tbResList Print — EGCG EGCG (Epigallocatechin Gallate)

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Product

EGCG EGCG (Epigallocatechin Gallate)
Description: <p><b>Epigallocatechin-3-gallate</b> — EGCG is a naturally occurring galloylated flavan-3-ol and the quantitatively dominant catechin in green tea leaves from <i>Camellia sinensis</i>. It is formally classified as a dietary polyphenol, catechin and investigational pleiotropic bioactive compound. EGCG has concentration-, oxidation-, metal- and cellular-context-dependent activity: it can function as an antioxidant and NRF2-associated cytoprotective agent in normal tissues, but may generate reactive oxygen species and induce stress-mediated death in susceptible cancer cells. It is not an approved anticancer drug, and purified high-dose extracts are pharmacologically and toxicologically distinct from brewed green tea.</p>

<p><b>Primary mechanisms (ranked):</b></p>
<ol>
<li>Biphasic redox modulation, including direct radical scavenging and metal chelation at lower exposure, but auto-oxidation, hydrogen-peroxide generation and pro-oxidant stress under permissive cancer-cell culture conditions.</li>
<li>Suppression of proliferative and survival signalling, particularly PI3K–AKT–mTOR, NF-κB, receptor tyrosine kinase, STAT and context-dependent MAPK pathways.</li>
<li>Mitochondrial dysfunction and intrinsic apoptosis through mitochondrial membrane-potential loss, cytochrome-c release and caspase activation.</li>
<li>Cell-cycle arrest through modulation of cyclins, cyclin-dependent kinases, p21, p27 and p53-associated signalling.</li>
<li>Inhibition of invasion, epithelial–mesenchymal transition and extracellular-matrix degradation through reduced FAK, MMP-2, MMP-9, uPA and related motility pathways.</li>
<li>Suppression of HIF-1α–VEGF signalling, angiogenesis and hypoxia adaptation.</li>
<li>Metabolic disruption involving reduced glycolysis, glucose transport and context-dependent mitochondrial energy production.</li>
<li>Epigenetic modulation, including experimental inhibition or altered expression of DNMTs, HDACs and EZH2.</li>
<li>Modulation of proteostasis, autophagy, endoplasmic-reticulum stress and unfolded-protein responses.</li>
<li>NRF2 activation as a secondary adaptive mechanism, generally cytoprotective in normal cells but potentially protective or treatment-resistant in some cancers.</li>
<li>Chemosensitization or radiosensitization in selected experimental models; treatment protection, antagonism or normal-tissue radioprotection can also occur depending on dose, schedule and therapy.</li>
</ol>

<p><b>Bioavailability / PK relevance:</b> Oral bioavailability is low and highly variable because EGCG is chemically unstable near neutral or alkaline pH, has limited intestinal permeability, undergoes extensive methylation, glucuronidation and sulfation, and is influenced by food and microbiota. Plasma concentrations after tea consumption are usually submicromolar, while large supplemental doses may transiently produce low-micromolar exposure. Fasting can increase systemic exposure but may also increase hepatic toxicity risk. Nanoencapsulation, lipid carriers and other delivery systems improve exposure experimentally but are not established anticancer treatments.</p>

<p><b>In-vitro vs systemic exposure relevance:</b> Many anticancer experiments use approximately 10–100 µM EGCG, whereas conventional oral administration generally produces submicromolar to low-micromolar plasma concentrations. Thus, many direct cytotoxic, glycolytic, mitochondrial and kinase effects occur at concentrations substantially exceeding typical achievable systemic exposure. EGCG can also oxidize in culture media and generate extracellular hydrogen peroxide, creating experimental effects that may not translate directly in vivo.</p>

<p><b>Clinical evidence status:</b> Extensive preclinical evidence; multiple small human biomarker, prevention and early-phase studies; limited randomized evidence for selected premalignant or recurrence-prevention settings; no established therapeutic efficacy against active cancer and no regulatory approval as an anticancer agent. A recent randomized colorectal adenoma study reported reduced recurrence, but this does not establish treatment efficacy for invasive colorectal cancer. Ongoing clinical studies continue to investigate prevention and adjunctive applications.</p>

<p><b>Safety and interactions:</b> Brewed green tea is generally well tolerated, whereas concentrated green-tea extracts and purified EGCG have been associated with dose-dependent aminotransferase elevations and rare clinically significant liver injury. Doses around 800 mg EGCG per day have generated a regulatory safety signal, and a universally safe supplemental dose has not been established. Risk may be higher with fasting administration, pre-existing liver disease or multi-ingredient weight-loss products. EGCG can bind non-heme iron, alter drug transporters or metabolic enzymes, and modify exposure to some medications; oncology use should therefore be reviewed for drug-specific interactions.</p>


<br><br>

<a href="https://www.medicinenet.com/egcg_epigallocatechin_gallate_benefits_dosage/article.htm">
<b>EGCG (Epigallocatechin Gallate)</b> is found in green tea. 100 times more effective than Vitamin C and 25 times more effective than Vitamin E at protecting cells from damage associated with oxidative stress. </a> <br>
EGCG Epigallocatechin Gallate (Green Tea) -Catechin<br>
Summary:<br>
1. Concentration is a factor that could determine whether green tea polyphenols act as antioxidants or pro-oxidants.<br>
2. Poor bioavailability: taking EGCG capsules without food was better.<br>
3. Cancer dosage 4g/day (2g twice per day)? with curcumin may help (another ref says 700–2100 mg/d). FDA says <800mg/day (hepatotoxicity)<br>
4. EGCG is susceptible to oxidative degradation.<br>
5. “As for the pH level, the acidic environments enhance the stability of EGCG”.<br>
6. “EGCG may enhance nanoparticle uptake by tumor cells”<br>
7. Might be iron chelator (removing iron from cancer cells)<br>
8. Claimed as synergistic effect with chemotherapy ( cisplatin, bleomycin, gemcitabine.<br>
9. May suppress glucose metabolism, interfere with VEGF, downregulate NF-κB and MMP-9, down-regulation of androgen-regulated miRNA-21.<br>
10. Take with red pepper powder, Capsicum ratio 25:1 (based on half life, they did every 4 hr) (chili pepper vanilloid capsaicin).<br>
11. EGCG mediated ROS formation can upregulate CTR1 expression via the ERK1/2/NEAT1 pathway, which can increase the intake of chemotherapeutic drugs such as cisplatin in NSCLC cells and act as a chemosensitizer [58]<br>
12. Matcha green tea has highest EGCG (2-3X) because consuming leaf.<br>
13. EGCG is an ENOX2 inhibitor.<br>
14. Nrf2 activator in both cancer and normal cells. This
<a href="https://nestronics.ca/dbx/tbResEdit.php?rid=3212"> example</a>
of lung cancer show both directions in different cell lines, but both toward optimim level.
<br>
Biological activity, EGCG has been reported to exhibit a range of effects, including:<br>
    Antioxidant activity: 10-50 μM<br>
     Anti-inflammatory activity: 20-50 μM<br>
     Anticancer activity: 50-100 μM<br>
     Cardiovascular health: 20-50 μM<br>
     Neuroprotective activity: 10-50 μM<br>
<br>
Drinking a cup (or two cups) of green tea (in which one might ingest roughly 50–100 mg of EGCG from brewed tea) generally results in peak plasma EGCG concentrations in the range of approximately 0.1 to 0.6 μM.<br>
<br>
With higher, supplement-type doses (e.g., oral doses in the 500 mg–800 mg range that are sometimes studied for clinical benefits), peak plasma concentrations in humans can reach the low micromolar range, often reported around ~1–2 μM and in some cases up to 5 μM.<br>
<br>
Reported values can range from about 25–50 mg of EGCG per gram of matcha powder.<br>
In cases where the matcha is exceptionally catechin-rich, the content could reach 200–250 mg or more in 5 g.<br>
<br>
-Peak plasma concentration roughly 1 to 2 hours after oral ingestion.<br>
-Elimination half-life of EGCG in plasma is commonly reported to be in the range of about 3 to 5 hours.<br>
<br>
Supplemental EGCG <br>
Dose (mg)   ≈ Peak Plasma EGCG (µM)<br>
~50 mg          ≈ 0.1–0.3 µM<br>
~100 mg         ≈ 0.2–0.6 µM<br>
~250 mg         ≈ 0.5–1.0 µM<br>
~500 mg         ≈ 1–2 µM<br>
~800 mg or higher  ≈ 1–5 µM<br>
<br>
50mg of EGCG in 1g of matcha tea(1/2 teaspoon) <br>
<br>
Studies on green tea extracts have employed doses roughly equivalent to 300–800 mg/day of EGCG. Excessive doses can cause liver toxicity in some cases.<br>
<br>
Methods to improve bioavailability<br>
-Lipid-based carriers or nanoemulsions<br>
-Polymer-based nanoparticles or encapsulation<br>
-Co-administration with ascorbic acid (vitamin C)<br>
-Co-administration of adjuvants like piperine (perhaps sunflower lecithin and chitosan)
-Using multiple smaller doses rather than one large single dose.<br>
-Taking EGCG on an empty stomach or under fasting conditions, or aligning dosing with optimal pH conditions in the GI tract, may improve its absorption.(acidic environment is generally more favorable for its stability and absorption).<br>
– EGCG is more stable under acidic conditions. In the stomach, where the pH is typically around 1.5 to 3.5, EGCG is less prone to degradation compared to the more neutral or basic environments of the small intestine.<br>
- At neutral (around pH 7) or alkaline pH, EGCG undergoes auto-oxidation, reducing the effective concentration available for absorption.<br>
– Although the stomach’s acidic pH helps maintain EGCG’s stability, most absorption occurs in the small intestine, where the pH is closer to neutral.<br>
– To counterbalance the inherent instability in the intestine, strategies such as co-administration of pH-modifying agents (like vitamin C) are sometimes used. These agents help to maintain a slightly acidic environment in the gut microenvironment, potentially improving EGCG stability during its transit and absorption.<br>
– The use of acidifiers or buffering agents in supplements may help preserve EGCG until it reaches the absorption sites.<br>



<br>
-Note <a href="tbResList.php?qv=73&tsv=1109&wNotes=on&exSp=open">half-life</a> 3–5 hours.<br>
- low <a href="tbResList.php?qv=73&tsv=792&wNotes=on&exSp=open">BioAv</a> 1%? despite its limited absorption, it is rapidly disseminated throughout the body
<br>
Pathways:<br>

<!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑-->
- induce
<a href="tbResList.php?qv=73&tsv=275&wNotes=on">ROS</a> production<br>
- ROS↑ related:
<a href="tbResList.php?qv=73&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm),
<a href="tbResList.php?qv=73&tsv=103&wNotes=on">ER Stress↑</a>,
<a href="tbResList.php?qv=73&tsv=459&wNotes=on">UPR↑</a>,
<a href="tbResList.php?qv=73&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=73&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>,
<a href="tbResList.php?qv=73&tsv=77&wNotes=on">Cyt‑c↑</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=Casp">Caspases↑</a>,
<a href="tbResList.php?qv=73&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>,
<a href="tbResList.php?qv=73&tsv=239&wNotes=on">cl-PARP↑</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=HSP">HSP↓</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=Prx">Prx</a>,<!-- mitochondrial antioxidant enzyme-->

<br>

<!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, -->
- Does NOT Lower AntiOxidant defense in Cancer Cells:
<a href="tbResList.php?qv=73&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>,
<a href="tbResList.php?qv=73&word=Trx&wNotes=on">TrxR↓**</a>,<!-- major antioxidant system -->
<a href="tbResList.php?qv=73&tsv=298&wNotes=on&word=SOD">SOD</a>,
<a href="tbResList.php?qv=73&tsv=137&wNotes=on&word=GSH">GSH</a>
<a href="tbResList.php?qv=73&tsv=46&wNotes=on">Catalase</a>
<a href="tbResList.php?qv=73&tsv=597&wNotes=on">HO1</a>
<a href="tbResList.php?qv=73&wNotes=on&word=GPx">GPx</a>


<br>

- Raises
<a href="tbResList.php?qv=73&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a>
defense in Normal Cells:
<a href="tbResList.php?qv=73&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>,
<a href="tbResList.php?qv=73&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>,
<a href="tbResList.php?qv=73&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>,
<a href="tbResList.php?qv=73&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>,
<a href="tbResList.php?qv=73&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>,
<br>

