Warburg Cancer Research Results

Warburg, Warburg Effect: Click to Expand ⟱
Source:
Type: effect

The Warburg effect (aerobic glycolysis) is a metabolic phenotype where many cancer cells use high glycolytic flux and lactate production even when oxygen is available. Tumors often contain hypoxic regions that further drive glycolysis, but Warburg metabolism can also occur under normoxic conditions (“pseudo-hypoxia”) via oncogenic signaling and metabolic rewiring.

Hypoxia-inducible factor 1 alpha (HIF-1α) is one important driver in hypoxic tumor regions. HIF-1α upregulates glycolytic genes (e.g., GLUT1, HK2, LDHA) and promotes reduced mitochondrial pyruvate oxidation in part through induction of PDK (which inhibits PDH), shifting carbon toward lactate.

Warburg effect (GLUT1, LDHA, HK2, and PKM2).
Classic HIF-Warburg axis: PDK1 and MCT4 (SLC16A3) (pyruvate gate + lactate export).

Here are some of the key pathways and potential targets:

Note: use database Filter to find inhibitors: Ex pick target HIF1α, and effect direction ↓

1.Glycolysis Inhibitors:(2-DG, 3-BP)
- HK2 Inhibitors: such as 2-deoxyglucose, can reduce glycolysis
-PFK1 Inhibitors: such as PFK-158, can reduce glycolysis
-PFKFB Inhibitors:
- PKM2 Inhibitors: (Shikonin)
-Can reduce glycolysis
- LDH Inhibitors: (Gossypol, FX11)
-Reducing the conversion of pyruvate to lactate.
-Inhibiting the production of ATP and NADH.
- GLUT1 Inhibitors: (phloretin, WZB117)
-A key transporter involved in glucose uptake.
-GLUT3 Inhibitors:
- PDK1 Inhibitors: (dichloroacetate)
- A key enzyme involved in the regulation of glycolysis. PDK inhibitors (e.g., DCA) activate PDH and shift pyruvate into TCA/OXPHOS, reducing lactate pressure.

2.Pentose phosphate pathway:
- G6PD Inhibitors: can reduce the pentose phosphate pathway

3.Hypoxia-inducible factor 1 alpha (HIF1α) pathway:
- HIF1α inhibitors: (PX-478,Shikonin)
-Reduce expression of glycolytic genes and inhibit cancer cell growth.

4.AMP-activated protein kinase (AMPK) pathway:
-AMPK activators: (metformin,AICAR,berberine)
-Can increase AMPK activity and inhibit cancer cell growth.

5.mTOR pathway:
- mTOR inhibitors:(rapamycin,everolimus)
-Can reduce mTOR activity and inhibit cancer cell growth.

Warburg Targeting Matrix (Cancer Metabolism)

