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Dihydroflavokawin B

CAS# 3791-76-2

Dihydroflavokawin B

Catalog No. BCN5272----Order now to get a substantial discount!

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Quality Control of Dihydroflavokawin B

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Chemical structure

Dihydroflavokawin B

3D structure

Chemical Properties of Dihydroflavokawin B

Cas No. 3791-76-2 SDF Download SDF
PubChem ID 270058 Appearance Powder
Formula C17H18O4 M.Wt 286.32
Type of Compound Chalcones Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name 1-(2-hydroxy-4,6-dimethoxyphenyl)-3-phenylpropan-1-one
SMILES COC1=CC(=C(C(=C1)OC)C(=O)CCC2=CC=CC=C2)O
Standard InChIKey JAJFQMZJIQDRSX-UHFFFAOYSA-N
Standard InChI InChI=1S/C17H18O4/c1-20-13-10-15(19)17(16(11-13)21-2)14(18)9-8-12-6-4-3-5-7-12/h3-7,10-11,19H,8-9H2,1-2H3
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.

Biological Activity of Dihydroflavokawin B

DescriptionFlavokawain A is an apoptotic inducer and immune- modulator ,it also shows anti-inflammatory, and anti-tumor activities.Flavokawain A can significantly reduce the expression of CDK1-inhibitory kinases, Myt1 and Wee1, and cause cyclin B1 protein accumulation leading to CDK1 activation in T24 cells.Flavokawain A may suppress LPS-induced expression of pro-inflammatory mediators via blockage of NF-κB-AP-1-JNK/p38 MAPK signaling pathways in the murine macrophages.
TargetsNF-kB | AP-1 | JNK | p38MAPK | TNF-α | CDK | NOS | COX | NO | PGE | IL Receptor | p53 | p21
In vitro

Suppression of iNOS and COX-2 expression by flavokawain A via blockade of NF-κB and AP-1 activation in RAW 264.7 macrophages.[Pubmed: 23727179 ]

Food Chem Toxicol. 2013 Aug;58:479-86.

Flavokawain A, a major constituent of chalcones derived from kava extracts, exerts various biological activities such as anti-tumor activities.
METHODS AND RESULTS:
In this study, we examined the suppressive effect of Flavokawain A on LPS-induced expression of pro-inflammatory mediators and the molecular mechanisms responsible for these activities in the murine macrophages. Flavokawain A significantly suppressed expression of iNOS and COX-2, as well as the subsequent production of NO and PGE2 in the LPS-stimulated RAW 264.7 cells. Flavokawain A significantly inhibited LPS-induced activation of NF-κB and AP-1 signaling pathways. In addition, Flavokawain A inhibited activation of JNK and p38 MAPK which was responsible for expression of iNOS and COX-2 in the LPS-stimulated RAW 264.7 cells. Furthermore, Flavokawain A suppressed LPS-induced expression of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6.
CONCLUSIONS:
These results suggest that Flavokawain A may exert anti-inflammatory responses by suppressing LPS-induced expression of pro-inflammatory mediators via blockage of NF-κB-AP-1-JNK/p38 MAPK signaling pathways in the murine macrophages.

Flavokawain A induces apoptosis in MCF-7 and MDA-MB231 and inhibits the metastatic process in vitro.[Pubmed: 25286005]

PLoS One. 2014 Oct 6;9(10):e105244.

The kava-kava plant (Piper methsyticum) is traditionally known as the pacific elixir by the pacific islanders for its role in a wide range of biological activities. The extract of the roots of this plant contains a variety of interesting molecules including Flavokawain A and this molecule is known to have anti-cancer properties. Breast cancer is still one of the leading diagnosed cancers in women today. The metastatic process is also very pertinent in the progression of tumorigenesis.
METHODS AND RESULTS:
MCF-7 and MDA-MB231 cells were treated with several concentrations of FKA. The apoptotic analysis was done through the MTT assay, BrdU assay, Annexin V analysis, cell cycle analysis, JC-1 mitochondrial dye, AO/PI dual staining, caspase 8/9 fluorometric assay, quantitative real time PCR and western blot. For the metastatic assays, the in vitro scratch assay, trans-well migration/invasion assay, HUVEC tube formation assay, ex vivo rat aortic ring assay, quantitative real time PCR and western blot were employed. We have investigated the effects of FKA on the apoptotic and metastatic process in two breast cancer cell lines. FKA induces apoptosis in both MCF-7 and MDA-MB231 in a dose dependent manner through the intrinsic mitochondrial pathway. Additionally, FKA selectively induces a G2/M arrest in the cell cycle machinery of MDA-MB231 and G1 arrest in MCF-7. This suggests that FKA's anti-cancer activity is dependent on the p53 status. Moreover, FKA also halted the migration and invasion process in MDA-MB231. The similar effects can be seen in the inhibition of the angiogenesis process as well.
CONCLUSIONS:
FKA managed to induce apoptosis and inhibit the metastatic process in two breast cancer cell lines, in vitro. Overall, FKA may serve as a promising candidate in the search of a new anti-cancer drug especially in halting the metastatic process but further in vivo evidence is needed.

