AcacetinCAS# 480-44-4 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 480-44-4 | SDF | Download SDF |
PubChem ID | 5280442 | Appearance | Yellow-ochre powder |
Formula | C16H12O5 | M.Wt | 284.3 |
Type of Compound | Flavonoids | Storage | Desiccate at -20°C |
Synonyms | Apigenin 4'-methyl ether; Buddleoflavonol; 5,7-Dihydroxy 4'-methoxyflavone; Linarigenin; 4'-Methylapigenin | ||
Solubility | DMSO : ≥ 37 mg/mL (130.16 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | 5,7-dihydroxy-2-(4-methoxyphenyl)chromen-4-one | ||
SMILES | COC1=CC=C(C=C1)C2=CC(=O)C3=C(C=C(C=C3O2)O)O | ||
Standard InChIKey | DANYIYRPLHHOCZ-UHFFFAOYSA-N | ||
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 | Acacetin is an atrium-selective agent that prolongs the atrial effective refractory period without prolonging the corrected QT interval and effectively prevents atrial fibrillation (AF) in anesthetized dogs after intraduodenal administration. Acacetin has anti-cancer, anti-mutagenic, spasmolytic and antinociceptive, anti-inflammatory and anti-peroxidative effects. |
Targets | NF-kB | IkB | Akt | Bcl-2/Bax | COX | PI3K | VEGFR | STAT | NOS | MMP(e.g.TIMP) | Calcium Channel | p38MAPK | JNK | IL Receptor | Potassium Channel | EGFR | IKK |
In vitro | Acacetin inhibits in vitro and in vivo angiogenesis and downregulates Stat signaling and VEGF expression.[Pubmed: 23943785]Cancer Prev Res (Phila). 2013 Oct;6(10):1128-39.Angiogenesis is an effective target in cancer control. The antiangiogenic efficacy and associated mechanisms of Acacetin, a plant flavone, are poorly known. Acacetin inhibits expression of matrix metalloproteinases via a MAPK-dependent mechanism in fibroblast-like synoviocytes.[Pubmed: 25856795]J Cell Mol Med. 2015 Aug;19(8):1910-5.It is well known that rheumatoid arthritis (RA) is an autoimmune joint disease in which fibroblast-like synoviocytes (FLSs) play a pivotal role. Acacetin, a natural flavone, selectively inhibits human atrial repolarization potassium currents and prevents atrial fibrillation in dogs.[Pubmed: 18458165 ]Circulation. 2008 May 13;117(19):2449-57.
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In vivo | Acacetin inhibits glutamate release and prevents kainic acid-induced neurotoxicity in rats.[Pubmed: 24520409]PLoS One. 2014 Feb 10;9(2):e88644.An excessive release of glutamate is considered to be a molecular mechanism associated with several neurological diseases that causes neuronal damage. Therefore, searching for compounds that reduce glutamate neurotoxicity is necessary. |
Kinase Assay | Acacetin suppressed LPS-induced up-expression of iNOS and COX-2 in murine macrophages and TPA-induced tumor promotion in mice.[Pubmed: 16949556 ]The P110 subunit of PI3-K is a therapeutic target of acacetin in skin cancer.[Pubmed: 23913940]Acacetin (5,7-dihydroxy-4'-methoxyflavone) exhibits in vitro and in vivo anticancer activity through the suppression of NF-κB/Akt signaling in prostate cancer cells.[Pubmed: 24285354]Int J Mol Med. 2014 Feb;33(2):317-24.Acacetin (5,7-dihydroxy-4'-methoxyflavone) is a flavonoid compound with antimutagenic, antiplasmodial, antiperoxidant, anti-inflammatory and anticancer effects. However, the molecular targets and pathways underlying the anticancer effects of Acacetin are yet to be elucidated. Carcinogenesis. 2014 Jan;35(1):123-30.The identification of primary molecular targets of cancer-preventive phytochemicals is essential for a comprehensive understanding of their mechanism of action. Biochem Pharmacol. 2006 Nov 15;72(10):1293-303.Acacetin (5,7-dihydroxy-4'-methoxyflavone), a flavonoid compound, has anti-peroxidative and anti-inflammatory effects. |
Animal Research | Dietary acacetin reduces airway hyperresponsiveness and eosinophil infiltration by modulating eotaxin-1 and th2 cytokines in a mouse model of asthma.[Pubmed: 23049614]Spasmolytic and antinociceptive activities of ursolic acid and acacetin identified in Agastache mexicana.[Pubmed: 22473340 ]Planta Med. 2012 May;78(8):793-6.Agastache mexicana is a plant in high demand that has long been used in Mexican folk medicine to treat anxiety, insomnia, and stomachache, among other afflictions. Ursolic acid and Acacetin were isolated and identified as two possible active compounds of A. mexicana aerial parts. Evid Based Complement Alternat Med. 2012;2012:910520.A previous study found that eosinophil infiltration and Th2 cell recruitment are important causes of chronic lung inflammation in asthma. The plant flavonoid Acacetin is known to have an anti-inflammatory effect in vitro. This study aims to investigate the anti-inflammatory effect of orally administered Acacetin in ovalbumin- (OVA-) sensitized asthmatic mice and its underlying molecular mechanism. |
