3-bromopyruvate / ROS Cancer Research Results

3BP, 3-bromopyruvate: Click to Expand ⟱
Features:
3BP, a small molecule, results in a remarkable therapeutic effect when it comes to treating cancers exhibiting a "Warburg effect."

3-Bromopyruvate — also written as 3BP or 3-BrPA — is a small, highly electrophilic pyruvate/lactate analog that acts as a metabolism-targeting alkylating agent (covalently modifying protein thiols) and is widely studied as an experimental anticancer compound. Functionally, it is best classified as a metabolic poison / anti-metabolite with multi-target effects centered on rapid ATP collapse (glycolysis + mitochondrial metabolism) and secondary oxidative and cell-death signaling. Cancer selectivity is often framed as higher uptake via MCT1 and higher reliance on glycolysis/Warburg metabolism, but the same chemical reactivity underlies a narrow safety margin unless formulated/delivered carefully.

Primary mechanisms (ranked):

  1. Covalent thiol alkylation of energy-metabolism enzymes (notably glycolytic nodes such as HK2 and other thiol-sensitive enzymes) → rapid ATP depletion
  2. Mitochondrial bioenergetic disruption (OXPHOS inhibition, permeability/ΔΨm collapse) → energetic crisis
  3. MCT1-facilitated uptake (context-dependent determinant of sensitivity and “selectivity”)
  4. Oxidative stress induction and redox-buffer depletion (ROS↑; GSH/thiols↓) (secondary but often decisive)
  5. Stress-response execution programs (AMPK activation; apoptosis/autophagy; ferroptosis context-dependent; sensitization to other therapies)

Bioavailability / PK relevance: Unformulated 3BP is chemically reactive and can be systemically toxic; practical translation has focused on formulation (e.g., cyclodextrin/microencapsulation) and/or locoregional delivery to improve tolerability and tumor exposure. Uptake can depend on transporter context (e.g., MCT1 expression) and extracellular pH/lactate milieu (context-dependent).

In-vitro vs systemic exposure relevance: Many in-vitro studies use µM–mM ranges; higher (mM) conditions may exceed what is plausibly achievable systemically without toxicity. Reported activity at low µM exists in some models (especially with optimized derivatives/formulations), but exposure/target-engagement in humans remains the central constraint.

Clinical evidence status: Not an approved drug. Evidence is predominantly preclinical (cell/animal). Human use has been limited and controversial, including safety incidents reported in non-standard clinical settings. A 3BP-derived clinical agent (e.g., KAT/3BP / KAT-101) is in early-phase clinical testing (HCC), but that is distinct from generic/unformulated 3BP.

Overall, 3BP attacks cancer cells by “starving” them of energy, leading to energetic collapse, oxidative damage, and eventual cell death.

- 3BP is known to inhibit enzymes involved in glycolysis, such as hexokinase II (HKII). Many cancer cells overexpress HKII and rely on glycolysis for ATP production. Inhibiting HKII leads to decreased ATP levels and energy depletion.
- Fermentation inhibitor:(inhibits conversion of pyruvate to lactate) NAD+ is compromised slowing Glycolysis leading to reduced ATP
- By depleting ATP, 3BP can impair mitochondrial functions indirectly.
- LDH converts pyruvate to lactate. In many cancers, lactate production is high (the Warburg effect). Inhibition of LDH disrupts lactate production and may contribute to an intracellular buildup of toxic metabolites.
- There is evidence indicating that, by interfering with glycolysis, 3BP might also indirectly affect the PPP. This reduces the production of NADPH, weakening the cancer cell’s ability to manage oxidative stress.
- Impairing energy metabolism, 3BP can indirectly affect mitochondrial function, potentially leading to an increase in ROS production.

Although 3BP shows promise as a metabolic inhibitor with anticancer properties, its transition from preclinical studies to approved clinical therapy has not yet been realized.