Flavokawain A, a novel chalcone from kava extract, induces apoptosis in bladder cancer cells by involvement of Bax protein-dependent and mitochondria-dependent apoptotic pathway and suppresses tumor growth in mice.[Pubmed: 15833884]

Cancer Res. 2005 Apr 15;65(8):3479-86.

Consumption of the traditional kava preparation was reported to correlate with low and uncustomary gender ratios (more cancer in women than men) of cancer incidences in three kava-drinking countries: Fiji, Vanuatu, and Western Samoa. We have identified Flavokawain A, B, and C but not the major kavalactone, kawain, in kava extracts as causing strong antiproliferative and apoptotic effect in human bladder cancer cells.
METHODS AND RESULTS:
Flavokawain A results in a significant loss of mitochondrial membrane potential and release of cytochrome c into the cytosol in an invasive bladder cancer cell line T24. These effects of Flavokawain A are accompanied by a time-dependent decrease in Bcl-x(L), a decrease in the association of Bcl-x(L) to Bax, and an increase in the active form of Bax protein. Using the primary mouse embryo fibroblasts Bax knockout and wild-type cells as well as a Bax inhibitor peptide derived from the Bax-binding domain of Ku70, we showed that Bax protein was, at least in part, required for the apoptotic effect of Flavokawain A. In addition, Flavokawain A down-regulates the expression of X-linked inhibitor of apoptosis and survivin.
CONCLUSIONS:
Because both X-linked inhibitor of apoptosis and survivin are main factors for apoptosis resistance and are overexpressed in bladder tumors, our data suggest that Flavokawain A may have a dual efficacy in induction of apoptosis preferentially in bladder tumors. Finally, the anticarcinogenic effect of Flavokawain A was evident in its inhibitory growth of bladder tumor cells in a nude mice model (57% of inhibition) and in soft agar.

In vivo

Kava chalcone, flavokawain A, inhibits urothelial tumorigenesis in the UPII-SV40T transgenic mouse model.[Pubmed: 24121102]

Cancer Prev Res (Phila). 2013 Dec;6(12):1365-75.

Flavokawain A (FKA) is the predominant chalcone identified from the kava plant. We have previously shown that FKA preferentially inhibits the growth of p53 defective bladder cancer cell lines.
METHODS AND RESULTS:
Here, we examined whether FKA could inhibit bladder cancer development and progression in vivo in the UPII-SV40T transgenic model that resembles human urothelial cell carcinoma (UCC) with defects in the p53 and the retinoblastoma (Rb) protein pathways. Genotyped UPII-SV40T mice were fed orally with vehicle control (AIN-93M) or FKA (6 g/kg food; 0.6%) for 318 days starting at 28 days of age. More than 64% of the male mice fed with FKA-containing food survived beyond 318 days of age, whereas only about 38% of the male mice fed with vehicle control food survived to that age (P = 0.0383). The mean bladder weights of surviving male transgenic mice with the control diet versus the FKA diet were 234.6 ± 72.5 versus 96.1 ± 69.4 mg (P = 0.0002). FKA was excreted primarily through the urinary tract and concentrated in the urine up to 8.4 μmol/L, averaging about 38 times (males) and 15 times (females) more concentrated than in the plasma (P = 0.0001). FKA treatment inhibited the occurrence of high-grade papillary UCC, a precursor to invasive urothelial cancer, by 42.1%. A decreased expression of Ki67, survivin, and X-linked inhibitor of apoptotic proteins (XIAP) and increased expression of p27 and DR5, and the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive apoptotic cells were observed in the urothelial tissue of FKA-fed mice.
CONCLUSIONS:
These results suggest a potential of FKA in preventing the recurrence and progression of non-muscle-invasive UCC.