Node What It Does (Warburg role) Representative Inhibitors / Modulators Mechanism Snapshot Typical Tumor Effects Best-Fit Tumor Context Common Constraints / Gotchas TSF Combination Logic
GLUT (glucose uptake)
GLUT1 (SLC2A1) focus		 Controls glucose entry; sets the upper bound on glycolytic flux. Research/repurposing: WZB117 (GLUT1), BAY-876 (GLUT1), STF-31 (GLUT1 tool), Fasentin (GLUT), Phloretin (broad, weak)
Dietary/indirect: some polyphenols reported to lower GLUT1 expression (context) 		Blocks glucose transport or reduces GLUT1 expression → less substrate for glycolysis & PPP. ATP stress (in highly glycolytic tumors), lactate ↓, growth slowdown; can sensitize to stressors. High-GLUT1 tumors; hypoxic / glycolysis-addicted phenotypes. Systemic glucose handling and glucose-dependent tissues; tumor compensation via alternate fuels. P, R Pairs with ROS/ETC stressors or LDH/MCT blockade; beware compensatory glutaminolysis/fatty acid oxidation.
Hexokinase (HK2)
first committed glycolysis step		 Traps glucose as G-6-P; HK2 often upregulated and mitochondria-associated in tumors. Clinical/adjunct interest: 2-Deoxyglucose (2-DG; glycolysis + glycosylation stress)
Research: Lonidamine-class glycolysis axis drugs (not “pure HK2”), 3-bromopyruvate (hazardous research agent; not for casual use) 		Competitive substrate mimic (2-DG) → 2-DG-6P accumulation; HK flux ↓; ER glycosylation stress ↑. ATP ↓, AMPK ↑, ER stress/UPR ↑, autophagy ↑, apoptosis (context); radiosensitization reported. Highly glycolytic tumors; tumors with strong HK2 dependence; hypoxic cores. Normal glucose-dependent tissues; ER-stress toxicities; dosing/tolerability limits in practice. P, R, G Pairs with radiation, pro-oxidant stress, or MCT/LDH blockade; watch systemic glucose effects.
LDH (LDHA/LDHB)
pyruvate ⇄ lactate		 Regenerates NAD+ to sustain glycolysis; LDHA supports lactate production and acidification. Tier A direct inhibitors: FX11, (R)-GNE-140, NCI-006, Oxamate, Galloflavin, Gossypol
Tier B indirect: polyphenols (often lactate/LDH expression ↓ rather than catalytic inhibition) 		Blocks LDH catalysis → NAD+ recycling ↓ → glycolysis throttles; pyruvate handling shifts; redox pressure ↑. Lactate ↓, glycolytic flux ↓, oxidative stress ↑ (often secondary), growth inhibition; immune microenvironment may improve if lactate decreases. LDHA-high tumors; lactate-driven immunosuppression; glycolysis-addicted phenotypes. Metabolic plasticity: tumors switch fuels; some LDH inhibitors have PK liabilities; “LDH release” ≠ LDH inhibition. R, G Pairs with MCT inhibition (trap lactate), NAD+ axis inhibitors, immune therapy (lactate suppression logic), and OXPHOS stressors (context).
MCT (lactate transport)
MCT1 (SLC16A1), MCT4 (SLC16A3)		 Exports lactate + H+ (acidifies TME); enables lactate shuttling between tumor subclones. Clinical-stage: AZD3965 (MCT1 inhibitor; clinical trials)
Research: AR-C155858 (MCT1/2), Syrosingopine (MCT1/4; repurposed), Lonidamine (MCT + MPC axis) 		Blocks lactate export/import → intracellular acid stress ↑ (in glycolytic cells) and lactate shuttling ↓. Acid stress, growth inhibition; may improve immune function by reducing lactate/acidic suppression (context). MCT1-high tumors; oxidative “lactate-using” tumor fractions; tumors with lactate shuttling. MCT4-driven export can bypass MCT1-only inhibitors; hypoxia upregulates MCT4; need target matching. P, R Pairs strongly with LDH inhibitors (cut production + block export), and with immune therapy rationale (lactate/acid microenvironment).
