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Catalogue Number : BF-R3006
Specification : 98%
CAS number : 84-26-4
Formula : C18H13N3O
Molecular Weight : 287.32
PUBCHEM ID : 65752
Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Tetradium ruticarpum

Structure Type



Standards;Natural Pytochemical;API




ruteacarpine/Rutecarpine/Indolo[2',3':3,4]pyrido[2,1-b]quinazolin-5(7H)-one, 8,13-dihydro-/RUTECARPINE 95+/8,13-Dihydroindolo[2',3':3,4]pyrido[2,1-b]quinazolin-5(7H)-one




1.5±0.1 g/cm3


Chloroform; Ethyl Acetate

Flash Point

286.5±32.9 °C

Boiling Point

550.1±60.0 °C at 760 mmHg

Melting Point

259.5 - 260ºC


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#:84-26-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Rutaecarpine is a bioactive alkaloid isolated from Evodia rutaecarpa (Wu Zhu Yu, Family: Rutaceae), a versatile medicinal herb which is clinically used to treat headache, abdominal pain, postpartum hemorrhage, dysentery, and amenorrhea in China. As one of the most representative indolopyridoquinazoline alkaloids of Evodia rutaecarpa, rutaecarpine has broad pharmacological actions in treating various cardiovascular, cerebrovascular, and metabolic diseases. The cardiovascular actions of rutaecarpine have aroused intense research interest due to its purported inotropic and chronotropic, vasodilatory, anti-platelet activation, anti-oxidant, anti-inflammatory, and lipid-lowering effects. Biochemical and pharmacological studies have illustrated the molecular targets of rutaecarpine, such as TRPV1, CGRP, AMPK, ABCA1, and β1-AR. Furthermore, several rutaecarpine derivatives (such as bromorutaecarpine and fluororutaecarpine) have been shown to possess cardioprotective and vasculoprotective effects with improved safety profile. Hereby, we provide a systematic overview of pharmacological actions, toxicological effects, and molecular targets of rutaecarpine in cardiovascular disease prevention/treatment, aiming to exploit the therapeutic potential of rutaecarpine and its derivatives in treating cardiovascular diseases.

Copyright © 2019 Elsevier Ltd. All rights reserved.


CGRP; Cardiovascular diseases; Dehydroevodiamine (PubChem CID: 9817839); Evodia rutaecarpa; Evodiamine (PubChem CID: 442088); Rutaecarpine; Rutaecarpine (PubChem CID: 65752); TRPV1; Therapeutics; Wu Zhu Yu


Rutaecarpine: A promising cardiovascular protective alkaloid from Evodia rutaecarpa (Wu Zhu Yu).


Tian KM1, Li JJ2, Xu SW3.

Publish date

2019 Mar




Sepsis is a life-threatening organ dysfunction disease caused by a dysregulated host response to infection. Rutaecarpine is an important alkaloid component of Evodia rutaecarpa. There has been no study on the therapeutic effects of rutaecarpine in sepsis.

Mice were randomly assigned into four groups: sham, sepsis, sepsis plus vehicle and sepsis plus rutaecarpine groups. Mice in sepsis were administered CLP surgery. Rutaecarpine or vehicle was injected intraperitoneally 1 h after CLP. The liver damage, bacterial infection, survival rate and weight loss were observed, and changes in the ratio of peritoneal resident macrophages were analyzed by flow cytometry and immunofluorescence microscopy. Western blotting was used to identify the levels of NF-κB signaling pathway, ER stress and apoptosis related proteins. TUNEL and Annexin V/PI assay were used to detect the apoptosis of liver tissues and peritoneal resident macrophages, respectively. ELISA and qRT-PCR were used to detect the inflammatory factors.

