Capsaicin / ROS Cancer Research Results

CAP, Capsaicin: Click to Expand ⟱
Features:
Capsaicin is a chemical compound that gives chili peppers their spicy flavor and heat.

Biological activity, capsaicin has been reported to exhibit a range of effects, including:
Pain relief: 10-50 μM
Anti-inflammatory activity: 20-50 μM
Antioxidant activity: 10-100 μM
Anti-cancer activity: 50-100 μM
Cardiovascular health: 20-50 μM

Approximate μM concentrations of capsaicin, the active compound in chili peppers, that can be achieved with different amounts of chili peppers:
1 teaspoon of dried chili pepper flakes (5g):~10-50 μM of capsaicin
1 tablespoon of dried chili pepper flakes (15g): ~30-150 μM of capsaicin
1 cup of fresh chili peppers (100g): ~100-500 μM of capsaicin
1 teaspoon of chili pepper extract (5g): ~100-500 μM of capsaicin
1 tablespoon of chili pepper extract (15g): ~300-1500 μM of capsaicin

Approximate μM concentrations of capsaicin in various foods that contain capsaicin:
Jalapeño peppers: 1 pepper (20g): ~20-100 μM of capsaicin 2–8 mg/100g of fresh Jalapeño
Serrano peppers: 1 pepper (10g): ~10-50 μM of capsaicin 5–15 mg/100g
Cayenne peppers: 1 pepper (10g): ~50-200 μM of capsaicin
Habanero peppers: 1 pepper (20g): ~100-500 μM of capsaicin 15–30 mg/100g
Ghost peppers: 1 pepper (20g): ~200-1000 μM of capsaicin
Hot sauce: 1 teaspoon (5g): ~10-50 μM of capsaicin
Chili flakes: 1 teaspoon (5g): ~10-50 μM of capsaicin
Spicy sauces and marinades: 1 tablespoon (15g): ~10-50 μM of capsaicin

Cayenne Pepper Powder – Approximate capsaicin content: roughly 5–20 mg/g (15-30g human for 100uM?)

-IC50 in Cancer Cell Lines: Approximately 50–300 µM (consume 150mg of capsaican not possible?)
-IC50 in Normal Cell Lines: Generally higher—often 2–3 times greater

Pathways:
-disrupting mitochondrial membrane potential, leading to cytochrome c release and subsequent activation of caspases
-Activation of TRPV1: resulting in increased intracellular calcium levels
-capsaicin can lead to increased production of ROS within cancer cells
-Inhibition of NF-κB
-Inhibit PI3K/AKT/mTOR signaling
-STAT3 Inhibition
-Cell Cycle Arrest
-reduce the expression of vascular endothelial growth factor (VEGF)
-COX-2
-capsaicin is a natural ADAM10 activator and shows potential to attenuate amyloid pathology and protect against AD

Capsaicin — capsaicin is a pungent vanilloid alkaloid phytochemical from Capsicum peppers and the principal TRPV1 agonist responsible for chili heat. It is best classified as a natural product / small-molecule vanilloid with approved topical analgesic use but no established anticancer indication. Standard abbreviations include CAP and CAPS. In cancer literature it is a pleiotropic stressor whose dominant preclinical effects usually converge on Ca2+ influx, mitochondrial dysfunction, ROS generation, suppression of pro-survival signaling, and apoptosis, but its biology is context- and concentration-dependent, with occasional low-dose pro-migratory / pro-metastatic signaling reported.

Primary mechanisms (ranked):

  1. TRPV-linked cation influx with intracellular Ca2+ dysregulation, variably via TRPV1 or other TRPV-family context such as TRPV6
  2. Mitochondrial injury with loss of membrane potential, cytochrome c release, and intrinsic apoptotic execution
  3. Mitochondrial and cellular ROS increase with redox stress exceeding tumor buffering capacity
  4. Suppression of STAT3 and related survival transcription programs in multiple models
  5. Suppression of NF-κB-centered inflammatory / survival signaling, with downstream anti-migratory and radiosensitizing implications in some settings
  6. PI3K/Akt/mTOR attenuation and cell-cycle restraint in responsive models
  7. Contextual induction of autophagy as a stress-adaptation program that may either accompany death or partially buffer it
  8. Anti-migratory / anti-invasive effects in many models, but with an important low-concentration exception in some colorectal systems

Bioavailability / PK relevance: Capsaicin is lipophilic, rapidly absorbed, and rapidly metabolized, with substantial first-pass limitation after oral exposure. Human oral PK from a capsicum preparation containing 26.6 mg capsaicin produced a Cmax of about 2.47 ng/mL at ~47 minutes, while the FDA-approved 8% topical system produced transient systemic exposure usually below 5 ng/mL, with a highest detected plasma level of 4.6 ng/mL. Delivery is therefore a major translation constraint for anticancer use, and formulation-based approaches are often invoked to overcome short half-life, irritancy, and exposure limits.

