989-51-5

Basic information

• Product Name: (-)-Epigallocatechin gallate
• Synonyms: TEA CATECHIN;(2R,3R)-2-(3,4,5-TRIHYDROXYPHENYL)-3,4-DIHYDRO-1(2H)-BENZOPYRAN-3,5,7-TRIOL 3-(3,4,5-TRIHYDROXYBENZOATE);3,4-DIHYDRO-5,7-DIHYDROXY-2R-(3,4,5-TRIHYDROXYPHENYL)-2H-1-BENZOPYRAN-3R-YL-3,4,5-TRIHYDROXY-BENZOATE;(-)-CIS-3,3',4',5,5',7-HEXAHYDROXY-FLAVANE-3-GALLATE;(-)-CIS-2-(3,4,5-TRIHYDROXYPHENYL)-3,4-DIHYDRO-1(2H)-BENZOPYRAN-3,5,7-TRIOL 3-GALLATE;(-)-CIS-3,4-DIHYDRO-5,7-DIHYDROXY-2-(3,4,5-TRIHYDROXYPHENYL)-1(2H)-BENZOPYRAN-3-YL GALLATE HYDRATE;(-)-EPIGALLOCATECHIN GALLATE;EPIGALLOCATECHIN GALLATE
• CAS NO: 989-51-5
• Molecular Formula: C₂₂H₁₈O₁₁
• Molecular Weight: 458.37
• EINECS: 479-560-7
• Product Categories: Pharmaceutical Raw Materials;Catechins & Tannins;All Inhibitors;Antioxidant;Biochemistry;Flavonoids;Standard extract;Natural Plant Extract;Inhibitors;Amyloid beta-peptide and related;Aromatics;Heterocycles;ProteasomeInhibitors;Plant extracts;Herb extract;Inhibitor;chemical reagent;pharmaceutical intermediate;phytochemical;reference standards from Chinese medicinal herbs (TCM).;standardized herbal extract
• Mol File: 989-51-5.mol
• Article Data: 35

Chemical Properties

• Melting Point: 222-224°C
• Boiling Point: 909.1 °C at 760 mmHg
• Flash Point: 320 °C
• Appearance: Solid
• Density: 1.9 g/cm³
• Vapor Pressure: 3.71E-35mmHg at 25°C
• Refractive Index: -175.5 ° (C=1, EtOH)
• Storage Temp.: 2-8°C
• Solubility: H2O: ≥5mg/mL, clear
• PKA: 7.75±0.25(Predicted)
• Water Solubility: Soluble in ethanol, dimethyl formamide, water.
• Stability: Stable, but may be light sensitive. Incompatible with strong oxidizing agents.
• Merck: 14,3526
• CAS DataBase Reference: (-)-Epigallocatechin gallate(CAS DataBase Reference)
• NIST Chemistry Reference: (-)-Epigallocatechin gallate(989-51-5)
• EPA Substance Registry System: (-)-Epigallocatechin gallate(989-51-5)

Safety Data

• Safety Statements: 24/25
• WGK Germany: 2
• RTECS: KB5200000
• F: 10-23
• Hazardous Substances Data: 989-51-5(Hazardous Substances Data)

Usage

Uses

Different sources of media describe the Uses of 989-51-5 differently. You can refer to the following data:
1. (-)-Epigallocatechin Gallate is a tumor-inhibiting constituent of green tea. (-)-Epigallocatechin Gallate alters the cleavage of amyloid precursor protein, decreasing production of amaloid-? and amaloid plaques in mice. This compound has neuroprotective properties.
2. telomerase inhibitor
3. An inhibitor of Bcl-2 and NOS2
4. (-)-Epigallocatechin Gallate is a tumor-inhibiting constituent of green tea. (-)-Epigallocatechin Gallate alters the cleavage of amyloid precursor protein, decreasing production of amaloid-β and amaloid plaques in mice. This compound has neuroprotective properties.
5. A tumor-inhibiting constituent of green tea. Alters the cleavage of amyloid precursor protein, decreasing production of amaloid- and amaloid plaques in mice

Chemical Properties

solid

General Description

Pharmaceutical secondary standards for application in quality control, provide pharma laboratories and manufacturers with a convenient and cost-effective alternative to the preparation of in-house working standards.Epigallocatechin gallate is a potent polyphenolic flavonoid which is found as a component of tea. It exhibits antioxidant, antimutagenic, antitumor and anti-inflammatory properties, thereby contributing to the health-beneficial actions. It finds potential use as a drug candidate in the pharmaceutical, cosmetic, and nutritional fields.

Hazard

Moderately toxic by ingestion.

