2',4-Dihydroxychalcone
Based on 1 Customer Validation
2',4-Dihydroxychalcone is an orally active natural chalcone flavonoid. 2',4-Dihydroxychalcone restores intestinal barrier integrity by upregulating tight junction proteins, regulates intestinal flora balance and alleviates inflammation. 2',4-Dihydroxychalcone induces GPX4 degradation, ferroptosis and apoptosis, triggers cell cycle arrest, and exhibits broad anti-tumor activity. 2',4-Dihydroxychalcone also possesses antifungal activity, antileishmanial activity, and reduces the hemolytic effect and virulence of Vibrio vulnificus.
For research use only. We do not sell to patients.
- CAS No.: 13323-66-5
- Formula: C15H12O3
- Molecular Weight:240.25
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Storage:
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HL-60 | IC50 |
7.1 μM
Compound: 5
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Cytotoxicity against human HL60 cells by MTT assay
Cytotoxicity against human HL60 cells by MTT assay
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[PMID: 25091929] |
| NALM-6 | IC50 |
40.6 μM
Compound: 5
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Cytotoxicity against human NALM6 cells by MTT assay
Cytotoxicity against human NALM6 cells by MTT assay
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[PMID: 25091929] |
| Neutrophil | IC50 |
1.5 μM
Compound: 22
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Inhibition of PMA-induce ROS/RNS generation in human neutrophils measured up to 30 mins in presence of 30 mM glucose by luminol-amplified chemiluminescence method
Inhibition of PMA-induce ROS/RNS generation in human neutrophils measured up to 30 mins in presence of 30 mM glucose by luminol-amplified chemiluminescence method
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[PMID: 33006891] |
| Neutrophil | IC50 |
1.6 μM
Compound: 22
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Inhibition of PMA-induce ROS/RNS generation in human neutrophils measured up to 30 mins in presence of 5.5 mM glucose by luminol-amplified chemiluminescence method
Inhibition of PMA-induce ROS/RNS generation in human neutrophils measured up to 30 mins in presence of 5.5 mM glucose by luminol-amplified chemiluminescence method
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[PMID: 33006891] |
| RBL-1 | IC50 |
42 μM
Compound: 4
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Inhibition of 5-lipoxygenase in rat RBL1 cells
Inhibition of 5-lipoxygenase in rat RBL1 cells
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10.1007/s00044-013-0745-7 |
| RBL-1 | IC50 |
42 μM
Compound: 5
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In vitro inhibition against 5-lipoxygenase in RBL-1 cells was determined
In vitro inhibition against 5-lipoxygenase in RBL-1 cells was determined
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[PMID: 8254620] |
| WM-115 | IC50 |
69.1 μM
Compound: 5
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Cytotoxicity against human WM115 cells by MTT assay
Cytotoxicity against human WM115 cells by MTT assay
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[PMID: 25091929] |
In Vitro
2',4-Dihydroxychalcone (1.25-40 μM; 1-2 h) selectively inhibits NLRP3 inflammasome activation in THP-1-derived macrophages and 774A.1 macrophages by blocking the cleavage of caspase-1 and Gasdermin D, and exhibits no cytotoxicity at concentrations up to 40 μM[1].
2',4-Dihydroxychalcone (25 μM; 1 h) potently inhibits Nigericin (HY-127019)-induced IL-1β secretion in THP-1-derived macrophages[1].
2',4-Dihydroxychalcone (12.5-50 µM; 24-72 h) potently inhibits the proliferation of HuCCT1 and QBC939 cholangiocarcinoma cells in a concentration-dependent manner[2].
2',4-Dihydroxychalcone (12.5-50 µM; 14 days) inhibits the colony-forming ability of HuCCT1 and QBC939 cholangiocarcinoma cells in a concentration-dependent manner[2].
2',4-Dihydroxychalcone (25 µM; 24 h) inhibits the proliferation of HuCCT1 and QBC939 cholangiocarcinoma cells by reducing EdU incorporation[2].
2',4-Dihydroxychalcone (12.5-50 µM; 48 h) inhibits horizontal and vertical migration of HuCCT1 and QBC939 cholangiocarcinoma cells in a concentration-dependent manner[2].
