Crocetin / ROS Cancer Research Results

Cro, Crocetin: Click to Expand ⟱

Features:

Crocetin is a carotenoid pigment found in saffron (Crocus sativus) and has been studied for its potential anti-cancer properties. Research has shown that crocetin may have anti-tumor and anti-proliferative effects, inhibiting the growth of various types of cancer cells.
Crocetin is a carotenoid dicarboxylic acid derived from saffron (Crocus sativus) and is a metabolite of crocin. It is lipophilic and more bioavailable than crocin. In cancer research, crocetin is studied mainly in preclinical models, where it appears to influence apoptosis, inflammation, angiogenesis, and redox signaling. It is not a primary cytotoxic chemotherapeutic, but a signaling and stress-modulating compound.

Mechanistic themes reported:
-NF-κB suppression
-PI3K/AKT pathway modulation
-MAPK signaling effects
-Apoptosis induction (mitochondrial pathway)
-Anti-angiogenic signaling (VEGF reduction)
-Redox modulation (context-dependent antioxidant / pro-oxidant behavior)

Evidence level: predominantly cell culture and animal models.

Reported to modulate glycolytic metabolism and lactate production (model-dependent); LDH5 inhibition has been reported preclinically, but clinical relevance and achievable tumor exposure are not established.

Crocetin — Crocetin is a saffron/gardenia-derived apocarotenoid dicarboxylic acid and the aglycone bioactive metabolite of crocin. It is formally a natural-product carotenoid derivative rather than an approved anticancer drug. Standard abbreviations include Cro and, less commonly, trans-crocetin or crocetic acid. It originates primarily from Crocus sativus stigma and Gardenia jasminoides fruit, with crocin serving as a glycosylated precursor that is hydrolyzed to crocetin after oral intake. In oncology, crocetin is best classified as a preclinical signaling, redox, metabolism, and apoptosis-modulating compound with limited direct human cancer-treatment evidence.

Primary mechanisms (ranked):

Mitochondrial apoptosis induction through Bax/Bcl-2 shift, caspase activation, mitochondrial membrane potential disruption, and cell-cycle checkpoint effects.
Suppression of inflammatory and survival signaling, especially NF-κB-linked cytokine, COX-2, VEGF, and invasion programs.
PI3K/AKT, MAPK, STAT3, SHH, and related growth-pathway modulation, with direction varying by cancer model.
Antiglycolytic activity through LDH5/LDHA-linked lactate metabolism effects; stronger as a preclinical metabolic hypothesis than as a clinically validated anticancer axis.
Anti-angiogenic and anti-invasive modulation, including VEGF, MMPs, EMT markers, and migration suppression in selected models.
Redox modulation, generally antioxidant/cytoprotective in normal-tissue injury models but context-dependent in cancer cells; NRF2/HO-1 activation is better supported in normal-cell injury models than as a core anticancer mechanism.
Adjunct chemosensitization, reported with vincristine and cisplatin in cell models, but not clinically established.

Bioavailability / PK relevance: Oral crocin is poorly absorbed intact and is largely converted to crocetin by intestinal and microbial glycosidase activity. Crocetin itself appears in plasma after oral crocin or crocetin exposure, often as free crocetin and glucuronide conjugates, but poor solubility, formulation dependence, intestinal metabolism, and uncertain tumor-tissue exposure constrain translation.

In-vitro vs systemic exposure relevance: Many anticancer cell studies use crocetin in the approximate 50–800 µM range, with several key studies around 60–240 µM or higher. These concentrations likely exceed typical exposure from dietary saffron or ordinary oral supplement use, so in-vitro cytotoxic and chemosensitizing effects should be treated as high-concentration/preclinical unless supported by formulation-specific PK data.

Clinical evidence status: Preclinical for oncology. There are cell-culture and animal tumor data, including pancreatic, colorectal, gastric, cervical/ovarian, prostate, and hepatocellular models, plus limited adjunct combination data. Human clinical evidence for isolated crocetin is mainly non-oncology or safety-oriented, while oncology-related human trials are more often crocin/saffron adjunctive or supportive-care contexts rather than crocetin as an anticancer therapy.

