Diclofenac / ROS Cancer Research Results

DFC, Diclofenac: Click to Expand ⟱
Features:
Diclofenac is a nonsteroidal anti-inflammatory drug (NSAID) commonly used to treat pain, inflammation, and fever.

Diclofenac — a synthetic phenylacetic-acid derivative and nonsteroidal anti-inflammatory drug used clinically for analgesic, anti-inflammatory, and antipyretic effects. It is a nonselective cyclooxygenase inhibitor with moderately greater functional inhibition of COX-2 than COX-1. Standard abbreviations include DCF, DIC, and Dicl. Diclofenac is approved in oral, topical, ophthalmic, rectal, and injectable formulations for non-cancer indications; its proposed anticancer use is drug repurposing and remains investigational.

Primary mechanisms (ranked):

  1. Inhibition of COX-2 and COX-1, reducing prostaglandin E2 production and downstream inflammatory, angiogenic, immunosuppressive, and tumor-promoting signalling.
  2. Suppression of MYC-dependent glucose metabolism, including reduced glucose uptake, glycolytic flux, lactate production, and expression of glycolysis-associated proteins.
  3. Disruption of tumor lactate handling through context-dependent inhibition of monocarboxylate transport and lactate dehydrogenase activity, potentially increasing intracellular metabolic stress and limiting extracellular acidification.
  4. Inhibition of angiogenesis through reduced VEGF expression and tumor vascularization.
  5. Microtubule destabilization, defective mitotic-spindle assembly, G2/M arrest, and mitotic cell death at sufficiently high concentrations.
  6. Mitochondrial dysfunction and ROS accumulation, causing loss of mitochondrial membrane potential and intrinsic apoptosis; this mechanism overlaps with diclofenac toxicity in normal hepatic and cardiac cells.
  7. Context-dependent chemosensitization and radiosensitization through suppression of prostaglandin signalling, tumor metabolism, angiogenesis, and lactate-associated antioxidant capacity.

Bioavailability / PK relevance: Oral diclofenac is extensively absorbed but undergoes substantial first-pass metabolism, producing approximately 50–55% systemic bioavailability. It reaches peak plasma concentration in roughly 2–3 hours, is more than 99% albumin-bound, and has a terminal plasma half-life of approximately 2 hours. Metabolism is primarily hepatic through CYP2C9, with additional CYP2C8, CYP3A4, and UGT2B7 contributions. High protein binding, short systemic exposure, and dose-limiting cardiovascular, gastrointestinal, renal, and hepatic toxicity constrain sustained anticancer exposure. Topical formulations provide high local tissue exposure but substantially lower systemic exposure.

In-vitro vs systemic exposure relevance: Many direct antiproliferative, mitochondrial, ROS, and microtubule effects are reported at approximately 50–500 µM and frequently exceed the sustained unbound concentrations achievable with standard oral dosing. Effects on COX/PGE2 signalling, MYC, lactate metabolism, angiogenesis, or treatment sensitization may occur at lower or intermittently achievable concentrations, but their dependence on tumor type, formulation, exposure duration, and protein content is substantial. High-concentration cytotoxic findings should not be interpreted as evidence that conventional analgesic dosing will directly kill tumors.

Clinical evidence status: Established approved NSAID for pain and inflammatory disorders; preclinical-to-early-human evidence for oncology repurposing. Animal studies and tumor-cell studies support metabolic, antiangiogenic, and cytotoxic activity. Human oncology evidence consists mainly of topical treatment studies in actinic keratosis, perioperative or supportive-care investigations, biomarker studies, and small or ongoing trials. A phase II study is evaluating systemic diclofenac in non-small-cell lung cancer, but diclofenac is not an approved systemic anticancer therapy and there is no established survival benefit from randomized oncology trials.