<!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, -->
- lowers
<a href="tbResList.php?qv=73&tsv=953&wNotes=on&word=Inflam">Inflammation</a> :
<a href="tbResList.php?qv=73&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>,
<a href="tbResList.php?qv=73&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>,
<a href="tbResList.php?qv=73&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines :
<a href="tbResList.php?qv=73&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>,
<a href="tbResList.php?qv=73&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>,
<a href="tbResList.php?qv=73&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>,
<a href="tbResList.php?qv=73&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>,
<a href="tbResList.php?qv=73&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a>
<br>



<!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓
inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.-->
- inhibit Growth/Metastases :
<a href="tbResList.php?qv=73&tsv=604&wNotes=on">TumMeta↓</a>,
<a href="tbResList.php?qv=73&tsv=323&wNotes=on">TumCG↓</a>,
<a href="tbResList.php?qv=73&tsv=96&wNotes=on">EMT↓</a>,
<a href="tbResList.php?qv=73&tsv=204&wNotes=on">MMPs↓</a>,
<a href="tbResList.php?qv=73&tsv=201&wNotes=on">MMP2↓</a>,
<a href="tbResList.php?qv=73&tsv=203&wNotes=on">MMP9↓</a>,
<!-- <a href="tbResList.php?qv=73&tsv=308&wNotes=on">TIMP2</a>, -->
<a href="tbResList.php?qv=73&tsv=415&wNotes=on">IGF-1↓</a>,
<a href="tbResList.php?qv=73&tsv=428&wNotes=on">uPA↓</a>,
<a href="tbResList.php?qv=73&tsv=334&wNotes=on">VEGF↓</a>,
<!-- <a href="tbResList.php?qv=73&tsv=1284&wNotes=on">ROCK1↓</a>, -->
<a href="tbResList.php?qv=73&tsv=110&wNotes=on">FAK↓</a>,
<a href="tbResList.php?qv=73&tsv=273&wNotes=on">RhoA↓</a>,
<a href="tbResList.php?qv=73&tsv=214&wNotes=on">NF-κB↓</a>,
<!-- <a href="tbResList.php?qv=73&tsv=79&wNotes=on">CXCR4↓</a>, -->
<!-- <a href="tbResList.php?qv=73&tsv=1247&wNotes=on">SDF1↓</a>, -->
<a href="tbResList.php?qv=73&tsv=304&wNotes=on">TGF-β↓</a>,
<a href="tbResList.php?qv=73&tsv=719&wNotes=on">α-SMA↓</a>,
<a href="tbResList.php?qv=73&tsv=105&wNotes=on">ERK↓</a>
<!-- <a href="tbResList.php?qv=73&tsv=1178&wNotes=on">MARK4↓</a> --><!-- contributing to tumor growth, invasion, and metastasis-->
<br>

<!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, -->
- reactivate genes thereby inhibiting cancer cell growth :
<a href="tbResList.php?qv=73&tsv=140&wNotes=on">HDAC↓</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=DNMT">DNMTs↓</a>,
<a href="tbResList.php?qv=73&tsv=108&wNotes=on">EZH2↓</a>,
<a href="tbResList.php?qv=73&tsv=236&wNotes=on">P53↑</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=HSP">HSP↓</a>,
<a href="tbResList.php?qv=73&tsv=506&wNotes=on">Sp proteins↓</a>,
<!-- <a href="tbResList.php?qv=73&wNotes=on&word=TET">TET↑</a> -->
<br>

<!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ -->
- cause Cell cycle arrest :
<a href="tbResList.php?qv=73&tsv=322&wNotes=on">TumCCA↑</a>,
<a href="tbResList.php?qv=73&tsv=73&wNotes=on">cyclin D1↓</a>,
<a href="tbResList.php?qv=73&tsv=378&wNotes=on">cyclin E↓</a>,
<a href="tbResList.php?qv=73&tsv=467&wNotes=on">CDK2↓</a>,
<a href="tbResList.php?qv=73&tsv=894&wNotes=on">CDK4↓</a>,
<a href="tbResList.php?qv=73&tsv=895&wNotes=on">CDK6↓</a>,
<br>

<!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, -->
- inhibits Migration/Invasion :
<a href="tbResList.php?qv=73&tsv=326&wNotes=on">TumCMig↓</a>,
<a href="tbResList.php?qv=73&tsv=324&wNotes=on">TumCI↓</a>,
<a href="tbResList.php?qv=73&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis -->
<a href="tbResList.php?qv=73&tsv=110&wNotes=on">FAK↓</a>,
<a href="tbResList.php?qv=73&tsv=105&wNotes=on">ERK↓</a>,
<a href="tbResList.php?qv=73&tsv=96&wNotes=on">EMT↓</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=TOP">TOP1↓</a>,
<!-- <a href="tbResList.php?qv=73&tsv=657&wNotes=on">TET1↓</a>, -->
<br>

<!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS -->
- inhibits
<a href="tbResList.php?qv=73&tsv=129&wNotes=on">glycolysis</a>
/<a href="tbResList.php?qv=73&tsv=947&wNotes=on">Warburg Effect</a> and
<a href="tbResList.php?qv=73&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> :
<a href="tbResList.php?qv=73&tsv=143&wNotes=on">HIF-1α↓</a>,
<a href="tbResList.php?qv=73&tsv=772&wNotes=on">PKM2↓</a>,
<a href="tbResList.php?qv=73&tsv=35&wNotes=on">cMyc↓</a>,
<a href="tbResList.php?qv=73&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>,
<a href="tbResList.php?qv=73&tsv=906&wNotes=on">LDH↓</a>,
<a href="tbResList.php?qv=73&tsv=175&wNotes=on&word=LDH">LDHA↓</a>,
<a href="tbResList.php?qv=73&tsv=773&wNotes=on">HK2↓</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=PFK">PFKs↓</a>,
<!-- <a href="tbResList.php?qv=73&wNotes=on&word=PDK">PDKs↓</a>, -->
<a href="tbResList.php?qv=73&tsv=847&wNotes=on">ECAR↓</a>,
<a href="tbResList.php?qv=73&tsv=230&wNotes=on">OXPHOS↓</a>,
<a href="tbResList.php?qv=73&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=73&tsv=1278&wNotes=on">Glucose↓</a>,
<a href="tbResList.php?qv=73&tsv=623&wNotes=on">GlucoseCon↓</a>
<br>


<!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)-->
- inhibits
<a href="tbResList.php?qv=73&tsv=447&wNotes=on">angiogenesis↓</a> :
<a href="tbResList.php?qv=73&tsv=334&wNotes=on">VEGF↓</a>,
<a href="tbResList.php?qv=73&tsv=143&wNotes=on">HIF-1α↓</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=NOTCH">Notch↓</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=FGF">FGF↓</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=PDGF">PDGF↓</a>,
<a href="tbResList.php?qv=73&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>,
<a href="tbResList.php?qv=73&&wNotes=on&word=ITG">Integrins↓</a>,
<br>

<!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, -->
- inhibits Cancer Stem Cells :
<a href="tbResList.php?qv=73&tsv=795&wNotes=on">CSC↓</a>,
<!-- <a href="tbResList.php?qv=73&tsv=524&wNotes=on">CK2↓</a>, -->
<a href="tbResList.php?qv=73&tsv=141&wNotes=on">Hh↓</a>,
<a href="tbResList.php?qv=73&tsv=434&wNotes=on">GLi↓</a>,
<a href="tbResList.php?qv=73&tsv=124&wNotes=on">GLi1↓</a>,
<a href="tbResList.php?qv=73&tsv=677&wNotes=on">CD133↓</a>,
<a href="tbResList.php?qv=73&tsv=655&wNotes=on">CD24↓</a>,
<a href="tbResList.php?qv=73&tsv=342&wNotes=on">β-catenin↓</a>,
<a href="tbResList.php?qv=73&tsv=357&wNotes=on">n-myc↓</a>,
<!-- <a href="tbResList.php?qv=73&tsv=656&wNotes=on">sox2↓</a>, -->
<a href="tbResList.php?qv=73&wNotes=on&word=NOTCH">Notch↓</a>,
<!-- <a href="tbResList.php?qv=73&tsv=1024&wNotes=on">nestin↓</a>, -->
<a href="tbResList.php?qv=73&tsv=508&wNotes=on">OCT4↓</a>,
<br>

<!-- OTHERS : -->
- Others: <a href="tbResList.php?qv=73&tsv=252&wNotes=on">PI3K↓</a>,
<a href="tbResList.php?qv=73&tsv=4&wNotes=on">AKT↓</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=JAK">JAK↓</a>,
<a href="tbResList.php?qv=73&wNotes=on&word=STAT">STAT↓</a>,
<a href="tbResList.php?qv=73&tsv=377&wNotes=on">Wnt↓</a>,
<a href="tbResList.php?qv=73&tsv=342&wNotes=on">β-catenin↓</a>,
<a href="tbResList.php?qv=73&tsv=9&wNotes=on">AMPK</a>,
<!-- <a href="tbResList.php?qv=73&tsv=475&wNotes=on">α↓</a>, -->
<a href="tbResList.php?qv=73&tsv=105&wNotes=on">ERK↓</a>,
<!-- <a href="tbResList.php?qv=73&tsv=1014&wNotes=on">5↓</a>, -->
<a href="tbResList.php?qv=73&tsv=168&wNotes=on">JNK</a>,


- <a href="tbResList.php?qv=73&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol).<br>


<!-- SYNERGIES : -->
- Synergies:
<a href="tbResList.php?qv=73&tsv=1106&wNotes=on">chemo-sensitization</a>,
<a href="tbResList.php?qv=73&tsv=1171&wNotes=on">chemoProtective</a>,
<a href="tbResList.php?qv=73&tsv=1107&wNotes=on">RadioSensitizer</a>,
<a href="tbResList.php?qv=73&tsv=1185&wNotes=on">RadioProtective</a>,
<a href="tbResList.php?qv=73&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>,
<a href="tbResList.php?qv=73&tsv=1105&wNotes=on">Neuroprotective</a>,
<a href="tbResList.php?qv=73&tsv=557&wNotes=on">Cognitive</a>,
<a href="tbResList.php?qv=73&tsv=1175&wNotes=on">Renoprotection</a>,
<a href="tbResList.php?qv=73&tsv=1179&wNotes=on">Hepatoprotective</a>(possible damage at high dose),
<a href="tbResList.php?&qv=73&tsv=1188&wNotes=on">CardioProtective</a>,

<br>
<br>
<!-- SELECTIVE: -->
- Selectivity:
<a href="tbResList.php?qv=73&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a><br>
<br>





