of the fruits of Evodia rutaecarpa Bentham Rutaceae, were evaluated on guinea pig isolated atria. Comparison with capsaicin, a vanilloid receptor agonist, revealed similar positive inotropic and chronotropic activity, as judged from antagonistic effects of the competitive vanilloid receptor (capsaicin receptor) antagonist capsazepine, the non-competitive vanilloid receptor antagonist ruthenium red, the calcitonin gene related peptide antagonist CGRP(8-37), the P2X purinoceptor antagonist PPADS, and various desensitization studies.
    Evodiamine and rutaecarpine produced transient positive inotropic and chronotropic effects on the guinea-pig isolated atria, followed by a desensitizing effect to additional administration. Dose-response relationships for Evodiamine, rutaecarpine and capsaicin were obtained. All the compounds evoked positive inotropic and chronotropic effects in a concentration-dependent manner. Maximal contractions for Evodiamine, rutaecarpine and capsaicin were observed at concentrations of 1 microM, 3 microM and 0.3 microM, respectively. The cardiotonic responses evoked by both Evodiamine and rutaecarpine were shifted to the right by capsazepine, an established antagonist of vanilloid receptor (capsaicin-receptor). The effects of both Evodiamine (1 microM) and rutaecarpine (3 microM) were abolished by pretreatment with a desensitizing dosage of capsaicin (1 microM), developing cross-tachyphylaxis between these compounds. The effects of Evodiamine (1 microM), rutaecarpine (3 microM) and capsaicin (0.3 microM) were also significantly reduced by pretreatment with ruthenium red (10 microM) and CGRP (8-37) (10 microM). The effects of Evodiamine, rutaecarpine and capsaicin were not affected by pretreatment with PPADS (100 microM), a highly selective P2X purinoceptor antagonist, and the possibility of the involvement of the P2X purinoceptor was excluded.
    These results suggest that the positive inotropic and chronotropic effects on the guinea-pig isolated right atria induced by both Evodiamine and rutaecarpine could be attributed to their interaction with vanilloid receptors and the resultant release of CGRP, a cardiotonic neurotransmitter, from capsaicin-sensitive nerves as with capsaicin.
    Planta Med. 2003 May;69(5):425-8.
    The nociceptive and anti-nociceptive effects of evodiamine from fruits of Evodia rutaecarpa in mice.[Pubmed: 12802723 ]
    Recently, the authors reported that Evodiamine, a major alkaloidal principle of Evodia fruits (Evodia rutaecarpa, Rutaceae), had vanilloid receptor agonistic activity comparable to capsaicin. In spite of the similarities in the actions of Evodiamine and capsaicin in vitro, the effects of Evodiamine on sensory neurons in vivo had not been investigated.
    We demonstrate here that Evodiamine sensitizes and desensitizes the capsaicin-sensitive sensory afferents in mice, resulting in nociceptive action and antinociceptive actions. The nociceptive action (paw licking behaviour) was dose dependently induced by intradermal injection (i.d.) of Evodiamine to the hind paw and was suppressed by the co-treatment with capsazepine, a vanilloid receptor specific agonist, in a dose-dependent manner. The treatment with higher dosages of Evodiamine showed sustained antinociceptive effects. The acetic acid-induced writhing was significantly suppressed by the intraperitoneal Evodiamine administration 3 days before, without any observable effects on spontaneous motor activity. The response of the isolated ileum from the mice with or without high dosages of Evodiamine administration indicated the sensory neuron specific desensitizing effect of Evodiamine. The isolated ileum from vehicle-treated mice contracted in response to both the sensory nerve stimulation by 10 microM capsaicin and the mimicked vagal stimulation by 2 microM carbachol. However, the isolated ileum from Evodiamine-treated mice lost its response to sensory nerve stimuli but retained its response to vagus nerve stimuli. The suppression of acetic acid-induced writhing and the desensitization of visceral sensory neurons strongly correlated [regression coefficient (r) = 0.955].
    Thus, we demonstrate that Evodiamine shows the analgesic action by desensitizing sensory nerves.
    Planta Med. 2001 Oct;67(7):628-33.
    Capsaicin-like anti-obese activities of evodiamine from fruits of Evodia rutaecarpa, a vanilloid receptor agonist.[Pubmed: 11582540 ]
    Evodiamine, a major alkaloidal principle of Evodia fruits (Evodia rutaecarpa, Rutaceae), showed vanilloid receptor agonistic activities comparable to capsaicin. The Chinese literature refers to Evodia fruits as a "hot nature" herb. In spite of the similarities in the actions of Evodiamine and capsaicin in vitro, Evodiamine has no perceptible taste, including a peppery hot taste. Therefore, the effectiveness of Evodiamine and the extract of Evodia fruits in preventing obesity on male C3H mice, or male SD rats were examined.
