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Flavokawain C is an orally active natural chalcone. Flavokawain C inhibits the proliferation of various cancer cells. Flavokawain C upregulates GADD153 in cancer cells, inhibits the phosphorylation of Akt and JNK, suppresses early ERK phosphorylation, activates late ERK phosphorylation, activates caspase related subtypes, induces PARP-1 cleavage, causes upregulation of p21 and p27, downregulation of mutant p53 and anti-apoptotic IAP proteins, elevates intracellular ROS levels, reduces SOD activity, and induces apoptosis. Flavokawain C downregulates FABP4, induces autophagy in cancer cells, and activates the AMPK/mTOR pathway. Flavokawain C decreases the expression of glycolysis-related proteins GLUT1 and HK2, and inhibits glycolysis in nasopharyngeal carcinoma cells. Flavokawain C inhibits the activation of the EGFR/PI3K/Akt/mTOR signaling pathway and reduces the expression of HSP90B1. Flavokawain C inhibits angiogenesis by decreasing the expression of angiogenic proteins Ang-1 and VEGF in human umbilical vein endothelial cells. Flavokawain C increases γ-H2AX levels in cells, inhibits the phosphorylation of FAK, PI3K and AKT in cells, and induces DNA damage in cells. Flavokawain C exerts anti-tumor activity in multiple tumor xenograft mouse models. Flavokawain C is applicable to research related to colorectal cancer, colon adenocarcinoma, nephroblastoma, nasopharyngeal carcinoma and liver cancer.
For research use only. We do not sell to patients.
FKC (Flavokawain C) inhibited the growth of G401 cells. The cell viability of G401 treated with different concentrations of FKC (0, 1, 5, 10, and 15 μM) was detected by CCK-8 assay.
G401 cells were treated with different concentrations of FKC (Flavokawain C; 0, 1, 5, and 10 μM), and the expression of epithelial-mesenchymal transition (EMT) markers was detected by western blot analysis.
The inhibitory effect of FKC (Flavokawain C; 10 μM) on the migration and invasion of G401 cells was detected by transwell assay. The bar graphs show the relative protein expression levels normalized to β-tubulin.
FKC (Flavokawain C) induced autophagy in G401 cells. G401 cells were treated with 10 μM FKC for different time (0, 4, 8, 12, 18, and 24 h), and the expression of LC3 was detected by western blot.
FKC (Flavokawain C) inhibited the growth and metastasis of nephroblastoma in vivo. Nude mice were subcutaneously injected with normal and oeNC or oeFABP4 infected G401 cells. One week after cell injection, mice in the treatment group were intraperitoneally administered 3 mg/kg FKC thrice a week for 4 weeks; control mice received the same volume of normal saline. The value of tumor volume and weight was quantified in each group.
FKC (Flavokawain C) inhibited the growth and metastasis of nephroblastoma in vivo. Nude mice were subcutaneously injected with normal and oeNC or oeFABP4 infected G401 cells. One week after cell injection, mice in the treatment group were intraperitoneally administered 3 mg/kg FKC thrice a week for 4 weeks; control mice received the same volume of normal saline. Tumor tissue sections stained with hematoxylin–eosin, the expression of Ki67, FABP4 and Vimentin by immunohistochemistry.
SUDHL-4 and OCI-Ly3 cells were treated with FKC (Flavokawain C; HY-N2445; 1.25-20 µg/mL) or Doxorubicin (HY-15142A; 10 µM) for 24 and 48 h. Cell viability was measured using the MTS assay. *P < 0.05, #P < 0.01, †P < 0.001, and ‡P < 0.0001 versus control at corresponding time points.SUDHL-4 (A), OCI-Ly3 (B), Raji (C), and Jeko-1 (D) cells were treated with FKA (1.25-20 µg/mL) or doxorubicin (10 µM) for 24 and 48 h. Cell viability was measured using the MTS assay. *P < 0.05, #P < 0.01, †P < 0.001, and ‡P < 0.0001 versus control at corresponding time points.