<h3>EGCG Mechanistic Profile</h3>
<table border="1" cellspacing="0" cellpadding="4">
<thead>
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer Cells</th>
<th>Normal Cells</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
</thead>
<tbody>
<tr>
<td>1</td>
<td>Biphasic redox modulation</td>
<td>↑ ROS or ↓ ROS (dose-dependent) (context-dependent)</td>
<td>↓ ROS; ↑ antioxidant buffering</td>
<td>P–R</td>
<td>Oxidative stress or antioxidant protection</td>
<td>Auto-oxidation and metal-catalysed peroxide formation may drive cancer-cell toxicity; culture-medium oxidation can exaggerate this mechanism.</td>
</tr>
<tr>
<td>2</td>
<td>PI3K AKT mTOR survival signalling</td>
<td>↓ PI3K; ↓ AKT; ↓ mTOR</td>
<td>↔ or adaptive modulation</td>
<td>R–G</td>
<td>Reduced proliferation and survival</td>
<td>Frequently reported across models, but direct target engagement at physiologically achievable concentrations remains uncertain.</td>
</tr>
<tr>
<td>3</td>
<td>Mitochondrial apoptosis</td>
<td>↓ ΔΨm; ↑ cytochrome c; ↑ caspase-9; ↑ caspase-3; ↑ PARP cleavage</td>
<td>↔ or preserved mitochondrial function</td>
<td>R–G</td>
<td>Intrinsic apoptotic death</td>
<td>Usually downstream of redox stress, calcium disturbance or survival-pathway inhibition.</td>
</tr>
<tr>
<td>4</td>
<td>NF-κB inflammatory survival signalling</td>
<td>↓ NF-κB; ↓ COX-2; ↓ inflammatory cytokines</td>
<td>↓ pathological inflammation</td>
<td>R–G</td>
<td>Reduced inflammatory and anti-apoptotic transcription</td>
<td>Potentially relevant to tumour-promoting inflammation and treatment resistance.</td>
</tr>
<tr>
<td>5</td>
<td>Cell-cycle regulation</td>
<td>↓ cyclin D1; ↓ cyclin E; ↓ CDK2; ↓ CDK4; ↓ CDK6; ↑ p21; ↑ arrest</td>
<td>↔ or transient arrest</td>
<td>G</td>
<td>Cytostatic growth inhibition</td>
<td>Arrest may occur at G1, S or G2/M depending on tumour type and concentration.</td>
</tr>
<tr>
<td>6</td>
<td>Invasion EMT and matrix remodelling</td>
<td>↓ EMT; ↓ FAK; ↓ uPA; ↓ MMP-2; ↓ MMP-9; ↓ migration</td>
<td>↔</td>
<td>G</td>
<td>Reduced invasion and metastatic phenotype</td>
<td>Predominantly supported by cellular and animal models.</td>
</tr>
<tr>
<td>7</td>
<td>HIF-1α VEGF angiogenesis axis</td>
<td>↓ HIF-1α; ↓ VEGF; ↓ angiogenic signalling</td>
<td>↔ or context-dependent vascular protection</td>
<td>G</td>
<td>Reduced hypoxia adaptation and angiogenesis</td>
<td>Responses depend on oxygen tension, cell type and exposure.</td>
</tr>
<tr>
<td>8</td>
<td>Glycolysis and energy metabolism</td>
<td>↓ GLUT1; ↓ HK2; ↓ PKM2; ↓ LDHA; ↓ ECAR; ↓ ATP (model-dependent)</td>
<td>↔ or improved metabolic homeostasis</td>
<td>R–G</td>
<td>Metabolic stress</td>
<td>Many metabolic findings use concentrations above typical human plasma exposure.</td>
</tr>
<tr>
<td>9</td>
<td>Calcium ER stress and proteostasis</td>
<td>↑ Ca²⁺; ↑ ER stress; ↑ UPR; ↑ GRP78 (context-dependent)</td>
<td>↔ or ↓ pathological ER stress</td>
<td>P–G</td>
<td>Proteotoxic stress and apoptosis</td>
<td>GRP78 and UPR activation may promote death or adaptation depending on intensity and duration.</td>
</tr>
<tr>
<td>10</td>
<td>Epigenetic regulation</td>
<td>↓ DNMT activity; ↓ HDAC signalling; ↓ EZH2 (model-dependent)</td>
<td>↔</td>
<td>G</td>
<td>Re-expression of suppressed genes</td>
<td>Biochemical inhibition and intracellular effects may require different concentrations.</td>
</tr>
<tr>
<td>11</td>
<td>NRF2 antioxidant response</td>
<td>↑ NRF2 or ↔ (context-dependent)</td>
<td>↑ NRF2; ↑ HO-1; ↑ GSH; ↑ antioxidant enzymes</td>
<td>R–G</td>
<td>Secondary adaptive cytoprotection</td>
<td>NRF2 can protect normal tissue but may also counteract EGCG-induced oxidative injury or support resistant cancer cells.</td>
</tr>
<tr>
<td>12</td>
<td>Cancer stemness signalling</td>
<td>↓ Wnt β-catenin; ↓ Hedgehog GLI; ↓ Notch; ↓ stem-cell markers</td>
<td>↔</td>
<td>G</td>
<td>Reduced self-renewal phenotype</td>
<td>Evidence remains predominantly preclinical and model-dependent.</td>
</tr>
<tr>
<td>13</td>
<td>Chemosensitization</td>
<td>↑ treatment response or ↓ resistance (drug-dependent)</td>
<td>↔ or ↑ tissue protection</td>
<td>R–G</td>
<td>Adjunctive modulation</td>
<td>Reported with several cytotoxic and targeted agents, but EGCG can also alter drug absorption, transport or stability; combinations require individual evaluation.</td>
</tr>
<tr>
<td>14</td>
<td>Radiosensitization and radioprotection</td>
<td>↑ radiosensitivity or ↔ (schedule-dependent)</td>
<td>↓ radiation injury in some models</td>
<td>R–G</td>
<td>Context-dependent radiation modulation</td>
<td>Opposing tumour and normal-tissue effects are possible; clinical evidence is insufficient for routine supplementation during radiotherapy.</td>
</tr>
<tr>
<td>15</td>
<td>Clinical Translation Constraint</td>
<td>Effective experimental exposure often not systemically achievable</td>
<td>↑ hepatic risk with concentrated high-dose extracts</td>
<td>G</td>
<td>Limited clinical translation</td>
<td>Poor oral bioavailability, rapid metabolism, instability, formulation heterogeneity, fasting-related exposure, liver toxicity and limited definitive oncology trials constrain deployment.</td>
</tr>
</tbody>
</table>
<p>P: 0–30 min&nbsp;&nbsp;&nbsp; R: 30 min–3 hr&nbsp;&nbsp;&nbsp; G: &gt;3 hr</p>


<br><br>
<p><b>Alzheimer’s disease relevance:</b> EGCG has substantial preclinical neuroprotective evidence but no established clinical efficacy for Alzheimer’s disease. Proposed actions include inhibition or remodelling of amyloid-β aggregation, altered amyloid precursor protein processing, metal chelation, reduced tau-associated injury, suppression of neuroinflammation, mitochondrial protection and activation of NRF2-associated antioxidant defences. Most positive findings derive from biochemical, cellular or animal models, and brain exposure after conventional oral administration is uncertain. EGCG should therefore be classified as preclinical or exploratory for Alzheimer’s disease rather than as a validated disease-modifying therapy.</p>



<h3>EGCG in Alzheimer’s Disease</h3>
<table border="1" cellspacing="0" cellpadding="4">
<thead>
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Modulation</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
</thead>
<tbody>
<tr>
<td>1</td>
<td>Amyloid beta aggregation</td>
<td>↓ fibril formation; ↑ non-toxic aggregate remodelling</td>
<td>Reduced amyloid-associated toxicity</td>
<td>Strong biochemical and preclinical rationale; effective brain exposure in humans remains uncertain.</td>
</tr>
<tr>
<td>2</td>
<td>Amyloid precursor protein processing</td>
<td>↑ non-amyloidogenic processing; ↓ amyloidogenic burden (model-dependent)</td>
<td>Reduced amyloid generation</td>
<td>Primarily demonstrated in cellular and animal systems.</td>
</tr>
<tr>
<td>3</td>
<td>Neuroinflammation</td>
<td>↓ NF-κB; ↓ NLRP3; ↓ inflammatory cytokines; ↓ microglial activation</td>
<td>Reduced inflammatory neurotoxicity</td>
<td>Inflammatory effects are context-, model- and dose-dependent.</td>
</tr>
<tr>
<td>4</td>
<td>Oxidative stress and NRF2</td>
<td>↓ ROS; ↑ NRF2; ↑ HO-1; ↑ endogenous antioxidant defence</td>
<td>Neuronal cytoprotection</td>
<td>Antioxidant signalling is more relevant at achievable exposure than many direct cytotoxic cancer mechanisms.</td>
</tr>
<tr>
<td>5</td>
<td>Mitochondrial function</td>
<td>↑ membrane stability; ↑ ATP preservation; ↓ mitochondrial ROS</td>
<td>Improved neuronal bioenergetics</td>
<td>Supported mainly by experimental injury and transgenic models.</td>
</tr>
<tr>
<td>6</td>
<td>Tau pathology</td>
<td>↓ tau phosphorylation or aggregation (model-dependent)</td>
<td>Reduced cytoskeletal and synaptic injury</td>
<td>Less developed evidence base than amyloid-related mechanisms.</td>
</tr>
<tr>
<td>7</td>
<td>Metal homeostasis</td>
<td>↓ redox-active iron and copper interactions</td>
<td>Reduced metal-promoted aggregation and oxidative injury</td>
<td>Chelation may contribute mechanistically but could also impair dietary non-heme iron absorption.</td>
</tr>
<tr>
<td>8</td>
<td>Clinical Translation Constraint</td>
<td>↓ oral and brain exposure; ↑ formulation variability</td>
<td>Uncertain human efficacy</td>
<td>No convincing evidence currently establishes EGCG as an Alzheimer’s disease-modifying treatment.</td>
</tr>
</tbody>
</table>



Pathway results for Effect on Cancer / Diseased Cells

Redox & Oxidative Stress(tgid=1)

Ceru↓, 1,   ENOX2↓, 3,   Fenton↑, 1,   Ferroptosis↑, 1,   GPx↑, 2,   GPx4↓, 1,   H2O2↑, 2,   HO-1↑, 1,   HO-1↓, 1,   Iron↑, 1,   Keap1↓, 2,   MDA↑, 1,   NADH↑, 1,   NADHdeh?, 1,   NQO1↑, 1,   NRF2↑, 6,   NRF2⇅, 1,   NRF2↓, 2,   OXPHOS↓, 1,   Prx↓, 1,   RNS↓, 1,   ROMO1↑, 1,   ROS↑, 6,   ROS⇅, 1,   ROS↓, 2,   mt-ROS↓, 1,   SOD↑, 1,   SOD1↑, 1,   SOD1↓, 1,   Trx↓, 1,   Trx1↓, 1,   TrxR↓, 1,  

Metal & Cofactor Biology(tgid=2)

FTH1↓, 1,   IronCh↑, 2,   TfR1/CD71↑, 1,  

Mitochondria & Bioenergetics(tgid=3)

ATP↝, 1,   ATP↓, 1,   EGF↓, 1,   MMP↓, 4,   MMP↑, 1,   mtDam↑, 3,   OCR↓, 1,   Raf↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4)

ACSL4↑, 1,   p‑AMPK↑, 1,   AMPK↑, 2,   cMyc↓, 1,   ECAR↓, 1,   GAPDH↓, 1,   GDH↓, 1,   GlucoseCon↓, 1,   GLUT2↓, 1,   GlutMet↓, 1,   Glycolysis↓, 2,   HK2↓, 6,   HK2∅, 1,   lactateProd↓, 1,   LDHA↓, 2,   LDHA∅, 1,   lipoGen↓, 1,   PDHA1↓, 1,   PFK↓, 3,   PFKP↓, 1,   PI3K/Akt↓, 1,   PI3k/Akt/mTOR↓, 1,   PKM2∅, 1,   PKM2↓, 2,   cl‑PPARα↓, 1,   Pyruv↓, 1,   RPSA↓, 1,   SIRT1↓, 1,   Warburg↓, 1,  

Cell Death(tgid=5)

Akt↓, 2,   p‑Akt↓, 3,   Apoptosis↑, 8,   Apoptosis↓, 1,   aSmase↑, 1,   BAD↓, 1,   BAD↑, 2,   Bak↑, 3,   BAX↑, 3,   BAX⇅, 1,   Bax:Bcl2↑, 3,   Bcl-2↓, 3,   Bcl-xL↓, 3,   BID↓, 1,   Casp↑, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp7↑, 5,   cl‑Casp7↑, 1,   Casp8↑, 1,   Casp8↓, 1,   Casp9↑, 5,   Cyt‑c↝, 1,   Cyt‑c↑, 4,   Diablo↑, 1,   Fas↑, 1,   Ferroptosis↑, 1,   HGF/c-Met↓, 1,   Hippo↓, 1,   hTERT/TERT↓, 2,   JNK↑, 1,   JNK↓, 1,   JWA↑, 1,   MAPK↓, 1,   Mcl-1↓, 1,   MDM2↓, 1,   MDM2↑, 1,   Myc↓, 1,   necrosis↑, 1,   p27/CDKN1B↑, 1,   p38↓, 1,   p38↑, 1,   Proteasome↓, 1,   SK↓, 1,   survivin↓, 1,   Telomerase↓, 3,   TumCD↓, 2,   YAP/TEAD↑, 1,  

Kinase & Signal Transduction(tgid=6)

HER2/EBBR2↓, 2,   miR-25-5p↓, 1,   Sp1/3/4↓, 3,   Sp1/3/4↑, 1,  

Transcription & Epigenetics(tgid=7)

EZH2↓, 2,   ac‑H3↑, 2,   H3↓, 1,   ac‑H4↑, 1,   HATs↓, 2,   miR-145↑, 1,   miR-21↓, 1,   other↑, 3,   other↝, 2,   other∅, 1,   p‑pRB↓, 1,   pRB↑, 1,   PRC2↓, 1,   tumCV↓, 2,   YMcells↑, 1,  