Acacetin Dilution Calculator
Acacetin Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.5174 mL | 17.5871 mL | 35.1741 mL | 70.3482 mL | 87.9353 mL |
5 mM | 0.7035 mL | 3.5174 mL | 7.0348 mL | 14.0696 mL | 17.5871 mL |
10 mM | 0.3517 mL | 1.7587 mL | 3.5174 mL | 7.0348 mL | 8.7935 mL |
50 mM | 0.0703 mL | 0.3517 mL | 0.7035 mL | 1.407 mL | 1.7587 mL |
100 mM | 0.0352 mL | 0.1759 mL | 0.3517 mL | 0.7035 mL | 0.8794 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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Spasmolytic and antinociceptive activities of ursolic acid and acacetin identified in Agastache mexicana.[Pubmed:22473340]
Planta Med. 2012 May;78(8):793-6.
Agastache mexicana is a plant in high demand that has long been used in Mexican folk medicine to treat anxiety, insomnia, and stomachache, among other afflictions. Ursolic acid and Acacetin were isolated and identified as two possible active compounds of A. mexicana aerial parts. An antinociceptive response was demonstrated in a significant and dose-dependent manner with ursolic acid and Acacetin (i. p. and p. o.) in comparison to the analgesic diclofenac by using the writhing test in mice. Moreover, Acacetin also produced a significant concentration-dependent spasmolytic response with major efficacy compared to ursolic acid and papaverine by using rings from the isolated guinea pig ileum. These results provide evidence of the presence of two active constituents of Agastache mexicana reinforcing its utility as a therapy for visceral pain as used in traditional medicine.
Acacetin (5,7-dihydroxy-4'-methoxyflavone) exhibits in vitro and in vivo anticancer activity through the suppression of NF-kappaB/Akt signaling in prostate cancer cells.[Pubmed:24285354]
Int J Mol Med. 2014 Feb;33(2):317-24.
Acacetin (5,7-dihydroxy-4'-methoxyflavone) is a flavonoid compound with antimutagenic, antiplasmodial, antiperoxidant, anti-inflammatory and anticancer effects. However, the molecular targets and pathways underlying the anticancer effects of Acacetin are yet to be elucidated. In this study, we investigated whether Acacetin induces apoptosis in the human prostate cancer cell line, DU145. The results of 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays revealed that cell viability decreased in a dose- and time-dependent manner in response to Acacetin. 4',6-Diamidino-2-phenylindole (DAPI) staining revealed that chromatin condensation significantly increased in a dose-dependent manner. Flow cytometric analysis indicated that Acacetin suppressed the viability of DU145 cells by inducing apoptosis. Western blot anlaysis of various markers of signaling pathways revealed that Acacetin targets the Akt and nuclear factor (NF)-kappaB signaling pathways by inhibiting the phosphorylation of IkappaBalpha and NF-kappaB in a dose-dependent manner. Consistent with its ability to induce apoptosis, the Acacetin-mediated inhibition of the pro-survival pathway, Akt, and of the NF-kappaB pathway was accompanied by a marked reduction in the levels of the NF-kappaBregulated anti-apoptotic proteins, Bcl-2 and X-linked inhibitor of apoptosis protein (XIAP), as well as of the proliferative protein, cyclooxygenase (COX)-2. We further evaluated the effects of Acacetin on prostate cancer using mice subcutaneously injected with DU145 prostate cancer cells. The Acacetin-treated nude mice bearing DU145 tumor xenografts exhibited significantly reduced tumor size and weight, due to the effects of Acacetin on cancer cell apoptosis, as determined by terminal deoxyribonucleotide transferase-mediated dUTP nick end-labeling (TUNEL) assay. Our findings suggest that Acacetin exerts antitumor effects by targeting the Akt/NF-kappaB signaling pathway. Rurther investigations on this flavonoid are warranted to evaluate its potential use in the prevention and therapy of prostate cancer.
Acacetin inhibits glutamate release and prevents kainic acid-induced neurotoxicity in rats.[Pubmed:24520409]
PLoS One. 2014 Feb 10;9(2):e88644.
An excessive release of glutamate is considered to be a molecular mechanism associated with several neurological diseases that causes neuronal damage. Therefore, searching for compounds that reduce glutamate neurotoxicity is necessary. In this study, the possibility that the natural flavone Acacetin derived from the traditional Chinese medicine Clerodendrum inerme (L.) Gaertn is a neuroprotective agent was investigated. The effect of Acacetin on endogenous glutamate release in rat hippocampal nerve terminals (synaptosomes) was also investigated. The results indicated that Acacetin inhibited depolarization-evoked glutamate release and cytosolic free Ca(2+) concentration ([Ca(2+)]C) in the hippocampal nerve terminals. However, Acacetin did not alter synaptosomal membrane potential. Furthermore, the inhibitory effect of Acacetin on evoked glutamate release was prevented by the Cav2.2 (N-type) and Cav2.1 (P/Q-type) channel blocker known as omega-conotoxin MVIIC. In a kainic acid (KA) rat model, an animal model used for excitotoxic neurodegeneration experiments, Acacetin (10 or 50 mg/kg) was administrated intraperitoneally to the rats 30 min before the KA (15 mg/kg) intraperitoneal injection, and subsequently induced the attenuation of KA-induced neuronal cell death and microglia activation in the CA3 region of the hippocampus. The present study demonstrates that the natural compound, Acacetin, inhibits glutamate release from hippocampal synaptosomes by attenuating voltage-dependent Ca(2+) entry and effectively prevents KA-induced in vivo excitotoxicity. Collectively, these data suggest that Acacetin has the therapeutic potential for treating neurological diseases associated with excitotoxicity.
Acacetin suppressed LPS-induced up-expression of iNOS and COX-2 in murine macrophages and TPA-induced tumor promotion in mice.[Pubmed:16949556]
Biochem Pharmacol. 2006 Nov 15;72(10):1293-303.
Acacetin (5,7-dihydroxy-4'-methoxyflavone), a flavonoid compound, has anti-peroxidative and anti-inflammatory effects. In this study, we investigated the inhibitory effects of Acacetin and a related compound, wogonin, on the induction of NO synthase (NOS) and COX-2 in RAW 264.7 cells activated with lipopolysaccharide (LPS). Acacetin markedly and actively inhibited the transcriptional activation of iNOS and COX-2. Western blotting, reverse transcription-polymerase chain reaction (PCR), and real-time PCR analyses demonstrated that Acacetin significantly blocked protein and mRNA expression of iNOS and COX-2 in LPS-inducted macrophages. Treatment with Acacetin reduced translocation of nuclear factor-kappa B (NF kappa B) subunit and the dependent transcriptional activity of NF kappa B. The activation of NF kappa B was inhibited by prevention of the degradation of inhibitor kappa B (I kappa B). Furthermore, Acacetin inhibited LPS-induced phosphorylation as well as degradation of I kappa B alpha. We further investigated the roles of tyrosine kinase, phosphatidylinositiol 3-kinase (PI3K)/Akt and mitogen-activated protein kinase (MAPK) in LPS-induced macrophages. We found that Acacetin also inhibited LPS-induced activation of PI3K/Akt and p44/42, but not p38 MAPK. After initiation of 7,12-dimethlybene[a]anthracene (DMBA), applying acacentin topically before each 12-O-tetradecanoylphorbol 13-acetat (TPA) treatment was found to reduce the number of papillomas at 20 weeks. Taken together, these results show that Acacetin down regulates inflammatory iNOS and COX-2 gene expression in macrophages by inhibiting the activation of NF kappa B by interfering with the activation PI3K/Akt/IKK and MAPK, suggesting that Acacetin is a functionally novel agent capable of preventing inflammation-associated tumorigenesis.
Acacetin inhibits in vitro and in vivo angiogenesis and downregulates Stat signaling and VEGF expression.[Pubmed:23943785]
Cancer Prev Res (Phila). 2013 Oct;6(10):1128-39.
Angiogenesis is an effective target in cancer control. The antiangiogenic efficacy and associated mechanisms of Acacetin, a plant flavone, are poorly known. In the present study, Acacetin inhibited growth and survival (up to 92%; P < 0.001), and capillary-like tube formation on Matrigel (up to 98%; P < 0.001) by human umbilical vein endothelial cells (HUVEC) in regular condition, as well as VEGF-induced and tumor cells conditioned medium-stimulated growth conditions. It caused retraction and disintegration of preformed capillary networks (up to 91%; P < 0.001). HUVEC migration and invasion were suppressed by 68% to 100% (P < 0.001). Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC. It also suppressed nuclear localization of pStat-3 (Tyr705). Acacetin strongly inhibited capillary sprouting and networking from rat aortic rings and fertilized chicken egg chorioallantoic membrane (CAM; approximately 71%; P < 0.001). Furthermore, it suppressed angiogenesis in Matrigel plugs implanted in Swiss albino mice. Acacetin also inhibited tyrosine phosphorylation of Stat-1 and -3, and expression of VEGF in cancer cells. Overall, Acacetin inhibits Stat signaling and suppresses angiogenesis in vitro, ex vivo, and in vivo, and therefore, it could be a potential agent to inhibit tumor angiogenesis and growth.
The P110 subunit of PI3-K is a therapeutic target of acacetin in skin cancer.[Pubmed:23913940]
Carcinogenesis. 2014 Jan;35(1):123-30.
The identification of primary molecular targets of cancer-preventive phytochemicals is essential for a comprehensive understanding of their mechanism of action. In the present study, we investigated the chemopreventive effects and molecular targets of Acacetin, a flavonoid found in Robinia p seudoacacia, also known as black locust. Acacetin treatment significantly suppressed epidermal growth factor (EGF)-induced cell transformation. Immunoblot analysis revealed that Acacetin attenuated EGF-induced phosphorylation of Akt and p70(S6K), which are downstream effectors of phosphatidylinositol 3-kinase (PI3-K). An immunoprecipitation kinase assay of PI3-K and pull-down assay results demonstrated that Acacetin substantially inhibits PI3-K activity by direct physical binding. Acacetin exhibited stronger inhibitory effects against anchorage-dependent and -independent cell growth in cells expressing higher PI3-K activity compared with those exhibiting relatively low PI3-K activity. Binding assay data combined with computational modeling suggest that Acacetin binds in an adenosine triphosphate (ATP)-competitive manner with the p110alpha subunit of PI3-K and interacts with Val828, Glu826, Asp911, Trp760, Ile777, Ile825, Tyr813, Ile910 and Met900 residues. Acacetin was also found to significantly reduce SK-MEL-28 tumor growth and Akt phosphorylation in vivo. Taken together, these results indicate that Acacetin is an ATP-competitive PI3-K inhibitor and a promising agent for melanoma chemoprevention.
Acacetin, a natural flavone, selectively inhibits human atrial repolarization potassium currents and prevents atrial fibrillation in dogs.[Pubmed:18458165]
Circulation. 2008 May 13;117(19):2449-57.