PDK (PDK1-4)
PDH gatekeeper		 PDK inhibits PDH → keeps pyruvate out of mitochondria; supports Warburg by favoring lactate. Prototype: Dichloroacetate (DCA; pan-PDK inhibitor “classic”)
Research: AZD7545 (PDK2 inhibitor; tool), newer PDK inhibitor series (research) 		Inhibits PDK → PDH active ↑ → pyruvate into TCA/OXPHOS ↑; lactate pressure ↓. Warburg reversal pressure (context), lactate ↓, mitochondrial flux ↑; can increase ROS in some settings (secondary). PDK-high tumors; tumors with suppressed PDH flux; “glycolysis locked” metabolic phenotype. Requires functional mitochondrial capacity; hypoxia can limit OXPHOS shift; effect is often modulatory rather than directly cytotoxic. R, G Pairs with therapies that exploit mitochondrial dependence or redox stress; can complement LDH/MCT strategies by reducing lactate drive.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (direct transport/enzyme flux effects begin)
  • R: 30 min–3 hr (acute ATP/NAD+/acid stress and signaling changes)
  • G: >3 hr (gene adaptation, phenotype outcomes, immune/TME effects)
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
5273- 3BP,    The promising anticancer drug 3-bromopyruvate is metabolized through glutathione conjugation which affects chemoresistance and clinical practice: An evidence-based view
- Review, Var, NA
AntiCan↑, ROS↑, angioG↓, CSCs↓, Warburg↓, GSH↓, Thiols↓,
5745- Buty,    Microbial Oncotarget: Bacterial-Produced Butyrate, Chemoprevention and Warburg Effect
- Review, Var, NA
selectivity↑, HDAC↓, TumCP↓, Apoptosis↑, Warburg↓, chemoPv↑,
1863- dietFMD,  Chemo,    Effect of fasting on cancer: A narrative review of scientific evidence
- Review, Var, NA
eff↑, ChemoSideEff↓, ChemoSen↑, Insulin↓, HDAC↓, IGF-1↓, STAT5↓, BG↓, MAPK↓, HO-1↓, ATG3↑, Beclin-1↑, p62↑, SIRT1↑, LAMP2↑, OXPHOS↑, ROS↑, P53↑, DNAdam↑, TumCD↑, ATP↑, Treg lymp↓, M2 MC↓, CD8+↑, Glycolysis↓, GutMicro↑, GutMicro↑, Warburg↓, Dose↝,
5069- dietSTF,    The Role of Intermittent Fasting in the Activation of Autophagy Processes in the Context of Cancer Diseases
- Review, Var, NA
Risk↓, ChemoSen↑, RadioS↑, *Dose↝, *Dose↝, *Dose↝, *LDL↓, *CRP↓, *TNF-α↓, TumAuto↓, GLUT1↓, GLUT2↓, glucose↓, IGF-1↓, Insulin↓, mTOR↓, mTORC1↓, AMPK↑, Warburg↓, OXPHOS↑, ROS↑, DNAdam↑, JAK1↓, STAT↓, TumCP↓, QoL↑,
649- EGCG,  CUR,  PI,    Targeting Cancer Hallmarks with Epigallocatechin Gallate (EGCG): Mechanistic Basis and Therapeutic Targets
- Review, Var, NA
*BioEnh↑, EGFR↓, HER2/EBBR2↓, IGF-1↓, MAPK↓, ERK↓, RAS↓, Raf↓, NF-kB↓, p‑pRB↓, TumCCA↑, Glycolysis↓, Warburg↓, HK2↓, Pyruv↓,
2313- Flav,    Flavonoids against the Warburg phenotype—concepts of predictive, preventive and personalised medicine to cut the Gordian knot of cancer cell metabolism
- Review, Var, NA
Warburg↓, antiOx↑, angioG↓, Glycolysis↓, PKM2↓, PKM2:PKM1↓, β-catenin/ZEB1↓, cMyc↓, HK2↓, Akt↓, mTOR↓, GLUT1↓, Hif1a↓,
2540- M-Blu,    Alternative mitochondrial electron transfer for the treatment of neurodegenerative diseases and cancers: Methylene blue connects the dots
- Review, Var, NA - Review, AD, NA
*OCR↑, *Glycolysis↓, *GlucoseCon↑, neuroP↑, Warburg↓, mt-OXPHOS↑, TumCCA↑, TumCP↓, ROS⇅, *cognitive↑, *mTOR↓, *mt-antiOx↑, *memory↑, *BBB↑, *eff↝, *ECAR↓, eff↑, lactateProd↓, NADPH↓, OXPHOS↑, AMPK↑, selectivity↑,