Protein Folding & ER Stress(tgid=8)

CHOP/DDIT3↑, 2,   CHOP/DDIT3↓, 1,   eIF2α↑, 1,   eIF2α↓, 1,   p‑eIF2α↑, 1,   ER Stress↑, 7,   GRP78/BiP↑, 5,   GRP78/BiP↓, 1,   HSP27↓, 1,   HSP70/HSPA5↓, 1,   HSP90↓, 1,   IRE1↑, 1,   NQO2↑, 1,   PERK↑, 1,   p‑PERK↓, 1,   UPR↓, 1,   UPR↑, 6,   XBP-1↑, 1,   XBP-1↝, 1,  

Autophagy & Lysosomes(tgid=9)

ATG5↝, 1,   ATG5↑, 1,   Beclin-1↝, 1,   Beclin-1↑, 1,   LC3B↑, 1,   LC3II↑, 1,   TumAuto↑, 3,  

DNA Damage & Repair(tgid=10)

DNAdam↑, 2,   DNMT1↓, 4,   DNMT3A↓, 1,   DNMTs↓, 6,   G9a↓, 1,   p16↑, 2,   P53↑, 2,   P53↓, 1,   cl‑PARP↑, 4,   PARP↑, 3,   PCNA↓, 1,   TP53↓, 1,   TP53↑, 1,   UHRF1↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11)

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   P21↑, 3,   TumCCA↑, 3,   TumCCA?, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

ALDH1A1↓, 1,   BMI1↓, 1,   CD133↓, 5,   CD24↓, 1,   CD44↓, 8,   CLOCK↓, 1,   CSCs↓, 15,   EMT↓, 1,   p‑ERK↓, 1,   p‑ERK↑, 1,   ERK↓, 4,   ERK↑, 1,   FGF↓, 1,   FOXO↓, 1,   FOXO↑, 1,   Gli↓, 1,   Gli1↓, 1,   p‑GSK‐3β↓, 1,   GSK‐3β↑, 1,   HDAC↓, 6,   HDAC1↓, 3,   HDAC2↓, 1,   HDAC3↓, 1,   HDAC4↓, 1,   HH↓, 1,   IGF-1↓, 1,   IGF-1R↑, 1,   IGFR↓, 1,   p‑IGFR↓, 1,   Jun↓, 1,   Let-7↑, 1,   miR-330-5p↑, 1,   miR-34a↑, 1,   p‑mTOR↓, 1,   mTOR↓, 2,   Nanog↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   NOTCH3↓, 1,   OCT4↓, 1,   PI3K↓, 1,   PTCH1↓, 3,   PTCH2↓, 1,   PTEN↑, 4,   RAS↓, 1,   SCF↓, 1,   Shh↓, 1,   Smo↓, 1,   SOX2↓, 2,   STAT↓, 1,   STAT1↓, 1,   STAT3↓, 1,   p‑STAT3↓, 2,   SUZ12↓, 1,   TCF↓, 1,   TOP1↑, 1,   TOP2↑, 1,   TumCG↓, 3,   Wnt↑, 1,   Wnt↓, 4,  

Migration(tgid=13)

67LR↓, 1,   AntiAg↑, 3,   AP-1↓, 4,   Ca+2↑, 1,   Ca+2↝, 1,   E-cadherin↓, 1,   ER-α36↓, 1,   FAK↓, 1,   Fibronectin↓, 1,   GLI2↓, 1,   ITGB3↓, 1,   Ki-67↓, 2,   KRAS↓, 1,   LEF1↓, 2,   miR-200c↑, 1,   miR-203↓, 1,   miR-485↑, 1,   MMP-10↓, 1,   MMP2↓, 3,   MMP2⇅, 1,   MMP7↓, 1,   MMP9↓, 2,   MMP9↑, 1,   MMP9⇅, 1,   MMPs↓, 4,   p‑PDGF↓, 1,   PDGF↓, 1,   PKA↓, 1,   RECK↑, 1,   Slug↓, 1,   Smad1↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   SMAD4↓, 1,   Snail↓, 1,   TGF-β↓, 3,   TIMP1↑, 1,   TIMP2↑, 1,   TIMP3↑, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 2,   TumCP↑, 1,   TumMeta↓, 3,   uPA↝, 1,   uPA↓, 2,   Vim↓, 5,   Zeb1↓, 1,   Zeb1↑, 1,   β-catenin/ZEB1↓, 10,  

Angiogenesis & Vasculature(tgid=14)

angioG↓, 4,   ATF4↑, 3,   EGFR↓, 2,   EPR↑, 1,   HIF-1↓, 1,   Hif1a↓, 2,   miR-210↑, 1,   miR-210↓, 1,   NO↑, 1,   PDGFR-BB↑, 1,   VEGF↓, 5,   VEGFR2/KDR/Flk1↓, 2,  

Barriers & Transport(tgid=15)

BBB↑, 1,   CTR1↑, 1,   GLUT1↓, 1,   GLUT3↑, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

COX1↓, 1,   COX2/PTGS2↓, 1,   IL1β↓, 1,   IL6↓, 3,   IL8↓, 1,   Imm↑, 1,   IκB↓, 1,   IκB↑, 1,   JAK↓, 1,   MCP1/CCL2↓, 1,   NF-kB↓, 5,   NF-kB↑, 1,   p50↓, 1,   PD-L1↓, 1,   PSA↓, 1,   RANTES?, 1,   TNF-α↓, 4,  

Cellular Microenvironment(tgid=17)

pH↓, 1,  

Hormonal & Nuclear Receptors(tgid=20)

AR↓, 2,   CDK6↓, 1,   COMT↓, 3,  

Drug Metabolism & Resistance(tgid=21)

BioAv↑, 5,   BioAv↓, 5,   BioAv∅, 1,   BioAv↝, 2,   ChemoSen↑, 7,   Dose?, 2,   Dose∅, 1,   Dose↑, 1,   Dose↝, 1,   eff↑, 24,   eff↓, 6,   Half-Life∅, 1,   Half-Life↝, 4,   MRP1/ABCC1↓, 1,   RadioS↑, 2,   selectivity↑, 7,  

Clinical Biomarkers(tgid=22)

AFP↓, 1,   ALC↓, 1,   AR↓, 2,   E6↓, 1,   E7↓, 1,   EGFR↓, 2,   EZH2↓, 2,   HER2/EBBR2↓, 2,   hTERT/TERT↓, 2,   IL6↓, 3,   Ki-67↓, 2,   KRAS↓, 1,   Myc↓, 1,   NOS2↓, 1,   PD-L1↓, 1,   PSA↓, 1,   SUZ12↓, 1,   TP53↓, 1,   TP53↑, 1,  

Functional Outcomes(tgid=23)

AntiCan↑, 2,   AntiTum↑, 1,   AntiTum↓, 1,   cardioP↑, 2,   chemoP↑, 3,   chemoPv↑, 3,   cognitive↑, 2,   OS↑, 2,   PARP16↓, 1,   Remission↑, 1,   Remission↓, 1,   Risk↓, 2,   toxicity↓, 1,   toxicity∅, 1,   TumVol↓, 2,   TumW↓, 2,   Weight∅, 1,  
Total Targets: 388

Pathway results for Effect on Normal Cells

NA, unassigned(tgid=0)

AntiBio↑, 3,  

Redox & Oxidative Stress(tgid=1)

antiOx↑, 15,   Catalase↑, 5,   GPx↑, 4,   GSH↑, 2,   GSTA1↑, 1,   GSTs↑, 1,   H2O2↓, 2,   H2O2↑, 1,   HO-1↑, 3,   lipid-P↓, 3,   MDA↓, 2,   MFN1↑, 2,   MFN2↑, 3,   MPO↓, 1,   NQO1↑, 1,   Nrf1↑, 2,   NRF2↑, 10,   OPA1↑, 2,   PARK2↑, 1,   RNS↓, 1,   ROS↓, 21,   SIRT3↑, 1,   SOD↑, 9,   SOD1↑, 1,   SOD2↑, 1,   Trx1↑, 1,  

Mitochondria & Bioenergetics(tgid=3)

mt-ATP↑, 1,   ATP↑, 1,   DRP1/DNM1L↓, 4,   FIS1↓, 7,   mitResp↑, 1,   MMP↑, 1,   mtDam↓, 1,   PGC-1α↑, 1,   PGC-1α↓, 1,   PINK1↑, 1,  

Core Metabolism/Glycolysis(tgid=4)

Acetyl-CoA↓, 1,   ALAT↑, 1,   AMPK↑, 1,   CRM↓, 1,   GDH↓, 1,   glucose↓, 1,   LDH↓, 1,   LDL↓, 4,   PDK1↓, 1,   PGC1A↑, 1,   PKM2↑, 1,   SIRT1↑, 4,   SREBP2↓, 1,  

Cell Death(tgid=5)

Apoptosis↓, 5,   BAX↓, 2,   Bcl-2↑, 2,   Casp1↓, 2,   Casp12↓, 1,   Casp3↓, 1,   Cyt‑c↓, 1,   iNOS↓, 2,   JNK↓, 1,  

Kinase & Signal Transduction(tgid=6)

AMPKα↑, 1,  

Transcription & Epigenetics(tgid=7)

Ach↑, 1,   other↓, 1,   other↑, 3,   other?, 2,  

Protein Folding & ER Stress(tgid=8)

CHOP/DDIT3↓, 2,   ER Stress↓, 1,   GRP78/BiP↓, 3,   IRE1↓, 1,   PERK↓, 1,   UPR↓, 2,  

Autophagy & Lysosomes(tgid=9)

ATG5↑, 1,   MitoP↑, 1,  

DNA Damage & Repair(tgid=10)

DNAdam↓, 1,   DNMTs↓, 1,   P53↓, 1,   p‑PARP↓, 1,  

Cell Cycle & Senescence(tgid=11)

cycD1/CCND1↓, 1,   E2Fs↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

FOXO↑, 1,   FOXO1↑, 1,   Gli1↑, 1,   GSK‐3β↓, 1,   HDAC↓, 2,   HDAC↑, 1,   HDAC1↓, 1,   IGF-1R↓, 1,   mTOR↓, 1,   mTORC1↓, 1,   n-MYC↑, 1,   neuroG↑, 2,   Shh↑, 1,   TCF-4↓, 1,   TOP2↑, 1,   VGCC↝, 1,  

Migration(tgid=13)

ACTA2↓, 1,   AntiAg↑, 2,   AP-1↓, 1,   APP↓, 1,   i-Ca+2↓, 1,   Ca+2↓, 4,   Ca+2?, 1,   COL1A1↓, 1,   MMP2↓, 2,   Rho↓, 2,   TXNIP↓, 1,   α-SMA↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14)

angioG↑, 1,   NO↓, 4,   PDGFR-BB↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15)

BBB↑, 3,   BBB∅, 1,  

Immune & Inflammatory Signaling(tgid=16)

ASC↓, 1,   COX2/PTGS2↓, 2,   IL1↓, 1,   IL18↓, 1,   IL1β↓, 2,   IL6↓, 6,   IL8↓, 2,   Imm↑, 1,   Inflam↓, 10,   JAK↓, 1,   NF-kB↓, 2,   TNF-α↓, 7,  

Synaptic & Neurotransmission(tgid=18)

AChE↓, 5,   BChE↓, 1,   BDNF↑, 1,   NGF↑, 1,   p‑tau↓, 4,   tau↓, 3,  

Protein Aggregation(tgid=19)

Aβ↓, 9,   BACE↓, 2,   NLRP3↓, 3,  

Hormonal & Nuclear Receptors(tgid=20)

GR↑, 1,  

Drug Metabolism & Resistance(tgid=21)

BioAv↑, 14,   BioAv↝, 2,   BioAv↓, 5,   BioEnh↑, 7,   Dose∅, 1,   Dose↝, 8,   Dose?, 1,   Dose↑, 1,   eff↓, 1,   eff↑, 4,   eff↝, 1,   Half-Life↝, 2,  

Clinical Biomarkers(tgid=22)

ALAT↑, 1,   AST↑, 1,   GutMicro↑, 3,   IL6↓, 6,   LDH↓, 1,  

Functional Outcomes(tgid=23)