Raji and Jeko-1 cells were treated with FKC (Flavokawain C; HY-N2445; 1.25-20 µg/mL) or Doxorubicin (HY-15142A; 10 µM) for 24 and 48 h. Cell viability was measured using the MTS assay. *P < 0.05, #P < 0.01, †P < 0.001, and ‡P < 0.0001 versus control at corresponding time points.SUDHL-4 (A), OCI-Ly3 (B), Raji (C), and Jeko-1 (D) cells were treated with FKA (1.25-20 µg/mL) or doxorubicin (10 µM) for 24 and 48 h. Cell viability was measured using the MTS assay. *P < 0.05, #P < 0.01, †P < 0.001, and ‡P < 0.0001 versus control at corresponding time points.
Flavokawain C is an orally active natural chalcone. Flavokawain C inhibits the proliferation of various cancer cells. Flavokawain C upregulates GADD153 in cancer cells, inhibits the phosphorylation of Akt and JNK, suppresses early ERK phosphorylation, activates late ERK phosphorylation, activates caspase related subtypes, induces PARP-1 cleavage, causes upregulation of p21 and p27, downregulation of mutant p53 and anti-apoptotic IAP proteins, elevates intracellular ROS levels, reduces SOD activity, and induces apoptosis. Flavokawain C downregulates FABP4, induces autophagy in cancer cells, and activates the AMPK/mTOR pathway. Flavokawain C decreases the expression of glycolysis-related proteins GLUT1 and HK2, and inhibits glycolysis in nasopharyngeal carcinoma cells. Flavokawain C inhibits the activation of the EGFR/PI3K/Akt/mTOR signaling pathway and reduces the expression of HSP90B1. Flavokawain C inhibits angiogenesis by decreasing the expression of angiogenic proteins Ang-1 and VEGF in human umbilical vein endothelial cells. Flavokawain C increases γ-H2AX levels in cells, inhibits the phosphorylation of FAK, PI3K and AKT in cells, and induces DNA damage in cells. Flavokawain C exerts anti-tumor activity in multiple tumor xenograft mouse models. Flavokawain C is applicable to research related to colorectal cancer, colon adenocarcinoma, nephroblastoma, nasopharyngeal carcinoma and liver cancer[1][2][3][4][5][6][7].
In Vitro
Flavokawain C (60 μM; 6-48 h) upregulates the endoplasmic reticulum stress marker GADD153, inhibits Akt phosphorylation, suppresses early ERK phosphorylation and late JNK phosphorylation, and activates late ERK phosphorylation in HCT 116 cells[1]. Flavokawain C (40-80 μM; 6-72 h) reduces the viability of HT-29 cells, induces apoptotic morphological and nuclear changes, triggers DNA fragmentation, increases the proportion of apoptotic cells, decreases mitochondrial membrane potential, and induces G2/M cell cycle arrest[2]. Flavokawain C (40-80 μM; 0-48 h) activates caspase-3, -8, and -9, induces PARP-1 cleavage, triggers p53-independent upregulation of p21 and p27, downregulation of mutant p53, upregulation of the endoplasmic reticulum stress marker GADD153, and downregulation of anti-apoptotic IAP proteins (XIAP, c-IAP1, c-IAP2), increases intracellular ROS levels, and decreases SOD activity in HT-29 cells[2]. Flavokawain C (1-15 μM; 24-72 h) inhibits the viability and proliferation of G401 cells, suppresses their colony-forming ability, and inhibits cell migration and invasion[3]. Flavokawain C (1-10 μM; 0-24 h) regulates the expression of EMT markers, downregulates FABP4, induces complete autophagic flux, and activates the AMPK/mTOR pathway in G401 cells[3]. Flavokawain C (0.5-4 μM; 48 h) inhibits the proliferation of human nasopharyngeal carcinoma HNE1 and CNE2 cells and increases the apoptotic rate of these cells[4]. Flavokawain C (4 μM; 48 h) inhibits glycolysis in human nasopharyngeal carcinoma HNE1 and CNE2 cells by reducing the extracellular acidification rate, glucose consumption and lactate production, as