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Catalogue Number : BF-D4012
Specification : 95%(HPLC)
CAS number : 483-15-8
Formula : C20H19NO4
Molecular Weight : 337.3692
PUBCHEM ID : 10217
Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow crystal

Botanical Source

tubers of Corydalis decumbens (Thunb.) Pers.

Structure Type



Standards;Natural Pytochemical;API




9,10-Dimethoxy-5,8-dihydro-6H-[1,3]dioxolo[4,5-g]isoquinolino[3,2-a]isoquinoline/Dihydroberbine/6H-1,3-Benzodioxolo[5,6-a]benzo[g]quinolizine, 5,8-dihydro-9,10-dimethoxy-/9,10-Dimethoxy-5,8-dihydro-6H-[1,3]dioxolo[4,5-g]isoquino[3,2-a]isoquinoline/Dihydroberberine




1.4±0.1 g/cm3


Soluble to 57.46 mg/l in water

Flash Point

170.7±27.3 °C

Boiling Point

557.8±50.0 °C at 760 mmHg

Melting Point

223-224ºC (dec.)



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#:483-15-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Highly effective and attenuated dose schedules are good regimens for drug research and development. Combination chemotherapy is a good strategy in cancer therapy. We evaluated the antitumour effects of dihydroberberine combined with sunitinib (DCS) on the human non-small cell lung cancer cell lines (NSCLC), A549, NCI-H460, and NCI-H1299 in vitro and in vivo. DCS showed synergic effects on NCI-H460 cell proliferation, colony formation and transplantable tumour growth, which suggested dihydroberberine increases the sensitivity of lung carcinoma to sunitinib. Further studies indicated that DCS down-regulated phosphorylation of JNK, p38, and NF-κB in NCI-H460 cells and tumours and suppressed the IκB and COX-2 expression. In addition, DCS reduced the secretion of the pro-inflammatory cytokine, interleukin-1 (IL-1), in tumours. Inhibition of p38 activation by DCS was a likely contributing factor in IL-1 and COX-2 down-regulation. Consistent with these results, a genomewide microarray analysis found that DCS induced the expression of cell cycle signal molecules that are known to be affected by JNK and p38. The change of cell cycle, in turn, led to down-regulation of JNK and p38, and further reduced IL-1 secretion. Collectively, these findings highlight potential molecular mechanisms of DCS chemotherapeutic activity and suggest that DCS is an efficacious strategy in NSCLC therapy.
© 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.


MAPK; NSCLC; anti-inflammation; combination therapy; dihydroberberine; sunitinib


Dihydroberberine exhibits synergistic effects with sunitinib on NSCLC NCI-H460 cells by repressing MAP kinase pathways and inflammatory mediators.


Dai B1, Ma Y1, Wang W1, Zhan Y1, Zhang D1, Liu R1, Zhang Y1.

Publish date

2017 Oct




The human ether-a-go-go-related gene (hERG) potassium channel conducts rapid delayed rectifier potassium currents (IKr) and contributes to phase III cardiac action potential repolarization. Drugs inhibit hERG channels by binding to aromatic residues in hERG helixes. Berberine (BBR) has multiple actions, and its hydrogenated derivative dihydroberberine (DHB) is a potential candidate for developing new drugs. Previous studies have demonstrated that BBR blocks hERG channels and prolongs action potential duration (APD). Our present study aimed to investigate the effects and mechanism of DHB on hERG channels. Protein expression and the hERG current were analyzed using western blotting and patch-clamp, respectively. DHB inhibited the hERG current concentration-dependently after instantaneous perfusion, accelerated channel inactivation by directly binding tyrosine (Tyr652) and phenylalanine (Phe656), and decreased mature (155-kDa) and simultaneously increased immature (135-kDa) hERG expression, respectively. This suggests disruption of forward trafficking of hERG channels. Besides, DHB remarkably reduced heat shock protein 90 (Hsp90) expression and its interaction with hERG, indicating that DHB disrupted hERG trafficking by impairing channel folding. Meanwhie, DHB enhanced the expression of cleaved activating transcription factor-6 (ATF-6), a biomarker of unfolded protein response (UPR). Expression of calnexin and calreticulin, chaperones activated by ATF-6 to facilitate channel folding, were also increased, which indicating UPR activation. Additionally, the degradation rate of mature 155-kDa hERG increased following DHB exposure. In conclusion, we demonstrated that DHB acutely blocked hERG channels by binding the aromatic Tyr652 and Phe656. DHB may decrease hERG plasma membrane expression through two pathways involving disruption of forward trafficking of immature hERG channels and enhanced degradation of mature hERG channels. Furthermore, forward trafficking was disrupted by impaired channel folding associated with altered interactions between hERG proteins and chaperones. Finally, trafficking inhibition activated UPR, and mature hERG channel degradation was increased by DHB.


Inhibitory effects and mechanism of dihydroberberine on hERG channels expressed in HEK293 cells.


Yu D1, Lv L1, Fang L1, Zhang B1, Wang J1, Zhan G1, Zhao L1, Zhao X1, Li B1.

Publish date

2017 Aug 1




Dihydroberberine (DHB), a hydrogenated derivative of berberine (BBR), has been firstly identified in Phellodendri Chinese Cortex (PC) by HPLC-ESI-MS/MS. Nowadays most researches on PC focus on its main components like BBR, however, the role of its naturally-occurring derivatives remains poorly defined heretofore. The present work aimed to comparatively evaluate the in vivo anti-inflammatory properties and mechanisms of DHB and BBR in three typical inflammatory murine models. The results showed that DHB effectively mitigated acetic acid-induced vascular permeability, xylene-elicited ear edema and carrageenan-caused paw edema. Meanwhile, DHB markedly attenuated the inflammatory cell infiltration in pathological sections of ears and paws. DHB was also observed to significantly decrease the production and mRNA expression levels of IL-6, IL-1β, TNF-α, NO (iNOS) and PGE2 (COX-2), increase the release of IL-10, and inhibit the activation of NF-κB and MAPK signaling pathways. The anti-inflammatory effect of DHB was weaker than that of BBR. The results might further contribute to unraveling the pharmacodynamic basis of PC and support its ethnomedical use in the treatment of inflammatory diseases. DHB possesses good potential to be further developed into a promising anti-inflammatory alternative, and can serve as a lead template for novel anti-inflammatory candidate.
Copyright © 2019 Elsevier B.V. All rights reserved.


Anti-inflammatory; Dihydroberberine; Inflammatory mediators; MAPK; NF-κB; Phellodendri Chinese Cortex


Dihydroberberine, a hydrogenated derivative of berberine firstly identified in Phellodendri Chinese Cortex, exerts anti-inflammatory effect via dual modulation of NF-κB and MAPK signaling pathways.


Tan L1, Wang Y1, Ai G1, Luo C1, Chen H2, Li C3, Zeng H3, Xie J4, Chen J5, Su Z6.

Publish date

2019 Oct