Fucoidan / ROS Cancer Research Results

Fuc, Fucoidan: Click to Expand ⟱
Features:
Fucoidan is found in brown algae. Extracted from the seaweed species Fucus vesiculosus, Cladosiphon okamuranus, Laminaria japonica and Undaria pinnatifida.
In oncology research, fucoidan is most consistently described as an immunomodulatory and anti-angiogenic compound with additional pro-apoptotic and anti-metastatic effects in preclinical models. Mechanistically, fucoidan has been reported to suppress NF-κB and PI3K/AKT signaling, reduce VEGF-mediated angiogenesis, inhibit tumor cell adhesion and invasion, and promote apoptosis through caspase activation and mitochondrial pathways. It may also enhance NK cell and macrophage activity, contributing to anti-tumor immune responses. Effects vary substantially depending on molecular weight, sulfation pattern, and source species. Human clinical data remain limited, and many anticancer claims are derived from in vitro and animal studies.

Fucoidan — a heterogeneous family of fucose-rich, sulfated polysaccharides obtained primarily from the cell walls of brown algae. It is classified as a marine-derived polysaccharide nutraceutical and experimental biologic rather than a single chemically defined drug. Standard abbreviations include FUC, FD, LMF or LMWF for low-molecular-weight fucoidan, and OF or oligo-fucoidan for depolymerized preparations. Major sources include Fucus vesiculosus, Undaria pinnatifida, Cladosiphon okamuranus, Saccharina japonica, and related brown seaweeds. Molecular weight, branching, sulfate content, monosaccharide composition, contaminants, and extraction method differ substantially among products and strongly affect biological activity.

Primary mechanisms (ranked):

  1. Induction of intrinsic and extrinsic apoptosis through mitochondrial dysfunction, Bax/Bcl-2-family modulation, death-receptor signaling, caspase activation, and suppression of survivin and XIAP.
  2. Suppression of tumor growth and survival signaling, particularly PI3K/AKT/mTOR, ERK/MAPK, NF-κB, and related translational-control pathways.
  3. Inhibition of angiogenesis through suppression of hypoxia-responsive HIF-1α/VEGF signaling and endothelial-cell migration.
  4. Inhibition of invasion and metastasis through reduced EMT, matrix-remodelling activity, selectin-mediated adhesion, migration, and tumor-cell interaction with extracellular matrix.
  5. Immune modulation involving NK cells, macrophages, dendritic cells, T cells, inflammatory cytokines, intestinal microbiota, and context-dependent effects on PD-L1 and antitumor immunity.
  6. Chemosensitization and radiosensitization in selected experimental models, with possible reduction of treatment-associated inflammation or toxicity in small clinical studies.
  7. Secondary redox modulation that may increase apoptosis-associated ROS in some tumor models while reducing inflammatory or oxidative injury in normal tissues; direction depends on preparation, dose, and cellular context.

Bioavailability / PK relevance: Intact high-molecular-weight fucoidan has limited and variable gastrointestinal absorption. Small quantities of orally administered fucoidan or fucoidan-derived fractions can be detected in human serum and urine, but systemic exposure is low, assay-dependent, and influenced by molecular weight, sulfation, source species, microbiota, and formulation. Low-molecular-weight and oligosaccharide preparations generally have greater absorption and tissue accessibility than native polymers. Local intestinal, microbiome-mediated, endothelial, and immune effects may therefore be more pharmacologically relevant than direct exposure of distant tumors after ordinary oral supplementation.

In-vitro vs systemic exposure relevance: Many direct anticancer experiments use approximately 50–1000 µg/mL fucoidan, concentrations that are unlikely to be reproduced as freely circulating intact polysaccharide after conventional oral dosing. Direct tumor-cell apoptosis and kinase inhibition demonstrated at these levels should therefore be considered high-concentration or formulation-dependent findings. Lower-concentration receptor, endothelial, coagulation, intestinal, and immune effects may be more clinically plausible. Nanoparticle, injectable, radiolabelled, and chemically depolymerized fucoidan preparations are not pharmacokinetically interchangeable with oral seaweed extracts.