well as downregulating the expression of glycolysis-related proteins GLUT1 and HK2[4]. Flavokawain C (4 μM; 48 h) inhibits the activation of the EGFR/PI3K/Akt/mTOR signaling pathway and reduces the expression of HSP90B1 in human nasopharyngeal carcinoma HNE1 and CNE2 cells[4]. Flavokawain C (4 μM; 48 h) inhibits angiogenesis in human nasopharyngeal carcinoma HNE1 and CNE2 cells by impairing the tube formation and migration capacities of human umbilical vein endothelial cells (HUVECs) and reducing the expression of angiogenic proteins Ang-1 and VEGF in HUVECs[4]. Flavokawain C (48 h) selectively inhibits the viability of Huh-7, Hep3B and HepG2 hepatocellular carcinoma cells, with IC50 values ranging from 23.42 μM to 30.71 μM; while it exhibits low toxicity to normal MIHA hepatocytes, with an IC50 of 53.95 μM[5]. Flavokawain C (2.0-8.0 μM; 2 weeks) inhibits colony formation of Huh-7, Hep3B and HepG2 hepatocellular carcinoma cells[5]. Flavokawain C (4.0-16.0 μM; 48 h) inhibits DNA replication, induces apoptosis, downregulates the expression of anti-apoptotic protein Bcl2, upregulates the expression of pro-apoptotic protein Bax, and promotes apoptosis by reducing the Bcl2/Bax ratio in Huh-7 and Hep3B hepatocellular carcinoma cells[5]. Flavokawain C (4.0-16.0 μM; 48 h) increases the level of γ-H2AX, a marker of DNA damage response, in Huh-7 and Hep3B cells, inhibits the phosphorylation of FAK, PI3K and AKT in cells, and induces DNA damage[5]. Flavokawain C (4.0-16.0 μM; 48 h) reduces extracellular matrix adhesion of Huh-7 and Hep3B cells and inhibits cell migration[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Induced time-dependent upregulation of GADD153 protein levels. Showed no GADD153 expression was detected in untreated control cells.\nCaused a transient increase in phosphorylated Akt levels at 6 hours. Induced time-dependent decrease in phosphorylated Akt levels through 48 hours. Showed no significant changes in total Akt protein levels were observed.\nCaused time-dependent decreases in phosphorylated ERK levels at 6, 12, and 18 hours. Induced dramatic increases in phosphorylated ERK levels at 24 and 48 hours. Showed total ERK levels remained unchanged. Caused small reductions in phosphorylated JNK levels at 24 and 48 hours. Showed no significant changes in total JNK, phosphorylated p38, or total p38 levels.
Reduced HT-29 cell viability in a dose- and time-dependent manner. Decreased cell viability from 644.51% (control) to 185.17%, 111.81%, and 104.94% at 40, 60, and 80 μM respectively after 72 h. Showed comparable inhibitory effect between 60 and 80 μM.
Induced dose-dependent apoptotic morphological changes, including cell shrinkage, surface blebbing, cytoplasmic vacuolation, chromatin condensation/fragmentation, and late apoptotic cells (pink fluorescence from propidium iodide staining).\nCaused a concentration-dependent increase in DNA fragmentation. Increased TUNEL-positive cells to 11.6% at 80 μM relative to control.
At 24 h, dose-dependently increased G2/M phase cell population (with a small G1 phase accumulation) and decreased S phase population. At 48 h, caused a marked dose-dependent increase in G2/M phase cell population, with the highest increase at 80 μM.
Increased the number of both yellow (autophagosomes) and red (autolysosomes) puncta per cell compared to control, indicating enhanced autophagic initiation and maturation.
Dose-dependently increased the number of 53BP1 foci (a marker of DNA damage response) in both cell lines. Increased average 53BP1 foci per cell to >15 in both cell lines at 16.0 μM, compared to ~1.5 foci per cell in untreated controls.
