Berbamine

CAS# 478-61-5

Berbamine

Catalog No. BCN5543----Order now to get a substantial discount!

Product Name & Size Price Stock
Berbamine: 5mg $23 In Stock
Berbamine: 10mg Please Inquire In Stock
Berbamine: 20mg Please Inquire Please Inquire
Berbamine: 50mg Please Inquire Please Inquire
Berbamine: 100mg Please Inquire Please Inquire
Berbamine: 200mg Please Inquire Please Inquire
Berbamine: 500mg Please Inquire Please Inquire
Berbamine: 1000mg Please Inquire Please Inquire

Quality Control of Berbamine

Number of papers citing our products

Chemical structure

Berbamine

3D structure

Chemical Properties of Berbamine

Cas No. 478-61-5 SDF Download SDF
PubChem ID 275182 Appearance Powder
Formula C37H40N2O6 M.Wt 608.7
Type of Compound Alkaloids Storage Desiccate at -20°C
Solubility DMSO : 125 mg/mL (205.35 mM; Need ultrasonic)
SMILES CN1CCC2=CC(=C3C=C2C1CC4=CC=C(C=C4)OC5=C(C=CC(=C5)CC6C7=C(O3)C(=C(C=C7CCN6C)OC)OC)O)OC
Standard InChIKey DFOCUWZXJBAUSQ-URLMMPGGSA-N
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Berbamine

The roots of Cocculus orbiculatus (L.) DC.

Biological Activity of Berbamine

DescriptionBerbamine is a novel inhibitor of bcr/abl fusion gene with potent anti-leukemia activity and also an inhibitor of NF-κB. Berbamine may be the first ATP-competitive inhibitor of CaMKII γ, could be as a new type of molecular targeted agent through inhibition of the CaMKII γ activity for treatment of leukemia.Berbamine confers cardioprotection against I/R injury by attenuating [Ca(2+)inf(i) overloading and preventing calpain activation through the activation of the PI3K-Akt-GSK3β pathway and, subsequently, opening of the mitoK(ATP) channel.
TargetsBcl-2/Bax | TGF-β/Smad | p21 | c-Myc | Calcium Channel | ATPase | Akt | GSK-3 | PI3K
In vitro

Berbamine enhances the antineoplastic activity of gemcitabine in pancreatic cancer cells by activating transforming growth factor-β/Smad signaling.[Pubmed: 24619961]

Anat Rec (Hoboken). 2014 May;297(5):802-9.

Drug-resistance to gemcitabine chemotherapy in pancreatic cancer is still an unsolved problem. Combinations of other chemotherapy drugs with gemcitabine have been shown to increase the efficacy of gemcitabine-based treatment.
METHODS AND RESULTS:
In this study, the effect of Berbamine on the antitumor activity of gemcitabine was evaluated in human pancreatic cancer cell lines Bxpc-3 and Panc-1, and the underlying mechanisms were explored. Our results demonstrated that Berbamine exhibited a time- and dose-dependent inhibitory effect in the pancreatic cancer cell lines. Berbamine enhanced gemcitabine-induced cell growth inhibition and apoptosis in these cells. Combined treatment of Berbamine and gemcitabine resulted in down-regulation of anti-apoptotic proteins (Bcl-2, Bcl-xL) and up-regulation of pro-apoptotic proteins (Bax, Bid). More importantly, Berbamine treatment in combination with gemcitabine activated the transforming growth factor-β/Smad (TGF-β/Smad) signaling pathway, as a result of a decrease in Smad7 and an increase in transforming growth factor-β receptor II (TβRII) expression. Changes in downstream targets of Smad7, such as up-regulation of p21 and down-regulation of c-Myc and Cyclin D1 were also observed. Therefore, Berbamine could enhance the antitumor activity of gemcitabine by inhibiting cell growth and inducing apoptosis, possibly through the regulation of the expression of apoptosis-related proteins and the activation of TGF-β/Smad signaling pathway.
CONCLUSIONS:
Our study indicates that Berbamine may be a promising candidate to be used in combination with gemcitabine for pancreatic cancer treatment.

