EGCG (Epigallocatechin Gallate) / PKM2 Cancer Research Results

EGCG, EGCG (Epigallocatechin Gallate): Click to Expand ⟱
Features:

Epigallocatechin-3-gallate — EGCG is a naturally occurring galloylated flavan-3-ol and the quantitatively dominant catechin in green tea leaves from Camellia sinensis. 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.

Primary mechanisms (ranked):

  1. 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.
  2. Suppression of proliferative and survival signalling, particularly PI3K–AKT–mTOR, NF-κB, receptor tyrosine kinase, STAT and context-dependent MAPK pathways.
  3. Mitochondrial dysfunction and intrinsic apoptosis through mitochondrial membrane-potential loss, cytochrome-c release and caspase activation.
  4. Cell-cycle arrest through modulation of cyclins, cyclin-dependent kinases, p21, p27 and p53-associated signalling.
  5. Inhibition of invasion, epithelial–mesenchymal transition and extracellular-matrix degradation through reduced FAK, MMP-2, MMP-9, uPA and related motility pathways.
  6. Suppression of HIF-1α–VEGF signalling, angiogenesis and hypoxia adaptation.
  7. Metabolic disruption involving reduced glycolysis, glucose transport and context-dependent mitochondrial energy production.
  8. Epigenetic modulation, including experimental inhibition or altered expression of DNMTs, HDACs and EZH2.
  9. Modulation of proteostasis, autophagy, endoplasmic-reticulum stress and unfolded-protein responses.
  10. NRF2 activation as a secondary adaptive mechanism, generally cytoprotective in normal cells but potentially protective or treatment-resistant in some cancers.
  11. Chemosensitization or radiosensitization in selected experimental models; treatment protection, antagonism or normal-tissue radioprotection can also occur depending on dose, schedule and therapy.

Bioavailability / PK relevance: 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.

In-vitro vs systemic exposure relevance: 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.

Clinical evidence status: 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.

Safety and interactions: 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.



EGCG (Epigallocatechin Gallate) 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.
EGCG Epigallocatechin Gallate (Green Tea) -Catechin
Summary:
1. Concentration is a factor that could determine whether green tea polyphenols act as antioxidants or pro-oxidants.
2. Poor bioavailability: taking EGCG capsules without food was better.
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)
4. EGCG is susceptible to oxidative degradation.
5. “As for the pH level, the acidic environments enhance the stability of EGCG”.
6. “EGCG may enhance nanoparticle uptake by tumor cells”
7. Might be iron chelator (removing iron from cancer cells)
8. Claimed as synergistic effect with chemotherapy ( cisplatin, bleomycin, gemcitabine.
9. May suppress glucose metabolism, interfere with VEGF, downregulate NF-κB and MMP-9, down-regulation of androgen-regulated miRNA-21.
10. Take with red pepper powder, Capsicum ratio 25:1 (based on half life, they did every 4 hr) (chili pepper vanilloid capsaicin).
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]
12. Matcha green tea has highest EGCG (2-3X) because consuming leaf.
13. EGCG is an ENOX2 inhibitor.
14. Nrf2 activator in both cancer and normal cells. This example of lung cancer show both directions in different cell lines, but both toward optimim level.
Biological activity, EGCG has been reported to exhibit a range of effects, including:
    Antioxidant activity: 10-50 μM
     Anti-inflammatory activity: 20-50 μM
     Anticancer activity: 50-100 μM
     Cardiovascular health: 20-50 μM
     Neuroprotective activity: 10-50 μM

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.

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.

Reported values can range from about 25–50 mg of EGCG per gram of matcha powder.
In cases where the matcha is exceptionally catechin-rich, the content could reach 200–250 mg or more in 5 g.

-Peak plasma concentration roughly 1 to 2 hours after oral ingestion.
-Elimination half-life of EGCG in plasma is commonly reported to be in the range of about 3 to 5 hours.

Supplemental EGCG
Dose (mg)   ≈ Peak Plasma EGCG (µM)
~50 mg          ≈ 0.1–0.3 µM
~100 mg         ≈ 0.2–0.6 µM
~250 mg         ≈ 0.5–1.0 µM
~500 mg         ≈ 1–2 µM
~800 mg or higher  ≈ 1–5 µM

50mg of EGCG in 1g of matcha tea(1/2 teaspoon)

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.

