Kazinol BCAS# 99624-27-8 |
Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
| Cas No. | 99624-27-8 | SDF | Download SDF |
| PubChem ID | 480869 | Appearance | Powder |
| Formula | C25H28O4 | M.Wt | 392.5 |
| Type of Compound | Flavonoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | 6-[(2S)-7-hydroxy-3,4-dihydro-2H-chromen-2-yl]-2,2-dimethyl-7-(3-methylbut-2-enyl)chromen-8-ol | ||
| SMILES | CC(=CCC1=C(C=C2C=CC(OC2=C1O)(C)C)C3CCC4=C(O3)C=C(C=C4)O)C | ||
| Standard InChIKey | QSCBHDIGHKHWKC-NRFANRHFSA-N | ||
| Standard InChI | InChI=1S/C25H28O4/c1-15(2)5-9-19-20(13-17-11-12-25(3,4)29-24(17)23(19)27)21-10-7-16-6-8-18(26)14-22(16)28-21/h5-6,8,11-14,21,26-27H,7,9-10H2,1-4H3/t21-/m0/s1 | ||
| 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. |
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| 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. |
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| 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. | ||
| Description | 1. Kazinol B inhibits the NO synthesis with an IC(50) of 21.6 microM. 2. Kazinol B can stimulate respiratory burst, is probably mediated by the synergism of PKC activation and [Ca2+]i elevation in rat neutrophils. 3. Kazinol B stimulates Ca(2+) release from internal Ca(2+) store, probably through the sphingosine 1-phosphate and IP(3) signaling, and activates external Ca(2+) influx mainly through a non-store-operated Ca(2+) entry (non-SOCE) pathway. 4. Kazinol B inhibits SOCE, is probably attributable to a break in the Ca(2+) driven force of mitochondria. 5. Kazinol B improves insulin sensitivity via Akt and AMPK activation in 3T3-L1 adipocytes, it might be a therapeutic candidate for diabetes mellitus. |
| Targets | Calcium Channel | Sodium Channel | ATPase | NOS | PI3K | PKC | p38MAPK | PPAR | GLUT | Akt | AMPK |
Kazinol B Dilution Calculator
Kazinol B Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.5478 mL | 12.7389 mL | 25.4777 mL | 50.9554 mL | 63.6943 mL |
| 5 mM | 0.5096 mL | 2.5478 mL | 5.0955 mL | 10.1911 mL | 12.7389 mL |
| 10 mM | 0.2548 mL | 1.2739 mL | 2.5478 mL | 5.0955 mL | 6.3694 mL |
| 50 mM | 0.051 mL | 0.2548 mL | 0.5096 mL | 1.0191 mL | 1.2739 mL |
| 100 mM | 0.0255 mL | 0.1274 mL | 0.2548 mL | 0.5096 mL | 0.6369 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. | |||||
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The signal transduction mechanism involved in kazinol B-stimulated superoxide anion generation in rat neutrophils.[Pubmed:9806335]
Br J Pharmacol. 1998 Oct;125(3):517-25.
1. In this study, the underlying mechanism of stimulation of respiratory burst by Kazinol B, a natural isoprenylated flavan, in rat neutrophils in vitro was investigated. 2. Kazinol B concentration-dependently stimulated the superoxide anion (O2*-) generation, with a lag but transient activation profile, in neutrophils but not in a cell-free system. The maximum response (13.2+/-1.4 nmol O2*- 10 min(-1) per 10(6) cells) was observed at 10 microM Kazinol B. 3. Pretreatment of neutrophils with phorbol 12-myristate 13-acetate (PMA) or formylmethionyl-leucyl-phenylalanine (fMLP) significantly enhanced the O2*- generation following the subsequent stimulation of cells with Kazinol B. 4. Cells pretreated with EGTA or a protein kinase inhibitor staurosporine effectively attenuated the Kazinol B-induced O2*- generation. However, a p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 and a phosphoinositide 3-kinase (PI3K) inhibitor wortmannin had no effect on the Kazinol B-induced response. 5. Kazinol B significantly stimulated [Ca2+]i elevation in neutrophils, with a lag and slow rate of rise activation profile, and this response was attenuated by a phospholipase C (PLC) inhibitor U73122. Kazinol B also stimulated the inositol bis- and trisphosphate (IP2 and IP3) formation with a 1 min lag time. 6. The membrane-associated PKC-alpha and PKC-theta but not PKC-iota were increased following the stimulation of neutrophils with Kazinol B. It was more rapid and sensitive in the activation of PKC-theta than PKC-alpha by Kazinol B. Kazinol B partially inhibited the [3H]phorbol 12,13-dibutyrate ([3H]PDB) binding to the neutrophil cytosolic PKC. 7. Neither the cellular mass of phosphatidic acid (PA) and phosphatidylethanol (PEt), in the presence of ethanol, nor the protein tyrosine phosphorylation were stimulated by Kazinol B. In addition, the Kazinol B-induced O2*- generation remained relatively unchanged in cells pretreated with ethanol or a tyrosine kinase inhibitor genistein. 8. Collectively, these results indicate that the stimulation of the respiratory burst by Kazinol B is probably mediated by the synergism of PKC activation and [Ca2+]i elevation in rat neutrophils.