Diclofenac Mechanistic Profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 COX and PGE2 signalling COX-2 activity ↓
PGE2 ↓
EP receptor signalling ↓		 Protective prostaglandins ↓ R–G Inflammatory and tumor-promoting signalling ↓ Core pharmacological mechanism. May reduce proliferation, angiogenesis, invasion, and immunosuppression, but normal-cell COX inhibition contributes to gastrointestinal, renal, and cardiovascular toxicity.
2 MYC and glucose metabolism MYC ↓
Glucose uptake ↓
Glycolysis ↓
Lactate production ↓		 Metabolic effects ↔ or ↓ (context-dependent) G Tumor bioenergetic capacity and proliferation ↓ Observed in melanoma, leukemia, carcinoma, glioma, and triple-negative breast-cancer models. Magnitude depends on dose and exposure duration.
3 Lactate transport and extracellular acidification MCT-dependent lactate transport ↓
LDHA activity ↓
Extracellular lactate ↓
Acidification ↓		 Lactate transport ↓ (context-dependent) R–G Metabolic stress ↑ and acidic tumor microenvironment ↓ Direct MCT4 inhibition by diclofenac remains model- and assay-dependent. Reduced lactate production through MYC and LDHA modulation may be equally or more important.
4 VEGF and angiogenesis VEGF ↓
Vascularization ↓
Endothelial recruitment ↓		 Angiogenic repair ↓ (context-dependent) G Tumor perfusion and growth ↓ Supported mainly by animal tumor models. Effects may derive from COX-2/PGE2 inhibition and altered tumor metabolism.
5 Microtubules and mitotic spindle Microtubule stability ↓
Spindle defects ↑
G2/M arrest ↑		 Mitotic injury ↑ (high concentration only) R–G Mitotic catastrophe and cell death ↑ COX-independent mechanism demonstrated in experimental cancer models, generally at concentrations above routine unbound clinical exposure.
6 Mitochondrial ROS and intrinsic apoptosis Mitochondrial ROS ↑
Membrane potential ↓
Cytochrome c release ↑
Caspase signalling ↑		 Hepatocyte and cardiomyocyte ROS ↑
Mitochondrial injury ↑		 R–G Apoptosis ↑ Potential anticancer leverage overlaps directly with recognized organ toxicity. Reactive metabolites and mitochondrial hydrogen peroxide are important in normal-cell injury.
7 NRF2 antioxidant response NRF2 response ↑ or overwhelmed (dose-dependent) NRF2 stress response ↑ R–G Adaptive antioxidant defence or oxidative death Secondary mechanism. NRF2 activation may protect cells at moderate stress, whereas severe mitochondrial oxidative injury can exceed antioxidant capacity.
8 PI3K AKT and MAPK survival signalling AKT phosphorylation ↓
ERK signalling ↓ or mixed
p38 and JNK stress signalling ↑		 Stress kinase signalling ↑ (context-dependent) R–G Survival signalling ↓ and apoptosis ↑ Reported in selected esophageal, neuroblastoma, and other experimental models; not established as a universal direct target.
9 Radiosensitization and chemosensitization Treatment sensitivity ↑ (context-dependent)
Lactate-mediated ROS buffering ↓		 Normal-tissue injury ↔ or ↑ G Response to radiation or chemotherapy ↑ Preclinical and limited translational evidence. Potential interaction with pemetrexed and other cytotoxic agents may increase renal, gastrointestinal, or marrow toxicity.
10 Clinical Translation Constraint Sustained free-drug exposure limited GI bleeding ↑
Cardiovascular thrombosis ↑
Renal injury ↑
Hepatotoxicity ↑		 G Therapeutic window narrowed Approximately 55% oral bioavailability, greater than 99% protein binding, short half-life, first-pass metabolism, CYP2C9 interactions, and systemic NSAID toxicity limit chronic high-dose oncology use. Local or reformulated delivery may improve exposure but remains investigational.