1782- MEL,    Melatonin in Cancer Treatment: Current Knowledge and Future Opportunities
- Review, Var, NA
AntiCan↑, Apoptosis↑, TumCP↓, TumCG↑, TumMeta↑, ChemoSideEff↓, radioP↑, ChemoSen↑, *ROS↓, *SOD↑, *GSH↑, *GPx↑, *Catalase↑, Dose∅, VEGF↓, eff↑, Hif1a↓, GLUT1↑, GLUT3↑, CAIX↑, P21↑, p27↑, PTEN↑, Warburg↓, PI3K↓, Akt↓, NF-kB↓, cycD1/CCND1↓, CDK4↓, CycB/CCNB1↓, CDK4↓, MAPK↑, IGF-1R↓, STAT3↓, MMP9↓, MMP2↓, MMP13↓, E-cadherin↑, Vim↓, RANKL↓, JNK↑, Bcl-2↓, P53↑, Casp3↑, Casp9↑, BAX↑, DNArepair↑, COX2↓, IL6↓, IL8↓, NO↓, T-Cell↑, NK cell↑, Treg lymp↓, FOXP3↓, CD4+↑, TNF-α↑, Th1 response↑, BioAv↝, RadioS↑, OS↑,
994- MET,    Tumor metabolism destruction via metformin-based glycolysis inhibition and glucose oxidase-mediated glucose deprivation for enhanced cancer therapy
- in-vitro, Var, NA
Glycolysis↓, HK2↓, ATP↓, AMPK↑, P53↑, Warburg↓, Apoptosis↑,
5254- NCL,    The magic bullet: Niclosamide
- Review, Var, NA
Wnt↓, β-catenin/ZEB1↓, RAS↓, STAT3↓, NOTCH↓, E2Fs↓, mTOR↓, eff↑, PD-1↓, PD-L1↓, BioAv↝, toxicity↓, BioAv↑, ETC↑, NADH:NAD↓, TCA↑, Warburg↓, Diff↑, AMPK↑, P53↑, PP2A↑, HIF-1↓, KRAS↓, Myc↓, RadioS↑, ChemoSen↑, Dose↝, Dose↑,
2332- RES,    Resveratrol’s Anti-Cancer Effects through the Modulation of Tumor Glucose Metabolism
- Review, Var, NA
Glycolysis↓, GLUT1↓, PFK1↓, Hif1a↓, ROS↑, PDH↑, AMPK↑, TumCG↓, TumCI↓, TumCP↓, p‑NF-kB↓, SIRT1↑, SIRT3↑, LDH↓, PI3K↓, mTOR↓, PKM2↓, R5P↝, G6PD↓, TKT↝, talin↓, HK2↓, GRP78/BiP↑, GlucoseCon↓, ER Stress↑, Warburg↓, PFK↓,
2441- RES,    Anti-Cancer Properties of Resveratrol: A Focus on Its Impact on Mitochondrial Functions
- Review, Var, NA
*toxicity↓, *BioAv↝, *Dose↝, *hepatoP↑, *neuroP↑, *AntiAg↑, *COX2↓, *antiOx↑, *ROS↓, *ROS↑, PI3K↓, Akt↓, NF-kB↓, Wnt↓, β-catenin/ZEB1↓, NRF2↑, GPx↑, HO-1↑, BioEnh?, PTEN↑, ChemoSen↑, eff↑, mt-ROS↑, Warburg↓, Glycolysis↓, GlucoseCon↓, GLUT1↓, lactateProd↓, HK2↓, EGFR↓, cMyc↓, ROS↝, MMPs↓, MMP7↓, survivin↓, TumCP↓, TumCMig↓, TumCI↓,
1748- RosA,    The Role of Rosmarinic Acid in Cancer Prevention and Therapy: Mechanisms of Antioxidant and Anticancer Activity
- Review, Var, NA
AntiCan↑, *BioAv↝, *CardioT↓, *Iron↓, *ROS↓, *SOD↑, *Catalase↑, *GPx↑, *NRF2↑, MARK4↓, MMP9↓, TumCCA↑, Bcl-2↓, BAX↑, Apoptosis↑, E-cadherin↑, N-cadherin↓, Vim↓, Gli1↓, HDAC2↓, Warburg↓, Hif1a↓, miR-155↓, p‑PI3K↑, ROS↑, *IronCh↑,
3003- RosA,    Comprehensive Insights into Biological Roles of Rosmarinic Acid: Implications in Diabetes, Cancer and Neurodegenerative Diseases
- Review, Var, NA - Review, AD, NA - Review, Park, NA
*Inflam↓, *antiOx↑, *neuroP↑, *IL6↓, *IL1β↓, *NF-kB↓, *PGE2↓, *COX2↓, *MMP↑, *memory↑, *ROS↓, *Aβ↓, *HMGB1↓, TumCG↓, MARK4↓, Zeb1↓, MDM2↓, BNIP3↑, ASC↑, NLRP3↓, PI3K↓, Akt↓, Casp1↓, E-cadherin↑, STAT3↓, TLR4↓, MMP↓, ICAM-1↓, AMPK↓, IL6↑, MMP2↓, Warburg↓, Bcl-xL↓, Bcl-2↓, TumCCA↑, EMT↓, TumMeta↓, mTOR↓, HSP27↓, Casp3↑, GlucoseCon↓, lactateProd↓, VEGF↓, p‑p65↓, GIT1↓, FOXM1↓, cycD1/CCND1↓, CDK4↓, MMP9↓, HDAC2↓,
3001- RosA,    Therapeutic Potential of Rosmarinic Acid: A Comprehensive Review
- Review, Var, NA
TumCP↓, Apoptosis↑, TumMeta↓, Inflam↓, *antiOx↑, *AntiAge↑, *ROS↓, BioAv↑, Dose↝, NRF2↑, P-gp↑, ATP↑, MMPs↓, cl‑PARP↓, Hif1a↓, GlucoseCon↓, lactateProd↓, Warburg↓, TNF-α↓, COX2↓, IL6↓, HDAC2↓, GSH↑, ROS↓, ChemoSen↑, *BG↓, *IL1β↓, *TNF-α↓, *IL6↓, *p‑JNK↓, *p38↓, *Catalase↑, *SOD↑, *GSTs↑, *VitC↑, *VitE↑, *GSH↑, *GutMicro↑, *cardioP↑, *ROS↓, *MMP↓, *lipid-P↓, *NRF2↑, *hepatoP↑, *neuroP↑, *P450↑, *HO-1↑, *AntiAge↑, *motorD↓,