In-vitro vs systemic exposure relevance: This is a major limitation. Many anticancer cell studies use roughly 10–300 µM, whereas reported human plasma exposures from oral or approved topical use are in the low ng/mL range, approximately ~0.008–0.015 µM, i.e., orders of magnitude lower than many cytotoxic in-vitro concentrations. Accordingly, direct systemic tumoricidal translation from standard dietary or approved topical exposure is weak unless local delivery, sustained-release systems, or substantially altered formulations are used.

Clinical evidence status: Anticancer evidence is predominantly preclinical, with in-vitro and some in-vivo support across several tumor types. There is no regulatory approval for cancer treatment. Human oncology use is currently much more credible as supportive care for neuropathic pain, especially chemotherapy-induced peripheral neuropathy, where topical high-concentration capsaicin patches are being studied and used off-label / investigationally, rather than as a direct antitumor therapy.

Mechanistic Table

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 TRPV-linked Ca2+ influx Ca2+ ↑; death signaling ↑ Sensory excitation ↑; irritancy ↑ P/R Upstream trigger Usually framed through TRPV1, but some tumor models show dependence on other TRPV-family context such as TRPV6; this is mechanistically central but not uniform across cancers.
2 Mitochondrial membrane potential MMP ↓; cytochrome c release ↑ ↔ / stress if exposed R Intrinsic apoptosis initiation Mitochondrial dysfunction is one of the most reproducible downstream events and often links Ca2+ overload with apoptosis.
3 Mitochondrial ROS increase ROS ↑; redox buffering overwhelmed ↔ / antioxidant response may compensate P/R Stress amplification Frequently sits upstream of mitochondrial collapse, DNA damage signaling, and apoptosis; cancer selectivity is often attributed to weaker redox reserve.
4 Intrinsic apoptosis machinery BAX/Bak ↑; Bcl-2/Bcl-xL ↓; caspase-3/9 ↑ ↔ / lower sensitivity in some comparisons R/G Execution-phase cell death Common endpoint across responsive models; often follows ROS and mitochondrial injury rather than acting as the primary initiating lesion.
5 STAT3 survival signaling STAT3 ↓ ↔ R/G Reduced survival and proliferation Well supported in multiple myeloma and other models, but not universal; note that a HepG2 context reported ROS-associated STAT3 activation coupled to autophagy.
6 NF-κB inflammatory survival axis NF-κB ↓ Inflammatory tone ↓ R/G Anti-survival; anti-migratory Important for invasion restraint and likely part of observed radiosensitization in some models.
7 PI3K Akt mTOR axis PI3K/Akt/mTOR ↓ ↔ R/G Growth suppression Seen in several responsive systems, but this axis is also part of the cautionary low-dose pro-metastatic literature in colorectal cancer.
8 Cell-cycle control G0/G1 or G1/S arrest ↑ ↔ G Proliferation blockade Usually secondary to upstream stress and survival-pathway suppression rather than the earliest event.
9 Autophagy stress program Autophagy ↑ (context-dependent) ↔ G Adaptive buffering or co-lethal stress In HepG2, autophagy appeared partially protective because inhibiting it enhanced capsaicin-induced apoptosis.
10 Migration invasion EMT phenotype Migration ↓; invasion ↓; EMT ↓ (context-dependent) ↔ G Anti-metastatic phenotype Frequently reported at active doses, often linked to AMPK activation and NF-κB suppression.
11 Low-dose paradox flag ROS ↑ with Akt/mTOR ↑ and STAT3 ↑ (model-dependent) ↔ G Potential pro-metastatic signaling Important caution: low-concentration capsaicin has been reported to enhance metastatic behavior in colorectal cancer models.
12 Radiosensitization or Chemosensitization Sensitivity ↑ (context-dependent) Unknown G Adjunct potential Preclinical support exists, especially via NF-κB and stress-pathway modulation, but this remains non-clinically established for direct cancer treatment.
13 Clinical Translation Constraint Required tumoricidal exposure often not reached systemically Irritation and tolerability limit escalation G Translation bottleneck Typical antitumor in-vitro concentrations greatly exceed known plasma exposure from standard oral intake or approved topical use; formulation, local delivery, and tumor heterogeneity are major constraints.

