3',4',7,8-TetrahydroxyflavoneCAS# 3440-24-2 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 3440-24-2 | SDF | Download SDF |
PubChem ID | 688798 | Appearance | Powder |
Formula | C15H10O6 | M.Wt | 286.2 |
Type of Compound | Flavonoids | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
Chemical Name | 2-(3,4-dihydroxyphenyl)-7,8-dihydroxychromen-4-one | ||
SMILES | C1=CC(=C(C=C1C2=CC(=O)C3=C(O2)C(=C(C=C3)O)O)O)O | ||
Standard InChIKey | ARYCMKPCDNHQCL-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C15H10O6/c16-9-3-1-7(5-12(9)19)13-6-11(18)8-2-4-10(17)14(20)15(8)21-13/h1-6,16-17,19-20H | ||
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. |
Description | 1. 2. 3',4',7,8-Tetrahydroxyflavone exhibits antibacterial activity against S. mutans. |
3',4',7,8-Tetrahydroxyflavone Dilution Calculator
3',4',7,8-Tetrahydroxyflavone Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.4941 mL | 17.4703 mL | 34.9406 mL | 69.8812 mL | 87.3515 mL |
5 mM | 0.6988 mL | 3.4941 mL | 6.9881 mL | 13.9762 mL | 17.4703 mL |
10 mM | 0.3494 mL | 1.747 mL | 3.4941 mL | 6.9881 mL | 8.7352 mL |
50 mM | 0.0699 mL | 0.3494 mL | 0.6988 mL | 1.3976 mL | 1.747 mL |
100 mM | 0.0349 mL | 0.1747 mL | 0.3494 mL | 0.6988 mL | 0.8735 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. |
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
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
- Ergocristine
Catalog No.:BCN0144
CAS No.:511-08-0
- cis-Aconitic acid
Catalog No.:BCN0143
CAS No.:585-84-2
- alpha-Bisabolol
Catalog No.:BCN0142
CAS No.:23089-26-1
- 7-Hydroxyflavonol
Catalog No.:BCN0141
CAS No.:492-00-2
- (+/-)-2-Methyl-1-butanol
Catalog No.:BCN0140
CAS No.:137-32-6
- Syringetin 3-O-galactoside
Catalog No.:BCN0139
CAS No.:55025-56-4
- Cynatratoside E
Catalog No.:BCN0138
CAS No.:
- Bidenoside C
Catalog No.:BCN0137
CAS No.:700877-55-0
- 5,7-Dihydroxy-3',4',5'-trimethoxyflavanone
Catalog No.:BCN0136
CAS No.:62252-10-2
- Protocetraric acid
Catalog No.:BCN0135
CAS No.:489-51-0
- Castalin
Catalog No.:BCN0134
CAS No.:19086-75-0
- 3',4',7,8-Tetramethoxyflavone
Catalog No.:BCN0133
CAS No.:65548-55-2
- Daphnin
Catalog No.:BCN0146
CAS No.:486-55-5
- 2',6'-Dihydroxy 4',4-dimethoxydihydrochalcone
Catalog No.:BCN0147
CAS No.:35241-54-4
- 2'-Hydroxyflavanone
Catalog No.:BCN0148
CAS No.:17348-76-4
- 3',4',7-Trihydroxyisoflavone
Catalog No.:BCN0149
CAS No.:485-63-2
- Maritimein
Catalog No.:BCN0150
CAS No.:490-54-0
- Candicine
Catalog No.:BCN0151
CAS No.:6656-13-9
- Comanthosid B
Catalog No.:BCN0153
CAS No.:70938-60-2
- Helenien
Catalog No.:BCN0154
CAS No.:547-17-1
- N-trans-caffeoyltyramine
Catalog No.:BCN0155
CAS No.:103188-48-3
- Lappaol B
Catalog No.:BCN0156
CAS No.:62359-60-8
- 2-Hydroxy-3-methoxybenzaldehyde
Catalog No.:BCN0157
CAS No.:148-53-8
- (E)-N-(2-Amino-4-fluorophenyl)-3-(1-cinnamyl-1H-pyrazol-4-yl)acrylamide
Catalog No.:BCN0158
CAS No.:1396841-57-8
3',4',7,8-Tetrahydroxyflavone inhibits RANKL-induced osteoclast formation and bone resorption.[Pubmed:29442051]
Pharmazie. 2017 Mar 1;72(3):161-166.