Methods to improve bioavailability
-Lipid-based carriers or nanoemulsions
-Polymer-based nanoparticles or encapsulation
-Co-administration with ascorbic acid (vitamin C)
-Co-administration of adjuvants like piperine (perhaps sunflower lecithin and chitosan) -Using multiple smaller doses rather than one large single dose.
-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).
– 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.
- At neutral (around pH 7) or alkaline pH, EGCG undergoes auto-oxidation, reducing the effective concentration available for absorption.
– 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.
– 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.
– The use of acidifiers or buffering agents in supplements may help preserve EGCG until it reaches the absorption sites.

-Note half-life 3–5 hours.
- low BioAv 1%? despite its limited absorption, it is rapidly disseminated throughout the body
Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Does NOT Lower AntiOxidant defense in Cancer Cells: NRF2↑, TrxR↓**, SOD, GSH Catalase HO1 GPx
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, FAK↓, RhoA↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, Hh↓, GLi↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, Notch↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective(possible damage at high dose), CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

EGCG Mechanistic Profile

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

P: 0–30 min    R: 30 min–3 hr    G: >3 hr



Alzheimer’s disease relevance: 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.

EGCG in Alzheimer’s Disease

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


PKM2, Pyruvate Kinase, Muscle 2: Click to Expand ⟱
Source:
Type: enzyme
PKM2 (Pyruvate Kinase, Muscle 2) is an enzyme that plays a crucial role in glycolysis, the process by which cells convert glucose into energy. PKM2 is a key regulatory enzyme in the glycolytic pathway, and it is primarily expressed in various tissues, including muscle, brain, and cancer cells.
-C-myc is a common oncogene that enhances aerobic glycolysis in the cancer cells by transcriptionally activating GLUT1, HK2, PKM2 and LDH-A
-PKM2 has been shown to be overexpressed in many types of tumors, including breast, lung, and colon cancer. This overexpression may contribute to the development and progression of cancer by promoting glycolysis and energy production in cancer cells.
-inhibition of PKM2 may cause ATP depletion and inhibiting glycolysis.
-PK exists in four isoforms: PKM1, PKM2, PKR, and PKL
-PKM2 plays a role in the regulation of glucose metabolism in diabetes.
-PKM2 is involved in the regulation of cell proliferation, apoptosis, and autophagy.
– Pyruvate kinase catalyzes the final, rate-limiting step of glycolysis, converting phosphoenolpyruvate (PEP) to pyruvate with the production of ATP.
– The PKM2 isoform is uniquely regulated and can exist in both highly active tetrameric and less active dimeric forms.
– Cancer cells often favor the dimeric form of PKM2 to slow pyruvate production, thereby accumulating upstream glycolytic intermediates that can be diverted into anabolic pathways to support cell growth and proliferation.
– Under low oxygen conditions, cancer cells rely on altered metabolic pathways in which PKM2 is a key player. – The shift to aerobic glycolysis (Warburg effect) orchestrated in part by PKM2 helps tumor cells survive and grow in hypoxic conditions.

– Elevated expression of PKM2 is frequently observed in many cancer types, including lung, breast, colorectal, and pancreatic cancers.
– High levels of PKM2 are often correlated with enhanced tumor aggressiveness, poor differentiation, and advanced clinical stage.

PKM2 in carcinogenesis and oncotherapy

Inhibitors of PKM2:
-Shikonin, Resveratrol, Baicalein, EGCG, Apigenin, Curcumin, Ursolic Acid, Citrate (best known as an allosteric inhibitor of phosphofructokinase-1 (PFK-1), a key rate-limiting enzyme in glycolysis) potential to directly inhibit or modulate PKM2 is less well established

Full List of PKM2 inhibitors from Database
-key connected observations: Glycolysis↓, lactateProd↓, ROS↑ in cancer cell, while some result for opposite effect on normal cells.
Tumor pyruvate kinase M2 modulators