Protocol of Dihydroflavokawin B

Kinase Assay

Effects of the kava chalcone flavokawain A differ in bladder cancer cells with wild-type versus mutant p53.[Pubmed: 19138991]

Cancer Prev Res (Phila). 2008 Nov;1(6):439-51.

Flavokawain A is the predominant chalcone from kava extract. We have assessed the mechanisms of Flavokawain A's action on cell cycle regulation.
METHODS AND RESULTS:
In a p53 wild-type, low-grade, and papillary bladder cancer cell line (RT4), Flavokawain A increased p21/WAF1 and p27/KIP1, which resulted in a decrease in cyclin-dependent kinase-2 (CDK2) kinase activity and subsequent G(1) arrest. The increase of p21/WAF1 protein corresponded to an increased mRNA level, whereas p27/KIP1 accumulation was associated with the down-regulation of SKP2, which then increased the stability of the p27/KIP1 protein. The accumulation of p21/WAF1 and p27/KIP1 was independent of cell cycle position and thus not a result of the cell cycle arrest. In contrast, Flavokawain A induced a G(2)-M arrest in six p53 mutant-type, high-grade bladder cancer cell lines (T24, UMUC3, TCCSUP, 5637, HT1376, and HT1197). Flavokawain A significantly reduced the expression of CDK1-inhibitory kinases, Myt1 and Wee1, and caused cyclin B1 protein accumulation leading to CDK1 activation in T24 cells. Suppression of p53 expression by small interfering RNA in RT4 cells restored Cdc25C expression and down-regulated p21/WAF1 expression, which allowed Cdc25C and CDK1 activation, which then led to a G(2)-M arrest and an enhanced growth-inhibitory effect by Flavokawain A. Consistently, Flavokawain A also caused a pronounced CDK1 activation and G(2)-M arrest in p53 knockout but not in p53 wild-type HCT116 cells.
CONCLUSIONS:
This selectivity of Flavokawain A for inducing a G(2)-M arrest in p53-defective cells deserves further investigation as a new mechanism for the prevention and treatment of bladder cancer.

Animal Research

In vitro Toxicity and in vivo Immunomodulatory Effects of Flavokawain A and Flavokawain B in Balb/C Mice.[Pubmed: 26411010]

Nat Prod Commun. 2015 Jul;10(7):1199-202.

Flavokawains are chalcones that can be found in the root extracts of the kava-kava (Piper methysticum) plant. Flavokawain A and flavokawain B are known to possess potential anti-inflammation and anti-cancer activities. Nevertheless, the effects of both these compounds on the normal function of the host have not been studied. There is a need to find agents that can enhance the functionality of the immune system without disturbing the homeostatic balance. This study aimed to determine the toxicity and immunomodulatory effects of Flavokawain A and flavokawain B on Balb/c mice.
METHODS AND RESULTS:
Several assays were conducted, the MTT viability assay, cytokine detection (IL-2 and TNF-α), immunophenotyping of important immune markers, serum biochemical analysis and detection of nitric oxide levels. Based on our results, Flavokawain A and B did not cause mortality and all mice were observed normal after the treatment period. Both flavokawains stimulated splenocyte proliferation, the secretion of IL-2 and TNF-α and raised the population of T cell subsets without significantly altering the level of several serum biochemical parameters.
CONCLUSIONS:
Overall, Flavokawain A and B could serve as potential immune-modulator drugs without causing any toxicity, however further in vivo evidence is needed.

Dihydroflavokawin B Dilution Calculator

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Dihydroflavokawin B Molarity Calculator

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Preparing Stock Solutions of Dihydroflavokawin B

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.4926 mL 17.463 mL 34.926 mL 69.8519 mL 87.3149 mL
5 mM 0.6985 mL 3.4926 mL 6.9852 mL 13.9704 mL 17.463 mL
10 mM 0.3493 mL 1.7463 mL 3.4926 mL 6.9852 mL 8.7315 mL
50 mM 0.0699 mL 0.3493 mL 0.6985 mL 1.397 mL 1.7463 mL
100 mM 0.0349 mL 0.1746 mL 0.3493 mL 0.6985 mL 0.8731 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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