AntiAge↑, 4,   AntiCan↑, 3,   cardioP↑, 6,   cognitive↑, 3,   hepatoP↓, 3,   hepatoP↑, 1,   memory↑, 6,   motorD↑, 1,   neuroP↑, 10,   Obesity↓, 1,   OS↑, 2,   Pain↓, 1,   radioP↑, 1,   RenoP↑, 2,   toxicity↓, 1,   toxicity∅, 2,   toxicity↑, 1,   toxicity↝, 4,   Weight∅, 1,  

Infection & Microbiome(tgid=24)

AntiViral↑, 2,   Bacteria↓, 3,  
Total Targets: 173

Research papers

Year Title Authors PMID Link Flag
2008Prospective cohort comparison of flavonoid treatment in patients with resected colorectal cancer to prevent recurrenceHarald HoenschPMC2703843https://pmc.ncbi.nlm.nih.gov/articles/PMC2703843/0
2015Increased chemopreventive effect by combining arctigenin, green tea polyphenol and curcumin in prostate and breast cancer cellsPiwen WangPMC4166488https://pmc.ncbi.nlm.nih.gov/articles/PMC4166488/0
2017Traditional Chinese medicinal herbs as potential AChE inhibitors for anti-Alzheimer’s disease: A reviewYingying Jianghttps://www.sciencedirect.com/science/article/abs/pii/S00452068173058490
2022Contribution of Non-Coding RNAs to Anticancer Effects of Dietary Polyphenols: Chlorogenic Acid, Curcumin, Epigallocatechin-3-Gallate, Genistein, Quercetin and ResveratrolSumio HayakawaPMC9774417https://pmc.ncbi.nlm.nih.gov/articles/PMC9774417/0
2011The anticancer flavonoid chrysin induces the unfolded protein response in hepatoma cellsXiangming SunPMC3822950https://pmc.ncbi.nlm.nih.gov/articles/PMC3822950/0
2014Caloric restriction mimetics: natural/physiological pharmacological autophagy inducersGuillermo MariñoPMC4502795https://pmc.ncbi.nlm.nih.gov/articles/PMC4502795/0
2026Targeting Cancer Stem Cells with Phytochemicals: Molecular Mechanisms and Therapeutic PotentialAshok Kumar Sahhttps://www.mdpi.com/2227-9059/14/1/2150
2022An update of Nrf2 activators and inhibitors in cancer prevention/promotionFarhad PouremamaliPMC9245222https://pmc.ncbi.nlm.nih.gov/articles/PMC9245222/0
2020Natural products targeting mitochondria: emerging therapeutics for age-associated neurological disordersZhibin LiangPMC8084865https://pmc.ncbi.nlm.nih.gov/articles/PMC8084865/0
2015Curcumin and epigallocatechin gallate inhibit the cancer stem cell phenotype via down-regulation of STAT3-NFκB signalingSeyung S ChungPMC4290892https://pmc.ncbi.nlm.nih.gov/articles/PMC4290892/0
2015Synergistic effect of curcumin on epigallocatechin gallate-induced anticancer action in PC3 prostate cancer cellsDae-Woon EomPMC4576954https://pmc.ncbi.nlm.nih.gov/articles/PMC4576954/0
2011Shattering the underpinnings of neoplastic architecture in LNCap: synergistic potential of nutraceuticals in dampening PDGFR/EGFR signaling and cellular proliferationAmmad Ahmad Farooqi 22070051https://pubmed.ncbi.nlm.nih.gov/22070051/0
2007The effects of tetrahydrocurcumin and green tea polyphenol on the survival of male C57BL/6 miceKenichi Kitani17516143https://pubmed.ncbi.nlm.nih.gov/17516143/0
2026Dietary (−)-Epigallocatechin Gallate (EGCG): State-of-the-Art Advances in Bioactivities, Bioavailability Enhancement Strategies, and Applications in Nutrition and HealthLi NiuPMC12844721https://pmc.ncbi.nlm.nih.gov/articles/PMC12844721/0
2025Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential Lucia Capassohttps://www.researchgate.net/publication/388669154_Epigallocatechin_Gallate_EGCG_Pharmacological_Properties_Biological_Activities_and_Therapeutic_Potential0
2025A systematic review and meta-analysis of the effects of green tea extracts and polyphenols in female hormone-dependent cancers for benefit-risk evaluationJin-jing HePMC12497591https://pmc.ncbi.nlm.nih.gov/articles/PMC12497591/0
2025Pharmacological and Genetic Approaches to Downregulate FIS1 Mitigate Neuropathic PainChang-Lei Zhuhttps://www.jneurosci.org/content/45/35/e05232520250
2025The Role of ER Stress and the Unfolded Protein Response in CancerROSE GHEMRAWIhttps://cgp.iiarjournals.org/content/22/3/3630
2025Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic PotentialLucia Capassohttps://pmc.ncbi.nlm.nih.gov/articles/PMC11821029/0
2025Nano-Engineered Epigallocatechin Gallate (EGCG) Delivery Systems: Overcoming Bioavailability Barriers to Unlock Clinical Potential in Cancer TherapyMohammad Qutubhttps://link.springer.com/article/10.1208/s12249-025-03145-00
2024Epigallocatechin‐3‐Gallate Ameliorates Diabetic Kidney Disease by Inhibiting the TXNIP/NLRP3/IL‐1β Signaling PathwayYinghui WangPMC11666909https://pmc.ncbi.nlm.nih.gov/articles/PMC11666909/0
2024Targeting Cancer Hallmarks with Epigallocatechin Gallate (EGCG): Mechanistic Basis and Therapeutic TargetsWamidh H TalibPMC10976257https://pmc.ncbi.nlm.nih.gov/articles/PMC10976257/0
2024Absorption, metabolism, bioactivity, and biotransformation of epigallocatechin gallateShuling Zhang36728926https://pubmed.ncbi.nlm.nih.gov/36728926/0
2024The Potential of Epigallocatechin Gallate in Targeting Cancer Stem Cells: A Comprehensive ReviewRupa Chaudhuri38243984https://pubmed.ncbi.nlm.nih.gov/38243984/0
2024EGCG inhibits diabetic nephrophathy through up regulation of PKM2genomediscovery.orghttps://genomediscovery.org/mmolecular-therapy-for-diabetic-nephropathy-dn-epigallocatechin-egcg-isolated-from-green-tea-increases-pyruvate-kinase-m2-pkm2-expression-decreases-toxic-glucose-metabolites-mitoc/0
2024Green Tea Epigallocatechin 3-Gallate Reduced Platelet Aggregation and Improved Anticoagulant Proteins in Patients with Transfusion-Dependent β-Thalassemia: A Randomized Placebo-Controlled Clinical TrialTouchwin PetiwathayakornPMC11640449https://pmc.ncbi.nlm.nih.gov/articles/PMC11640449/0
2024Immunomodulatory Effects of Green Tea Catechins and Their Ring Fission Metabolites in a Tumor Microenvironment PerspectiveEmmanuele D S AndradePMC11478201https://pmc.ncbi.nlm.nih.gov/articles/PMC11478201/0
2024Epigallocatechin-3-gallate at the nanoscale: a new strategy for cancer treatmentWenxue SunPMC11443569https://pmc.ncbi.nlm.nih.gov/articles/PMC11443569/0
2024Chemoprophylaxis Effect of EGCG on the Recurrence of Colorectal Cancer: A Systematic Review and Meta-AnalysisBenyu He38988171https://pubmed.ncbi.nlm.nih.gov/38988171/0
2024EGCG-induced selective death of cancer cells through autophagy-dependent regulation of the p62-mediated antioxidant survival pathwayHo Woon Leehttps://www.sciencedirect.com/science/article/pii/S01674889240000280
2024Epigallocatechin gallate modulates ferroptosis through downregulation of tsRNA-13502 in non-small cell lung cancerShun Wanghttps://cancerci.biomedcentral.com/articles/10.1186/s12935-024-03391-50
2023Epigallocatechin-3-gallate and its nanoformulation in cervical cancer therapy: the role of genes, MicroRNA and DNA methylation patternsGuichun Wanghttps://cancerci.biomedcentral.com/articles/10.1186/s12935-023-03161-90
2023Epigallocatechin-3-gallate and cancer: focus on the role of microRNAsChunguang Wanghttps://cancerci.biomedcentral.com/articles/10.1186/s12935-023-03081-80
2023Improving the anti-tumor effect of EGCG in colorectal cancer cells by blocking EGCG-induced YAP activationYu Wanghttps://www.researchgate.net/publication/370713821_Improving_the_anti-tumor_effect_of_EGCG_in_colorectal_cancer_cells_by_blocking_EGCG-induced_YAP_activation0
2023EGCG: The antioxidant powerhouse in lung cancer management and chemotherapy enhancementAmit Sehgalhttps://www.sciencedirect.com/science/article/pii/S26671379230002550
2023The Potential Role of Epigallocatechin-3-Gallate (EGCG) in Breast Cancer TreatmentVíctor MarínPMC10341956https://pmc.ncbi.nlm.nih.gov/articles/PMC10341956/0
2023Epigallocatechin-3-gallate restores mitochondrial homeostasis impairment by inhibiting HDAC1-mediated NRF1 histone deacetylation in cardiac hypertrophyGu Lihttps://link.springer.com/article/10.1007/s11010-023-04768-20
2023Targeting fibrotic signaling pathways by EGCG as a therapeutic strategy for uterine fibroidsMd Soriful Islam2023https://www.nature.com/articles/s41598-023-35212-60
2023Effectiveness of epigallocatechin gallate nanoparticles on the in-vivo treatment of Alzheimer's disease in a rat/mouse model: a systematic reviewMaha K A KhalifaPMC11087435https://pmc.ncbi.nlm.nih.gov/articles/PMC11087435/0
2023The Effects of Green Tea Catechins in Hematological MalignanciesFernanda Isabel Della ViaPMC10385775https://pmc.ncbi.nlm.nih.gov/articles/PMC10385775/0
2023Cardioprotective effect of epigallocatechin gallate in myocardial ischemia/reperfusion injury and myocardial infarction: a meta-analysis in preclinical animal studiesXin-Yu WeiPMC10462709https://pmc.ncbi.nlm.nih.gov/articles/PMC10462709/0
2023Effects of Epigallocatechin-3-Gallate on Matrix Metalloproteinases in Terms of Its Anticancer ActivityHiroki Tanabehttps://pmc.ncbi.nlm.nih.gov/articles/PMC9862901/0
2023Epigallocatechin-3-Gallate Prevents the Acquisition of a Cancer Stem Cell Phenotype in Ovarian Cancer Tumorspheres through the Inhibition of Src/JAK/STAT3 SignalingSahily Rodriguez Torreshttps://www.mdpi.com/2227-9059/11/4/10000
2023Epigallocatechin-3-Gallate Therapeutic Potential in Cancer: Mechanism of Action and Clinical ImplicationsMateusz Kciukhttps://pmc.ncbi.nlm.nih.gov/articles/PMC10343677/pdf/molecules-28-05246.pdf0
2023An Update on Impacts of Epigallocatechin Gallate Co-administration in Modulating Pharmacokinetics of Statins, Calcium Channel Blockers, and Beta-blockersLee Siew-Keah37328148https://pubmed.ncbi.nlm.nih.gov/37328148/0
2022Antioxidation Function of EGCG by Activating Nrf2/HO-1 Pathway in Mice with Coronary Heart DiseaseXiaoyi HuangPMC9293516https://pmc.ncbi.nlm.nih.gov/articles/PMC9293516/0
2022Structure-based discovery of small molecules that disaggregate Alzheimer’s disease tissue derived tau fibrils in vitroPaul M SeidlerPMC9481533https://pmc.ncbi.nlm.nih.gov/articles/PMC9481533/0
2022EGCG-coated silver nanoparticles self-assemble with selenium nanowires for treatment of drug-resistant bacterial infections by generating ROS and disrupting biofilmsChenhao Yanghttps://www.semanticscholar.org/paper/EGCG-coated-silver-nanoparticles-self-assemble-with-Yang-Wang/36ea7fc4cf689f9c6637599e8374ae35fdaef86f0
2022Identification of plant-based hexokinase 2 inhibitors: combined molecular docking and dynamics simulation studiesAsifa Khan34176437https://pubmed.ncbi.nlm.nih.gov/34176437/0
2022Epigallocatechin gallate triggers apoptosis by suppressing de novo lipogenesis in colorectal carcinoma cellsPhuriwat KhiewkamroPMC9063442https://pmc.ncbi.nlm.nih.gov/articles/PMC9063442/0
