160096-59-3

Basic information

• Product Name: VERATRYLCURCUMINOID
• Synonyms: VERATRYLCURCUMINOID;Dimethoxycurcumin;(1E,4Z,6E)-1,7-bis(3,4-dimethoxyphenyl)-5-hydroxyhepta-1,4,6-trien-3-one;Dimethoxycurcumin(DiMC);Dimethoxycurcumin(DMC)
• CAS NO: 160096-59-3
• Molecular Formula: C₂₃H₂₄O₆
• Molecular Weight: 396.43306
• Mol File: 160096-59-3.mol
• Article Data: 15

Chemical Properties

• Boiling Point: 587.007°C at 760 mmHg
• Flash Point: 254.399°C
• Appearance: /
• Density: 1.169g/cm³
• Vapor Pressure: 0mmHg at 25°C
• Refractive Index: 1.585
• CAS DataBase Reference: VERATRYLCURCUMINOID(CAS DataBase Reference)
• NIST Chemistry Reference: VERATRYLCURCUMINOID(160096-59-3)
• EPA Substance Registry System: VERATRYLCURCUMINOID(160096-59-3)

Safety Data

• Hazardous Substances Data: 160096-59-3(Hazardous Substances Data)

Usage

Uses

Used in Pharmaceutical Industry:
VERATRYLCURCUMINOID is used as an anti-inflammatory agent for its ability to inhibit mitogen-induced proliferation of CD4+ T cells, CD8+ T cells, and B cells, as well as the secretion of various cytokines such as IL-2, IL-4, IL-6, and IFN-γ in isolated human lymphocytes.
VERATRYLCURCUMINOID is also used as an antioxidant agent for its ability to inhibit LPS-induced nitric oxide (NO) production and expression of inducible nitric oxide synthase (iNOS) in RAW 264.7 cells, as well as to inhibit hemolysis of isolated human red blood cells (RBCs) induced by AAPH.
Used in Cancer Treatment:
VERATRYLCURCUMINOID is used as an anticancer agent for its effectiveness at suppressing HCT116 tumor cells, which is more potent than its parent compound, curcumin. It may have potential applications in the development of novel drug delivery systems to enhance its bioavailability and therapeutic outcomes in cancer treatment.

InChI:InChI=1/C23H24O6/c1-26-20-11-7-16(13-22(20)28-3)5-9-18(24)15-19(25)10-6-17-8-12-21(27-2)23(14-17)29-4/h5-14H,15H2,1-4H3/b9-5+,10-6+

Upstream product

• 120-14-9 3,4-dimethoxy-benzaldehyde 
• 111-30-8 Glutaraldehyde 
• 123-54-6 acetylacetone 
• 15001-27-1 O-methyldehydrozingerone 
• 39856-08-1 (E)-3,4-dimethoxycinnamic chloride 
• 458-37-7 curcumin 
• 74-88-4 methyl iodide 
• 77-78-1 dimethyl sulfate 

Downstream Products

• 52328-97-9 (1E,6E)-1,7-bis(3,4-dimethoxyphenyl)-4,4-dimethylhepta-1,6-diene-3,5-dione 
• 1226895-15-3 FLLL₃₂ 
• 1118765-36-8 (2E,6E)-ethyl-7-(3,4-dimethoxyphenyl)-4-((E)-3-(3,4-dimethoxyphenyl)acryloyl)-5-oxohepta-2,6-dienoate 
• 478919-25-4 (E,E)-3,5-bis(3,4-dimethoxystyryl)-1H-pyrazole 
• 1118765-46-0 (E,E)-3,5-bis(3,4-dimethoxystyryl)isoxazole 
• 1118765-35-7 (2E,6E)-methyl-7-(3,4-dimethoxyphenyl)-4-((E)-(3,4-dimethoxyphenyl)acryloyl)-5-oxohepta-2,6-dienoate 
• 1118765-37-9 (2E,6E)-7-(3,4-dimethoxyphenyl)-4-((E)-3-(3,4-dimethoxyphenyl)acryloyl)-5-oxohepta-2,6-dienamide 
• 52328-98-0 O,O-dimethyl-curcumin 
• 55094-78-5 di-O-methyltetrahydrocurcumin 

Relevant articles and documents

Curcumin-Cu(II) Ensemble-Based Fluorescence "turn-On" Mode Sensing the Plant Defensive Hormone Salicylic Acid in Situ and in Vivo

Salicylic acid (SA), a crucial, plant-derived signal molecule, is capable of launching global transcriptional reprogramming to assist plants in obtaining the systemic acquired resistance (SAR) mechanism. Thus, the accurate detection of SA will not only si

A PERSONAL CARE COMPOSITION

Disclosed is a personal care composition and a method of providing antiperspirant and anti-inflammation using certain curcuminoid derivatives. The composition comprises: (i) a compound of the Formula 1 Ar-CHnCHn-X.C(R)2-X.CHnCHn-Ar (Formula 1) wherein Ar is a substituted or unsubstituted phenyl group; R is H or CH3; X is CH(OH) group or C=O group; n has the value 1 or 2; and, (ii) a topically acceptable base comprising at least 0.1% of a fragrance wherein, when n=1, the compound of (Formula 1) is 1E,6E)-1,7-bis(3,4- dimethoxyphenyl)-4,4-dimethylhepta-1,6-diene-3,5-dione (Formula 2), and when n=2, the compound of (Formula 1) is 1,7-bis(4-hydroxy-3- methoxyphenyl) heptane-3,5-diol (Formula 4) or is 1,7-bis (3,4-dimethoxyphenyl)-4,4-dimethylheptane-3,5-diol (Formula 5).