Berbamine protects the heart from ischemia/reperfusion injury by maintaining cytosolic Ca(2+) homeostasis and preventing calpain activation.[Pubmed: 22664727]

Circ J. 2012;76(8):1993-2002. Epub 2012 May 15.

Berbamine, a natural compound from Barberry, was reported to protect myocardium from ischemia/reperfusion (I/R) injury, but the underlying mechanisms are largely unknown.
METHODS AND RESULTS:
Berbamine pretreatment from 10 to 100nmol/L concentration-dependently improved post-ischemic myocardial function. Similar protection was confirmed in isolated cardiomyocytes characterized by the attenuation of I/R-induced intracellular free Ca(2+) concentration ([Ca(2+)](i)) overloading and the depression of cell shortening and Ca(2+) transients, which were partially mimicked but not augmented by calpain inhibitor calpeptin and abolished by mitochondrial ATP-sensitive potassium (mitoK(ATP) channel inhibitor 5-hydroxydecanoate (5-HD) and phosphoinositide 3-kinase (PI3K) inhibitor wortmannin. Consistently, I/R-induced increase of calpain activity and decrease of sarcoplasmic reticulum Ca(2+) ATPase (SERCA2) activity; and protein expression of SERCA2a, desmin, calpastatin and Akt was significantly attenuated by Berbamine. In addition, I/R-decreased Akt protein was reversed by calpeptin. Moreover, Berbamine further increased I/R-enhanced phosphorylation of Akt and glycogen synthase kinase-3β (GSK3β). These protections were abolished by wortmannin. Furthermore, Berbamine significantly attenuated I/R-induced lactate dehydrogenase release, infarct size and contractile dysfunction, and such cardioprotective actions were abolished by wortmannin and 5-HD or mimicked by glycogen synthase kinase-3β (GSK3β) inhibitor SB216763 but without additive effect.
CONCLUSIONS:
These findings suggest that Berbamine confers cardioprotection against I/R injury by attenuating [Ca(2+)inf(i) overloading and preventing calpain activation through the activation of the PI3K-Akt-GSK3β pathway and, subsequently, opening of the mitoK(ATP) channel.

In vivo

Berbamine inhibits the growth of liver cancer cells and cancer-initiating cells by targeting Ca2⁺/calmodulin-dependent protein kinase II.[Pubmed: 23960096 ]

Mol Cancer Ther. 2013 Oct;12(10):2067-77.

Liver cancer is the third leading cause of cancer deaths worldwide but no effective treatment toward liver cancer is available so far. Therefore, there is an unmet medical need to identify novel therapies to efficiently treat liver cancer and improve the prognosis of this disease.
METHODS AND RESULTS:
Here, we report that Berbamine and one of its derivatives, bbd24, potently suppressed liver cancer cell proliferation and induced cancer cell death by targeting Ca(2+)/calmodulin-dependent protein kinase II (CAMKII). Furthermore, Berbamine inhibited the in vivo tumorigenicity of liver cancer cells in NOD/SCID mice and downregulated the self-renewal abilities of liver cancer-initiating cells. Chemical inhibition or short hairpin RNA-mediated knockdown of CAMKII recapitulated the effects of Berbamine, whereas overexpression of CAMKII promoted cancer cell proliferation and increased the resistance of liver cancer cells to Berbamine treatments. Western blot analyses of human liver cancer specimens showed that CAMKII was hyperphosphorylated in liver tumors compared with the paired peritumor tissues, which supports a role of CAMKII in promoting human liver cancer progression and the potential clinical use of Berbamine for liver cancer therapies.
CONCLUSIONS:
Our data suggest that Berbamine and its derivatives are promising agents to suppress liver cancer growth by targeting CAMKII.

Protocol of Berbamine

Kinase Assay

CaMKII γ, a critical regulator of CML stem/progenitor cells, is a target of the natural product berbamine.CaMKII γ, a critical regulator of CML stem/progenitor cells, is a target of the natural product berbamine.[Pubmed: 23074277]

Blood. 2012 Dec 6;120(24):4829-39.

