76666-32-5

Basic information

• Product Name: 3-HYDROXY-3'-METHOXYFLAVONE
• Synonyms: 3-HYDROXY-3'-METHOXYFLAVONE
• CAS NO: 76666-32-5
• Molecular Formula: C₁₆H₁₂O₄
• Molecular Weight: 268.26
• Product Categories: Di-substituted Flavones
• Mol File: 76666-32-5.mol
• Article Data: 11

Chemical Properties

• Melting Point: 130-131°C
• Appearance: /
• CAS DataBase Reference: 3-HYDROXY-3'-METHOXYFLAVONE(CAS DataBase Reference)
• NIST Chemistry Reference: 3-HYDROXY-3'-METHOXYFLAVONE(76666-32-5)
• EPA Substance Registry System: 3-HYDROXY-3'-METHOXYFLAVONE(76666-32-5)

Safety Data

• Hazardous Substances Data: 76666-32-5(Hazardous Substances Data)

Usage

Uses

3''-Methoxyflavonol, is a selective agonist of neuromedin U 2 receptor (NMU2R).

Upstream product

• 34000-28-7 2'-hydroxy-3-methoxy-chalcone 
• 118-93-4 o-hydroxyacetophenone 
• 591-31-1 3-methoxy-benzaldehyde 
• 67765-54-2 2,3-dihydro-2-(3-methoxyphenyl)-4H-1-benzopyran-4-one 
• 7146-86-3 3-methoxy-2'-hydroxychalcone 

Downstream Products

• 69799-39-9 3-β-D-glucopyranosyloxy-2-(3-methoxy-phenyl)-chromen-4-one 
• 119621-52-2 2-(3-methoxy-phenyl)-3-(tetra-O-acetyl-β-D-glucopyranosyloxy)-chromen-4-one 
• 55977-09-8 3'-hydroxyflavonol 
• 53906-83-5 3'-methoxyflavone 

Relevant articles and documents

Synthesis, inverse docking-assisted identification and in vitro biological characterization of Flavonol-based analogs of fisetin as c-Kit, CDK2 and mTOR inhibitors against melanoma and non-melanoma skin cancers

Due to hurdles, including resistance, adverse effects, and poor bioavailability, among others linked with existing therapies, there is an urgent unmet need to devise new, safe, and more effective treatment modalities for skin cancers. Herein, a series of flavonol-based derivatives of fisetin, a plant-based flavonoid identified as an anti-tumorigenic agent targeting the mammalian targets of rapamycin (mTOR)-regulated pathways, were synthesized and fully characterized. New potential inhibitors of receptor tyrosine kinases (c-KITs), cyclin-dependent kinase-2 (CDK2), and mTOR, representing attractive therapeutic targets for melanoma and non-melanoma skin cancers (NMSCs) treatment, were identified using inverse-docking, in vitro kinase activity and various cell-based anticancer screening assays. Eleven compounds exhibited significant inhibitory activities greater than the parent molecule against four human skin cancer cell lines, including melanoma (A375 and SK-Mel-28) and NMSCs (A431 and UWBCC1), with IC50 values ranging from 0.12 to 15 μM. Seven compounds were identified as potentially potent single, dual or multi-kinase c-KITs, CDK2, and mTOR kinase inhibitors after inverse-docking and screening against twelve known cancer targets, followed by kinase activity profiling. Moreover, the potent compound F20, and the multi-kinase F9 and F17 targeted compounds, markedly decreased scratch wound closure, colony formation, and heightened expression levels of key cancer-promoting pathway molecular targets c-Kit, CDK2, and mTOR. In addition, these compounds downregulated Bcl-2 levels and upregulated Bax and cleaved caspase-3/7/8 and PARP levels, thus inducing apoptosis of A375 and A431 cells in a dose-dependent manner. Overall, compounds F20, F9 and F17, were identified as promising c-Kit, CDK2 and mTOR inhibitors, worthy of further investigation as therapeutics, or as adjuvants to standard therapies for the control of melanoma and NMSCs.

Discovery of a Prenylated Flavonol Derivative as a Pin1 Inhibitor to Suppress Hepatocellular Carcinoma by Modulating MicroRNA Biogenesis

Peptidyl-prolyl cis-trans isomerase Pin1 plays a crucial role in the development of human cancers. Recently, we have disclosed that Pin1 regulates the biogenesis of miRNA, which is aberrantly expressed in HCC and promotes HCC progression, indicating the therapeutic role of Pin1 in HCC therapy. Here, 7-(benzyloxy)-3,5-dihydroxy-2-(4-methoxyphenyl)-8-(3-methylbut-2-en-1-yl)-4H-chromen-4-one (AF-39) was identified as a novel Pin1 inhibitor. Biochemical tests indicate that AF-39 potently inhibits Pin1 activity with an IC50 values of 1.008 μm, and also displays high selectivity for Pin1 among peptidyl prolyl isomerases. Furthermore, AF-39 significantly suppresses cell proliferation of HCC cells in a dose- and time-dependent manner. Mechanistically, AF-39 regulates the subcellular distribution of XPO5 and increases miRNAs biogenesis in HCC cells. This work provides a promising lead compound for HCC treatment, highlighting the therapeutic potential of miRNA-based therapy against human cancer.

Profiling of flavonol derivatives for the development of antitrypanosomatidic drugs

Flavonoids represent a potential source of new antitrypanosomatidic leads. Starting from a library of natural products, we combined target-based screening on pteridine reductase 1 with phenotypic screening on Trypanosoma brucei for hit identification. Flavonols were identified as hits, and a library of 16 derivatives was synthesized. Twelve compounds showed EC50 values against T. brucei below 10 μM. Four X-ray crystal structures and docking studies explained the observed structure-activity relationships. Compound 2 (3,6-dihydroxy-2-(3-hydroxyphenyl)-4H-chromen-4-one) was selected for pharmacokinetic studies. Encapsulation of compound 2 in PLGA nanoparticles or cyclodextrins resulted in lower in vitro toxicity when compared to the free compound. Combination studies with methotrexate revealed that compound 13 (3-hydroxy-6-methoxy-2-(4-methoxyphenyl)-4H-chromen-4-one) has the highest synergistic effect at concentration of 1.3 μM, 11.7-fold dose reduction index and no toxicity toward host cells. Our results provide the basis for further chemical modifications aimed at identifying novel antitrypanosomatidic agents showing higher potency toward PTR1 and increased metabolic stability.