Clinical evidence status: Predominantly preclinical, with several small human studies and randomized adjunct trials. Small colorectal and rectal cancer studies have reported possible improvements in disease control, treatment tolerance, quality of life, or selected inflammatory outcomes, and a 2025 randomized trial reported improved outcomes when low-molecular-weight fucoidan was added to transarterial chemoembolization for unresectable hepatocellular carcinoma. However, studies remain heterogeneous, generally small, formulation-specific, and insufficient to establish fucoidan as an anticancer treatment. Additional randomized phase II studies are registered for cancer-related fatigue, cachexia, chemoradiotherapy, and other supportive indications. Fucoidan is not an approved anticancer drug and no oncology guideline currently recommends routine therapeutic use.

Safety and interaction constraints: Oral preparations have generally been well tolerated in small studies, but safety cannot be generalized across poorly standardized extracts. Fucoidan can exhibit anticoagulant, antiplatelet, or fibrinolytic activity depending on molecular weight and sulfation; caution is appropriate with warfarin, heparins, direct oral anticoagulants, antiplatelet drugs, bleeding disorders, or perioperative use. Seaweed-derived products may also contain variable iodine, sodium, heavy metals, or other polysaccharides. Potential interactions with chemotherapy, immunotherapy, and drug absorption remain incompletely characterized.


Fucoidan Mechanistic Profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial and death-receptor apoptosis Apoptosis ↑; Bax and Bak ↑; Bcl-2 and Mcl-1 ↓; Fas and BID ↑; caspase-3, caspase-7, caspase-8 and caspase-9 ↑; survivin and XIAP ↓ Apoptosis generally ↔ at lower exposures; cytoprotection reported in injury models (dose-dependent) R, G Programmed tumor-cell death One of the most recurrent direct anticancer findings, but often demonstrated at high in-vitro concentrations and strongly dependent on molecular weight, sulfate content, and cancer model.
2 PI3K AKT mTOR survival signaling PI3K ↓; AKT phosphorylation ↓; mTOR signaling ↓; p70S6K ↓; 4E-BP1 phosphorylation ↓; proliferation ↓ ↔ or protective signaling modulation (context-dependent) R, G Growth and survival suppression Central pathway reported across several tumor models; direct target engagement in humans has not been established.
3 HIF-1α VEGF angiogenesis HIF-1α ↓; VEGF ↓; endothelial recruitment ↓; tumor angiogenesis ↓ Pathological angiogenesis ↓; physiological vascular effects mixed (context-dependent) R, G Anti-angiogenic activity Best characterized for selected low-molecular-weight preparations under hypoxic conditions; some preparations or concentrations can produce different VEGF responses.
4 EMT adhesion invasion and metastasis EMT ↓; Snail ↓; Slug ↓; Twist ↓; migration ↓; invasion ↓; selectin-mediated adhesion ↓ Inflammatory leukocyte adhesion ↓ (context-dependent) R, G Anti-invasive and anti-metastatic activity Sulfated polysaccharide structure may interfere with selectins, extracellular-matrix binding, proteases, and EMT signaling.
5 Innate and adaptive antitumor immunity NK-cell activity ↑; macrophage and dendritic-cell activation ↑; T-cell responses ↑; immune surveillance ↑ Host immune responsiveness ↑; excessive inflammatory signaling may ↓ R, G Immune modulation Effects may be mediated partly through pattern-recognition receptors and intestinal microbiota. Responses are preparation-dependent and should not be interpreted as uniform immune stimulation.
6 NF-κB inflammatory and survival signaling NF-κB activation ↓; inflammatory cytokines ↓; anti-apoptotic signaling ↓ IL-1β ↓; IL-6 ↓; TNF-α ↓; inflammatory injury ↓ (context-dependent) R, G Anti-inflammatory and anti-survival activity Small human studies support reduced circulating inflammatory cytokines, but lack adequate controls for definitive antitumor attribution.
7 ERK MAPK proliferation signaling ERK phosphorylation ↓; proliferation ↓; cell-cycle progression ↓ ↔ or stress-response normalization (model-dependent) R, G Antiproliferative activity Direction can vary with cell type, receptor engagement, and fucoidan structure.
8 Cell-cycle control G0/G1 or G2/M arrest ↑; cyclins and CDKs ↓; p21 or p27 ↑ (model-dependent) Proliferation usually ↔ at moderate exposure G Growth arrest The arrest point is not uniform across cancers
9 PD-L1 and immune-checkpoint responsiveness PD-L1 surface expression ↓; response to PD-1 blockade ↑ (model-dependent) Antitumor immune activation ↑; systemic effects uncertain G Immunotherapy adjunct potential Evidence is primarily cellular and animal-based, including microbiome-associated enhancement of anti-PD-1 activity. Clinical benefit with checkpoint inhibitors remains unproven.
10 Mitochondrial ROS and redox modulation ROS ↑ during apoptosis in some models; ROS ↓ in other inflammatory or oxidative models (context-dependent) ROS and lipid peroxidation ↓; antioxidant defences ↑ (model-dependent) P, R Secondary redox modulation Fucoidan is not consistently a direct pro-oxidant. ROS direction depends on tumor type, preparation, concentration, and whether apoptosis or cytoprotection is being studied.
11 Chemosensitization Chemotherapy response ↑; drug-resistant cell survival ↓ (model-dependent) Chemotherapy-associated fatigue, hepatic injury, or toxicity may ↓ G Adjunct treatment potential Clinical findings are preliminary and formulation-specific. Fucoidan should not replace standard chemotherapy or justify empiric dose reduction.
12 Radiosensitization and radioprotection Radiation response ↑ in selected tumor models Radiation-associated inflammatory or tissue injury ↓ in selected models G Context-dependent radiation modulation Potentially useful differential effects have not been sufficiently established clinically; timing and preparation may determine whether sensitization or protection predominates.
13 Gut microbiota and systemic immune signaling Microbiome-associated antitumor immunity ↑; tumor growth ↓ (model-dependent) Microbial diversity and barrier function may ↑ G Indirect host-mediated activity May be especially relevant after oral administration because systemic absorption of intact high-molecular-weight fucoidan is limited.
14 Coagulation and platelet interactions Tumor-associated thrombosis and selectin-mediated dissemination may ↓ Coagulation ↓; platelet activity ↓; bleeding tendency may ↑ (preparation-dependent) P, R Antithrombotic activity and safety constraint Anticoagulant potency increases with particular sulfation patterns and molecular structures. Oral clinical significance is uncertain but warrants caution with anticoagulant or antiplatelet therapy.
15 Clinical Translation Constraint Direct tumor exposure after oral dosing is low and uncertain Safety and contaminant profiles vary among products G Translation and standardization constraint Fucoidan is a family of non-equivalent polymers. Source species, molecular weight, sulfate pattern, purity, iodine and metal contamination, extraction, dose, and route must be specified before comparing studies.