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⟱
5841- CAP,    The red pepper’s spicy ingredient capsaicin activates AMPK in HepG2 cells through CaMKKβ
- in-vitro, HCC, HepG2
AMPK↑, CaMKII ↑, tumCV↓, Akt↓, mTOR↓, ROS↑,
5842- CAP,    Capsaicin: Current Understanding of Its Mechanisms and Therapy of Pain and Other Pre-Clinical and Clinical Uses
- Review, Nor, NA - Review, Diabetic, NA
*Pain↓, *TRPV1↑, AMPK↑, ROS↑, TumCP↑, Apoptosis↑, TumCCA↑, Casp3↑, BAX↑, Bak↑, cl‑PARP↑, Bcl-2↓, RNS↑, *glucose↓, *Insulin↑, *BP↓, *AntiAg↑, ER Stress↑, Hif1a↓, chemoPv↑,
5838- CAP,    Capsaicin Induces Autophagy and Apoptosis in Human Nasopharyngeal Carcinoma Cells by Downregulating the PI3K/AKT/mTOR Pathway
- in-vitro, NPC, NA
TumCG↓, TumCCA↑, TumAuto↑, Casp3↑, Ca+2↑, ROS↑, MMP↓, LC3‑Ⅱ/LC3‑Ⅰ↑, ATG5↑, p62↓, Fap1↓, PI3K↓, DNAdam↑,
5836- CAP,    In vitro and in vivo induction of apoptosis by capsaicin in pancreatic cancer cells is mediated through ROS generation and mitochondrial death pathway
- vitro+vivo, PC, AsPC-1 - in-vitro, PC, Bxpc-3
tumCV↓, Apoptosis↑, ROS↑, MMP↓, eff↓, BAX↑, Bcl-2↓, survivin↓, Cyt‑c↑, AIF↑, selectivity↑, JNK↑, TumCG↓,
5835- CAP,    Capsaicin and dihydrocapsaicin induce apoptosis in human glioma cells via ROS and Ca2+-mediated mitochondrial pathway
- in-vitro, GBM, U251
tumCV↓, Apoptosis↑, selectivity↑, ROS↑, Ca+2↑, MMP↓, Cyt‑c↑, Casp↑, eff↑, MPT↑, ETC↓, Casp3↑, Casp9↑,
5834- CAP,    Capsaicin and TRPV1: A Novel Therapeutic Approach to Mitigate Vascular Aging
- Study, Nor, NA
*AntiCan↑, *Inflam↓, *antiOx↑, *TRPV1↑, *AMPK↑, *SIRT1↑, *NADPH↓, *ROS↓, *MAPK↓, *eNOS↑, *Wnt/(β-catenin)↓, RenoP↑,
5833- CAP,    Capsaicin: From Plants to a Cancer-Suppressing Agent
- Review, Var, NA
chemoPv↑, TumCCA↑, Apoptosis↑, ROS↑, MMP↓, Ca+2↑, JNK↑, Casp3↑, NADH↓, CDK2↓, CDK4↓, CDK6↓, P53↑,
5831- CAP,    Unraveling TRPV1’s Role in Cancer: Expression, Modulation, and Therapeutic Opportunities with Capsaicin
TRPV1↑, Ca+2↑, AntiCan↑, TumCP↓, Pain↓, TumCG↓, ChemoSen↑, Apoptosis↑, ROS↑, MMP↓, Cyt‑c↑, Casp↑,
5830- CAP,    Inhibition of pyroptosis and apoptosis by capsaicin protects against LPS-induced acute kidney injury through TRPV1/UCP2 axis in vitro
- in-vitro, Nor, HK-2
*IL1β↓, *IL18↓, *TRPV1↑, *ROS↓, *MMP↑, *Apoptosis↓, *RenoP↑, *Inflam↓, *UCPs↑,
5826- CAP,    Capsaicin induces mitochondrial dysfunction and apoptosis in anaplastic thyroid carcinoma cells via TRPV1-mediated mitochondrial calcium overload
- in-vitro, Thyroid, NA
TRPV1↑, tumCV↓, Ca+2↑, mtDam↑, ROS↑, MMP↓, MPT↑, Cyt‑c↑, Casp↑, Apoptosis↑,
5860- CAP,    Beneficial Effects of Capsaicin in Disorders of the Central Nervous System