A dimethoxy curcumin polymer micelle and its preparation method and medical use

The invention relates to a dimethoxycurcumin polymer micelle and a preparation method, an injection or oral administration system for the polymer micelle, and medical application of the polymer micelle. The drug-loaded micelle employs an amphiphilic segmented copolymer as a carrier material and forms a typical core-shell structure in an aqueous solution through self-assembly; and the structure has uniform particle size distribution,solubility and thermodynamic stability of dimethoxycurcumin in an aqueous medium are substantially improved, leakage, degradation and metabolism of dimethoxycurcumin in the body are effectively reduced, and long circulation and tumor tissue passive targeting are realized, so drug effect and security are improved. According to specific needs of clinical indications, freeze-dried powder or preparations of other dosage forms can be prepared from the drug-loaded micelle provided by the invention for injection or oral administration of the micelle; and the micelle is used for resisting tumors, oxidation, inflammation, bacteria and aging, realizing immunoloregulation, reducing blood fat, resisting atherosclerosis and senile dementia, etc., and is especially applicable to combination with tumor radiotherapeutics and chemotherapeutics to exert sensitivity-enhancing, efficiency-improving and toxicity-attenuating effects.

Structure activity relationship study of curcumin analogues toward the amyloid-beta aggregation inhibitor

Inhibition of the amyloid β aggregation process could possibly prevent the onset of Alzheimer's disease. In this article, we report a structure-activity relationship study of curcumin analogues for anti amyloid β aggregation activity. Compound 7, the ideal amyloid β aggregation inhibitor in vitro among synthesized curcumin analogues, has not only potent anti amyloid β aggregation effects, but also water solubility more than 160 times that of curcumin. In addition, new approaches to improve water solubility of curcumin-type compounds are proposed.

Synthesis and evaluation of curcumin derivatives toward an inhibitor of beta-site amyloid precursor protein cleaving enzyme 1

To research a new non-peptidyl inhibitor of beta-site amyloid precursor protein cleaving enzyme 1, we focused on the curcumin framework, two phenolic groups combined with an sp2 carbon spacer for low-molecular and high lipophilicity. The structure-activity relationship study of curcumin derivatives is described. Our results indicate that phenolic hydroxy groups and an alkenyl spacer are important structural factors for the inhibition of beta-site amyloid precursor protein cleaving enzyme 1 and, furthermore, non-competitive inhibition of enzyme activity is anticipated from an inhibitory kinetics experiment and docking simulation.

Autoxidative and cyclooxygenase-2 catalyzed transformation of the dietary chemopreventive agent curcumin

The efficacy of the diphenol curcumin as a cancer chemopreventive agent is limited by its chemical and metabolic instability. Non-enzymatic degradation has been described to yield vanillin, ferulic acid, and feruloylmethane through cleavage of the heptadienone chain connecting the phenolic rings. Here we provide evidence for an alternative mechanism, resulting in autoxidative cyclization of the heptadienone moiety as a major pathway of degradation. Autoxidative transformation of curcumin was pH-dependent with the highest rate at pH 8 (2.2 μM/min) and associated with stoichiometric uptake of O 2. Oxidation was also catalyzed by recombinant cyclooxygenase-2 (COX-2) (50 nM; 7.5 μM/min), and the rate was increased ≈10-fold by the addition of 300 μM H2O2. The COX-2 catalyzed transformation was inhibited by acetaminophen but not indomethacin, suggesting catalysis occurred by the peroxidase activity. We propose a mechanism of enzymatic or autoxidative hydrogen abstraction from a phenolic hydroxyl to give a quinone methide and a delocalized radical in the heptadienone chain that undergoes 5-exo cyclization and oxygenation. Hydration of the quinone methide (measured by the incorporation of O-18 from H218O) and rearrangement under loss of water gives the final dioxygenated bicyclopentadione product. When curcumin was added to RAW264.7 cells, the bicyclopentadione was increased 1.8-fold in cells activated by LPS; vanillin and other putative cleavage products were negligible. Oxidation to a reactive quinone methide is the mechanistic basis of many phenolic anti-cancer drugs. It is possible, therefore, that oxidative transformation of curcumin, a prominent but previously unrecognized reaction, contributes to its cancer chemopreventive activity.