2',4-Dihydroxychalcone (12.5-50 µM; 24 h) increases intracellular ROS levels in HuCCT1 and QBC939 cholangiocarcinoma cells in a concentration-dependent manner[2].
2',4-Dihydroxychalcone (12.5-50 µM; 24 h) induces ferroptosis in HuCCT1 and QBC939 cholangiocarcinoma cells[2].
2',4-Dihydroxychalcone (12.5-50 µM; 24 h) inhibits epithelial-mesenchymal transition in HuCCT1 and QBC939 cholangiocarcinoma cells, while downregulating the PI3K/AKT/mTOR signaling pathway and ferroptosis-related markers SLC7A11 and GPX4[2].
2',4-Dihydroxychalcone (12.5-50 µM) downregulates the expression of ERO1A in HuCCT1 and QBC939 cholangiocarcinoma cells in a concentration-dependent manner[2].
2',4-Dihydroxychalcone (0.06-256 μg/mL; 48 h) inhibits the metabolic activity and hyphal growth of Aspergillus fumigatus Af293, with an MIC50 ranging from 64 to 128 μg/mL, and significantly reduces hyphal growth at a concentration of 256 μg/mL[3].
2',4-Dihydroxychalcone (8 μg/mL; 48 h) inhibits the radial growth of Aspergillus fumigatus Af293 by 20%, blocks its sporulation process, and reduces the expression levels of sporulation-related genes brlA, abaA and wetA by 3-5 folds[3].
2',4-Dihydroxychalcone (8 μg/mL; 48 h) reduces the expression levels of calcineurin pathway genes cnaA and crzA in Aspergillus fumigatus Af293[3].
2',4-Dihydroxychalcone (4-256 μg/mL; 48 h) enhances the antifungal activity of Itraconazole (HY-17514) and Caspofungin (HY-17006A) against Aspergillus fumigatus Af293[3].
2',4-Dihydroxychalcone (0.195-100.0 µg/mL; 72 h) potently inhibits the growth of Leishmania amazonensis promastigotes, with an IC50 of 0.4 μM, and this compound shows high selectivity for parasites over mammalian cells[4].
2',4-Dihydroxychalcone (24 h) exhibits low cytotoxicity against mouse peritoneal macrophages, with a CC50 of 416.7 μM[4].
2',4-Dihydroxychalcone (5-20 μg/mL; 48 h) induces morphological changes associated with apoptosis in human gastric cancer MGC-803 cells, with severe cell detachment and nuclear damage observed at the highest concentration[5].
2',4-Dihydroxychalcone (5-20 μg/mL; 48 h) induces cell cycle arrest in human gastric cancer MGC-803 cells: it triggers S-phase arrest at 5 μg/mL, induces G2/M-phase arrest in a dose-dependent manner as the concentration increases to 10 μg/mL, while the G2/M-phase arrest effect attenuates at 20 μg/mL[5].
2',4-Dihydroxychalcone (2.5-20 μg/mL; 48 h) increases the activity of caspase-3 in human gastric cancer MGC-803 cells in a dose-dependent manner[5].
2',4-Dihydroxychalcone (5-20 μg/mL; 48 h) downregulates the expression of survivin mRNA in human gastric cancer MGC-803 cells in a dose-dependent manner[5].
2',4-Dihydroxychalcone (0.2-5 μM; cultured to an OD600 of 1.8-2.0) potently reduces the transcription levels of HlyU-regulated toxin genes rtxA1 and vvhA in wild-type Vibrio vulnificus MO6-24/O, without altering the expression of hlyU or hns[6].
2',4-Dihydroxychalcone (2-8 μM) inhibits the hemolytic activity of wild-type *Vibrio vulnificus* MO6-24/O in a concentration-dependent manner, and at the concentration of 8 μM, the hemolysis level decreases to a level comparable to that of the ΔhlyU mutant[6].
2',4-Dihydroxychalcone exhibits low cytotoxicity against HeLa and HEK293 cells, with IC50 values of 100.3 μM and 60.0 μM, respectively, which are much higher than the maximum working concentration of 8 μM[6].