Showing Research Papers: 1 to 15 of 15

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GPx↑, 1,   GSH↓, 1,   GSH↑, 1,   HO-1↓, 1,   HO-1↑, 1,   NRF2↑, 2,   OXPHOS↑, 3,   mt-OXPHOS↑, 1,   ROS↓, 1,   ROS↑, 5,   ROS⇅, 1,   ROS↝, 1,   mt-ROS↑, 1,   SIRT3↑, 1,   Thiols↓, 1,   TKT↝, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ATP↑, 2,   ETC↑, 1,   Insulin↓, 2,   MMP↓, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↓, 1,   AMPK↑, 5,   CAIX↑, 1,   cMyc↓, 2,   G6PD↓, 1,   glucose↓, 1,   GlucoseCon↓, 4,   GLUT2↓, 1,   Glycolysis↓, 6,   HK2↓, 5,   lactateProd↓, 4,   LDH↓, 1,   NADH:NAD↓, 1,   NADPH↓, 1,   PDH↑, 1,   PFK↓, 1,   PFK1↓, 1,   PKM2↓, 2,   PKM2:PKM1↓, 1,   Pyruv↓, 1,   R5P↝, 1,   SIRT1↑, 2,   TCA↑, 1,   Warburg↓, 15,  

Cell Death ⓘ

Akt↓, 4,   Apoptosis↑, 5,   BAX↑, 2,   Bcl-2↓, 3,   Bcl-xL↓, 1,   Casp1↓, 1,   Casp3↑, 2,   Casp9↑, 1,   JNK↑, 1,   MAPK↓, 2,   MAPK↑, 1,   MDM2↓, 1,   Myc↓, 1,   p27↑, 1,   survivin↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

p‑pRB↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   GRP78/BiP↑, 1,   HSP27↓, 1,  

Autophagy & Lysosomes ⓘ

ATG3↑, 1,   Beclin-1↑, 1,   BNIP3↑, 1,   LAMP2↑, 1,   p62↑, 1,   TumAuto↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   DNArepair↑, 1,   P53↑, 4,   cl‑PARP↓, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 3,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 2,   E2Fs↓, 1,   P21↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   Diff↑, 1,   EMT↓, 1,   ERK↓, 1,   FOXM1↓, 1,   Gli1↓, 1,   HDAC↓, 2,   HDAC2↓, 3,   IGF-1↓, 3,   IGF-1R↓, 1,   mTOR↓, 5,   mTORC1↓, 1,   NOTCH↓, 1,   PI3K↓, 4,   p‑PI3K↑, 1,   PTEN↑, 2,   RAS↓, 2,   STAT↓, 1,   STAT3↓, 3,   STAT5↓, 1,   TumCG↓, 2,   TumCG↑, 1,   Wnt↓, 2,  