Biological Activity

(-)-epigallocatechin gallate (egcg), the major catechin accounting for 59% of the total catechins in green tea, is a powerful antioxidant as well as an antiangiogenic and antitumor agent. egcg has been studied for its role in the chemoprevention of a wild range of cancers, including liver, stomach, skin, lung, mammary gland and colon cancers. study results show that egcg is able to induce apoptosis, promote cell growth arrest and block carcinogenesis by affecting signal transduction pathways. moreover, egcg exhibits inhibition against a variety of viruses, including hcv, hiv-1, hbv, hsv-1, hsv-2, ebv, adenovirus, influenza virus and enterovirus, as well as several enzymes, including dnmts, proteases and dhfr.singh bn, shankar s, srivastava rk. green tea catechin, epigallocatechin-3-gallate (egcg): mechanisms, perspectives and clinical applications. biochem pharmacol. 2011; 82(12):1807-1821.steinmann j, buer j, pietschmann t, steinmann e. anti-infective properties of epigallocatechin-3-gallate (egcg), a component of green tea. br j pharmacol. 2013; 168(5):1059-1073

Biochem/physiol Actions

(-)-Epigallocatechin gallate (EGCG), an antioxidant polyphenol flavonoid exerts anti-tumor properties by inhibiting telomerase and DNA methyltransferase activity. EGCG inhibits the expression of matrix metalloproteinase-2 (MMP-2), MMP-9 and reduces the invasiveness. EGCG blocks the activation of epidermal growth factor (EGF) receptors and human epidermal growth factor receptor-2 (HER-2). EGCG increases bone mineral density and reduces bone resorption. EGCG inhibits osteoclastogenesis by inhibiting receptor activator of nuclear factor κ-B ligand (RANKL) induced nuclear factor κ B (NF-κB) transcriptional activity. EGCG reduces skeletal muscle atrophy. EGCG has anti-aging property and increases myogenic differentiation. EGCG inhibits fatty acid synthase and glutamate dehydrogenase activity.

Anticancer Research

Different sources of media describe the Anticancer Research of 989-51-5 differently. You can refer to the following data:
1. EGCG and EGC are the active polyphenol compounds found in green tea, found toinhibit p-glycoprotein transport activities in Chinese hamster ovary (p-gp+) cells.EGCG facilitates the retraction of MDR phenotype by reducing cellular drug effluxwhen given in combination with vinblastine or doxorubicin. Hesperetin, quercetin,daidzein, silymarin, naringenin, and resveratrol also inhibit the MRP1, MRP4, andMRP5 (Kawasaki et al. 2008). Curcumin increases the cellular accumulation ofanticancer agents like cisplatin, tamoxifen, daunorubicin, vincristine, anddoxorubicin and thereby effectively sensitizes the drug-resistant cancer cells. Areduction in MDR1B expression in L1210/Adr cells (mouse leukemic MDR cells)by curcumin is mediated by PI3K, Akt, and NF-κB pathways. It also inhibits theABCG2 transporter activity. In addition curcumin facilitates the accumulation ofmitoxantrone and doxorubicin in ABCG2-expressing HEK cells and hence reversesMDR (Kawasaki et al. 2008; Dandawate et al. 2013).
2. EGCG is an ester of gallic acid and epigallocatechin and is a catechin compound(Murakami et al. 1996). It is found most abundantly in green tea. It can be used to treat brain, prostate, cervical, and bladder cancers (Wang et al. 2012). It suppressesthe ornithine decarboxylase action, an enzyme that leads to rapid proliferation andfurthermore circumvents apoptosis (Singh et al. 2016a). It suppresses nuclear factor(NF-κB) activation and expression of Bcl-2 (B-cell lymphoma 2) as well as COX-2(cyclooxygenase-2) in prostate cancer cells and causes induction of apoptosis. Ithamper the matrix metallopeptidase-9 (MMP-9) activation in bladder and lungcancer cells and suppresses the synthesis of VGEF (vascular endothelial growthfactor) in head and neck cancers. It prevents ERK (extracellular signal-regulatedkinase) phosphorylation and MMP-2 and MMP-9 activation and suppresses ERK,c-Jun N-terminal kinase (JNK), and MMP-9 expressions in gastric carcinoma cells(Singh et al. 2016a). It is binding and inhibits the antiapoptotic protein Bcl-xL,interferes with EGFR (epidermal growth factor receptor) signaling, and inhibitshepatocyte growth factor-induced cell proliferation and MAPK (mitogen-activatedprotein kinase), CDK (cyclin-dependent kinase), and cell signaling linked to growthfactors (Wang et al. 2012; Du et al. 2012).Green tea constitutes the rich amount of EGCG which aids in cancer chemoprevention(Fujiki et al. 1998). EGCG improved the impacts of ginseng compoundin the restraint of colon tumor cell development, showing that green tea could bea successful synergist with an anticancer agent for malignancy chemoprevention.It obstructs the PDGF-initiated proliferation and migration of rodent pancreaticstellate cells (Masamune et al. 2005). The soluble and plasma membrane-integratedEGCG straightforwardly communicates with PDGF-BB and in this wayputs off precise receptor binding promoting the inhibitory impacts of EGCG onplatelet-derivedgrowth factor-incited cell signaling and mitogens (Weber et al.2004).