2',4-Dihydroxychalcone (150-300 μM) inhibits the specific DNA-binding activity of purified wild-type Vibrio vulnificus HlyU protein with the PrtxA1 promoter, and prevents the formation of specific high-mobility DNA-protein complexes[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Human cholangiocarcinoma HuCCT1 and QBC939 cells
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Concentration:12.5, 25 and 50 µM
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Incubation Time:24 h, 48 h, 72 h
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Result:Resulted in significant, concentration-dependent inhibition of HuCCT1 and QBC939 cell proliferation at all time points, compared to untreated controls.
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Cell Line:Human cholangiocarcinoma HuCCT1 and QBC939 cells
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Concentration:12.5, 25 and 50 µM
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Incubation Time:14 days
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Result:Caused a significant, concentration-dependent reduction in colony number for both HuCCT1 and QBC939 cells, compared to untreated controls.
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Cell Line:Human cholangiocarcinoma HuCCT1 and QBC939 cells
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Concentration:25 µM
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Incubation Time:24 h
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Result:Inhibited DNA synthesis (EdU incorporation) in CCA cells, indicating reduced proliferation.
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Cell Line:Human cholangiocarcinoma HuCCT1 and QBC939 cells
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Concentration:12.5, 25 and 50 µM
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Incubation Time:48 h
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Result:Caused a significant, concentration-dependent reduction in wound closure (horizontal migration) for both HuCCT1 and QBC939 cells, compared to untreated controls.\nCaused a significant, concentration-dependent reduction in the number of migrated cells (vertical migration) for both HuCCT1 and QBC939 cells, compared to untreated controls.
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Cell Line:Human cholangiocarcinoma HuCCT1 and QBC939 cells
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Concentration:12.5, 25 and 50 µM
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Incubation Time:24 h
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Result:Caused a significant, concentration-dependent increase in epithelial marker E-cadherin levels in both HuCCT1 and QBC939 cells, compared to untreated controls.
Caused a significant, concentration-dependent decrease in mesenchymal markers (Vimentin, Snail, Slug) and matrix metalloproteinases (MMP2, MMP9) levels in both HuCCT1 and QBC939 cells, compared to untreated controls.
Reduced protein levels of phosphorylated PI3K, AKT, and mTOR in both HuCCT1 and QBC939 cells, compared to untreated controls.
Downregulated ferroptosis-related markers SLC7A11 and GPX4 in both HuCCT1 and QBC939 cells, compared to untreated controls.
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Cell Line:human gastric cancer MGC-803 cells
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Concentration:5 μg/mL, 10 μg/mL, 20 μg/mL
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Incubation Time:48 h
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Result:Induced marked nuclear condensation, nuclear fragmentation, and apoptotic body formation at 5 μg/mL and 10 μg/mL.
Caused most cells to detach from coverslips and float in the medium, with complete destruction of nuclear morphology in remaining adherent cells at 20 μg/mL.
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Cell Line:human gastric cancer MGC-803 cells
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Concentration:5 μg/mL, 10 μg/mL, 20 μg/mL
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Incubation Time:48 h
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Result:Increased the percentage of cells in S-phase from 30.51% (control) to 44.72%, and increased the percentage of cells in G2/M phase from 18.36% (control) to 26.71% at 5 μg/mL.
Caused a dose-dependent increase in G2/M phase cells to 60.53%, with a corresponding decrease in S-phase cells to 8.92% at 10 μg/mL.
Reduced the percentage of G2/M phase cells to 30.60%, with S-phase cells at 23.90% at 20 μg/mL.
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Cell Line:human gastric cancer MGC-803 cells
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Concentration:5 μg/mL, 10 μg/mL, 20 μg/mL
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Incubation Time:48 h
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Result:Reduced survivin mRNA expression to ~85% of control at 5 μg/mL.
Reduced survivin mRNA expression to ~40% of control (P < 0.05) at 10 μg/mL.
Reduced survivin mRNA expression to ~15% of control (P < 0.05) at 20 μg/mL.