Migration ⓘ

E-cadherin↑, 3,   GIT1↓, 1,   KRAS↓, 1,   MARK4↓, 2,   miR-155↓, 1,   MMP13↓, 1,   MMP2↓, 2,   MMP7↓, 1,   MMP9↓, 3,   MMPs↓, 2,   N-cadherin↓, 1,   talin↓, 1,   Treg lymp↓, 2,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 7,   TumMeta↓, 2,   TumMeta↑, 1,   Vim↓, 2,   Zeb1↓, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   EGFR↓, 2,   HIF-1↓, 1,   Hif1a↓, 5,   NO↓, 1,   VEGF↓, 2,  

Barriers & Transport ⓘ

GLUT1↓, 4,   GLUT1↑, 1,   GLUT3↑, 1,   P-gp↑, 1,  

Immune & Inflammatory Signaling ⓘ

ASC↑, 1,   CD4+↑, 1,   COX2↓, 2,   FOXP3↓, 1,   ICAM-1↓, 1,   IL6↓, 2,   IL6↑, 1,   IL8↓, 1,   Inflam↓, 1,   JAK1↓, 1,   M2 MC↓, 1,   NF-kB↓, 3,   p‑NF-kB↓, 1,   NK cell↑, 1,   p‑p65↓, 1,   PD-1↓, 1,   PD-L1↓, 1,   T-Cell↑, 1,   Th1 response↑, 1,   TLR4↓, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,   PP2A↑, 1,  

Hormonal & Nuclear Receptors ⓘ

RANKL↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   BioAv↝, 2,   BioEnh?, 1,   ChemoSen↑, 6,   Dose↑, 1,   Dose↝, 3,   Dose∅, 1,   eff↑, 5,   RadioS↑, 3,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

BG↓, 1,   EGFR↓, 2,   FOXM1↓, 1,   GutMicro↑, 2,   HER2/EBBR2↓, 1,   IL6↓, 2,   IL6↑, 1,   KRAS↓, 1,   LDH↓, 1,   Myc↓, 1,   PD-L1↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 3,   chemoPv↑, 1,   ChemoSideEff↓, 2,   neuroP↑, 1,   OS↑, 1,   QoL↑, 1,   radioP↑, 1,   Risk↓, 1,   toxicity↓, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 194

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   mt-antiOx↑, 1,   Catalase↑, 3,   GPx↑, 2,   GSH↑, 2,   GSTs↑, 1,   HO-1↑, 1,   Iron↓, 1,   lipid-P↓, 1,   NRF2↑, 2,   ROS↓, 6,   ROS↑, 1,   SOD↑, 3,   VitC↑, 1,   VitE↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   MMP↑, 1,   OCR↑, 1,  

Core Metabolism/Glycolysis ⓘ

ECAR↓, 1,   GlucoseCon↑, 1,   Glycolysis↓, 1,   LDL↓, 1,  

Cell Death ⓘ

p‑JNK↓, 1,   p38↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,  

Migration ⓘ

AntiAg↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   CRP↓, 1,   HMGB1↓, 1,   IL1β↓, 2,   IL6↓, 2,   Inflam↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 2,   BioEnh↑, 1,   Dose↝, 4,   eff↝, 1,   P450↑, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,   CRP↓, 1,   GutMicro↑, 1,   IL6↓, 2,  

Functional Outcomes ⓘ

AntiAge↑, 2,   cardioP↑, 1,   CardioT↓, 1,   cognitive↑, 1,   hepatoP↑, 2,   memory↑, 2,   motorD↓, 1,   neuroP↑, 3,   toxicity↓, 1,  
Total Targets: 56

Scientific Paper Hit Count for: Warburg, Warburg Effect
3 Rosmarinic acid
2 Resveratrol
1 3-bromopyruvate
1 Butyrate
1 diet FMD Fasting Mimicking Diet
1 Chemotherapy
1 diet Short Term Fasting
1 EGCG (Epigallocatechin Gallate)
1 Curcumin
1 Piperine
1 flavonoids
1 Methylene blue
1 Melatonin
1 Metformin
1 Niclosamide (Niclocide)
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:26  Cells:%  prod#:%  Target#:947  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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