Bcr-Abl tyrosine kinase inhibitors (TKIs) have been a remarkable success for the treatment of Ph(+) chronic myeloid leukemia (CML). However, a significant proportion of patients treated with TKIs develop resistance because of leukemia stem cells (LSCs) and T315I mutant Bcr-Abl.
METHODS AND RESULTS:
Here we describe the unknown activity of the natural product Berbamine that efficiently eradicates LSCs and T315I mutant Bcr-Abl clones. Unexpectedly, we identify CaMKII γ as a specific and critical target of Berbamine for its antileukemia activity. Berbamine specifically binds to the ATP-binding pocket of CaMKII γ, inhibits its phosphorylation and triggers apoptosis of leukemia cells. More importantly, CaMKII γ is highly activated in LSCs but not in normal hematopoietic stem cells and coactivates LSC-related β-catenin and Stat3 signaling networks. The identification of CaMKII γ as a specific target of Berbamine and as a critical molecular switch regulating multiple LSC-related signaling pathways can explain the unique antileukemia activity of Berbamine.
CONCLUSIONS:
These findings also suggest that Berbamine may be the first ATP-competitive inhibitor of CaMKII γ, and potentially, can serve as a new type of molecular targeted agent through inhibition of the CaMKII γ activity for treatment of leukemia.

Structure Identification
Rapid Commun Mass Spectrom. 2014 Jan 15;28(1):143-7.

Electrospray ionization mass spectrometry probing of binding affinity of berbamine, a flexible cyclic alkaloid from traditional Chinese medicine, with G-quadruplex DNA.[Pubmed: 24285399]

Classic G-quadruplex binders typically have a large aromatic core and interact with G-quadruplexes through π-π stacking with the quartets. There are rather few reports on natural flexible cyclic molecule from traditional Chinese medicine which has high binding affinity with G-quadruplex.
METHODS AND RESULTS:
Electrospray ionization mass spectrometry (ESI-MS) experiments were performed to evaluate the binding affinities of a natural alkaloid, Berbamine, with seven G-quadruplexes. Furthermore, we utilized autodock4 analysis to uncover the binding mode of Berbamine with the G-quadruplex. ESI-MS experiments showed that Berbamine has the best binding affinity toward the (GGA)8  G-quadruplex compared with the other six G-quadruplexes. Autodock4 analysis indicated that Berbamine interacted with the (GGA)8  G-quadruplex through hydrogen bonding and van der Waals forces with a binding site at the lateral groove formed by DG8-DA9-DA15-DG16.
CONCLUSIONS:
In this study, we discovered a novel G-quadruplex binder, Berbamine, which has high binding affinity toward the (GGA)8  G-quadruplex. This study provided important clues regarding the probing of small molecule from traditional Chinese medicine which can target the G-quadruplex with high affinity.

Berbamine Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Berbamine Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Berbamine

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.6428 mL 8.2142 mL 16.4285 mL 32.8569 mL 41.0711 mL
5 mM 0.3286 mL 1.6428 mL 3.2857 mL 6.5714 mL 8.2142 mL
10 mM 0.1643 mL 0.8214 mL 1.6428 mL 3.2857 mL 4.1071 mL
50 mM 0.0329 mL 0.1643 mL 0.3286 mL 0.6571 mL 0.8214 mL
100 mM 0.0164 mL 0.0821 mL 0.1643 mL 0.3286 mL 0.4107 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University
Featured Products
New Products
 

References on Berbamine

CaMKII gamma, a critical regulator of CML stem/progenitor cells, is a target of the natural product berbamine.[Pubmed:23074277]

Blood. 2012 Dec 6;120(24):4829-39.