Stimulation of cellular free Ca2+ elevation and inhibition of store-operated Ca2+ entry by kazinol B in neutrophils.[Pubmed:15558242]
Naunyn Schmiedebergs Arch Pharmacol. 2004 Dec;370(6):500-9.
Kazinol B, a natural isoprenylated flavan, stimulated the [Ca(2+)](i) elevation in the presence or absence of Ca(2+) in the medium. Treatment with chymotrypsin or phorbol 12-myristate 13-acetate to shedding of L: -selectin had no effect on subsequent Kazinol B-induced Ca(2+) response. Upon initial cyclopiazonic acid (CPA) treatment in the absence of external Ca(2+), the subsequent [Ca(2+)](i) rise followed by challenge with Kazinol B was greatly diminished. The ryanodine receptor blockers, 8-bromo-cyclic ADP-ribose and ruthenium red did not affect Kazinol B-evoked Ca(2+) release from internal stores. However, the inhibitors of sphingosine kinase, dimethylsphingosine, but not dihydrosphingosine, inhibited Kazinol B-induced Ca(2+) release. Kazinol B-induced [Ca(2+)](i) rise was not affected by two nitric oxidase inhibitors, N-(3-aminomethyl)benzylacetamidine (1400W) and 7-nitroindazole, cytochalasin B and Na(+)-deprivation. This response was slightly attenuated by 2-aminoethyldiphenyl borate (2-APB), a D: -myo-inositol 1,4,5-trisphosphate (IP(3)) receptor blocker, and by genistein, a general tyrosine kinase inhibitor. However, the Ca(2+) response was greatly diminished by two actin filament reorganizers, calyculin A and jasplakinolide, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY 294002), an inhibitor of phosphoinositide 3-kinase, N-(3-aminomethyl)benzylacetamidine (SB 203580), the p38 mitogen-activated protein kinase inhibitor, 1-[6-[17beta-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dio ne (U-73122), the inhibitor of phospholipase C-coupled processes, and by 0.3 mM La(3+) or Ni(2+). Kazinol B did not evoke any appreciable Ba(2+) and Sr(2+) entry into cells. The Ca(2+) entry blockers, 1-[beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole (SKF-96365), but not cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine (MDL-12,330A), inhibited a Kazinol B-induced [Ca(2+)](i) rise. Kazinol B had no effect on the pharmacologically isolated plasma membrane Ca(2+)-ATPase activity. In a Ca(2+)-free medium, Kazinol B inhibited the subsequent Ca(2+) addition, resulting in robust entry in CPA- and formyl peptide-activated cells. Kazinol B produced a concentration-dependent reduction in the mitochondrial membrane potential. These results indicate that Kazinol B stimulates Ca(2+) release from internal Ca(2+) store, probably through the sphingosine 1-phosphate and IP(3) signaling, and activates external Ca(2+) influx mainly through a non-store-operated Ca(2+) entry (non-SOCE) pathway. Inhibition of SOCE by Kazinol B is probably attributable to a break in the Ca(2+) driven force of mitochondria.
Kazinol B from Broussonetia kazinoki improves insulin sensitivity via Akt and AMPK activation in 3T3-L1 adipocytes.[Pubmed:27223849]
Fitoterapia. 2016 Jul;112:90-6.
In this study, we evaluated the insulin-sensitizing effect of flavans purified from Broussonetia kazinoki Siebold (BK) on 3T3-L1 adipocytes. Among the tested compounds, Kazinol B enhanced intracellular lipid accumulation, gene expression of proliferator-activated receptorgamma (PPARgamma) and CCAAT/enhancer binding protein-alpha (C/EBPalpha), and consistently induced PPARgamma transcriptional activation. To further investigate the insulin-sensitizing effect of Kazinol B, we measured glucose analogue uptake by fully differentiated adipocytes and myotubes. Kazinol B increased 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-d-glucose (2-NBDG) uptake by cells by upregulating the gene expression and translocation of glucose transporter 4 (GLUT-4) into the plasma membrane in adipocytes. Kazinol B stimulated the gene expression and secretion of adiponectin, which is associated with a low risk of types 1 and 2 diabetes mellitus. We also suggested the mechanism of the antidiabetic effect of Kazinol B by assaying Akt and AMP-activated protein kinase (AMPK) phosphorylation. In conclusion, Kazinol B isolated from BK improved insulin sensitivity by enhancing glucose uptake via the insulin-Akt signaling pathway and AMPK activation. These results suggest that Kazinol B might be a therapeutic candidate for diabetes mellitus.
Inhibition of nitric oxide production on LPS-activated macrophages by kazinol B from Broussonetia kazinoki.[Pubmed:12781805]
Fitoterapia. 2003 Jun;74(4):350-4.
The ethyl acetate soluble fraction of Broussonetia kazinoki at 50 microg/ml showed a significant inhibition (78.2%) of nitric oxide (NO) in lipopolysaccharide activated macrophages. Kazinol B, an isoprenylated flavan, was identified as the active principle. It inhibits the NO synthesis with an IC(50) of 21.6 microM.