2022Epigallocatechin-3-gallate Delivered in Nanoparticles Increases Cytotoxicity in Three Breast Carcinoma Cell LinesFulvia Farabegolihttps://pubs.acs.org/doi/10.1021/acsomega.2c01829#0
2022Laminin Receptor-Mediated Nanoparticle Uptake by Tumor Cells: Interplay of Epigallocatechin Gallate and Magnetic Force at Nano-Bio InterfaceSheng-Chieh HsuPMC9330565https://pmc.ncbi.nlm.nih.gov/articles/PMC9330565/0
2022When Natural Compounds Meet Nanotechnology: Nature-Inspired Nanomedicines for Cancer ImmunotherapyLinna Yuhttps://www.researchgate.net/publication/362395636_When_Natural_Compounds_Meet_Nanotechnology_Nature-Inspired_Nanomedicines_for_Cancer_Immunotherapy0
2022The Potential of Epigallocatechin Gallate (EGCG) in Targeting Autophagy for Cancer Treatment: A Narrative ReviewElena Ferrarihttps://www.researchgate.net/publication/360934968_The_Potential_of_Epigallocatechin_Gallate_EGCG_in_Targeting_Autophagy_for_Cancer_Treatment_A_Narrative_Review0
2022Epigallocatechin-3-gallate suppresses hemin-aggravated colon carcinogenesis through Nrf2-inhibited mitochondrial reactive oxygen species accumulationJu Hyung SeokPMC9523342https://pmc.ncbi.nlm.nih.gov/articles/PMC9523342/0
2022Characterization of mesenchymal stem cells with augmented internalization of magnetic nanoparticles: The implication of therapeutic potentialChing-Hui Chienhttps://www.sciencedirect.com/science/article/abs/pii/S03048853220094530
2022EGCG Enhances the Chemosensitivity of Colorectal Cancer to Irinotecan through GRP78-MediatedEndoplasmic Reticulum StressWenbing Wuhttps://onlinelibrary.wiley.com/doi/full/10.1155/2022/70995890
2021Simple Approach to Enhance Green Tea Epigallocatechin Gallate Stability in Aqueous Solutions and Bioavailability: Experimental and Theoretical CharacterizationsPhilippe-Henri SecretanPMC8706847https://pmc.ncbi.nlm.nih.gov/articles/PMC8706847/0
2021Thymoquinone Is a Multitarget Single Epidrug That Inhibits the UHRF1 Protein ComplexOmeima AbdullahPMC8143546https://pmc.ncbi.nlm.nih.gov/articles/PMC8143546/0
2021Epigallocatechin-3-Gallate Provides Protection Against Alzheimer's Disease-Induced Learning and Memory Impairments in RatsShanji NanPMC8128347https://pmc.ncbi.nlm.nih.gov/articles/PMC8128347/0
2021Flavonoids Targeting HIF-1: Implications on Cancer MetabolismMarek SamecPMC7794792https://pmc.ncbi.nlm.nih.gov/articles/PMC7794792/0
2020Epigallocatechin gallate inhibits HeLa cells by modulation of epigenetics and signaling pathwaysMadhumitha Kedhari SundaramPMC7584697https://pmc.ncbi.nlm.nih.gov/articles/PMC7584697/0
2020Prooxidant Effects of Epigallocatechin-3-Gallate in Health Benefits and Potential Adverse EffectJie OuyangPMC7441425https://pmc.ncbi.nlm.nih.gov/articles/PMC7441425/0
2020Epigallocatechin-3-gallate inhibits self-renewal ability of lung cancer stem-like cells through inhibition of CLOCKPan JiangPMC7595654https://pmc.ncbi.nlm.nih.gov/articles/PMC7595654/0
2020Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of CancerSaleh A. Almatroodihttps://www.mdpi.com/1420-3049/25/14/31460
2020Epigallocatechin-3-gallate (EGCG) Alters Histone Acetylation and Methylation and Impacts Chromatin Architecture Profile in Human Endothelial CellsOskar CiesielskiPMC7287656https://pmc.ncbi.nlm.nih.gov/articles/PMC7287656/0
2020Preclinical Pharmacological Activities of Epigallocatechin-3-gallate in Signaling Pathways: An Update on CancerMehdi Sharifi-Radhttps://www.researchgate.net/publication/338741198_Preclinical_Pharmacological_Activities_of_Epigallocatechin-3-gallate_in_Signaling_Pathways_An_Update_on_Cancer0
2020The pharmacological activity of epigallocatechin-3-gallate (EGCG) on Alzheimer's disease animal model: A systematic reviewShuang Zhang32942205https://pubmed.ncbi.nlm.nih.gov/32942205/0
2020Health Benefits and Chemical Composition of Matcha Green Tea: A ReviewJoanna KochmanPMC7796401https://pmc.ncbi.nlm.nih.gov/articles/PMC7796401/0
2020Protective Effect of Epigallocatechin-3-Gallate in Hydrogen Peroxide-Induced Oxidative Damage in Chicken LymphocytesXiaoqing ChiPMC7790551https://pmc.ncbi.nlm.nih.gov/articles/PMC7790551/0
2020Bioavailability of Epigallocatechin Gallate Administered With Different Nutritional Strategies in Healthy VolunteersVicente Andreu-Fernándezhttps://www.researchgate.net/publication/341598633_Bioavailability_of_Epigallocatechin_Gallate_Administered_With_Different_Nutritional_Strategies_in_Healthy_Volunteers0
2020Epigallocatechin-3-gallate downregulates PDHA1 interfering the metabolic pathways in human herpesvirus 8 harboring primary effusion lymphoma cellsLing-Chun Yehhttps://www.sciencedirect.com/science/article/abs/pii/S08872333193062410
2020Epigallocatechin Gallate (EGCG)https://www.alzforum.org/therapeutics/epigallocatechin-gallate-egcg0
2020The Role of EGCG in Breast Cancer Prevention and TherapyAdriana Romanohttps://www.researchgate.net/publication/347873100_The_Role_of_EGCG_in_Breast_Cancer_Prevention_and_Therapy0
2020EGCG impedes human Tau aggregation and interacts with TauShweta Kishor SonawanePMC7387440https://pmc.ncbi.nlm.nih.gov/articles/PMC7387440/0
2020Advanced Nanovehicles-Enabled Delivery Systems of Epigallocatechin Gallate for Cancer TherapyKai LiPMC7645157https://pmc.ncbi.nlm.nih.gov/articles/PMC7645157/0
2020The Epigenetic Modification of Epigallocatechin Gallate (EGCG) on CancerLinqi Yanghttps://www.researchgate.net/publication/341133182_The_Epigenetic_Modification_of_Epigallocatechin_Gallate_EGCG_on_Cancer0
2020Anticancer effects of epigallocatechin-3-gallate nanoemulsion on lung cancer cells through the activation of AMP-activated protein kinase signaling pathwayBing-Huei Chenhttps://www.nature.com/articles/s41598-020-62136-20
2020Iron Chelation Properties of Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Analysis on Tfr/Fth Regulations and Molecular DockingZarith Nameyrrahttps://www.researchgate.net/publication/340088640_Iron_Chelation_Properties_of_Green_Tea_Epigallocatechin-3-Gallate_EGCG_in_Colorectal_Cancer_Cells_Analysis_on_TfrFth_Regulations_and_Molecular_Docking0
2020Epigallocatechin-3-Gallate-Loaded Gold Nanoparticles: Preparation and Evaluation of Anticancer Efficacy in Ehrlich Tumor-Bearing MiceMohamed A SafwatPMC7559993https://pmc.ncbi.nlm.nih.gov/articles/PMC7559993/0
2020The “Big Five” Phytochemicals Targeting Cancer Stem Cells: Curcumin, EGCG, Sulforaphane, Resveratrol and GenisteinCord Naujokathttps://www.researchgate.net/publication/339583519_The_Big_Five_Phytochemicals_Targeting_Cancer_Stem_Cells_Curcumin_EGCG_Sulforaphane_Resveratrol_and_Genistein0
2020The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human DiseasShuangshuang ZhangPMC7504867https://pmc.ncbi.nlm.nih.gov/articles/PMC7504867/0
2019Epigallocatechin gallate (EGCG) suppresses epithelial-Mesenchymal transition (EMT) and invasion in anaplastic thyroid carcinoma cells through blocking of TGF-β1/Smad signaling pathwaysTingting LiPMC6650192https://pmc.ncbi.nlm.nih.gov/articles/PMC6650192/0
2019Induction of Endoplasmic Reticulum Stress Pathway by Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Activation of PERK/p-eIF2 α /ATF4 and IRE1 αZarith Nameyrra Md Nesrahttps://www.researchgate.net/publication/338109917_Induction_of_Endoplasmic_Reticulum_Stress_Pathway_by_Green_Tea_Epigallocatechin-3-Gallate_EGCG_in_Colorectal_Cancer_Cells_Activation_of_PERKp-eIF2_a_ATF4_and_IRE1_a0
2019Epigallocatechin-3-Gallate Prevents Acute Gout by Suppressing NLRP3 Inflammasome Activation and Mitochondrial DNA SynthesisHye Eun LeePMC6600669https://pmc.ncbi.nlm.nih.gov/articles/PMC6600669/0
2019EGCG maintained Nrf2-mediated redox homeostasis and minimized etoposide resistance in lung cancer cellsSuchisnigdhahttps://www.sciencedirect.com/science/article/abs/pii/S17564646193047730
2019Induction of Endoplasmic Reticulum Stress Pathway by Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Activation of PERK/p-eIF2α/ATF4 and IRE1αZarith Nameyrra Md NesranPMC6942794https://pmc.ncbi.nlm.nih.gov/articles/PMC6942794/0
2019Epigallocatechin-3-Gallate (EGCG) Suppresses Pancreatic Cancer Cell Growth, Invasion, and Migration partly through the Inhibition of Akt Pathway and Epithelial–Mesenchymal Transition: Enhanced Efficacy When Combined with GemcitabineRan Weihttps://www.researchgate.net/publication/335091666_Epigallocatechin-3-Gallate_EGCG_Suppresses_Pancreatic_Cancer_Cell_Growth_Invasion_and_Migration_partly_through_the_Inhibition_of_Akt_Pathway_and_Epithelial-Mesenchymal_Transition_Enhanced_Efficacy_whe0
2019Targeting Glycolysis with Epigallocatechin-3-Gallate Enhances the Efficacy of Chemotherapeutics in Pancreatic Cancer Cells and XenograftsRan WeiPMC6826788https://pmc.ncbi.nlm.nih.gov/articles/PMC6826788/0
2018Epigallocatechin-3-gallate Enhances Radiation Sensitivity in Colorectal Cancer Cells Through Nrf2 Activation and AutophagyTumenjin Enkhbat30396944https://pubmed.ncbi.nlm.nih.gov/30396944/0
2018Anti-fibrosis activity of combination therapy with epigallocatechin gallate, taurine and genistein by regulating glycolysis, gluconeogenesis, and ribosomal and lysosomal signaling pathways in HSC-T6 cellsYan LiPMC6257822https://pmc.ncbi.nlm.nih.gov/articles/PMC6257822/0
2018(-)- Epigallocatechin-3-gallate induces GRP78 accumulation in the ER and shifts mesothelioma constitutive UPR into proapoptotic ER stressSimona Martinotti29744892https://pubmed.ncbi.nlm.nih.gov/29744892/0
2018Nano-chemotherapeutic efficacy of (−) -epigallocatechin 3-gallate mediating apoptosis in A549 cells: Involvement of reactive oxygen species mediated Nrf2/Keap1signalingBakthavatchalam Velavanhttps://www.sciencedirect.com/science/article/abs/pii/S0006291X183160730
2018Evaluation of the neuroprotective effect of EGCG: a potential mechanism of mitochondrial dysfunction and mitochondrial dynamics after subarachnoid hemorrhageYing Chen30452052https://pubmed.ncbi.nlm.nih.gov/30452052/0
2018EGCG inhibits CSC-like properties through targeting miR-485/CD44 axis in A549-cisplatin resistant cellsPan Jiang30182373https://pubmed.ncbi.nlm.nih.gov/30182373/0
2018Green Tea Catechin Is an Alternative Immune Checkpoint Inhibitor that Inhibits PD-L1 Expression and Lung Tumor GrowthAnchalee RawangkanPMC6222340https://pmc.ncbi.nlm.nih.gov/articles/PMC6222340/0
2018(−)-Epigallocatechin-3-gallate protects PC12 cells against corticosterone-induced neurotoxicity via the hedgehog signaling pathwaySha FengPMC5920970https://pmc.ncbi.nlm.nih.gov/articles/PMC5920970/0