Decreased expression in a dose-dependent manner.
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Cell Line:wild-type Vibrio vulnificus MO6-24/O cells
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Concentration:0.2, 0.5, 1, 2 and 5 μM.
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Incubation Time:grown to OD600 1.8-2.0
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Result:Reduced rtxA1 transcript levels by more than 30-fold compared to the DMSO control at 5 μM.
Caused concentration-dependent reductions in the transcript levels of rtxA1 and vvhA at 0.2, 0.5, 1, and 2 μM.
Left hlyU transcript levels unchanged at 0.2, 0.5, 1, and 2 μM.
Caused no significant change in hns gene expression at 0.2, 0.5, 1, and 2 μM.
In Vivo
2',4-Dihydroxychalcone (6.25-12.5 mg/kg; i.p.; repeated dosing schedule) significantly inhibits cholangiocarcinoma xenograft tumor growth with minimal organ toxicity[2].
2',4-Dihydroxychalcone (15 mg/kg; injection; single dose) provides ~50% protection to Galleria mellonella larvae against Vibrio vulnificus infection[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (6-week-old male, specific pathogen-free, DSS-induced acute ulcerative colitis)[1]
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Dosage:10 mg/kg; 30 mg/kg
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Administration:i.g.; daily; 10 days
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Result:Significantly mitigated body weight loss (30 mg/kg group showed greater preservation) and reduced disease activity index (DAI) scores compared to DSS model group.
Preserved colon length, alleviated colon mucosal ulceration, crypt loss, and epithelial damage, and reduced histological scores.
Inhibited NLRP3 inflammasome activation in colon tissue, as shown by reduced NLRP3, cleaved caspase-1, cleaved Gasdermin D, IL-1β, and IL-6 levels.
Increased mRNA and protein levels of tight junction proteins occludin and ZO-1, restoring gut barrier integrity.
Showed no abnormal lesions in major organs (heart, liver, spleen, lung, kidney), indicating no organ toxicity.
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Animal Model:BALB/c nude (female, 4 weeks old, specific pathogen-free housing)[2]
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Dosage:6.25 mg/kg; 12.5 mg/kg
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Administration:i.p.; repeated dosing schedule
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Result:Significantly reduced tumor weight and volume compared to the control group.
Produced a more pronounced reduction in tumor weight and volume at 12.5 mg/kg than at 6.25 mg/kg.
Markedly decreased Ki-67 and ERO1A expression in tumor tissues, with greater reduction in the 12.5 mg/kg group than the 6.25 mg/kg group.
Showed no histopathological changes in liver and kidney tissues, indicating minimal toxicity.
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Animal Model:wax-worm larvae (130 mg)[6]
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Dosage:15 mg/kg
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Administration:injection; single dose
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Result:Increased larval survival to ~50% by 30 hours post-infection, compared to 10% in the untreated infected group.
Improved health index based on motility, cocoon formation, melanization, and survival.
Chemical Information
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CAS No. 13323-66-5
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Appearance Solid
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Molecular Weight 240.25
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Formula C15H12O3
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Color Light yellow to yellow
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SMILES
O=C(C1=CC=CC=C1O)/C=C/C2=CC=C(O)C=C2
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (416.23 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
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 (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
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 (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- 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.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL (10.41 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 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.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: 2.5 mg/mL (10.41 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 2.5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
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).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
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.