Rutaecarpine alleviated weight loss, bacterial infection and liver injury, and regulated inflammation homeostasis, enhancing survival rate induced by sepsis. Population of peritoneal resident macrophages (CD11b+F4/80hiMHCIIlow) was significantly decreased in sepsis mice, which was resulted from ER stress-induced apoptosis through caspase-12 signaling pathway. Rutaecarpine restored the ratio of peritoneal resident macrophages and the level of GATA6 in CD11b+ peritoneal macrophages. Rutaecarpine could also attenuate sepsis-induced inflammatory responses through inhibiting the activation of ER stress/NF-κB pathway.

Rutaecarpine ameliorated sepsis-induced peritoneal resident macrophages apoptosis and inflammation responses through inhibition of ER stress-mediated caspase-12 and NF-κB pathways. Our study provided new insights for drug development against sepsis.

Copyright © 2019 Elsevier Inc. All rights reserved.


Apoptosis; Endoplasmic reticulum stress; Inflammation; Peritoneal resident macrophages; Rutaecarpine; Sepsis


Rutaecarpine ameliorated sepsis-induced peritoneal resident macrophages apoptosis and inflammation responses.


Li Z1, Yang M1, Peng Y1, Gao M1, Yang B2.

Publish date

2019 Jul 1




Objective: To determine the therapic effects of rutaecarpine in dextran sodium sulfate (DSS)induced experimental colitis and explore whether the protective role of rutaecarpine is related to the synthesis and release of CGRP. Methods: Fifty female BABL/c strain mice were randomly divided into untreated model control group and DSS-exposed groups.DSS-exposed groups were given administration of 5% DSS for 7 days and respectively treated with vehicle, rutacarpine(30 mg/kg, 100 mg/kg) , prednisone by intragastric administration from day 8 to day 14.The disease activity index (DAI) scores, the histological scores, the mRNA and protein concentrations of CGRP in colonic tissues were measured. Results: On day 7, the DAI scores of the DSS-exposed groups[vehicle group (8.9±0.9), low-dose Rut group(8.9±0.6), high-dose Rut group(8.2±0.8), prednisone group(8.7±1.6)] were much higher, compared with the untreated model control group(0±0)(P<0.01). The DAI scores on day 14 of the vehicle, rutaecarpine or prednisone treated groups were respectively markedly lower than on day 7(3.2±0.6, 0.9±0.6, 3.1±0.7 vs 8.9±0.6, 8.2±0.8, 8.7±1.6, P<0.05). The DAI score of mice treated with high-dose rutaecarpine was significantly lower, compared with those treated with low-dose rutaecarpine and prednisone.Compared to the untreated model control group, the histological scores in other four groups significantly increased.Comparisons of values among the post-treatment groups had statistical significance (0.2±0.4 vs 6.9±0.9, 4.5±0.9, 2.8±0.8, 5.7±0.7, P<0.01), while the high-dose rutaecarpine group presented the lowest score.The colonic mucosal CGRP mRNA and CGRP protein expressions in groups receiving vehicle, low-dose rutaecarpine and prednisone were significantly reduced than those in the untreated model control group(0.32±0.03 vs 0.15±0.02, 0.18±0.01, 0.22±0.01, P<0.01). The CGRP mRNA and CGRP protein expressions in the untreated model control group was similar to those in the DSS+ high-dose rutaecarpine group with no statistic significance between them(0.32±0.03 vs 0.31±0.02, P>0.05). Pearson correlation analysis between CGRP mRNA levels, CGRP immunohistochemisty levels and DAI, histological scores showed a statistically negative relationship respectively(r=-0.797, -0.819, -0.863, -0.845, all P<0.01). Conclusions: Rutaecarpine can ameliorate the DAI scores and histological scores of ulcerative colitis in mice.Rutaecarpine can upregulate the expressions of CGRP mRNA and CGRP protein.Correlation between CGRP mRNA, CGRP protein levels and DAI scores, histological scores respectively showed a statistically negative relationship.


Calcitonin gene-related peptide; Dextran sodium sulfate; Rutaecarpine; Ulcerative colitis


[Therapeutic effects of rutaecarpine on dextran sodium sulfate-induced experimental colitis in mice].


Luo DN1, Li FJ, Zou YY.

Publish date

2018 Feb 13