In Vivo
Flavokawain C (3 mg/kg; i.p.; thrice weekly; 4 weeks) inhibits nephroblastoma xenograft growth in BALB/c nude mice, with significant reductions in tumor volume and weight that are partially reversed by FABP4 overexpression[3]. Flavokawain C (3 mg/kg; i.p.; 4 weeks (subcutaneous tumor model); 8 weeks (liver metastasis model)) reduces subcutaneous nasopharyngeal carcinoma tumor volume and weight, inhibits liver metastasis, and downregulates glycolysis, angiogenesis, and EGFR/PI3K/Akt/mTOR pathway activation in vivo, with effects enhanced by HSP90B1 knockdown and reversed by HSP90B1 overexpression[4]. Flavokawain C (16 mg/kg; i.p.; daily; 14 days) significantly inhibits Huh-7 liver cancer xenograft growth in nude mice without causing notable body weight loss, via reduced tumor cell proliferation and induced DNA damage[5]. Flavokawain C (1-3 mg/kg; i.p.; thrice weekly; 19 days) dose-dependently inhibits HCT 116 colon carcinoma xenograft growth in BALB/c nude mice, with the 3 mg/kg dose achieving up to 52.17% tumor volume inhibition, via induction of apoptosis and reduction of cell proliferation, without causing significant organ toxicity[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
BALB/c nude (5-week-old male, weight range 19.0g to 22.3g at euthanasia, subcutaneous nephroblastoma xenograft model)[3]
Dosage:
3 mg/kg
Administration:
i.p.; thrice weekly; 4 weeks
Result:
Significantly reduced tumor volume and tumor weight compared to the control group. Reduced expression of Ki67, FABP4, and Vimentin in tumor tissues. Increased expression of E-cadherin in tumor tissues. Induced loose tumor structure and increased inflammatory cell infiltration in tumor samples. Had its tumor growth inhibition effect partially reversed by FABP4 overexpression.
Reduced subcutaneous tumor volume and weight compared to vehicle control. Downregulated the expression of HSP90B1, GLUT1, HK2, Ang-1, and VEGF in tumor tissues. Inhibited the phosphorylation of EGFR, PI3K, Akt, and mTOR in tumor tissues. Inhibited liver metastasis of NPC tumors, as measured by reduced bioluminescence signal from luciferase-expressing tumor cells. Enhanced inhibitory effect on tumor growth and pathway suppression was observed with HSP90B1 knockdown. Reversed inhibitory effect on tumor growth and pathway suppression was observed with HSP90B1 overexpression.
Significantly reduced tumor growth rate, final tumor volume, and final tumor weight relative to controls. Caused no significant changes in mouse body weight during treatment. Induced cytoplasmic-nuclear separation and nuclear fragmentation (cell death) in tumor tissues via H&E staining. Reduced Ki67 (proliferation marker) levels in treated tumor tissues. Increased γ-H2AX (DNA damage marker) levels in treated tumor tissues.
Reduced final mean tumor volume to 658.19 mm3 (600% growth from initial 84.48 mm3) with 18.73-23.99% tumor volume inhibition (%T/C) over days 3-19 at 1 mg/kg. Reduced final mean tumor volume to 411.31 mm3 (300% growth from initial 86.56 mm3) with 23.43-52.17% tumor volume inhibition (%T/C) over days 3-19 at 3 mg/kg. Increased tumor necrotic area significantly (p < 0.05 vs control) at 3 mg/kg. Increased TUNEL-positive cells significantly (p < 0.05 vs control) at 3 mg/kg. Increased cleaved caspase-3 immunoreactivity score significantly (p < 0.05 vs control) at 3 mg/kg. Decreased Ki67 immunoreactivity score significantly (p < 0.05 vs control) at 3 mg/kg. Up-regulated Ig mu chain C region (secreted form) and down-regulated GRP78, hemopexin, kininogen-1, and apolipoprotein E compared to vehicle controls, with levels returning to near normal ranges at 3 mg/kg. Caused no significant body weight loss in either dose group; kept serum liver (AST, ALT, ALP) and kidney (creatine, urea) function parameters within normal limits, with only mild urea elevation in the 1 mg/kg group; caused no pathological damage to major organs (heart, spleen, liver, lungs, kidneys).