Protocols
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Flow cytometric DNA-content cell-cycle staining
Flow cytometric DNA-content cell-cycle staining measures the fluorescence intensity of DNA-bound fluorochromes in single cells or nuclei to estimate DNA content distributions, allowing assignment of populations to G0/G1, S, and G2/M phases by DNA histogram deconvolution. Propidium iodide (PI) intercalates into DNA, and PI fluorescence is proportional to cellular DNA content when staining is performed under conditions that make DNA accessible and minimize non-DNA signal. Cells with G2/M DNA content are expected to show approximately twice the fluorescence intensity of G0/G1 cells, while S-phase cells occupy intermediate fluorescence values. PI-based DNA-content analysis can also detect cells with fractional DNA content, often reported as sub-G1, when DNA fragmentation and extraction during staining reduce retained DNA signal in apoptotic cells. DAPI is an alternative DNA fluorochrome for univariate DNA-content analysis, while bivariate approaches combining DNA content with proliferation
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
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Transepithelial/transendothelial electrical resistance assay
TEER measures electrical resistance across epithelial or endothelial monolayers cultured on permeable supports, and the readout reflects ionic conductance through the cell barrier, especially the paracellular pathway regulated by junctional integrity. TEER can be measured without destroying the monolayer and is commonly used before or during transport, permeability, barrier-disruption, and barrier-maturation experiments. TEER values are influenced by biological maturation and technical conditions; reported factors include temperature, medium formulation, passage number, electrode geometry, membrane properties, and junctional length during early monolayer maturation. Therefore, TEER should be interpreted with blank-insert subtraction, area normalization, repeated readings, and, when possible, orthogonal barrier readouts such as FITC-dextran flux or tight-junction staining.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
Purity & Documentation
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Data Sheet (302 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
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Handling Instructions (2659 KB)
References
[1]. Zhang G, et al. 2',4'-dihydroxychalcone alleviates inflammatory bowel disease by inhibiting NLRP3 inflammasome and modulating gut microbiota. Frontiers in immunology. 2026;17:1751218. [Content Brief]
[2]. Wang T, et al. 2',4'-dihydroxychalcone induces ferroptosis through ERO1A/GPX4 regulatory axis in cholangiocarcinoma. Phytomedicine : international journal of phytotherapy and phytopharmacology. 2025 Nov;147:157192. [Content Brief]
[3]. Seo YH, et al. In Vitro Antifungal Activity and Mode of Action of 2',4'-Dihydroxychalcone against Aspergillus fumigatus. Mycobiology. 2015 Jun;43(2):150-6. [Content Brief]
[4]. Passalacqua TG, et al. The 2',4'-dihydroxychalcone could be explored to develop new inhibitors against the glycerol-3-phosphate dehydrogenase from Leishmania species. Bioorganic & medicinal chemistry letters. 2015 Sep 01;25(17):3564-8. [Content Brief]
[5]. Lou C, et al. 2',4'-Dihydroxychalcone-induced apoptosis of human gastric cancer MGC-803 cells via down-regulation of survivin mRNA. Toxicology in vitro : an international journal published in association with BIBRA. 2010 Aug;24(5):1333-7. [Content Brief]
[6].
Imdad S, et al. Identification of 2',4'-Dihydroxychalcone as an Antivirulence Agent Targeting HlyU, a Master Virulence Regulator in Vibrio vulnificus. Molecules. 2018 Jun 20;23(6):1492.
[Content Brief]
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 (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 4.1623 mL | 20.8117 mL | 41.6233 mL | 104.0583 mL |
| 5 mM | 0.8325 mL | 4.1623 mL | 8.3247 mL | 20.8117 mL | |
| 10 mM | 0.4162 mL | 2.0812 mL | 4.1623 mL | 10.4058 mL | |
| 15 mM | 0.2775 mL | 1.3874 mL | 2.7749 mL | 6.9372 mL | |
| 20 mM | 0.2081 mL | 1.0406 mL | 2.0812 mL | 5.2029 mL | |
| 25 mM | 0.1665 mL | 0.8325 mL | 1.6649 mL | 4.1623 mL | |
| 30 mM | 0.1387 mL | 0.6937 mL | 1.3874 mL | 3.4686 mL | |
| 40 mM | 0.1041 mL | 0.5203 mL | 1.0406 mL | 2.6015 mL | |
| 50 mM | 0.0832 mL | 0.4162 mL | 0.8325 mL | 2.0812 mL | |
| 60 mM | 0.0694 mL | 0.3469 mL | 0.6937 mL | 1.7343 mL | |
| 80 mM | 0.0520 mL | 0.2601 mL | 0.5203 mL | 1.3007 mL | |
| 100 mM | 0.0416 mL | 0.2081 mL | 0.4162 mL | 1.0406 mL |
2',4-Dihydroxychalcone Related Classifications
HY-141462 Related Classifications
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