Osteoclasts, which are specialized bone multinuclear cells, are responsible for bone lytic diseases such as osteoporosis. 3',4',7,8-tetrahydroxyflavone is a flavonoid from Acacia confusa. In the present study, we found that 3',4',7,8-tetrahydroxyflavone markedly inhibited receptor activator of nuclear factor kappa B ligand (RANKL)-induced osteoclastic differentiation from mouse bone marrow-derived macrophages (BMMs). 3',4',7,8-tetrahydroxyflavone also reduced the mRNA expression levels of osteoclastic marker genes including the calcitonin receptor (CTR) and cathepsin K. In addition, 3',4',7,8-tetrahydroxyflavone decreased the bone resorption activity of osteoclasts on dentin slices. We found that 3',4',7,8-tetrahydroxyflavone inhibited RANKL-induced expression of c-Fos and nuclear factor of activated T cells c1 (NFATc1), a key transcription factor of osteoclast differentiation. Furthermore, ectopic overexpression of a constitutively active form of NFATc1 completely rescued the anti-osteoclastogenic effect of 3',4',7,8-tetrahydroxyflavone, suggesting that the anti-osteoclastogenic effect was mainly attributed to the reduction in NFATc1 expression. Taken together, our data suggest that 3',4',7,8-tetrahydroxyflavone inhibits osteoclast differentiation and bone loss and may therefore be considered a promising drug candidate for treating or preventing bone-lytic diseases.
Antiproliferative plant and synthetic polyphenolics are specific inhibitors of vertebrate inositol-1,4,5-trisphosphate 3-kinases and inositol polyphosphate multikinase.[Pubmed:15659385]
J Biol Chem. 2005 Apr 8;280(14):13229-40.
Inositol-1,4,5-trisphosphate 3-kinases (IP3K) A, B, and C as well as inositol polyphosphate multikinase (IPMK) catalyze the first step in the formation of the higher phosphorylated inositols InsP5 and InsP6 by metabolizing Ins(1,4,5)P3 to Ins(1,3,4,5)P4. In order to clarify the special role of these InsP3 phosphorylating enzymes and of subsequent anabolic inositol phosphate reactions, a search was conducted for potent enzyme inhibitors starting with a fully active IP3K-A catalytic domain. Seven polyphenolic compounds could be identified as potent inhibitors with IC50 < 200 nM (IC50 given): ellagic acid (36 nM), gossypol (58 nM), (-)-epicatechin-3-gallate (94 nM), (-)-epigallocatechin-3-gallate (EGCG, 120 nM), aurintricarboxylic acid (ATA, 150 nM), hypericin (170 nM), and quercetin (180 nM). All inhibitors displayed a mixed-type inhibition with respect to ATP and a non-competitive inhibition with respect to Ins(1,4,5)P3. Examination of these inhibitors toward IP3K-A, -B, and -C and IPMK from mammals revealed that ATA potently inhibits all kinases while the other inhibitors do not markedly affect IPMK but differentially inhibit IP3K isoforms. We identified chlorogenic acid as a specific IPMK inhibitor whereas the flavonoids myricetin, 3',4',7,8-tetrahydroxyflavone and EGCG inhibit preferentially IP3K-A and IP3K-C. Mutagenesis studies revealed that both the calmodulin binding and the ATP [corrected] binding domain in IP3K are involved in inhibitor binding. Their absence in IPMK and the presence of a unique insertion in IPMK were found to be important for selectivity differences from IP3K. The fact that all identified IP3K and IPMK inhibitors have been reported as antiproliferative agents and that IP3Ks or IPMK often are the best binding targets deserves further investigation concerning their antitumor potential.