Bcr-Abl tyrosine kinase inhibitors (TKIs) have been a remarkable success for the treatment of Ph(+) chronic myeloid leukemia (CML). However, a significant proportion of patients treated with TKIs develop resistance because of leukemia stem cells (LSCs) and T315I mutant Bcr-Abl. Here we describe the unknown activity of the natural product Berbamine that efficiently eradicates LSCs and T315I mutant Bcr-Abl clones. Unexpectedly, we identify CaMKII gamma as a specific and critical target of Berbamine for its antileukemia activity. Berbamine specifically binds to the ATP-binding pocket of CaMKII gamma, inhibits its phosphorylation and triggers apoptosis of leukemia cells. More importantly, CaMKII gamma is highly activated in LSCs but not in normal hematopoietic stem cells and coactivates LSC-related beta-catenin and Stat3 signaling networks. The identification of CaMKII gamma as a specific target of Berbamine and as a critical molecular switch regulating multiple LSC-related signaling pathways can explain the unique antileukemia activity of Berbamine. These findings also suggest that Berbamine may be the first ATP-competitive inhibitor of CaMKII gamma, and potentially, can serve as a new type of molecular targeted agent through inhibition of the CaMKII gamma activity for treatment of leukemia.

Electrospray ionization mass spectrometry probing of binding affinity of berbamine, a flexible cyclic alkaloid from traditional Chinese medicine, with G-quadruplex DNA.[Pubmed:24285399]

Rapid Commun Mass Spectrom. 2014 Jan 15;28(1):143-7.

RATIONALE: Classic G-quadruplex binders typically have a large aromatic core and interact with G-quadruplexes through pi-pi stacking with the quartets. There are rather few reports on natural flexible cyclic molecule from traditional Chinese medicine which has high binding affinity with G-quadruplex. METHODS: Electrospray ionization mass spectrometry (ESI-MS) experiments were performed to evaluate the binding affinities of a natural alkaloid, Berbamine, with seven G-quadruplexes. Furthermore, we utilized autodock4 analysis to uncover the binding mode of Berbamine with the G-quadruplex. RESULTS: ESI-MS experiments showed that Berbamine has the best binding affinity toward the (GGA)8 G-quadruplex compared with the other six G-quadruplexes. Autodock4 analysis indicated that Berbamine interacted with the (GGA)8 G-quadruplex through hydrogen bonding and van der Waals forces with a binding site at the lateral groove formed by DG8-DA9-DA15-DG16. CONCLUSIONS: In this study, we discovered a novel G-quadruplex binder, Berbamine, which has high binding affinity toward the (GGA)8 G-quadruplex. This study provided important clues regarding the probing of small molecule from traditional Chinese medicine which can target the G-quadruplex with high affinity.

Berbamine enhances the antineoplastic activity of gemcitabine in pancreatic cancer cells by activating transforming growth factor-beta/Smad signaling.[Pubmed:24619961]

Anat Rec (Hoboken). 2014 May;297(5):802-9.

Drug-resistance to gemcitabine chemotherapy in pancreatic cancer is still an unsolved problem. Combinations of other chemotherapy drugs with gemcitabine have been shown to increase the efficacy of gemcitabine-based treatment. In this study, the effect of Berbamine on the antitumor activity of gemcitabine was evaluated in human pancreatic cancer cell lines Bxpc-3 and Panc-1, and the underlying mechanisms were explored. Our results demonstrated that Berbamine exhibited a time- and dose-dependent inhibitory effect in the pancreatic cancer cell lines. Berbamine enhanced gemcitabine-induced cell growth inhibition and apoptosis in these cells. Combined treatment of Berbamine and gemcitabine resulted in down-regulation of anti-apoptotic proteins (Bcl-2, Bcl-xL) and up-regulation of pro-apoptotic proteins (Bax, Bid). More importantly, Berbamine treatment in combination with gemcitabine activated the transforming growth factor-beta/Smad (TGF-beta/Smad) signaling pathway, as a result of a decrease in Smad7 and an increase in transforming growth factor-beta receptor II (TbetaRII) expression. Changes in downstream targets of Smad7, such as up-regulation of p21 and down-regulation of c-Myc and Cyclin D1 were also observed. Therefore, Berbamine could enhance the antitumor activity of gemcitabine by inhibiting cell growth and inducing apoptosis, possibly through the regulation of the expression of apoptosis-related proteins and the activation of TGF-beta/Smad signaling pathway. Our study indicates that Berbamine may be a promising candidate to be used in combination with gemcitabine for pancreatic cancer treatment.

