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Rotundic acid


Catalogue Number : BF-I4008
Specification : 98%(HPLC)
CAS number : 20137-37-5
Formula : C30H48O5
Molecular Weight : 488.7
PUBCHEM ID : 12315075
Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White powder

Botanical Source

Gardenia jasminoides,Ilex cornuta,Nauclea officinalis,Ilex rotunda

Structure Type



Standards;Natural Pytochemical;API




(3β)-3,19,23-Trihydroxyurs-12-en-28-oic acid/Rotundic acid/Urs-12-en-28-oic acid, 3,19,23-trihydroxy-, (3β)-


(1R,2R,4aS,6aR,6aS,6bR,8aR,9R,10S,12aR,14bS)-1,10-dihydroxy-9-(hydroxymethyl)-1,2,6a,6b,9,12a-hexamethyl-2,3,4,5,6,6a,7,8,8a,10,11,12,13,14b-tetradecahydropicene-4a-carboxylic acid


1.2±0.1 g/cm3



Flash Point

344.5±28.0 °C

Boiling Point

622.8±55.0 °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#:20137-37-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Rotundic acid (RA) is a major triterpene constituent in the barks of Ilex rotunda Thunb, which have been widely used to make herbal tea for health care in southern China. RA has a variety of bioactivities such as anti-inflammation and lipid-lowering effect. However, little is known about the effects and mechanisms of RA on metabolic disturbance in type 2 diabetes (T2D) and its effect on gut microbiota. A T2D rat model induced by high fat diet (HFD) feeding and low-dose streptozotocin (STZ) injection was employed and RA showed multipronged effects on T2D and its complications, including improving glucolipid metabolism, lowering blood pressure, protecting against cardiovascular and hepatorenal injuries, and alleviating oxidative stress and inflammation. Furthermore, 16s rRNA gene sequencing was carried out on an Illumina HiSeq 2500 platform and RA treatment could restore the gut microbial dysbiosis in T2D rats to a certain extent. RA treatment significantly enhanced the richness and diversity of gut microbiota. At the genus level, beneficial or commensal bacteria Prevotella, Ruminococcus, Leuconostoc and Streptococcus were significantly increased by RA treatment, while RA-treated rats had a lower abundance of opportunistic pathogen Klebsiella and Proteus. Spearman’s correlation analysis showed that the abundances of these bacteria were strongly correlated with various biochemical parameters, suggesting that the improvement of gut microbiota might help to prevent or attenuate T2D and its complication. In conclusion, our findings support RA as a nutraceutical agent or plant foods rich in this compound might be helpful for the alleviation of T2D and its complications through improving gut microbiota.


diabetic complications; gut microbiota; metabolic disturbance; rotundic acid; type 2 diabetes.


Rotundic Acid Protects Against Metabolic Disturbance and Improves Gut Microbiota in Type 2 Diabetes Rats


Zenghao Yan 1 , Hao Wu 1 , Hongliang Yao 1 2 3 , Wenjun Pan 1 , Minmin Su 1 , Taobin Chen 1 2 , Weiwei Su 1 , Yonggang Wang 1

Publish date

2019 Dec 26




In the present study, the functions and mechanisms of rotundic acid (RA) underlying its induction of apoptosis in caspase-3-transfected MCF-7 human breast cancer cells (Cas3-MCF-7 cells) were investigated. RA induced apoptosis in Cas3-MCF-7 cells more efficiently compared with that in MCF-7 cells transfected with control plasmid. The results from an MTT assay demonstrated that RA effectively inhibited Cas3-MCF-7 cell viability in a dose-dependent manner and induced cell apoptosis via caspase-3 activity within 12 to 48 h. Western blotting and fluorescence-activated cell sorting demonstrated that RA initiated Cas3-MCF-7 cell apoptosis via p53 activation. The silencing of the p53 gene in the Cas3-MCF-7 cell line led to decreased RA-induced Cas3-MCF-7 cell caspase-3 activity and cell apoptosis. Collectively, the results of the present study indicate that caspase-3 serves a critical function in rotundic acid-induced apoptosis, and suggest that caspase-3 deficiency may contribute to the chemotherapy-resistance of breast cancer. Reconstitution of caspase-3 sensitizes MCF-7 breast cancer cells to chemotherapy. RA has the potential for development as a novel drug combined with reconstitution of caspase-3 gene therapy for the treatment of human breast cancer with caspase-3 deficiency.


diabetic complications; gut microbiota; metabolic disturbance; rotundic acid; type 2 diabetes.


Rotundic Acid Induces Cas3-MCF-7 Cell Apoptosis Through the p53 Pathway


Min-Lun Nan 1 , Xue Wang 2 , Hai-Jun Li 3 , De-Hai Yu 4 , Wen-Yi Sun 5 , Hong-Mei Xu 6 , Yu-Fang He 1 7 , Quan-Cheng Zhao 1

Publish date

2019 Jan;




Although radiation therapy is a powerful anticancer modality, radiation- induced stress response and gene expression with adaptive resistance may severely compromise the effectiveness of radiation. The function of rotundic acid (RA) on inducing apoptosis in the human breast cancer cell line MCF-7 has been investigated in a previous study. In the present study, the combined effect of chemotherapy and radiotherapy on reducing side effects was examined. The results of an MTT assay revealed that radiation (0.5, 2 and 10 Gy) effectively inhibit MCF-7 cell viability in a dose-dependent manner, consistent with the effects of RA (2, 5 and 12.5 µM). Interestingly, a lower dose of radiation (1 Gy) combined with RA (5 µM) exhibited a greater inhibition efficiency compared with a high dose of radiation alone. Flow cytometry revealed that radiation combined with RA induced the apoptosis of MCF-7 cells. Using western blotting, it was demonstrated that radiation induced the expression of ataxia-telangiectasia mutated (ATM) and p53 protein, and that RA enhanced this effect. On examining the potential underlying mechanism, it was revealed that radiation and RA combined induce Bcl-2-associated X protein expression and cell apoptosis in MCF-7 cells. An ATM inhibitor was able to restore the effect of radiation and RA on inducing MCF-7 cell apoptosis. These results suggest that the ATM/p53 pathway directly participates in radiation and RA-induced apoptosis in MCF-7 cells. RA has the potential for development as a novel drug for the treatment of human breast cancer combined with radiation therapy, given that the combined side effects are reduced.


Rotundic Acid Enhances the Impact of Radiological Toxicity on MCF-7 Cells Through the ATM/p53 Pathway


Zhong-Feng Wang 1 , Wen-Yi Sun 2 , De-Hai Yu 3 , Yan Zhao 4 , Hong-Mei Xu 5 , Yu-Fang He 6 , Hai-Jun Li 1

Publish date

2018 Nov