2018Matcha green tea (MGT) inhibits the propagation of cancer stem cells (CSCs), by targeting mitochondrial metabolism, glycolysis and multiple cell signalling pathwaysGloria BonuccelliPMC6128439https://pmc.ncbi.nlm.nih.gov/articles/PMC6128439/0
2018The Effect of Ultrasound, Oxygen and Sunlight on the Stability of (−)-Epigallocatechin GallateJiajun ZengPMC6225204https://pmc.ncbi.nlm.nih.gov/articles/PMC6225204/0
2018Epigallocatechin gallate suppresses hepatic cholesterol synthesis by targeting SREBP-2 through SIRT1/FOXO1 signaling pathwayYongnan Li29446047https://pubmed.ncbi.nlm.nih.gov/29446047/0
2018Suppressive Effects of EGCG on Cervical CancerYing-Qi Wanghttps://www.researchgate.net/publication/327610816_Suppressive_Effects_of_EGCG_on_Cervical_Cancer0
2018Interaction of poly-l-lysine coating and heparan sulfate proteoglycan on magnetic nanoparticle uptake by tumor cellsWei Xiong Siowhttps://www.researchgate.net/publication/323871065_Interaction_of_poly-l-lysine_coating_and_heparan_sulfate_proteoglycan_on_magnetic_nanoparticle_uptake_by_tumor_cells0
2018Suppressing glucose metabolism with epigallocatechin-3-gallate (EGCG) reduces breast cancer cell growth in preclinical modelsRan Weihttps://www.researchgate.net/publication/328236054_Suppressing_glucose_metabolism_with_epigallocatechin-3-gallate_EGCG_reduces_breast_cancer_cell_growth_in_preclinical_models0
2018Cancer preventive and therapeutic effects of EGCG, the major polyphenol in green teaIslam Radyhttps://www.researchgate.net/publication/321911600_Cancer_preventive_and_therapeutic_effects_of_EGCG_the_major_polyphenol_in_green_tea0
2018Scientific opinion on the safety of green tea catechinsEFSA Panel on Food Additiveshttps://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2018.52390
2018Cancer Prevention with Green Tea and Its Principal Constituent, EGCG: from Early Investigations to Current Focus on Human Cancer Stem CellsHirota FujikiPMC5824026https://pmc.ncbi.nlm.nih.gov/articles/PMC5824026/0
2018Case Report of Unexpectedly Long Survival of Patient With Chronic Lymphocytic Leukemia: Why Integrative Methods MatterGregory HaskinPMC6380985https://pmc.ncbi.nlm.nih.gov/articles/PMC6380985/0
2018Molecular Targets of Epigallocatechin—Gallate (EGCG): A Special Focus on Signal Transduction and CancerAide NegriPMC6315581https://pmc.ncbi.nlm.nih.gov/articles/PMC6315581/0
2017Epigallocatechin-3-gallate enhances ER stress-induced cancer cell apoptosis by directly targeting PARP16 activityJuanjuan WangPMC5502302https://pmc.ncbi.nlm.nih.gov/articles/PMC5502302/0
2017(-)-Epigallocatechin-3-gallate ameliorates memory impairment and rescues the abnormal synaptic protein levels in the frontal cortex and hippocampus in a mouse model of Alzheimer's diseaseYufang Guo28520620https://pubmed.ncbi.nlm.nih.gov/28520620/0
2017Epigallocatechin gallate upregulates NRF2 to prevent diabetic nephropathy via disabling KEAP1Weixia Sun28457936https://pubmed.ncbi.nlm.nih.gov/28457936/0
2017Insights on the involvement of (-)-epigallocatechin gallate in ER stress-mediated apoptosis in age-related macular degenerationBose Karthikeyan27778132https://pubmed.ncbi.nlm.nih.gov/27778132/0
2017(−)-Epigallocatechin-3-Gallate Inhibits Colorectal Cancer Stem Cells by Suppressing Wnt/β-Catenin PathwayYue ChenPMC5490551https://pmc.ncbi.nlm.nih.gov/articles/PMC5490551/0
2017Epigallocatechin gallate has pleiotropic effects on transmembrane signaling by altering the embedding of transmembrane domainsFeng YePMC5473239https://pmc.ncbi.nlm.nih.gov/articles/PMC5473239/0
2017Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallateHirota FujikiPMC5693978https://pmc.ncbi.nlm.nih.gov/articles/PMC5693978/0
2017Epigallocatechin-3-gallate promotes angiogenesis via up-regulation of Nfr2 signaling pathway in a mouse model of ischemic strokeQian Baihttps://www.sciencedirect.com/science/article/abs/pii/S01664328163078720
2017EGCG, a tea polyphenol, as a potential mitigator of hematopoietic radiation injury in miceMrinalini Tiwarihttps://www.sciencedirect.com/science/article/abs/pii/S07533322163266950
2017Anti-platelet effects of epigallocatechin-3-gallate in addition to the concomitant aspirin, clopidogrel or ticagrelor treatmentHyung Joon JooPMC5943656https://pmc.ncbi.nlm.nih.gov/articles/PMC5943656/0
2017Comparative efficacy of epigallocatechin-3-gallate against H2O2-induced ROS in cervical cancer biopsies and HeLa cell linesSohail Hussainhttps://pmc.ncbi.nlm.nih.gov/articles/PMC5701581/0
2017A new molecular mechanism underlying the EGCG-mediated autophagic modulation of AFP in HepG2 cellsLin Zhaohttps://www.nature.com/articles/cddis20175630
2016Tea polyphenols EGCG and TF restrict tongue and liver carcinogenesis simultaneously induced by N-nitrosodiethylamine in miceSubhayan Sur27058323https://pubmed.ncbi.nlm.nih.gov/27058323/0
2016Epigallocatechin gallate and mitochondria—A story of life and deathMarcos Roberto de Oliveirahttps://www.sciencedirect.com/science/article/abs/pii/S10436618153015600
2016Protective effect of epigallocatechin-3-gallate (EGCG) via Nrf2 pathway against oxalate-induced epithelial mesenchymal transition (EMT) of renal tubular cellsRattiyaporn Kanlayahttps://www.nature.com/articles/srep302330
2016EGCG inhibited bladder cancer SW780 cell proliferation and migration both in vitro and in vivo via down regulation of NF-κB and MMP-9Ke-Wang Luohttps://www.researchgate.net/publication/311782892_EGCG_inhibited_bladder_cancer_SW780_cell_proliferation_and_migration_both_in_vitro_and_in_vivo_via_down_regulation_of_NF-kB_and_MMP-90
2016Epigallocatechin-3-gallate targets cancer stem-like cells and enhances 5-fluorouracil chemosensitivity in colorectal cancerShusuke Todenhttps://www.researchgate.net/publication/304940512_Epigallocatechin-3-gallate_targets_cancer_stem-like_cells_and_enhances_5-fluorouracil_chemosensitivity_in_colorectal_cancer0
2016In vitro and in vivo study of epigallocatechin-3-gallate-induced apoptosis in aerobic glycolytic hepatocellular carcinoma cells involving inhibition of phosphofructokinase activitySainan LiPMC4923908https://pmc.ncbi.nlm.nih.gov/articles/PMC4923908/0
2016Anti-cancer effect of EGCG and its mechanismsMotofumi Kumazoehttps://www.researchgate.net/publication/318469094_Anti-cancer_effect_of_EGCG_and_its_mechanisms0
2016Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapyPiwen Wanghttps://www.researchgate.net/publication/301933430_Green_tea_and_quercetin_sensitize_PC-3_xenograft_prostate_tumors_to_docetaxel_chemotherapy0
2015EGCG antagonizes Bortezomib cytotoxicity in prostate cancer cells by an autophagic mechanismAlice ModernelliPMC4607952https://pmc.ncbi.nlm.nih.gov/articles/PMC4607952/0
2015A Case of Complete and Durable Molecular Remission of Chronic Lymphocytic Leukemia Following Treatment with Epigallocatechin-3-gallate, an Extract of Green TeaDawn Lemanne, Keith I. Blockhttps://pmc.ncbi.nlm.nih.gov/articles/PMC4739749/pdf/cureus-0007-000000000441.pdf0
2015Estrogen receptor-α36 is involved in epigallocatechin-3-gallate induced growth inhibition of ER-negative breast cancer stem/progenitor cellsXiaohua Panhttps://www.researchgate.net/publication/289992020_Estrogen_receptor-a36_is_involved_in_epigallocatechin-3-gallate_induced_growth_inhibition_of_ER-negative_breast_cancer_stemprogenitor_cells0
2015Food Inhibits the Oral Bioavailability of the Major Green Tea Antioxidant Epigallocatechin Gallate in HumansNenad Naumovskihttps://www.mdpi.com/2076-3921/4/2/3730
2015Epigallocatechin-3-gallate treatment to promote neuroprotection and functional recovery after nervous system injuryPere Boadas-VaelloPMC4625495https://pmc.ncbi.nlm.nih.gov/articles/PMC4625495/0
2015A Case of Complete and Durable Molecular Remission of Chronic Lymphocytic Leukemia Following Treatment with Epigallocatechin-3-gallate, an Extract of Green TeaDawn Lemannehttps://glennsabin.com/wp-content/uploads/2016/01/Glenn_Sabin_Cureus_case_report.pdf0
2015Biocompatible and biodegradable nanoparticles for enhancement of anti-cancer activities of phytochemicalsChuan LIhttps://www.researchgate.net/publication/282316276_Biocompatible_and_biodegradable_nanoparticles_for_enhancement_of_anti-cancer_activities_of_phytochemicals0
2015(-)-Epigallocatechin-3-gallate attenuates cognitive deterioration in Alzheimer's disease model mice by upregulating neprilysin expressionXiang Chang25882496https://pubmed.ncbi.nlm.nih.gov/25882496/0
2015Molecular mechanisms for inhibition of colon cancer cells by combined epigenetic-modulating epigallocatechin gallate and sodium butyrateSabita N SaldanhaPMC4043227https://pmc.ncbi.nlm.nih.gov/articles/PMC4043227/0
2015(−)-Epigallocatechin-3-gallate attenuates cognitive deterioration in Alzheimer׳s disease model mice by upregulating neprilysin expressionXiang Changhttps://www.sciencedirect.com/science/article/abs/pii/S00144827150013660
2015Epigallocatechin gallate inhibits human tongue carcinoma cells via HK2‑mediated glycolysisFeng Gao25591943https://pubmed.ncbi.nlm.nih.gov/25591943/0
2015Metabolic Consequences of LDHA inhibition by Epigallocatechin Gallate and Oxamate in MIA PaCa-2 Pancreatic Cancer CellsQing-Yi LuPMC4523095https://pmc.ncbi.nlm.nih.gov/articles/PMC4523095/0
2015(-)-Epigallocatechin-3-gallate reverses the expression of various tumor-suppressor genes by inhibiting DNA methyltransferases and histone deacetylases in human cervical cancer cellsMunawwar Ali Khan25682960https://pubmed.ncbi.nlm.nih.gov/25682960/0
2014The antimicrobial possibilities of green teaWanda C ReygaertPMC4138486https://pmc.ncbi.nlm.nih.gov/articles/PMC4138486/0
2014Green tea catechins potentiate the neuritogenic action of brain-derived neurotrophic factor: role of 67-kDa laminin receptor and hydrogen peroxideUsha Gundimeda24508265https://pubmed.ncbi.nlm.nih.gov/24508265/0
2014Epigallocatechin-3-gallate (EGCG)-stabilized selenium nanoparticles coated with Tet-1 peptide to reduce amyloid-β aggregation and cytotoxicityJingnan Zhang24758520https://pubmed.ncbi.nlm.nih.gov/24758520/0
2014Augmented cellular uptake of nanoparticles using tea catechins: effect of surface modification on nanoparticle-cell interactionYi-Ching Lu25069428https://pubmed.ncbi.nlm.nih.gov/25069428/0
2014Phase 2 Trial of Daily, Oral Polyphenon E in Patients with Asymptomatic, Rai Stage 0-II Chronic Lymphocytic Leukemia(CLL)Tait D ShanafeltPMC3902473https://pmc.ncbi.nlm.nih.gov/articles/PMC3902473/0
2014New insights into the mechanisms of polyphenols beyond antioxidant properties; lessons from the green tea polyphenol, epigallocatechin 3-gallateHae-Suk KimPMC3909779https://pmc.ncbi.nlm.nih.gov/articles/PMC3909779/0