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*neuroP↑, *memory↑, *Pain↓, *TRPV1↑, *Aβ↓, *tau↓, *cognitive↑, *Risk↓, *motorD↓, *ROS↓, *TNF-α↓, *IL1β↓, *eff↑, *Risk↓,
5859- CAP,    Are We Ready to Recommend Capsaicin for Disorders Other Than Neuropathic Pain?
- Review, Var, NA
*TRPV1↑, *Ca+2↑, *Na+↑, *UCPs↑, *SIRT1↑, *PPARγ↑, *Inflam↓, *lipid-P↑, *IL6↓, *TNF-α↓, *NF-kB↓, *p‑Akt↑, *NRF2↑, *HO-1↑, *ROS↑, *GutMicro↑,
5858- CAP,    Capsaicin as a Microbiome Modulator: Metabolic Interactions and Implications for Host Health
- Review, Nor, NA - Review, AD, NA
*BBB↓, *GutMicro↑, Obesity↓, *Inflam↓, *AntiCan↑, *TRPV1↑, *Ca+2↑, *antiOx↑, *cardioP↑, *BioAv↓, *Half-Life↓, *BioAv↝, *BioAv↑, *neuroP↑, Apoptosis↑, p38↑, ROS↑, MMP↓, MPT↑, Cyt‑c↑, Casp↑, TRIB3↑, NADH↓, SIRT1↓, TumCG↓, TumCMig↓, TOP1↓, TOP2↓, β-catenin/ZEB1↓, *ROS↓, *Aβ↓,
5854- CAP,    Pharmacological activity of capsaicin: Mechanisms and controversies (Review)
- Review, Var, NA - Review, AD, NA
Obesity↓, Half-Life↓, antiOx↑, TRPV1↑, STAT3↓, Ca+2↑, ROS↑, MMP↓, *neuroP↑, *tau↓, *Inflam↓, *ROS?,
5850- CAP,    Anticancer Activity of Natural and Synthetic Capsaicin Analogs
- Review, Var, NA
TRPV1↑, Ca+2↑, ROS↑, mitResp↓, ChemoSen↑, P-gp↓,
5849- CAP,    The Impact of TRPV1 on Cancer Pathogenesis and Therapy: A Systematic Review
- Review, Var, NA
TRPV1↑, Ca+2↑, TumCD↑, TumCCA↑, Apoptosis↑, P53↑, Fas↑, PI3K↑, AR↑, STAT3↓, ROS↑, MMP↓, ATP↓, CHOP↑, TumCMig↓, Twist↓, Snail↓, MMP2↓, MMP9↓, E-cadherin↑,
5847- CAP,    An updated review on molecular mechanisms underlying the anticancer effects of capsaicin
- in-vitro, Liver, HepG2
HO-1↑, ROS↑, NRF2↑, *lipid-P↓, *SOD↑, *Catalase↑, *GPx↑, *GSR↑, *PGE2↓, *COX2↓, *iNOS↓, TumCP↓, TumCCA↑, cycE/CCNE↓, CDK4↓, MMP↓, P53↑, P21↑, BAX↑, SIRT1↑, angioG↓, P-gp↓, ChemoSen↑,
5845- CAP,    Unveiling the Molecular Mechanisms Driving the Capsaicin-Induced Immunomodulatory Effects on PD-L1 Expression in Bladder and Renal Cancer Cell Lines
- in-vivo, RCC, A498 - in-vitro, RCC, T24/HTB-9 - NA, Bladder, 5637
TRPV1↑, TumCP↓, Casp↑, Apoptosis↑, SIRT1↓, MMP2↓, MMP9↓, TumCMig↓, TumCCA↑, ROS↑, DNAdam↑, PD-L1↑, eff↓,
5843- CAP,    The Effects of Capsaicin on Gastrointestinal Cancers
- Review, GC, NA
*BioAv↑, ROS↑, Apoptosis↑, Glycolysis↓, HK2↓, MMP9↓, AMPK↑, TumCP↓, Casp3↑, Bcl-2↓, P53↑, BAX↑,
2019- CAP,    Capsaicin: A Two-Decade Systematic Review of Global Research Output and Recent Advances Against Human Cancer
- Review, Var, NA
chemoPv↑, Ca+2↑, antiOx↑, *ROS↓, *MMP∅, *Cyt‑c∅, *Casp3∅, *eff↑, *Inflam↓, *NF-kB↓, *COX2↓, iNOS↓, TRPV1↑, i-Ca+2?, MMP↓, Cyt‑c↑, Bax:Bcl2↑, P53↑, JNK↑, PI3K↓, Akt↓, mTOR↓, LC3II↑, ATG5↑, p62↑, Fap1↓, Casp3↑, Apoptosis↑, ROS↑, MMP9↓, eff↑, eff↓, eff↑, selectivity↑, eff↑, ChemoSen↑,