    When Evodiamine was supplemented at 0.03% of the diet and fed to mice for 12 days, the perirenal fat weight became significantly lower than in the control group. The epididymal fat mass was also decreased in the Evodiamine diet group. When Evodiamine was supplemented at 0.02% in the form of ethanol extract of Evodia fruits to the high-fat diet and fed to rats for 21 days, the body weight, the perirenal fat weight, epididymal fat weight, the levels of serum free fatty acid, total lipids in the liver, triglyceride in the liver, and cholesterol level in the liver were significantly reduced as compared with the control diet group. Furthermore, both lipolytic activity in the perirenal fat tissue and specific GDP binding in brown adipose tissue mitochondria, as the biological index of enhanced heat production, were significantly increased in the Evodiamine fed rats. Fasting mice subcutaneously administered 1-3 mg/kg Evodiamine showed decreased core body temperature by 1-2 degrees C. This hypothermic effect was prevented by the pretreatment of intraperitoneally administered 10 mg/kg capsazepine, a vanilloid receptor antagonist. On the other hand, food-sated mice subcutaneously administered 1-3 mg/kg Evodiamine showed unchanged core body temperature and increased tail skin temperature by more than 5 degrees C, suggesting the increased energy expenditure by enhanced heat dissipation.
    In conclusion, we have demonstrated that a novel non-pungent vanilloid receptor agonist, Evodiamine, mimics the characteristic anti-obese effects induced by capsaicin. Evodiamine would induce heat loss and heat production at the same time and dissipate food energy, preventing the accumulation of perivisceral fat and the body weight increase.
    Oncol Lett. 2015 Feb;9(2):801-805.
    Inhibitory effects of evodiamine on human osteosarcoma cell proliferation and apoptosis.[Pubmed: 25621054]
    The aim of the present study was to investigate the effect of Evodiamine on osteosarcoma cell proliferation and apoptosis, and explore the associated underlying molecular mechanism. A Cell Counting Kit 8 assay was performed to detect the effects of Evodiamine on the proliferation of human osteosarcoma U2OS cells. Annexin V-fluorescein isothiocyanate/propidium iodide staining was performed to analyze the apoptotic rate of the cells. The effect of Evodiamine on the protein expression levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3 and survivin were detected by performing western blot analysis. Evodiamine inhibited the growth of human osteosarcoma U2OS cells by inhibiting cell proliferation and inducing cell apoptosis. Western blotting demonstrated that Evodiamine effectively inhibited proliferation and induced apoptosis of osteosarcoma cells in a dose-dependent manner via downregulation of Bcl-2, caspase-3 and survivin protein expression levels and upregulation of Bax protein expression levels.
    Toxicol In Vitro. 2010 Apr;24(3):898-904.
    Evodiamine-induced human melanoma A375-S2 cell death was mediated by PI3K/Akt/caspase and Fas-L/NF-kappaB signaling pathways and augmented by ubiquitin-proteasome inhibition.[Pubmed: 20005289 ]
    Evodiamine, a major alkaloidal component of Evodiae fructus exhibits anti-tumor activities. We have previously reported that Evodiamine has a marked inhibitory effect on IL-1 sensitive human melanoma A375-S2 cells proliferation, and this action might be through inactivation of PI3K signaling. However, the detailed molecular mechanisms of Evodiamine-induced cell death remains poorly understood.
    In present study, we further confirmed that Akt is the main effector molecule involved in this pathway. Evodiamine also led to IkappaBalpha phosphorylation and degradation that reflect translocation of NF-kappaB. Pretreatment of A375-S2 cells with ubiquitin-proteasome inhibitor MG132 was shown to aggregate the Evodiamine caused cell death at 24h. In addition, MG132 reduced ERK phosphorylation, increased caspase-3 activation, Fas-L expression and Bcl-2 cleavage in Evodiamine-treated A375-S2 cells.
    These results suggested the PI3K/Akt/caspase and Fas-L/NF-kappaB signaling pathways might account for the responses of A375-S2 cell death induced by Evodiamine, and these signals could be augmented by ubiquitin-proteasome pathway.
    Neurosci Lett. 2015 Feb 19;588:154-8.
    Antidepressant-like effect of evodiamine on chronic unpredictable mild stress rats.[Pubmed: 25545553]
    Evodiamine is a major alkaloid compound extracted from the dry unripened fruit Evodia fructus (Evodia rutaecarpa Benth., Rutaceae), which has a variety of pharmacological activities. The present study aims to determine the antidepressant-like effect of Evodiamine in a rat model of chronic unpredictable mild stress (CUMS).
    We identified that Evodiamine could reverse the following CUMS-induced behavioural deficits and biochemical changes in rats: the decreases of sucrose preference, number of crossings, 5-HT and NA levels, as well as the increase of immobility time. Evodiamine treatments also ameliorated the corticosterone hypersecretion induced by CUMS. Furthermore, we found that Evodiamine was able to up-regulate the expression of brain-derived neurotrophic factor (BDNF) and phosphorylated tropomyosin-related kinase B (pTrkB) without altering TrkB.
    This study suggests potential antidepressant-like effect of Evodiamine on CUMS rats, and its underlying mechanisms can be potentially linked to their modulating effects on the monoamine transmitters and BDNF-TrkB signaling in the hippocampus.
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