DMSO : 125 mg/mL (416.24 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
3.3299 mL
16.6495 mL
33.2989 mL
5 mM
0.6660 mL
3.3299 mL
6.6598 mL
10 mM
0.3330 mL
1.6649 mL
3.3299 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
This protocol yields a clear solution of ≥ 1.25 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (12.5 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
This protocol yields a clear solution of ≥ 1.25 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (12.5 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
Customer Validation
FKC (Flavokawain C) inhibited the growth of G401 cells. The cell viability of G401 treated with different concentrations of FKC (0, 1, 5, 10, and 15 μM) was detected by CCK-8 assay.
Customer Validation
G401 cells were treated with different concentrations of FKC (Flavokawain C; 0, 1, 5, and 10 μM), and the expression of epithelial-mesenchymal transition (EMT) markers was detected by western blot analysis.
Customer Validation
The inhibitory effect of FKC (Flavokawain C; 10 μM) on the migration and invasion of G401 cells was detected by transwell assay. The bar graphs show the relative protein expression levels normalized to β-tubulin.
Customer Validation
FKC (Flavokawain C) induced autophagy in G401 cells. G401 cells were treated with 10 μM FKC for different time (0, 4, 8, 12, 18, and 24 h), and the expression of LC3 was detected by western blot.
Customer Validation
FKC (Flavokawain C) inhibited the growth and metastasis of nephroblastoma in vivo. Nude mice were subcutaneously injected with normal and oeNC or oeFABP4 infected G401 cells. One week after cell injection, mice in the treatment group were intraperitoneally administered 3 mg/kg FKC thrice a week for 4 weeks; control mice received the same volume of normal saline. The value of tumor volume and weight was quantified in each group.
Customer Validation
FKC (Flavokawain C) inhibited the growth and metastasis of nephroblastoma in vivo. Nude mice were subcutaneously injected with normal and oeNC or oeFABP4 infected G401 cells. One week after cell injection, mice in the treatment group were intraperitoneally administered 3 mg/kg FKC thrice a week for 4 weeks; control mice received the same volume of normal saline. Tumor tissue sections stained with hematoxylin–eosin, the expression of Ki67, FABP4 and Vimentin by immunohistochemistry.
Customer Validation
SUDHL-4 and OCI-Ly3 cells were treated with FKC (Flavokawain C; HY-N2445; 1.25-20 µg/mL) or Doxorubicin (HY-15142A; 10 µM) for 24 and 48 h. Cell viability was measured using the MTS assay. *P < 0.05, #P < 0.01, †P < 0.001, and ‡P < 0.0001 versus control at corresponding time points.SUDHL-4 (A), OCI-Ly3 (B), Raji (C), and Jeko-1 (D) cells were treated with FKA (1.25-20 µg/mL) or doxorubicin (10 µM) for 24 and 48 h. Cell viability was measured using the MTS assay. *P < 0.05, #P < 0.01, †P < 0.001, and ‡P < 0.0001 versus control at corresponding time points.
Customer Validation
Raji and Jeko-1 cells were treated with FKC (Flavokawain C; HY-N2445; 1.25-20 µg/mL) or Doxorubicin (HY-15142A; 10 µM) for 24 and 48 h. Cell viability was measured using the MTS assay. *P < 0.05, #P < 0.01, †P < 0.001, and ‡P < 0.0001 versus control at corresponding time points.SUDHL-4 (A), OCI-Ly3 (B), Raji (C), and Jeko-1 (D) cells were treated with FKA (1.25-20 µg/mL) or doxorubicin (10 µM) for 24 and 48 h. Cell viability was measured using the MTS assay. *P < 0.05, #P < 0.01, †P < 0.001, and ‡P < 0.0001 versus control at corresponding time points.
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