P: 0–30 min    R: 30 min–3 hr    G: >3 hr
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⟱
6697- DFC,    Diclofenac induces apoptosis in hepatocytes by alteration of mitochondrial function and generation of ROS
Inflam↓, Casp3↑, Casp8↑, Casp9↑, MPT↑, mt-ROS↑,
6707- DFC,    Markers of mitochondrial dysfunction during the diclofenac-induced apoptosis in melanoma cell lines
- in-vitro, Melanoma, NA
TumCP↓, ROS↑, Bax:Bcl2↑, Casp3↑, SOD2↑, Cyt‑c↑,
6705- DFC,    Development and Challenges of Diclofenac-Based Novel Therapeutics: Targeting Cancer and Complex Diseases
- Review, Var, NA
*Inflam↓, *Pain↓, *COX1↓, *COX2↓, *toxicity↝, *BioAv↑, *AntiAg↑, *neuroP↑, ROS↑, p73↑, Myc↓, lactateProd↓, TumCCA↑, PI3K↓, Akt↓, NF-kB↓, SOD2↓, *neuroP↑,
6701- DFC,    Intracellular pH and calcium signaling as molecular targets of diclofenac-induced apoptosis against colon cancer
- in-vivo, Colon, NA
COX2↓, Inflam↓, chemoPv↑, Apoptosis↑, pH↓, ROS↑, Ca+2↑, MMP↓, APAF1↑,
6699- DFC,    Mitochondrial H2O2 Is a Central Mediator of Diclofenac-Induced Hepatocellular Injury
- vitro+vivo, Nor, NA
*ROS↑, *hepatoP↓, *eff↑, *ATP↓, OXPHOS↓, *ETC↓, *compI↓, *compIII↓,
6698- DFC,    Diclofenac induces proteasome and mitochondrial dysfunction in murine cardiomyocytes and hearts
- in-vivo, Nor, NA
*cardioP↓, *ROS↑, MMP↓, compIII↓,
6695- DFC,    Inhibition of lactate dehydrogenase A by diclofenac sodium induces apoptosis in HeLa cells through activation of AMPK
- in-vitro, Cerv, HeLa
other↝, Glycolysis↓, LDHA↓, Hypoxia↓, Apoptosis↑, lactateProd↓, ATP↓, mt-ROS↑, DNAdam↑, lipid-P↑, AMPK↑, p‑S6K↓, TumCP↓, Dose↝, selectivity↑, i-MDA↑, mtDam↑,
6690- DFC,    Diclofenac: A Nonsteroidal Anti-Inflammatory Drug Inducing Cancer Cell Death by Inhibiting Microtubule Polymerization and Autophagy Flux
- in-vitro, Cerv, HeLa
Inflam↓, ROS↑, mitA↑, ChemoSen↑,
6689- DFC,    Diclofenac-Induced Apoptosis in the Neuroblastoma Cell Line SH-SY5Y: Possible Involvement of the Mitochondrial Superoxide Dismutase
- in-vitro, neuroblastoma, SH-SY5Y
Apoptosis↑, mtDam↑, ROS↑, SOD2↓, MMP↓, Cyt‑c↑, Dose↝, BBB↑,

Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

lipid-P↑, 1,   i-MDA↑, 1,   OXPHOS↓, 1,   ROS↑, 5,   mt-ROS↑, 2,   SOD2↓, 2,   SOD2↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   compIII↓, 1,   MMP↓, 3,   MPT↑, 1,   mtDam↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   Glycolysis↓, 1,   lactateProd↓, 2,   LDHA↓, 1,   p‑S6K↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   APAF1↑, 1,   Apoptosis↑, 3,   Bax:Bcl2↑, 1,   Casp3↑, 2,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 2,   Myc↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   p73↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

mitA↑, 1,   TumCCA↑, 1,  

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

PI3K↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   TumCP↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hypoxia↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   Inflam↓, 3,   NF-kB↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

pH↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   Dose↝, 2,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

Myc↓, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoPv↑, 1,  
Total Targets: 45

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

compI↓, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   compIII↓, 1,   ETC↓, 1,  

Migration(tgid=13) ⓘ

AntiAg↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2↓, 1,   Inflam↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   eff↑, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↓, 1,   hepatoP↓, 1,   neuroP↑, 2,   Pain↓, 1,   toxicity↝, 1,  
Total Targets: 16

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
9 Diclofenac
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#:200  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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