2014Cancer prevention trial of a synergistic mixture of green tea concentrate plus Capsicum (CAPSOL-T) in a random population of subjects ages 40-84Claudia HanauPMC3901999https://pmc.ncbi.nlm.nih.gov/articles/PMC3901999/0
2014Green Tea Polyphenol Epigallocatechin 3-Gallate, Contributes to the Degradation of DNMT3A and HDAC3 in HCT 116 Human Colon Cancer CellsVONDINA R MOSELEYPMC4017340https://pmc.ncbi.nlm.nih.gov/articles/PMC4017340/0
2014Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applicationsBrahma N SinghPMC4082721https://pmc.ncbi.nlm.nih.gov/articles/PMC4082721/0
2013Inhibition of sonic hedgehog pathway and pluripotency maintaining factors regulate human pancreatic cancer stem cell characteristicsSu-Ni TangPMC3480310https://pmc.ncbi.nlm.nih.gov/articles/PMC3480310/0
2013Antioxidant effects of green teaSARAH C FORESTERPMC3679539https://pmc.ncbi.nlm.nih.gov/articles/PMC3679539/0
2013(-)-Epigallocatechin-3-gallate induces apoptosis in human endometrial adenocarcinoma cells via ROS generation and p38 MAP kinase activationMurli Manohar22959059https://pubmed.ncbi.nlm.nih.gov/22959059/0
2013Epigallocatechin-3-gallate-capped Ag nanoparticles: preparation and characterizationShokit Hussainhttps://link.springer.com/article/10.1007/s00449-013-1094-00
2013EGCG, a major green tea catechin suppresses breast tumor angiogenesis and growth via inhibiting the activation of HIF-1α and NFκB, and VEGF expressionJian-Wei GuPMC3649947https://pmc.ncbi.nlm.nih.gov/articles/PMC3649947/0
2013Targeting the AMP-Activated Protein Kinase for Cancer Prevention and TherapyInyoung Kimhttps://www.researchgate.net/publication/250926581_Targeting_the_AMP-Activated_Protein_Kinase_for_Cancer_Prevention_and_Therapy0
2013Bioactivity-Guided Identification and Cell Signaling Technology to Delineate the Lactate Dehydrogenase A Inhibition Effects of Spatholobus suberectus on Breast CancerZhiyu WangPMC3572989https://pmc.ncbi.nlm.nih.gov/articles/PMC3572989/0
2013Novel epigallocatechin gallate (EGCG) analogs activate AMP-activated protein kinase pathway and target cancer stem cellsDi ChenPMC3334407https://pmc.ncbi.nlm.nih.gov/articles/PMC3334407/0
2012Epigallocathechin gallate, polyphenol present in green tea, inhibits stem-like characteristics and epithelial-mesenchymal transition in nasopharyngeal cancer cell linesChien-Hung LinPMC3575296https://pmc.ncbi.nlm.nih.gov/articles/PMC3575296/0
2012Prevention effect of EGCG in rat's lung cancer induced by benzopyreneQ.-X. Fenghttps://www.researchgate.net/publication/287947721_Prevention_effect_of_EGCG_in_rat's_lung_cancer_induced_by_benzopyrene0
2012Quercetin Increased the Antiproliferative Activity of Green Tea Polyphenol (-)-Epigallocatechin Gallate in Prostate Cancer CellsPiwen Wanghttps://www.tandfonline.com/doi/abs/10.1080/01635581.2012.6615140
2012Epigallocatechin Gallate (EGCG) Is the Most Effective Cancer Chemopreventive Polyphenol in Green TeaGuang-Jian DuPMC3509513https://pmc.ncbi.nlm.nih.gov/articles/PMC3509513/0
2011Epigallocatechin-3-gallate (EGCG) for Clinical Trials: More Pitfalls than Promises?Derliz MerelesPMC3189735https://pmc.ncbi.nlm.nih.gov/articles/PMC3189735/0
2011Dietary Epicatechin Promotes Survival of Obese Diabetic Mice and Drosophila melanogasterHongwei SiPMC3095141https://pmc.ncbi.nlm.nih.gov/articles/PMC3095141/0
2011Metabolite modulation of HeLa cell response to ENOX2 inhibitors EGCG and phenoxodiolLian-Ying Wuhttps://www.sciencedirect.com/science/article/abs/pii/S03044165110009360
2011Green tea constituents (−)-epigallocatechin-3-gallate (EGCG) and gallic acid induce topoisomerase I– and topoisomerase II–DNA complexes in cells mediated by pyrogallol-induced hydrogen peroxideMiguel López-Lázarohttps://academic.oup.com/mutage/article-abstract/26/4/489/1189168?redirectedFrom=fulltext&login=false0
2010The antioxidant and pro-oxidant activities of green tea polyphenols: a role in cancer preventionJoshua D LambertPMC2946098https://pmc.ncbi.nlm.nih.gov/articles/PMC2946098/0
2010Epigenetic targets of bioactive dietary components for cancer prevention and therapySyed M MeeranPMC3024548https://pmc.ncbi.nlm.nih.gov/articles/PMC3024548/0
2010Reciprocal Relationship Between Cytosolic NADH and ENOX2 Inhibition Triggers Sphingolipid-Induced Apoptosis in HeLa CellsThomas De Lucahttps://www.researchgate.net/publication/44644721_Reciprocal_Relationship_Between_Cytosolic_NADH_and_ENOX2_Inhibition_Triggers_Sphingolipid-Induced_Apoptosis_in_HeLa_Cells0
2010Molecular bases of thioredoxin and thioredoxin reductase-mediated prooxidant actions of (-)-epigallocatechin-3-gallateHuihui Zhang20951799https://pubmed.ncbi.nlm.nih.gov/20951799/0
2010(−)-Epigallocatechin Gallate, A Major Constituent of Green Tea, Poisons Human Type II TopoisomerasesOmari J BandelePMC2893035https://pmc.ncbi.nlm.nih.gov/articles/PMC2893035/0
2010Green tea polyphenol EGCG blunts androgen receptor function in prostate cancerImtiaz A Siddiqui https://www.researchgate.net/publication/49701530_Green_tea_polyphenol_EGCG_blunts_androgen_receptor_function_in_prostate_cancer0
2010(-)-Epigallocatechin-3-gallate induces apoptosis and suppresses proliferation by inhibiting the human Indian Hedgehog pathway in human chondrosarcoma cellsGuo-Qing Tang20127255https://pubmed.ncbi.nlm.nih.gov/20127255/0
2009Targeting CWR22Rv1 prostate cancer cell proliferation and gene expression by combinations of the phytochemicals EGCG, genistein and quercetinHsieh, T.-CPMC3641843https://pmc.ncbi.nlm.nih.gov/articles/PMC3641843/0
2008Epigallocatechin-3-gallate exhibits anti-tumor effect by perturbing redox homeostasis, modulating the release of pro-inflammatory mediators and decreasing the invasiveness of glioblastoma cellsAnindita Agarwal21479441https://pubmed.ncbi.nlm.nih.gov/21479441/0
2008Dual Roles of Nrf2 in CancerAlexandria LauPMC2652397https://pmc.ncbi.nlm.nih.gov/articles/PMC2652397/0
2007Epigallocatechin-3-gallate inhibits secretion of TNF-alpha, IL-6 and IL-8 through the attenuation of ERK and NF-kappaB in HMC-1 cellsHye-Young Shin17135765https://pubmed.ncbi.nlm.nih.gov/17135765/0
2006Green tea polyphenols modulate insulin secretion by inhibiting glutamate dehydrogenaseChanghong Li16476731https://pubmed.ncbi.nlm.nih.gov/16476731/0
2005Epigallocatechin-3-gallate, a green-tea polyphenol, suppresses Rho signaling in TWNT-4 human hepatic stellate cellsNobuhiko Higashi15976760https://pubmed.ncbi.nlm.nih.gov/15976760/0
2005EGCG upregulates phase-2 detoxifying and antioxidant enzymes via the Nrf2 signaling pathway in human breast epithelial cellsHye-Kyung Nahttps://aacrjournals.org/cancerres/article/65/9_Supplement/367/519963/EGCG-upregulates-phase-2-detoxifying-and0
2004Piperine enhances the bioavailability of the tea polyphenol (-)-epigallocatechin-3-gallate in miceJoshua D Lambert15284381https://pubmed.ncbi.nlm.nih.gov/15284381/0
2003Green tea epigallocatechin-3-gallate inhibits platelet signalling pathways triggered by both proteolytic and non-proteolytic agonistsRenzo Deana12719785https://pubmed.ncbi.nlm.nih.gov/12719785/0
2002Pharmacokinetics of tea catechins after ingestion of green tea and (-)-epigallocatechin-3-gallate by humans: formation of different metabolites and individual variabilityMao-Jung Lee12376503https://pubmed.ncbi.nlm.nih.gov/12376503/0
2002Inhibition of beta-catenin/Tcf activity by white tea, green tea, and epigallocatechin-3-gallate (EGCG): minor contribution of H(2)O(2) at physiologically relevant EGCG concentrationsWan-Mohaiza Dashwood12176021https://pubmed.ncbi.nlm.nih.gov/12176021/0
2002Cellular thiol status-dependent inhibition of tumor cell growth via modulation of retinoblastoma protein phosphorylation by (-)-epigallocatechinDavid Opare Kennedy11880178https://pubmed.ncbi.nlm.nih.gov/11880178/0
2000Tea polyphenols down-regulate the expression of the androgen receptor in LNCaP prostate cancer cellsFengge Renhttps://www.nature.com/articles/12035110
2000Preferential inhibition by (-)-epigallocatechin-3-gallate of the cell surface NADH oxidase and growth of transformed cells in cultureD. James Morre´0
2022Targeting cancer stem cells by nutraceuticals for cancer therapyMan Chuhttps://www.sciencedirect.com/science/article/abs/pii/S1044579X210020290
2010Common botanical compounds inhibit the hedgehog signaling pathway in prostate cancerAnna Slusarz20395211https://pubmed.ncbi.nlm.nih.gov/20395211/0
2012Antiproliferative and Apoptotic Effects Triggered by Grape Seed Extract (GSE) versus Epigallocatechin and Procyanidins on Colon Cancer Cell LinesSimona DinicolaPMC3269711https://pmc.ncbi.nlm.nih.gov/articles/PMC3269711/0
2013Plant polyphenol induced cell death in human cancer cells involves mobilization of intracellular copper ions and reactive oxygen species generation: a mechanism for cancer chemopreventive actionHusain Yar Khan24123728https://pubmed.ncbi.nlm.nih.gov/24123728/0
2020Prospective randomized trial evaluating blood and prostate tissue concentrations of green tea polyphenols and quercetin in men with prostate cancerSusanne M. Henninghttps://pubs.rsc.org/en/content/articlelanding/2020/fo/d0fo00565g0
2013Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green teaPiwen WangPMC3858726https://pmc.ncbi.nlm.nih.gov/articles/PMC3858726/0
2010The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transitionSu-Ni TangPMC2933702https://pmc.ncbi.nlm.nih.gov/articles/PMC2933702/0
2010The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transitionSu-Ni Tanghttps://link.springer.com/article/10.1186/1750-2187-5-140
2025Targeting aging pathways with natural compounds: a review of curcumin, epigallocatechin gallate, thymoquinone, and resveratrolMohamed AhmedPMC12225039https://pmc.ncbi.nlm.nih.gov/articles/PMC12225039/0
2010Antithrombotic effects of naturally derived products on coagulation and platelet functionShaker A Mousa20617421https://pubmed.ncbi.nlm.nih.gov/20617421/0
2022A Combination Therapy of Urolithin A+EGCG Has Stronger Protective Effects than Single Drug Urolithin A in a Humanized Amyloid Beta Knockin Mice for Late-Onset Alzheimer’s DiseaseSudhir KshirsagarPMC9454743https://pmc.ncbi.nlm.nih.gov/articles/PMC9454743/0
2022A Combination Therapy of Urolithin A+EGCG Has Stronger Protective Effects than Single Drug Urolithin A in a Humanized Amyloid Beta Knockin Mice for Late-Onset Alzheimer's DiseaseSudhir KshirsagarPMC9454743https://pmc.ncbi.nlm.nih.gov/articles/PMC9454743/0