ferumoxytol / ROS Cancer Research Results

Fer, ferumoxytol: Click to Expand ⟱

Features:

Ferumoxytol is an intravenous iron replacement product composed of superparamagnetic iron oxide nanoparticles coated with a carbohydrate shell. It was primarily developed to treat iron deficiency anemia, particularly in patients with chronic kidney disease (CKD). The nanoparticle formulation offers both therapeutic iron supplementation and a potential role as a magnetic resonance imaging (MRI) contrast agent because of its unique magnetic properties.

Because iron is essential for cell proliferation, there has been some concern about the theoretical risk of providing additional iron to environments where tumor cells might use it for growth. Nevertheless, the clinical significance of this in the context of ferumoxytol administration remains controversial and is not clearly established by current evidence.

There has been some research combining Ferumoxytol with high dose Vitamin C. Some laboratory studies have examined whether the combination of ferumoxytol and vitamin C can enhance anticancer effects. For instance, exposure of cancer cell lines or tumor models to this combination has been evaluated to see if there is an increase in ROS-mediated cytotoxicity compared to using either agent alone.

Ferumoxytol — an intravenously administered, carbohydrate-coated superparamagnetic iron oxide nanoparticle used as an iron-replacement drug. It consists of a non-stoichiometric magnetite core surrounded by a polyglucose sorbitol carboxymethylether coating, with an overall colloidal particle size of approximately 17–31 nm. The principal US brand is Feraheme, with additional ferumoxytol products now approved. Clinically, ferumoxytol is used to treat iron-deficiency anemia in adults with chronic kidney disease or intolerance or inadequate response to oral iron. Its strong magnetic susceptibility also permits off-label blood-pool, vascular, inflammatory and tumor-associated macrophage MRI, although it is not FDA-approved as an MRI contrast agent. Experimental anticancer activity is distinct from its approved hematologic use and remains investigational.

Primary mechanisms (ranked):

Macrophage uptake and tumor-associated macrophage repolarization toward a pro-inflammatory, tumor-inhibitory M1-like phenotype in responsive preclinical tumor models.
Iron-dependent Fenton chemistry and ROS generation after nanoparticle degradation, producing oxidative injury, mitochondrial dysfunction and cancer-cell death, particularly when combined with pharmacologic ascorbate.
Enhancement of oxidative stress-mediated radiosensitization and chemosensitization when combined experimentally with high-dose intravenous ascorbate, radiation and temozolomide.
Ferroptosis-related lipid peroxidation and iron-dependent membrane injury reported for iron oxide nanoparticle systems; direct attribution to clinically dosed ferumoxytol remains model-dependent.
Preferential phagocytic accumulation in macrophages and reticuloendothelial tissues, enabling MRI detection of tumor-associated macrophages, inflammation and vascular compartments.
Systemic iron delivery through macrophage processing of the nanoparticle coating and incorporation of released iron into ferritin, transferrin and hemoglobin.

Bioavailability / PK relevance: Ferumoxytol must be administered intravenously and has no meaningful oral bioavailability. The nanoparticle initially remains largely within the vascular compartment and is subsequently cleared primarily by macrophages of the reticuloendothelial system. Its apparent plasma half-life is approximately 15 hours at therapeutic doses, while intracellular iron persists much longer after macrophage uptake. The standard labeled regimen is 510 mg elemental iron followed by a second 510 mg infusion 3–8 days later. Tumor delivery depends on vascular permeability, perfusion, macrophage abundance and phagocytic uptake; heterogeneous intratumoral accumulation limits extrapolation from cell culture or highly macrophage-rich animal tumors.

In-vitro vs systemic exposure relevance: Free iron concentrations and direct nanoparticle-to-cell ratios used in many mechanistic studies do not reproduce the protein corona, vascular compartmentalization, macrophage sequestration and regulated iron handling occurring in patients. Direct cancer-cell cytotoxicity often requires high local nanoparticle exposure, prolonged incubation or an added pro-oxidant such as pharmacologic ascorbate. Clinically achievable ferumoxytol exposure is sufficient for iron replacement and prolonged MRI effects, but autonomous anticancer activity at approved anemia doses has not been established.

Clinical evidence status: Approved intravenous treatment for iron-deficiency anemia; off-label human MRI experience is substantial but does not constitute an approved imaging indication. Anticancer evidence is predominantly cellular and animal-model based. A first-in-human phase I glioblastoma study is evaluating ferumoxytol plus pharmacologic ascorbate with radiation and temozolomide, primarily for safety, tolerability and dose determination. There is presently no randomized evidence demonstrating improved cancer survival, and ferumoxytol should not be classified as an established anticancer drug or standard radiosensitizer.