-Combining metabolic inhibitors like 3BP with agents that modulate ROS levels could represent a synergistic approach in cancer therapy. By simultaneously disrupting energy production and exacerbating oxidative stress, such combinations may more effectively induce cancer cell death while sparing normal cells.

In advanced cancer it has been known to kill the cancer too fast, causing liver failure and death.

3-Bromopyruvate (3BP, 3-BrPA) — mechanistic axes (oncology)

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Glycolysis inhibition via thiol-alkylation of glycolytic enzymes ↓ glycolytic flux; ↓ ATP (often rapid) ↔ to ↓ (model-dependent) P/R Energetic collapse Often framed around HK2, but 3BP is broadly thiol-reactive; glycolysis collapse is a convergent phenotype rather than a single-enzyme story.
2 Mitochondrial bioenergetics disruption ↓ OXPHOS; ↓ ΔΨm; ↑ MPTP (context-dependent) ↔ to ↓ (dose-dependent) P/R ATP depletion + mitochondrial stress Dual hit (glycolysis + mitochondria) is a major reason for potency in high-glycolytic tumors; also a toxicity driver if exposure is systemic.
3 MCT1-dependent uptake ↑ uptake and sensitivity when MCT1-high ↔ (varies by tissue MCT1) P Determinant of selectivity MCT1 has been shown as a key sensitivity node in multiple models; “selectivity” claims are strongest when transporter context is documented.
4 Redox buffering and thiol pool depletion ↓ GSH/thiols; redox crisis ↔ to ↓ (dose-dependent) R/G Lowered antioxidant capacity Because 3BP alkylates thiols, GSH depletion can be both direct and indirect; can amplify downstream death pathways and resistance phenotypes.
5 ROS axis ↑ ROS (often); oxidative damage (context-dependent) ↔ (dose- and context-dependent) R Oxidative stress amplification ROS changes are frequently secondary to mitochondrial disruption + thiol depletion; can be decisive for apoptosis/ferroptosis engagement.
6 AMPK energy-stress signaling ↑ AMPK; ↓ anabolic signaling (context-dependent) ↑ AMPK (protective or adaptive) R Stress adaptation vs death priming Energetic collapse typically triggers AMPK; downstream outcomes depend on baseline metabolic state and co-treatments.
7 Cell-death programs: apoptosis and autophagy ↑ apoptosis; ↑ autophagy (context-dependent) ↔ to ↑ stress responses G Execution of cytotoxicity Multiple reports show mixed death phenotypes; autophagy can be cytoprotective or contribute to death depending on context and timing.
8 Ferroptosis axis ↑ ferroptosis susceptibility (context-dependent) ↔ (context-dependent) G Lipid-peroxidation-driven death Most consistent when redox buffering is weakened and/or combined with agents that tilt iron/lipid-ROS balance.
9 NRF2 axis ↔ (model-dependent; often stress-activated) ↔ (model-dependent) G Adaptive antioxidant response NRF2 behavior varies: oxidative stress can activate NRF2, but thiol-alkylation/redox collapse can also overwhelm defenses; treat as context-dependent.
10 Chemosensitization / radiosensitization ↑ sensitization (context-dependent) ↔ R/G Combination leverage Reported synergy with targeted therapy/chemo/radiation in some models, typically via metabolic stress + redox imbalance.
11 Clinical Translation Constraint Formulation/delivery-limited; systemic toxicity risk Off-target injury risk — Therapeutic index limitation Unformulated 3BP has significant toxicity concerns; translation efforts emphasize formulation (e.g., cyclodextrin/microencapsulation) and/or locoregional strategies and derivatives now entering early clinical trials.


ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
5277- 3BP,    3-Bromopyruvate inhibits pancreatic tumor growth by stalling glycolysis, and dismantling mitochondria in a syngeneic mouse model
- in-vivo, PC, Panc02
HK2↓, selectivity↑, ATP↓, mtDam↑, Dose↝, TumCG↓, Casp3↑, Glycolysis↓, NADPH↓, ATP↓, ROS↑, DNAdam↑, GSH↓, Bcl-2↓, Casp↑, lactateProd↓,
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↓,
5272- 3BP,    The efficacy of the anticancer 3-bromopyruvate is potentiated by antimycin and menadione by unbalancing mitochondrial ROS production and disposal in U118 glioblastoma cells
- in-vitro, GBM, U87MG - in-vitro, Nor, HEK293
Glycolysis↓, ROS↑, GPx↓, eff↓, OXPHOS↓, HK2↓, ATP↓, ROS↑, ER Stress↑, BioAv↓, Cyt‑c↑, eff↑,
5271- 3BP,    The anticancer agent 3-bromopyruvate: a simple but powerful molecule taken from the lab to the bedside
- Review, Var, NA
selectivity↑, selectivity↑, ATP↓, Glycolysis↓, HK2↓, mt-OXPHOS↓, GAPDH↓, mtDam↑, GSH↓, ROS↑, ER Stress↑, TumAuto↑, LC3‑Ⅱ/LC3‑Ⅰ↑, p62↓, Akt↓, HDAC↓, TumCA↑, Bcl-2↓, cMyc↓, Casp3↑, Cyt‑c↑, Mcl-1↓, PARP↓, ChemoSen↑,
5263- 3BP,  CET,    3-Bromopyruvate overcomes cetuximab resistance in human colorectal cancer cells by inducing autophagy-dependent ferroptosis
- in-vitro, CRC, DLD1 - NA, NA, HCT116
eff↑, Ferroptosis↓, TumAuto↑, Apoptosis↑, FOXO3↑, AMPKα↑, p‑Beclin-1↑, HK2↓, ATP↓, ROS↑, Dose↝, TumVol↓, TumW↓, xCT↑, GSH↓, eff↓, MDA↑,
5257- 3BP,    Tumor Energy Metabolism and Potential of 3-Bromopyruvate as an Inhibitor of Aerobic Glycolysis: Implications in Tumor Treatment
- Review, Var, NA
Glycolysis↓, mt-OXPHOS↓, HK2↓, Cyt‑c↑, Casp3↓, Bcl-2↓, Mcl-1↓, GAPDH↓, LDH↓, PDH↓, TCA↓, GlutaM↓, GSH↓, ATP↓, mitResp↓, ROS↑, ChemoSen↑, toxicity↝,
1341- 3BP,    The HK2 Dependent “Warburg Effect” and Mitochondrial Oxidative Phosphorylation in Cancer: Targets for Effective Therapy with 3-Bromopyruvate
- Review, NA, NA
Glycolysis↓, OXPHOS↓, *toxicity↓, ROS↑, GSH↓, eff↑,

Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↓, 1,   GPx↓, 1,   GSH↓, 6,   MDA↑, 1,   OXPHOS↓, 2,   mt-OXPHOS↓, 2,   ROS↑, 8,   Thiols↓, 1,   xCT↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 6,   mitResp↓, 1,   mtDam↑, 2,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   GAPDH↓, 2,   GlutaM↓, 1,   Glycolysis↓, 5,   HK2↓, 5,   lactateProd↓, 1,   LDH↓, 1,   NADPH↓, 1,   PDH↓, 1,   TCA↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,   Bcl-2↓, 3,   Casp↑, 1,   Casp3↓, 1,   Casp3↑, 2,   Cyt‑c↑, 3,   Ferroptosis↓, 1,   Mcl-1↓, 2,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 2,  

Autophagy & Lysosomes ⓘ

p‑Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   p62↓, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   PARP↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   FOXO3↑, 1,   HDAC↓, 1,   TumCG↓, 1,  

Migration ⓘ

TumCA↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 2,   Dose↝, 2,   eff↓, 2,   eff↑, 3,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

LDH↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   toxicity↝, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 57

Pathway results for Effect on Normal Cells:


Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 1

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
7 3-bromopyruvate
1 cetuximab
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#:20  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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