Synthesis and identification of new 4-arylidene curcumin analogues as potential anticancer agents targeting nuclear factor-κB signaling pathway

A series of curcumin analogues including new 4-arylidene curcumin analogues (4-arylidene-1,7-bisarylhepta-1,6-diene-3,5-diones) were synthesized. Cell growth inhibition assays revealed that most 4-arylidene curcumin analogues can effectively decrease the growth of a panel of lung cancer cells at submicromolar and low micromolar concentrations. High content analysis technology coupled with biochemical studies showed that this new class of 4-arylidene curcumin analogues exhibits significantly improved NF-κB inhibition activity over the parent compound curcumin, at least in part by inhibiting IκB phosphorylation and degradation via IKK blockage; selected 4-arylidene curcumin analogues also reduced the tumorigenic potential of cancer cells in a clonogenic assay.

CURCUMIN ANALOGS AS DUAL JAK2/STAT3 INHIBITORS AND METHODS OF MAKING AND USING THE SAME

Curcumin analogues and methods of making and using the same are disclosed.

Isoxazole analogs of curcuminoids with highly potent multidrug-resistant antimycobacterial activity

Curcumin (1), demethoxycurcumin (2) and bisdemethoxycurcumin (3), the curcuminoid constituents of the medicinal plant Curcuma longa L., have been structurally modified to 55 analogs and antimycobacterial activity against Mycobacterium tuberculosis has been evaluated. Among the highly active curcuminoids, the isoxazole analogs are the most active group, with mono-O-methylcurcumin isoxazole (53) being the most active compound (MIC 0.09 μg/mL). It was 1131-fold more active than curcumin (1), the parent compound, and was approximately 18 and 2-fold more active than the standard drugs kanamycin and isoniazid, respectively. Compound 53 also exhibited high activity against the multidrug-resistant M. tuberculosis clinical isolates, with the MICs of 0.195-3.125 μg/mL. The structural requirements for a curcuminoid analog to exhibit antimycobacterial activity are the presence of an isoxazole ring and two unsaturated bonds on the heptyl chain. The presence of a suitable para-alkoxyl group on the aromatic ring which is attached in close proximity to the nitrogen function of the isoxazole ring and a free para-hydroxyl group on another aromatic ring enhances the biological activity.

Curcuminoid analogs with potent activity against Trypanosoma and Leishmania species

The natural curcuminoids curcumin (1), demethoxycurcumin (2) and bisdemethoxycurcumin (3) have been chemically modified to give 46 analogs and 8 pairs of 1:1 mixture of curcuminoid analogs and these parent curcuminoids and their analogs were assessed against protozoa of the Trypanosoma and Leishmania species. The parent curcuminoids exhibited low antitrypanosomal activity (EC50 for our drug-sensitive Trypanosoma brucei brucei line (WT) of compounds 1, 2 and 3 are 2.5, 4.6 and 7.7 μM, respectively). Among 43 curcuminoid analogs and 8 pairs of 1:1 mixture of curcuminoid analogs tested, 8 pure analogs and 5 isomeric mixtures of analogs exhibited high antitrypanosomal activity in submicromolar order of magnitude. Among these highly active analogs, 1,7-bis(4-hydroxy-3-methoxyphenyl)hept-4-en-3-one (40) was the most active compound, with an EC50 value of 0.053 ± 0.007 μM; it was about 2-fold more active than the standard veterinary drug diminazene aceturate (EC50 0.12 ± 0.01 μM). Using a previously characterized diminazene-resistant T. b. brucei (TbAT1-KO) and a derived multi-drug resistant line (B48), no cross-resistance of curcuminoids was observed to the diamidine and melaminophenyl arsenical drugs that are the current treatments. Indeed, curcuminoids carrying a conjugated keto (enone) motif, including 40, were significantly more active against T. b. brucei B48. This enone motif was found to contribute to particularly high trypanocidal activity against all Trypanosoma species and strains tested. The parent curcuminoids showed low antileishmanial activity (EC50 values of compounds 1 and 2 for Leishmania mexicana amastigotes are 16 ± 3 and 37 ± 6 μM, respectively) while the control drug, pentamidine, displayed an EC50 of 16 ± 2 μM. Among the active curcuminoid analogs, four compounds exhibited EC50 values of less than 5 μM against Leishmania major promastigotes and four against L. mexicana amastigotes. No significant difference in sensitivity to curcuminoids between L. major promastigotes and L. mexicana amastigotes was observed. The parent curcuminoids and most of their analogs were also tested for their toxicity against human embryonic kidney (HEK) cells. All the curcuminoids exhibited lower toxicity to HEK cells than to T. b. brucei bloodstream forms and only one of the tested compounds showed significantly higher activity against HEK cells than curcumin (1). The selectivity index for T. b. brucei ranged from 3-fold to 1500-fold. The selectivity index for the most active analog, the enone 40, was 453-fold.