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)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"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⟱
7016- Fuc,    Therapies from Fucoidan: New Developments
- Review, Var, NA
*Bacteria↓, *BioAv↓, *Dose↝, *GutMicro↑, PD-1↝, ROS⇅, cl‑Casp↑, cl‑PARP↑, RadioS↑, *radioP↑, *neuroP↑, *Aβ↓,
7006- Fuc,    Seaweeds in the Oncology Arena: Anti-Cancer Potential of Fucoidan as a Drug—A Review
- Review, Var, NA
*toxicity↓, *AntiViral↑, *antiOx↑, *Imm⇅, AntiCan↑, TumCCA↑, Apoptosis↑, TumMeta↓, angioG↓, antiNeop↑, VEGF↓, MMPs↓, BioAv↑, BioAv↑, ROS⇅, cl‑PARP↑, Casp3↑, Casp7↑, ROS↑, GSH↓, MMP↓, PI3K↓, ERK↓, MAPK↑, TumCP↓, Bax:Bcl2↑, TJ↑, ZO-1↑, OCLN↑, CLDN1↑, IBI↑, GutMicro↑, NK cell↑, STAT3↓, eff↑,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

GSH↓, 1,   ROS↑, 1,   ROS⇅, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Bax:Bcl2↑, 1,   cl‑Casp↑, 1,   Casp3↑, 1,   Casp7↑, 1,   MAPK↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

ERK↓, 1,   PI3K↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

CLDN1↑, 1,   MMPs↓, 1,   TJ↑, 1,   TumCP↓, 1,   TumMeta↓, 1,   ZO-1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

IBI↑, 1,   OCLN↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NK cell↑, 1,   PD-1↝, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   eff↑, 1,   RadioS↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

GutMicro↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   antiNeop↑, 1,  
Total Targets: 33

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm⇅, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

GutMicro↑, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 1,   radioP↑, 1,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,   Bacteria↓, 1,  
Total Targets: 11

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
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#:81  Target#:275  State#:%  Dir#:3
  wNotes=0  sortOrder:rid,rpid

 

Home Page