Crocetin Cancer Mechanism Table

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	Mitochondrial apoptosis and cell-cycle checkpoints	Bax ↑; Bcl-2 ↓; caspase-3/9 ↑; p21 ↑; G1/S/G2-M arrest ↑ (model-dependent)	Apoptosis ↓ in injury models; mitochondrial protection ↑ (context-dependent)	G	Apoptosis induction and cytostasis	Core anticancer mechanism across multiple models; normal-cell effects often move in the opposite protective direction under oxidative or inflammatory injury.
2	NF-κB inflammatory survival signaling	NF-κB ↓; IL-6 ↓; IL-8 ↓; COX-2 ↓; iNOS ↓; inflammatory transcription ↓	NF-κB-driven inflammation ↓	R, G	Anti-inflammatory tumor suppression	Central to anti-invasive and anti-angiogenic interpretations; strongest where inflammation-linked tumor progression is active.
3	PI3K / AKT and survival kinase signaling	p-AKT ↓ or pathway suppression ↑ (model-dependent); survival signaling ↓	p-AKT ↑ in some endothelial/cardioprotective injury models	R, G	Growth and survival pathway modulation	Direction is highly context-dependent; cancer-cell suppression should not be generalized to all normal tissues.
4	MAPK stress signaling	p38 MAPK ↑; ERK/JNK effects variable; migration ↓ in HCT-116 models	↔ or stress signaling normalization (context-dependent)	P, R, G	Stress-pathway reprogramming	Important in colorectal models, but direction and therapeutic implication vary by tumor genotype and drug context.
5	LDH5 / lactate metabolism	LDH5 activity ↓; LDHA protein ↓; lactate production ↓; glycolytic phenotype ↓ (model-dependent)	↔	R, G	Antiglycolytic pressure	Mechanistically attractive because LDH5 is a Warburg-metabolism target, but evidence is still mainly biochemical and preclinical.
6	Angiogenesis and VEGF axis	VEGF ↓; EGFR phosphorylation ↓; angiogenic signaling ↓	↔ or vascular protection ↑ in injury models	G	Anti-angiogenic support	Usually secondary to NF-κB, AKT, EGFR, and inflammatory pathway changes rather than a uniquely direct anti-VEGF drug-like mechanism.
7	Migration / invasion and EMT	MMP-2 ↓; MMP-9 ↓; uPA ↓; N-cadherin ↓; β-catenin ↓; E-cadherin ↑	↔	G	Anti-invasive phenotype	Relevant to metastasis biology but mostly based on in-vitro migration/invasion and selected xenograft models.
8	ROS and oxidative stress balance	ROS effects mixed; oxidative stress ↓ in some melanoma/cancer models; apoptosis may occur without a simple ROS ↑ pattern	ROS ↓; MDA ↓; lipid peroxidation ↓; SOD/GPx/GSH defenses ↑	P, R, G	Redox buffering and stress modulation	More clearly cytoprotective in normal-cell injury models than selectively pro-oxidant in cancer. Not a universal cancer ROS increaser.
9	NRF2 / HO-1 antioxidant response	↔ or uncertain; cancer-specific NRF2 direction is not well established	NRF2 ↑; HO-1 ↑ in oxidative/inflammatory injury models	R, G	Normal-tissue cytoprotection	Relevant as a protective/stress-response axis. Because sustained NRF2 activation can support therapy resistance in some cancers, this is a context-sensitive translation issue.
10	STAT3 / JAK / Src signaling	STAT3 activation ↓; nuclear accumulation ↓; upstream Src/JAK signaling ↓ (reported in hepatocellular models)	↔	R, G	Proliferation and inflammatory transcription suppression	Secondary but potentially meaningful where STAT3-driven inflammation/survival signaling is dominant.
11	SHH / Gli cancer stem and gastric signaling	SHH ↓; Gli1 ↓; DCLK1 ↓; cancer stem phenotype ↓ (model-dependent)	↔	G	Stemness and developmental pathway modulation	Potentially relevant in pancreatic and gastric contexts, but not yet a broad validated crocetin mechanism.
12	Chemosensitization	Vincristine sensitivity ↑; cisplatin-induced apoptosis ↑ in selected models	Normal-tissue protection possible but not established for oncology treatment protocols	G	Adjunct sensitization	Combination evidence is preclinical. Antioxidant and NRF2-linked effects make timing, concentration, and chemotherapy mechanism important.
13	Clinical Translation Constraint	Effective in-vitro concentrations often high; tumor exposure uncertain; human oncology efficacy not established	Generally tolerated in limited human non-oncology studies, but cancer-treatment safety is not established	G	Evidence and delivery limitation	Key constraints are poor solubility, formulation dependence, metabolism from crocin to crocetin, uncertain achievable tumor concentration, and lack of definitive anticancer trials.

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

P: 0–30 min (early redox and signaling interactions)
R: 30 min–3 hr (NF-κB / PI3K / MAPK modulation)
G: >3 hr (apoptosis, angiogenesis, and phenotype-level outcomes)

Crocetin and Alzheimer’s disease context — Crocetin is relevant to AD mainly as part of the saffron/crocin/crocetin evidence cluster rather than as a clinically established isolated AD drug. Mechanistic support includes antioxidant protection, anti-inflammatory signaling, Aβ-related effects, AChE inhibition signals from saffron constituents, ER-stress/apoptosis reduction, and possible BBB/gut-microbiome-mediated effects. Human RCT evidence is stronger for saffron extract than for purified crocetin.