Flavonoids effect on PKM2
Compounds name IC50/AC50uM Effect
Flavonols
1. Fisetin 0.90uM Inhibition
2. Rutin 7.80uM Inhibition
3. Galangin 8.27uM Inhibition
4. Quercetin 9.24uM Inhibition
5. Kaempferol 9.88uM Inhibition
6. Morin hydrate 37.20uM Inhibition
7. Myricetin 0.51uM Activation
8. Quercetin 3-b- D-glucoside 1.34uM Activation
9. Quercetin 3-D -galactoside 27-107uM Ineffective
Flavanons
10. Neoeriocitrin 0.65uM Inhibition
11. Neohesperidin 14.20uM Inhibition
12. Naringin 16.60uM Inhibition
13. Hesperidin 17.30uM Inhibition
14. Hesperitin 29.10uM Inhibition
15. Naringenin 70.80uM Activation
Flavanonols
16. (-)-Catechin gallateuM 0.85 Inhibition
17. (±)-Taxifolin 1.16uM Inhibition
18. (-)-Epicatechin 1.33uM Inhibition
19. (+)-Gallocatechin 4-16uM Ineffective
Phenolic acids
20. Ferulic 11.4uM Inhibition
21. Syringic and 13.8uM Inhibition
22. Caffeic acid 36.3uM Inhibition
23. 3,4-Dihydroxybenzoic acid 78.7uM Inhibition
24. Gallic acid 332.6uM Inhibition
25. Shikimic acid 990uM Inhibition
26. p-Coumaric acid 22.2uM Activation
27. Sinapinic acids 26.2uM Activation
28. Vanillic 607.9uM Activation


Scientific Papers found: Click to Expand⟱
2302- EGCG,    Flavonoids Targeting HIF-1: Implications on Cancer Metabolism
- Review, Var, NA
TumCP↓, Hif1a↓, LDHA↓, PFK↓, cardioP↑, Glycolysis↓, PKM2↓,
2309- EGCG,  Chemo,    Targeting Glycolysis with Epigallocatechin-3-Gallate Enhances the Efficacy of Chemotherapeutics in Pancreatic Cancer Cells and Xenografts
- in-vitro, PC, MIA PaCa-2 - in-vitro, Nor, HPNE - in-vitro, PC, PANC1 - in-vivo, NA, NA
TumCG↓, eff↑, ROS↑, ECAR↓, ChemoSen↑, selectivity↑, Glycolysis↓, PFK↓, PKA↓, HK2∅, LDHA∅, PFKP↓, PKM2↓, H2O2↑, TumW↓,
2395- EGCG,    EGCG inhibits diabetic nephrophathy through up regulation of PKM2
- Study, Diabetic, NA
*PKM2↑, *Apoptosis↓, *PGC-1α↑,
989- EGCG,  Citrate,    In vitro and in vivo study of epigallocatechin-3-gallate-induced apoptosis in aerobic glycolytic hepatocellular carcinoma cells involving inhibition of phosphofructokinase activity
- in-vitro, HCC, NA - in-vivo, NA, NA
PFK↓, Glycolysis↓, lactateProd↓, GlucoseCon↓, TumCP↓, TumCCA↑, Casp3↑, cl‑PARP↑, Apoptosis↑, Casp8↑, Casp9↑, Cyt‑c↝, MMP↓, BAD↑, GLUT2↓, PKM2∅,

Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

H2O2↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ECAR↓, 1,   GlucoseCon↓, 1,   GLUT2↓, 1,   Glycolysis↓, 3,   HK2∅, 1,   lactateProd↓, 1,   LDHA↓, 1,   LDHA∅, 1,   PFK↓, 3,   PFKP↓, 1,   PKM2↓, 2,   PKM2∅, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   BAD↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↝, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

TumCG↓, 1,  

Migration(tgid=13) ⓘ

PKA↓, 1,   TumCP↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   eff↑, 1,   selectivity↑, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   TumW↓, 1,  
Total Targets: 32

Pathway results for Effect on Normal Cells:


Mitochondria & Bioenergetics(tgid=3) ⓘ

PGC-1α↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PKM2↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,  
Total Targets: 3

Scientific Paper Hit Count for: PKM2, Pyruvate Kinase, Muscle 2
4 EGCG (Epigallocatechin Gallate)
1 Chemotherapy
1 Citric Acid
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:73  Target#:772  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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