Berbamine protects the heart from ischemia/reperfusion injury by maintaining cytosolic Ca(2+) homeostasis and preventing calpain activation.[Pubmed:22664727]

Circ J. 2012;76(8):1993-2002. Epub 2012 May 15.

BACKGROUND: Berbamine, a natural compound from Barberry, was reported to protect myocardium from ischemia/reperfusion (I/R) injury, but the underlying mechanisms are largely unknown. METHODS AND RESULTS: Berbamine pretreatment from 10 to 100nmol/L concentration-dependently improved post-ischemic myocardial function. Similar protection was confirmed in isolated cardiomyocytes characterized by the attenuation of I/R-induced intracellular free Ca(2+) concentration ([Ca(2+)](i)) overloading and the depression of cell shortening and Ca(2+) transients, which were partially mimicked but not augmented by calpain inhibitor calpeptin and abolished by mitochondrial ATP-sensitive potassium (mitoK(ATP) channel inhibitor 5-hydroxydecanoate (5-HD) and phosphoinositide 3-kinase (PI3K) inhibitor wortmannin. Consistently, I/R-induced increase of calpain activity and decrease of sarcoplasmic reticulum Ca(2+) ATPase (SERCA2) activity; and protein expression of SERCA2a, desmin, calpastatin and Akt was significantly attenuated by Berbamine. In addition, I/R-decreased Akt protein was reversed by calpeptin. Moreover, Berbamine further increased I/R-enhanced phosphorylation of Akt and glycogen synthase kinase-3beta (GSK3beta). These protections were abolished by wortmannin. Furthermore, Berbamine significantly attenuated I/R-induced lactate dehydrogenase release, infarct size and contractile dysfunction, and such cardioprotective actions were abolished by wortmannin and 5-HD or mimicked by glycogen synthase kinase-3beta (GSK3beta) inhibitor SB216763 but without additive effect. CONCLUSIONS: These findings suggest that Berbamine confers cardioprotection against I/R injury by attenuating [Ca(2+)inf(i) overloading and preventing calpain activation through the activation of the PI3K-Akt-GSK3beta pathway and, subsequently, opening of the mitoK(ATP) channel.

Berbamine inhibits the growth of liver cancer cells and cancer-initiating cells by targeting Ca(2)(+)/calmodulin-dependent protein kinase II.[Pubmed:23960096]

Mol Cancer Ther. 2013 Oct;12(10):2067-77.

Liver cancer is the third leading cause of cancer deaths worldwide but no effective treatment toward liver cancer is available so far. Therefore, there is an unmet medical need to identify novel therapies to efficiently treat liver cancer and improve the prognosis of this disease. Here, we report that Berbamine and one of its derivatives, bbd24, potently suppressed liver cancer cell proliferation and induced cancer cell death by targeting Ca(2+)/calmodulin-dependent protein kinase II (CAMKII). Furthermore, Berbamine inhibited the in vivo tumorigenicity of liver cancer cells in NOD/SCID mice and downregulated the self-renewal abilities of liver cancer-initiating cells. Chemical inhibition or short hairpin RNA-mediated knockdown of CAMKII recapitulated the effects of Berbamine, whereas overexpression of CAMKII promoted cancer cell proliferation and increased the resistance of liver cancer cells to Berbamine treatments. Western blot analyses of human liver cancer specimens showed that CAMKII was hyperphosphorylated in liver tumors compared with the paired peritumor tissues, which supports a role of CAMKII in promoting human liver cancer progression and the potential clinical use of Berbamine for liver cancer therapies. Our data suggest that Berbamine and its derivatives are promising agents to suppress liver cancer growth by targeting CAMKII. Mol Cancer Ther; 12(10); 2067-77. (c)2013 AACR.

Description

Berbamine is a natural compound extracted from traditional Chinese medicine Barberry with anti-tumor, immunomodulatory and cardiovascular effects. Berbamine is a calcium channel blocker.

Keywords:

Berbamine,478-61-5,Natural Products, buy Berbamine , Berbamine supplier , purchase Berbamine , Berbamine cost , Berbamine manufacturer , order Berbamine , high purity Berbamine

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: