Product Details
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1131-62-0 Name |
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Name |
3,4-Dimethoxyacetophenone |
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Synonym |
Dimethoxyacetophenone;3,4-Dimethoxyacetoph;3,4-DIMETHOXYACETOPHENONE FOR SYNTHESIS;3,4-Dimethoxyacetophenone≥ 99% (GC);3',4'-DIMETHOXYACETOPHENONE;3,4-DIMETHOXYACETOPHENONE;3,4-dimethoxyacetophenone (acetoveratrone);3',4'-Dimethoxyacetophenone 1-(3,4-Dimethoxyphenyl)ethan-1-one 3,4-Dimethoxyacetophenone |
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1131-62-0 Chemical & Physical Properties |
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Melting point |
47-54 °C(lit.) |
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Boiling point |
287.0±0.0 °C at 760 mmHg |
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Density |
1.1±0.1 g/cm3 |
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Molecular Formula |
C10H12O3 |
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Molecular Weight |
180.201 |
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Flash Point |
113.4±8.2 °C |
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PSA |
35.53000 |
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LogP |
1.82 |
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Exact Mass |
180.078644 |
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Vapour Pressure |
0.0±0.6 mmHg at 25°C |
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Index of Refraction |
1.499 |
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Water Solubility |
SOLUBLE IN HOT WATER |
3,4-Dimethoxyacetophenone is a chemical compound that has been studied in various scholarly articles for its potential applications. One of its primary uses is as an intermediate in the synthesis of pharmaceuticals and agrochemicals. It can be used as a starting material for the synthesis of various compounds, including analgesics, antipyretics, and anti-inflammatory agents. Additionally, 3,4-Dimethoxyacetophenone has been investigated for its potential biological activities, such as antimicrobial and antifungal properties. It has also been studied as a potential agent for the treatment of cancer, as it has been found to induce apoptosis in cancer cells. However, further research is needed to fully explore and understand the extent of its applications and potential benefits in these areas.
Dysregulated HGF/c-Met signalling has been associated with many human cancers, poor clinical outcomes, and even resistance acquisition to some approved targeted therapies. As such, c-Met kinase has emerged as an attractive target for anticancer drug discovery. Herein, a series of 6,7-disubstitued-4-(2-fluorophenoxy)quinoline derivatives bearing α-acyloxycarboxamide moiety were designed, synthesized via Passerini reaction as the key step, and evaluated for their in vitro biological activities against c-Met kinase and five selected cancer cell lines. The preliminary structure-activity relationship demonstrated that α-acyloxycarboxamide as the 5-atom linker maintained the potent antitumor potency. Among these compounds, compound 25s (c-Met IC50 = 4.06 nmol/L) was identified as the most promising lead compound and displayed the most potent antiproliferative activities against A549, HT-29 and MDA-MB-231 cell lines with IC50 of 0.39, 0.20, and 0.58 μmol/L, which were 1.3-, 1.4- and 1.2-fold superior to foretinib, respectively. The further studies indicated that compound 25s can induce apoptosis of A549 cells and arrest efficiently the cell cycle distribution in G2/M phase of A549 cells. Moreover, compound 25s can also inhibit c-Met phosphorylation in A549 cells by a dose-dependent manner. Collectively, these results indicated that compound 25s could be a potential anticancer lead compound deserving for further development.
Contrary to previous reports, the reaction mechanism of chlorine dioxide (OClOC·) with benzyl alcohols involves both radical cation and benzyl radical mechanisms dependent on pH. The primary reaction product between OClOC· and 1-(3,4-dimethoxy-phenyl) ethanol at pH 8 is 3,4-dimethoxyacetophenone. At pH 4 no acetophenone was observed; the majority of the degradation products were chlorinated and aromatic ring-oxidized compounds. A primary kinetic isotope effect (kH/kD = 2.05) was observed in the reaction of OClOC· with 1-(3,4-dimethoxy-phenyl)-(1-2H) ethanol at pH 8, but was absent at pH 4 (kH/kD ≈ 1). Similarly, the corresponding methyl ether (4-(1-methoxy)ethyl-1,2-dimethoxybenzene) was substantially less reactive at pH > 6. On the basis of these results, competing pH-dependent reaction mechanisms have been proposed, where at high pH OClOC· reacts with benzyl alcohols via a OClOC·-benzyl alcohol complex.
The c-Met kinase has emerged as a promising target for the development of small molecule antitumor agents because of its close relationship with the progression of many human cancers, poor clinical outcomes and even drug resistance. In this study, two novel series of 6,7-disubstitued-4-(2-fluorophenoxy)quinoline derivatives containing α-acyloxycarboxamide or α-acylaminoamide scaffolds were designed, synthesized, and evaluated for their in vitro biological activities against c-Met kinase and four cancer cell lines (H460, HT-29, MKN-45, and MDA-MB-231). Most of the target compounds exhibited moderate to significant potency and possessed selectivity for H460 and HT-29 cancer cell lines. The preliminary structure-activity relationships indicated that α-acyloxycarboxamide or α-acylaminoamide as 5-atom linker contributed to the antitumor potency. Among these compounds, compound 10m (c-Met IC50 = 2.43 nM, a multitarget tyrosine kinase inhibitor) exhibited the most potent inhibitory activities against H460, HT-29 and MDA-MB-231 cell lines with IC50 of 0.14 ± 0.03 μM, 0.20 ± 0.02 μM and 0.42 ± 0.03 μM, which were 1.7-, 1.3- and 1.6-fold more active than foretinib, respectively. In addition, concentration-dependent assay and time-dependent assay indicated compound 10m can inhibit the proliferation of H460 cell in a time and concentration dependent manner. Moreover, docking studies revealed the common mode of interaction with the c-Met binding site, suggesting that 10m is a potential candidate for cancer therapy deserving further study.
Herein, a catalytic reductive fractionation of lignocellulose is presented using a heterogeneous cobalt catalyst and formic acid or formate as a hydrogen donor. The catalytic reductive fractionation of untreated birch wood yields monophenolic compounds in up to 34 wt % yield of total lignin, which corresponds to 76 % of the theoretical maximum yield. Model compound studies revealed that the main role of the cobalt catalyst is to stabilize the reactive intermediates formed during the organosolv pulping by transfer hydrogenation and hydrogenolysis reactions. Additionally, the cobalt catalyst is responsible for depolymerization reactions of lignin fragments through transfer hydrogenolysis reactions, which target the β-O-4′ bond. The catalyst could be recycled three times with only negligible decrease in efficiency, showing the robustness of the system.
Laccase, a blue copper oxidase, in view of its moderate redox potential can oxidise only phenolic compounds by electron-transfer. However, in the presence of ABTS (2,2'-azinobis(3-ethylbenzthiazoline-6-sulfonate) as a redox mediator, laccase reacts with the more difficult to oxidise non-phenolic substrates, such as benzyl alcohols. The role of ABTS in these mediated oxidations is investigated. Redox interaction with laccase could produce in situ two reactive intermediates from ABTS, namely ABTS++ or ABTS ?+. These species have been independently generated by oxidation with Ce(IV) or Co(III) salts, respectively, and their efficiency as monoelectronic oxidants tested in a kinetic study towards a series of non-phenolic substrates; a Marcus treatment is provided in the case of ABTS ++. On these grounds, intervention of ABTS++ as a reactive intermediate in laccase-ABTS oxidations appears unlikely, because the experimental conditions under which ABTS++ is unambiguously generated, and survives long enough to serve as a diffusible mediator, are too harsh (2 M H2SO4 solution) and incompatible with the operation of the enzyme. Likewise, ABTS?+ seems an intermediate of limited importance in laccase-ABTS oxidations, because this weaker monoelectronic oxidant is unable to react directly with many of the non-phenolic substrates that laccase-ABTS can oxidise. To solve this paradox, it is alternatively suggested that degradation by-products of either ABTS ++ or ABTS?+ are formed in situ by hydrolysis during the laccase-ABTS reactions, and may be responsible for the observed oxidation of non-phenolics. The Royal Society of Chemistry 2005.
The liquid phase of acetylation of 1,2-dimethoxybenzene with acetic anhydride has been investigated over a series of acid nickel-mesoporous materials (Ni-MCM-41) synthesized by the microwave irradiation method with different Si/Ni ratios (Si/Ni = 80, 50, 10) and characterized by several spectroscopic techniques such as: N2 physical adsorption, ICP, XRD, TEM, FT-IR, and a temperature programmed desorption (TPD) of pyridine. In fact, the catalyst Ni-MCM-41 (10) showed better performance in the acid-catalyzed acetylation of 1,2-dimethoxybenzene employing acetic anhydride as an acylating agent. Furthermore, the kinetics of the acetylation of 1,2-dimethoxybenzene over these catalysts have also been investigated.
From the microbiological reduction of ethyl 3-oxo-3-(3,4-dimethoxyphenyl)-propionate, (+)-(3R)-ethyl 3-hydroxy-3-(3,4-dimethoxyphenyl)propionate was prepared on a quantitative scale. The absolute configuration was assigned by X-ray structural determination of the crystallized camphanate derivative.
We examined the inhibitory effects of curcumin and tetrahydrocurcumin (THC), one of the major metabolites of curcumin, on the lipid peroxidation of erythrocyte membrane ghosts induced by tert-butylhydroperoxide. The results demonstrated that THC showed a greater inhibitory effect than curcumin. To investigate the mechanism of antioxidative activity, we examined the effects of several inhibitors, such as antioxidant enzymes, hydroxyl radical scavengers, 1O2 quencher, and chelating agents for metal ions. Given that all inhibitors failed to inhibit membrane peroxidation, THC must scavenge radicals such as tert-butoxyl radical and peroxyl radical. To clarify the antioxidative mechanism of THC, in particular the role of the β-diketone moiety, dimethylated THC was incubated with peroxyl radicals generated by thermolysis of 2,2'-azobis(2,4-dimethylvaleronitrile). Four oxidation products were detected, three of which were identified as 3,4-dimethoxybenzoic acid, 3',4'-dimethoxyacetophenone, and 3-(3,4-dimethoxyphenyl)-propionic acid. The fourth oxidation product seems to be an unstable intermediate, and its detailed structure has not been determined. These results suggest that the β-diketone moiety of THC must exhibit antioxidative activity by cleavage of the C-C bond at the active methylene carbon between two carbonyls in the β-diketone moiety. Because THC is one of the major metabolites of curcumin, it may also exhibit the same physiological and pharmacological properties as the active form of curcumin in vivo by means of the β-diketone moiety as well as phenolic hydroxy groups.
Herein, we report a new protocol for the dehydrogenative oxidation of aryl methanols using the cheap and commercially available catalyst CuSeO3·2H2O. Oxygen-bridged [Cu-O-Se] bimetallic catalysts are not only less expensive than other catalysts used for the dehydrogenative oxidation of aryl alcohols, but they are also effective under mild conditions and at low concentrations. The title reaction proceeds with a variety of aromatic and heteroaromatic methanol examples, obtaining the corresponding carbonyls in high yields. This is the first example using an oxygen-bridged copper-based bimetallic catalyst [Cu-O-Se] for dehydrogenative benzylic oxidation. Computational DFT studies reveal simultaneous H-transfer and Cu-O bond breaking, with a transition-state barrier height of 29.3 kcal mol?1
1-(3,4-dimethoxyphenyl)ethanol
2-methoxy-1,4-benzoquinone
4,5-dimethoxy-1,2-benzoquinone
![2-(1-Hydroxy-ethyl)-5-methoxy-[1,4]benzoquinone](/upload/2023/1\758f4fcf-3a08-4791-9989-f3446fdb596a.png)
2-(1-Hydroxy-ethyl)-5-methoxy-[1,4]benzoquinone
(2-methyl-6-oxo-6H-pyran-3-ylidene)acetic acid methyl ester
1-(3,4-dimethoxyphenyl)ethanone
| Conditions | Yield |
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With chlorine dioxide; sodium sulfate; In water; at 20 - 40 ℃; Thermodynamic data; Mechanism; Kinetics; E(excit.); var. of pH, ionic strength; reaction in presence of chloride;
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1-(3,4-dimethoxyphenyl)-2-(methoxyphenoxy)propane-1,3-diol
2-methoxyphenoxy-3',4'-dimethoxyacetophenone
ethyl 3,4-dimethoxyphenyl ketone
2-(2-methoxyphenoxy)ethanol
3,4-dimethoxy-benzaldehyde
2-methoxy-phenol
1-(3,4-dimethoxyphenyl)ethanone
| Conditions | Yield |
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With 1-hydroxytetraphenylcyclopentadienyl(tetraphenyl-2,4-cyclopentadien-1-one)-μ-hydrotetracarbonyldiruthenium(II); In 1,3,5-trimethyl-benzene; at 140 ℃; for 20h; Reagent/catalyst; Temperature; Inert atmosphere;
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14.3 %Chromat. 6.1 %Chromat. 7.2 %Chromat. 25 %Chromat. 20.8 %Chromat. 27.7 %Chromat. |
Ketene
1,2-dimethoxybenzene
4-isopropenyl-1,2-dimethoxybenzene
2-(3,4-dimethoxyphenyl)propanoic acid
(3,4-dimethoxy-phenyl)-thioacetic acid methylamide
N-<3,4-dimethoxyphenyl(thioacetyl)>morpholine
isonicotinic acid-[1-(3,4-dimethoxy-phenyl)-ethylidenehydrazide]
(E)-1-(3,4-dimethoxyphenyl)-3-(3,4-methylenedioxyphenyl)-prop-2-en-1-one
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