Crocetin AD-Relevant Mechanism Table

Rank	Pathway / Axis	Modulation	TSF	Primary Effect	Notes / Interpretation
1	Oxidative stress and lipid peroxidation	ROS ↓; MDA ↓; SOD/GPx/GSH ↑	P, R, G	Neuroprotection	Most consistent non-cancer mechanism; often demonstrated in injury or neurodegeneration models using saffron, crocin, or crocetin-related exposure.
2	Neuroinflammation	NF-κB ↓; TNF-α ↓; IL-1β ↓; inflammatory tone ↓	R, G	Anti-inflammatory support	Likely contributes to cognitive and neuroprotective outcomes, but source specificity may vary between saffron extract, crocin, and crocetin.
3	Aβ aggregation / amyloid burden	Aβ aggregation ↓; amyloid toxicity ↓ (model-dependent)	G	Protein aggregation modulation	Relevant for AD indexing, but human clinical claims should be tied to saffron/crocin trial evidence rather than isolated crocetin unless directly tested.
4	Cholinergic signaling	AChE ↓; ChAT ↑ (reported)	R, G	Neurotransmission support	AChE inhibition is plausible for saffron constituents; compound-specific potency and clinical relevance require careful source attribution.
5	ER stress and apoptosis	CHOP ↓; GRP78/BiP ↓; caspase-3 ↓; Bax ↓; Bcl-2 ↑	G	Stress and cell-death reduction	Protective direction is opposite to the desired cancer-cell apoptosis direction, so disease context must be explicit.
6	PK / CNS exposure constraint	Crocin → crocetin; plasma crocetin ↑; BBB exposure uncertain	R, G	Translation constraint	Recent metabolism data support intestinal conversion to crocetin, but direct brain exposure and active metabolites remain incompletely resolved.

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

P: 0–30 min (early redox and signaling interactions)
R: 30 min–3 hr (NF-κB / PI3K / MAPK modulation)
G: >3 hr (apoptosis, angiogenesis, and phenotype-level outcomes)

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
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⟱

6300-

Cro,

Interaction of saffron and its constituents with Nrf2 signaling pathway: A review

Review,

Nor,

Review,

Arthritis,

*antiOx↑, *Inflam↓, *AntiTum↑, *hepatoP↑, *cardioP↑, *neuroP↑, *NRF2↑, *NF-kB↓, *iNOS↓, *COX2↓, *IL6↓, *IL10↓, *IL1β↓, *TNF-α↓, *HO-1↑, ROS↑, NQO1↑, NRF2↑, HO-1↑, NQO2↑, LDHA↓, ATP↓, *hepatoP↑, *SOD↑, *Catalase↑, *GPx↑, *NRF2↑, *ROS↓, *cardioP↑, *ER Stress↓, *GRP78/BiP↓, *CHOP↓, *Apoptosis↓, *miR-34a↓, *SIRT1↑, chemoP↑,

6309-

Cro,

Crocin exerts anti-tumor effect in colon cancer cells via repressing the JaK pathway

in-vitro,

CRC,

HCT116

tumCV↓, TumCP↓, Ki-67↓, Apoptosis↓, Inflam↓, ROS↑, MMP↓, JAK2↓, STAT3↓, ERK↓, MIP2↓, IL6↓, MCP1↓, IL8↓, IL1β↓, TNF-α↓, SOD↓, Catalase↓, GSH↓, ROS↑, mtDam↑,

6313-

Cro,

Review,

Covid,

Review,

Var,

Review,

Stroke,

RadioS↑, *other↑, *other↑, *OCR↑, *neuroP↑, ChemoSen↑, ROS↑,

6314-

Cro,

Crocin promotes ferroptosis in gastric cancer via the Nrf2/GGTLC2 pathway

in-vitro,

GC,

TumCP↓, TumCMig↓, TumCI↓, Apoptosis↓, antiOx↓, Ferroptosis↑, NRF2↑, P53↑, TumCCA↑, ChemoSen↑, EMT↓, Hif1a↓, ROS↑,

Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

chemoP↑, 1,
Total Targets: 40

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Catalase↑, 1, GPx↑, 1, HO-1↑, 1, NRF2↑, 2, ROS↓, 1, SOD↑, 1,

Mitochondria & Bioenergetics ⓘ

OCR↑, 1,

Core Metabolism/Glycolysis ⓘ

SIRT1↑, 1,

Cell Death ⓘ

Apoptosis↓, 1, iNOS↓, 1,

Transcription & Epigenetics ⓘ

other↑, 2,

Protein Folding & ER Stress ⓘ

CHOP↓, 1, ER Stress↓, 1, GRP78/BiP↓, 1,

Proliferation, Differentiation & Cell State ⓘ

miR-34a↓, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, IL10↓, 1, IL1β↓, 1, IL6↓, 1, Inflam↓, 1, NF-kB↓, 1, TNF-α↓, 1,

Clinical Biomarkers ⓘ

IL6↓, 1,

Functional Outcomes ⓘ

AntiTum↑, 1, cardioP↑, 2, hepatoP↑, 2, neuroP↑, 2,
Total Targets: 28

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

4 Crocetin

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#:249  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

Crocetin / ROS Cancer Research Results

Crocetin Cancer Mechanism Table

Crocetin AD-Relevant Mechanism Table

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Proliferation, Differentiation & Cell State ⓘ

Immune & Inflammatory Signaling ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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