Ferumoxytol Mechanistic Profile

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	Tumor-associated macrophage polarization	Indirect ↓ survival and growth	↑ macrophage inflammatory activation (context-dependent)	G	↑ M1-like macrophage phenotype and antitumor innate immunity	Best-supported ferumoxytol-specific anticancer mechanism, but demonstrated principally in murine tumor models. Response depends on macrophage abundance and tumor microenvironment.
2	Iron-dependent Fenton chemistry	↑ hydroxyl-radical stress and cytotoxicity	↑ oxidative burden if antioxidant capacity is exceeded	R/G	Conversion of peroxide into highly reactive oxygen species	Requires intracellular nanoparticle degradation and available peroxide. Strongly enhanced by pharmacologic ascorbate or other pro-oxidant conditions.
3	Pharmacologic ascorbate interaction	↑ H₂O₂-mediated killing	↔ or modest injury under controlled exposure	R	Ferumoxytol-derived iron accelerates ascorbate-driven oxidative chemistry	Investigational combination. Selectivity is proposed to arise from differences in peroxide metabolism and redox buffering, not from tumor-exclusive nanoparticle uptake.
4	Radiosensitization	↑ radiation-associated oxidative damage (requires external trigger)	Potential ↑ normal-tissue oxidative injury	R/G	Amplification of radiation-induced ROS and macromolecular damage	Being tested with pharmacologic ascorbate, radiation and temozolomide in glioblastoma. Ferumoxytol-alone radiosensitization is not clinically established.
5	Chemosensitization	↑ temozolomide-associated cytotoxicity (context-dependent)	Potential ↑ treatment toxicity	G	Oxidative augmentation of DNA-damaging therapy	Evidence is primarily combination-based and cannot be separated cleanly from the effects of pharmacologic ascorbate and radiation.
6	Mitochondrial ROS and dysfunction	↑ ROS, ↓ membrane potential and ↑ apoptosis	↔ at regulated iron exposure; ↑ injury with overload	R/G	Oxidative impairment of mitochondrial function	Often secondary to iron release and Fenton chemistry rather than a direct nanoparticle receptor-mediated effect.
7	Ferroptosis and lipid peroxidation	↑ lipid ROS and ferroptotic susceptibility (model-dependent)	↑ susceptibility during iron overload or depleted antioxidant defenses	G	Iron-dependent oxidative membrane damage	Well described for iron oxide nanoparticle platforms, but ferumoxytol-specific evidence is less mature than the macrophage-polarization mechanism.
8	NRF2 antioxidant response	↑ adaptive NRF2 signaling or ↓ cytotoxicity (context-dependent)	↑ antioxidant defense	G	Compensatory response to nanoparticle-induced oxidative stress	Secondary mechanism. NRF2 activation may protect cells and reduce oxidative treatment efficacy rather than function as the principal therapeutic action.
9	Macrophage and reticuloendothelial uptake	↑ tumor-associated macrophage labeling	↑ hepatic, splenic and marrow macrophage uptake	G	Phagocytic sequestration and gradual iron processing	Central to iron delivery and off-label MRI. Uptake does not itself prove antitumor activity.
10	Iron availability and erythropoiesis	Potential ↑ iron availability (context-dependent)	↑ transferrin iron, ferritin and hemoglobin synthesis	G	Correction of iron-deficiency anemia	Established clinical mechanism. Theoretical concern that iron could support tumor metabolism has not established a clinically meaningful tumor-promoting effect from appropriately indicated ferumoxytol therapy.
11	Magnetic resonance signal modulation	↓ T2 and T2-star signal in nanoparticle-rich regions	↓ signal in blood pool and reticuloendothelial tissues	R/G	Prolonged susceptibility-based MRI contrast	Useful for vascular and macrophage imaging but off-label. Ferumoxytol can alter MRI findings for weeks to months and may obscure or mimic pathology.
12	Clinical Translation Constraint	↔ uncertain therapeutic exposure	Risk of hypersensitivity, hypotension, iron overload and extravasation staining	R/G	Limits oncology deployment outside controlled trials	Anticancer effects are unproven in randomized trials. Administration requires infusion over at least 15 minutes, immediate availability of anaphylaxis treatment and observation for at least 30 minutes. Tumor uptake is heterogeneous, and approved anemia dosing cannot be assumed to reproduce experimental intratumoral concentrations.

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
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



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



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



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



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



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



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

Scientific Papers found: Click to Expand⟱

6890-

Fer,

Iron oxide nanoparticles inhibit tumour growth by inducing pro-inflammatory macrophage polarization in tumour tissues

vitro+vivo,

Var,

TumMeta↓, TumCD∅, Casp3↑, ROS↑, H2O2↑, TumCG↓, Dose↝, other↑,

6891-

Fer,

Iron oxide nanoparticles inhibit tumor growth by ferroptosis in diffuse large B-cell lymphoma

vitro+vivo,

lymphoma,

female nude mice

TumCG↓, Ferroptosis↑, i-Iron↑, lipid-P↑, GPx4↓, ROS↑, Fenton↑, TfR1/CD71↝, FPN↝, LIP↑, TumCP↓, Apoptosis↑, TumCG↓,

6893-

Fer,

VitC,

MRI Detection and Therapeutic Enhancement of Ferumoxytol Internalization in Glioblastoma Cells

in-vitro,

GBM,

U87MG

in-vitro,

GBM,

U251

in-vitro,

GBM,

U118MG

eff↑, i-Iron↑, AntiCan↑, ROS↓, H2O2↑,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,
Total Targets: 22

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

3 ferumoxytol
1 Vitamin C (Ascorbic Acid)

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:285  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

ferumoxytol / ROS Cancer Research Results

Ferumoxytol Mechanistic Profile

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

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

Migration(tgid=13) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

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