InChI:InChI=1/C22H18O11/c23-10-5-12(24)11-7-18(33-22(31)9-3-15(27)20(30)16(28)4-9)21(32-17(11)6-10)8-1-13(25)19(29)14(26)2-8/h1-6,18,21,23-30H,7H2/t18-,21-/m1/s1

Upstream product

• 108-98-5 thiophenol 
• 121795-67-3 assamicain C 
• 2596-50-1 (-)-epigallocathechin gallate 
• 50-99-7 D-glucose 
• 528852-04-2 C₇₈H₆₆O₁₁ 
• 333796-77-3 (E)-1-[2,4-bis(benzyloxy)-6-hydroxyphenyl]-3-[3,4,5-tris(benzyloxy)phenyl]propenone 
• 333796-78-4 5,7-dibenzyloxy-2-[3,4,5-tris(benzyloxy)phenyl]-2H-chromene 
• 18065-05-9 1-[2,4-bis(benzyloxy)-6-hydroxyphenyl]ethanone 
• 896121-45-2 5,7-bis-benzyloxy-2-(3,4,5-tris-benzyloxy-phenyl)-chroman-3-ol 
• 108-73-6 3,5-dihydroxyphenol 
• 1359849-48-1 epigallocatechin-3-O-p-hydroxybenzoate-(4β->8)-epigallocatechin-3-O-gallate 
• 100-53-8 phenylmethanethiol 
• 989-51-5 (-)-gallocatechin 3-gallate 
• 148707-39-5 (-)-epigallocatechin 3-O-galloylperacetate 

Downstream Products

• 1707-75-1 2,2-diphenyl-1-picrylhydrazine 
• 5146-12-3 purpurogallin-4-carboxylic acid 
• 102067-92-5 epitheaflagallin 3-O-gallate 
• 149-91-7 3,4,5-trihydroxybenzoic acid 
• 989-51-5 (-)-gallocatechin 3-gallate 
• 30462-35-2 theaflavin-3,3'-di-o-gallate 
• 126716-06-1 oolong homobisflavan C 
• 126737-60-8 oolonghomobisflavan A 
• 176107-91-8 oolonghomobisflavan B 
• 1093758-49-6 C₄₃H₂₉NO₁₆S 

Relevant articles and documents

Study on in Vitro Preparation and Taste Properties of N-Ethyl-2-Pyrrolidinone-Substituted Flavan-3-Ols

N-ethyl-2-pyrrolidinone-substituted flavan-3-ols (EPSFs) were prepared by an in vitro model reaction, and the taste thresholds of EPSFs and their dose-over-threshold factors in large-leaf yellow tea (LYT) were investigated. The effects of initial reactant

Molecular Mechanism by Which Tea Catechins Decrease the Micellar Solubility of Cholesterol

Tea polyphenols lower the levels of cholesterol in the blood by decreasing the cholesterol micellar solubility. To clarify this mechanism, the interactions between taurocholic acid and (-)-epigallocatechin gallate (EGCg) and its derivatives were investigated. 13C NMR studies revealed remarkable chemical-shift changes for the carbonyl carbon atom and the 1″- and 4″-positions in the galloyl moiety. Furthermore, 1H NMR studies using (-)-EGCg derivatives showed that the number of hydroxyl groups on the B ring did not affect these interactions, whereas the carbonyl carbon atom and the aromatic ring of the galloyl moiety had remarkable effects. The configuration at the 2- and 3-positions of the catechin also influenced these interactions, with the trans-configuration resulting in stronger inhibition activity than the cis-configuration. Additionally, a 1:1 component ratio for the catechin-taurocholic acid complex was determined by electrospray ionization-mass spectrometry. These molecular mechanisms contribute to the development of cholesterol-absorption inhibitors.

Oligomerization mechanism of tea catechins during tea roasting

Roasting of green tea causes oligomerization of tea catechins, which decreases the astringency. The aim of this study was to elucidate the oligomerization mechanism. The 13C NMR spectrum of the oligomer fraction showed signals arising from catechin and sugar residues. Heating of epigallocatechin-3-O-gallate with 13C-labeled glucose (150 °C for 2 h) suggested that condensation of sugars with catechin A-rings caused the oligomerization. The dimeric product obtained by heating for a shorter period (30 min) suggested cross-linking occurred between sugars and catechin A-rings. Furthermore, heating of phloroglucinol, a catechin A-ring mimic, with glucose, methylglyoxal, and dihydroxyacetone, confirmed that the basic mechanism included reaction of the catechin A-ring methine carbons with carbonyl carbons of glucose and their pyrolysis products.