BACKGROUND: The development of atrium-selective antiarrhythmic agents is a current strategy for inhibiting atrial fibrillation (AF). The present study investigated whether the natural flavone Acacetin from the traditional Chinese medicine Xuelianhua would be an atrium-selective anti-AF agent. METHODS AND RESULTS: The effects of Acacetin on human atrial ultrarapid delayed rectifier K(+) current (I(Kur)) and other cardiac ionic currents were studied with a whole-cell patch technique. Acacetin suppressed I(Kur) and the transient outward K(+) current (IC(50) 3.2 and 9.2 mumol/L, respectively) and prolonged action potential duration in human atrial myocytes. The compound blocked the acetylcholine-activated K(+) current; however, it had no effect on the Na(+) current, L-type Ca(2+) current, or inward-rectifier K(+) current in guinea pig cardiac myocytes. Although Acacetin caused a weak reduction in the hERG and hKCNQ1/hKCNE1 channels stably expressed in HEK 293 cells, it did not prolong the corrected QT interval in rabbit hearts. In anesthetized dogs, Acacetin (5 mg/kg) prolonged the atrial effective refractory period in both the right and left atria 1 to 4 hours after intraduodenal administration without prolongation of the corrected QT interval, whereas sotalol at 5 mg/kg prolonged both the atrial effective refractory period and the corrected QT interval. Acacetin prevented AF induction at doses of 2.5 mg/kg (50%), 5 mg/kg (85.7%), and 10 mg/kg (85.7%). Sotalol 5 mg/kg also prevented AF induction (60%). CONCLUSIONS: The present study demonstrates that the natural compound Acacetin is an atrium-selective agent that prolongs the atrial effective refractory period without prolonging the corrected QT interval and effectively prevents AF in anesthetized dogs after intraduodenal administration. These results indicate that oral Acacetin is a promising atrium-selective agent for the treatment of AF.
Dietary acacetin reduces airway hyperresponsiveness and eosinophil infiltration by modulating eotaxin-1 and th2 cytokines in a mouse model of asthma.[Pubmed:23049614]
Evid Based Complement Alternat Med. 2012;2012:910520.
A previous study found that eosinophil infiltration and Th2 cell recruitment are important causes of chronic lung inflammation in asthma. The plant flavonoid Acacetin is known to have an anti-inflammatory effect in vitro. This study aims to investigate the anti-inflammatory effect of orally administered Acacetin in ovalbumin- (OVA-) sensitized asthmatic mice and its underlying molecular mechanism. BALB/c mice were sensitized by intraperitoneal OVA injection. OVA-sensitized mice were fed Acacetin from days 21 to 27. Acacetin treatment attenuated airway hyperresponsiveness and reduced eosinophil infiltration and goblet cell hyperplasia in lung tissue. Additionally, eotaxin-1- and Th2-associated cytokines were inhibited in bronchoalveolar lavage fluid and suppressed the level of OVA-IgE in serum. Human bronchial epithelial (BEAS-2B) cells were used to examine the effect of Acacetin on proinflammatory cytokines, chemokines, and cell adhesion molecule production in vitro. At the molecular level, Acacetin significantly reduced IL-6, IL-8, intercellular adhesion molecule-1, and eotaxin-1 in activated BEAS-2B cells. Acacetin also significantly suppressed the ability of eosinophils to adhere to inflammatory BEAS-2B cells. These results suggest that dietary Acacetin may improve asthma symptoms in OVA-sensitized mice.
Acacetin inhibits expression of matrix metalloproteinases via a MAPK-dependent mechanism in fibroblast-like synoviocytes.[Pubmed:25856795]
J Cell Mol Med. 2015 Aug;19(8):1910-5.
It is well known that rheumatoid arthritis (RA) is an autoimmune joint disease in which fibroblast-like synoviocytes (FLSs) play a pivotal role. In this study, we investigated the anti-arthritic properties of Acacetin in FLSs. The expression of matrix metalloproteinase (MMP)-1, MMP-3 and MMP-13 were investigated by quantitative RT-PCR and western blot at gene and protein levels. At the same time, the phosphorylation of mitogen-activated protein kinases (MAPK) was investigated. The DNA-binding activity of NF-kappaB was investigated by electrophoretic mobility shift assay. We found that Acacetin inhibits p38 and JNK phosphorylation and reduces MMP-1, MMP-3 and MMP-13 expression in interleukin-1beta-induced FLSs. Our results suggest that Acacetin has antiarthritic effects in FLSs. Thus, Acacetin should be further studied for the treatment of arthritis.