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  • Brand : BIOFRON

  • Catalogue Number : AV-F03676

  • Specification : 98%

  • CAS number : 54260-72-9

  • Formula : C21H20ClNO4

  • Molecular Weight : 385.84

  • PUBCHEM ID : 148670

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Coptidis rhizoma

Structure Type



Standards;Natural Pytochemical;API




dehydrothalictricavine chloride/13-Methylberberinium chlorid/13-methylberberine chloride





Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

Boiling Point

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#:54260-72-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




High mobility group box 1 (HMGB1), a late phase cytokine of sepsis, is viewed as a potential target for the treatment of sepsis. The authors considered that 13-methylberberine (13-MB) might reduce circulating HMGB1 levels and increase survival in a mouse model of sepsis by activating AMP-activated protein kinase (AMPK). Western blot analysis and vascular contraction testing were performed using RAW264.7 cells and rat thoracic aorta, respectively. The mechanisms responsible were investigated using various signal inhibitors and small interfering RNA techniques. 13-MB significantly reduced HMGB1 release by LPS-activated RAW264.7 cells, and this was prevented by silencing AMPK or p38, or by pretreating cells with p38 MAPKinase inhibitor, suggesting that the activations of p38 and AMPK were responsible for the observed reduction in HMGB1 release. As was expected, 13-MB increased the phosphorylations of p38 and AMPK. Interestingly, phosphorylations of p38 by 13-MB were inhibited by AMPKsiRNA, indicating that AMPK lies upstream of p38. Furthermore, 13-MB concentration-dependently inhibited IκB phosphorylation in LPS-activated RAW264.7 cells, and in aortic rings, co-treatment with 13-MB and LPS for 8h, in vitro, significantly restored the isometric contraction induced by phenylephrine. Importantly, 13-MB significantly increased the survival rate of LPS-induced endotoxemic mice. These results suggest 13-MB may be useful for treating diseases in which HMGB1 is viewed as a target.


13-methylberberine; AMPK; HMGB1; Inflammation; Sepsis; p38MAPK.


13-Methylberberine Reduces HMGB1 Release in LPS-activated RAW264.7 Cells and Increases the Survival of Septic Mice Through AMPK/P38 MAPK Activation


Ki Churl Chang 1 , Young Shin Ko 1 , Hye Jung Kim 1 , Da-Yeong Nam 2 , Dong-Ung Lee 3

Publish date

2016 Nov




Lipid metabolism modulation is a main focus of metabolic syndrome research, an area in which many natural and synthetic chemicals are constantly being screened for in vitro and in vivo activity. Berberine, a benzylisoquinoline plant alkaloid, has been extensively investigated for its anti-obesity effects and as a potential cholesterol and triglyceride-lowering drug. We screened 11 protoberberine and 2 benzophenanthridine alkaloids for their anti-adipogenic effects on 3T3-L1 adipocytes and found that 13-methylberberine exhibited the most potent activity. 13-Methylberberine down-regulated the expression of the main adipocyte differentiation transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT enhancer binding protein alpha (C/EBPα), as well as their target genes. PPARγ, C/EBPα, and sterol regulatory element binding protein 1 (SREBP-1) protein levels were reduced, and this lipid-reducing effect was attenuated by an AMP-activated protein kinase (AMPK) inhibitor, indicating that the effect of this compound requires the AMPK signaling pathway. Decreased Akt phosphorylation suggested reduced de novo lipid synthesis. C-13 methyl substitution of berberine increased its accumulation in treated cells, suggesting that 13-methylberberine has improved absorption and higher accumulation compared to berberine. Our findings suggest that 13-methylberberine has potential as an anti-obesity drug.


13-Methylberberine, a Berberine Analogue With Stronger Anti-Adipogenic Effects on Mouse 3T3-L1 Cells


Yit-Lai Chow 1 , Mami Sogame 1 , Fumihiko Sato 1

Publish date

2016 Dec 5




Background: Atherosclerosis, the underlying cause of the majority of cardiovascular diseases, is a lipid-driven, inflammatory disease of the large arteries. Atherosclerotic cardiovascular disease (ASCVD) threatens human lives due to high morbidity and mortality. Many studies have demonstrated that atherosclerosis is accelerated via activation of the NLRP3 inflammasome. The NLRP3 inflammasome plays a critical role in the development of vascular inflammation and atherosclerosis. In atherosclerotic plaques, excessive generation of reactive oxygen species (ROS) activates the NLRP3 inflammasome. 13-Methylberberine (13-MB) is a newly synthesized compound used in traditional Chinese medicine that has outstanding antibacterial, antitumor, and antiobesity activities, especially anti-inflammatory activity. However, the role of 13-MB in atherosclerosis needs to be explored.
Methods: CCK-8 assays and flow cytometry were conducted to determine the cell viability and apoptotic profiles of human umbilical vein endothelial cells (HUVECs) treated with 13-MB. Carboxy-DCFH-DA and JC-10 assays were used to measure ROS and determine mitochondrial membrane potential. Western blot analysis was performed to investigate proteins that are associated with the NLRP3 inflammasome and autophagy. ELISA was used to detect and quantify inflammatory cytokines related to the NLRP3 inflammasome. Transfection and confocal microscopy were conducted to observe autophagy.
Results: Pretreatment with 13-MB markedly reduced cytotoxicity and apoptosis, as well as intracellular ROS production, in H2O2-induced HUVECs. Moreover, 13-MB showed a protective effect in maintaining mitochondrial membrane potential. 13-MB also suppressed NLRP3 inflammasome activation and promoted autophagy induction in HUVECs.
Conclusion: 13-MB exerts cytoprotective effects in an H2O2-induced cell injury model by inhibiting NLRP3 inflammasome activation via autophagy induction in HUVECs. These anti-inflammatory and autophagy induction activities may provide valuable evidence for further investigating the potential role of 13-MB in atherosclerosis.


13-Methylberberine; Anti-inflammatory; Atherosclerosis; Autophagy inducer; NLRP3 inflammasome.


13-Methylberberine Improves Endothelial Dysfunction by Inhibiting NLRP3 Inflammasome Activation via Autophagy Induction in Human Umbilical Vein Endothelial Cells


Zhihua Peng # 1 2 3 , Hong Zhan # 1 , Yijia Shao 2 , Yan Xiong 1 , Lijin Zeng 1 2 3 , Cong Zhang 1 2 3 , Zhihao Liu 1 , Zhenhua Huang 1 , Huanxing Su 4 , Zhen Yang 1 2 3

Publish date

2020 Jan 22

Description :

13-Methylberberine chloride (13-Methylberberinium chloride), a berberine analogue, has anti-adipogenic and antitumor activities. 13-Methylberberine chloride (13-Methylberberinium chloride) increases production of IL-12 and inhibits the expression of iNOS at posttranscriptional level in macrophages activated with LPS[1][2][3].