2018- CAP,  MF,    Capsaicin: Effects on the Pathogenesis of Hepatocellular Carcinoma
- Review, HCC, NA
TRPV1↑, eff↑, Akt↓, mTOR↓, p‑STAT3↑, MMP2↑, ER Stress↑, Ca+2↑, ROS↑, selectivity↑, MMP↓, eff↑,
2014- CAP,    Role of Mitochondrial Electron Transport Chain Complexes in Capsaicin Mediated Oxidative Stress Leading to Apoptosis in Pancreatic Cancer Cells
- in-vitro, PC, Bxpc-3 - in-vitro, Nor, HPDE-6 - in-vivo, PC, AsPC-1
ROS↑, *ROS∅, selectivity↑, compI↓, compIII↓, eff↑, selectivity↑, ATP↓, Cyt‑c↑, Casp9↑, Casp3↑, MMP↓, SOD↓, GSH/GSSG↓, Apoptosis↑, *toxicity∅, GSH↓, Catalase↓, GPx↓, Dose↝,
2012- CAP,    Capsaicin induces cytotoxicity in human osteosarcoma MG63 cells through TRPV1-dependent and -independent pathways
- NA, OS, MG63
AntiTum↑, Apoptosis↑, TRPV1↑, ROS↑, SOD↓, AMPK↑, P53↑, JNK↑, Bcl-2↓, Cyt‑c↑, cl‑Casp3↑, cl‑PARP↑, Ca+2↑, MMP↓,
1517- CAP,    Capsaicin Inhibits Multiple Bladder Cancer Cell Phenotypes by Inhibiting Tumor-Associated NADH Oxidase (tNOX) and Sirtuin1 (SIRT1)
- in-vitro, Bladder, TSGH8301 - in-vitro, CRC, T24/HTB-9
ENOX2↓, TumCCA↑, ERK↓, p‑FAK↓, p‑pax↓, TumCMig↓, EMT↓, SIRT1↓, Dose∅, ROS↑, MMP↓, Bcl-2↓, Bak↑, cl‑PARP↑, Casp3↑, SIRT1↓, ac‑P53↑, BIM↑, p‑RB1↓, cycD1/CCND1↓, Dose∅, β-catenin/ZEB1↓, N-cadherin↓, E-cadherin↑,
1259- CAP,    Capsaicin inhibits HIF-1α accumulation through suppression of mitochondrial respiration in lung cancer cells
- in-vitro, Lung, H1299 - in-vitro, Lung, A549 - in-vitro, Lung, H23 - in-vitro, Lung, H2009
Hif1a↓, PDK1↓, GLUT1↓, ROS↑, mitResp↓, ATP↓,
5204- CAP,    Low-concentration capsaicin promotes colorectal cancer metastasis by triggering ROS production and modulating Akt/mTOR and STAT-3 pathways
- in-vitro, Colon, SW480 - in-vitro, Colon, CT26
TumCP↓, TumCMig↑, TumCI↑, EMT↑, MMP2↓, MMP9↑, STAT3↑, TumMeta↑, ROS↑,
5202- CAP,    Capsaicin Suppresses Cell Proliferation, Induces Cell Cycle Arrest and ROS Production in Bladder Cancer Cells through FOXO3a-Mediated Pathways
- vitro+vivo, Bladder, 5637 - in-vitro, Bladder, T24/HTB-9
antiOx↑, Inflam↓, AntiCan↓, TRPV1↑, TumCP↓, TumCCA↑, ROS↑, FOXO3↑, TumCMig↓,
5201- CAP,    Inhibiting ROS-STAT3-dependent autophagy enhanced capsaicin-induced apoptosis in human hepatocellular carcinoma cells
- NA, HCC, HepG2
AntiCan↓, Apoptosis↑, cl‑PARP↑, Bcl-2↑, TumAuto↑, LC3II↑, eff↑, STAT3↑, ROS↑, eff↓,
5198- CAP,    Capsaicin induces apoptosis by generating reactive oxygen species and disrupting mitochondrial transmembrane potential in human colon cancer cell lines
- in-vitro, CRC, LoVo - in-vitro, CRC, Colo320
tumCV↓, DNAdam↑, Apoptosis↑, ROS↑, MMP↑, Casp3↑, chemoPv↑,
2652- CAP,    Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
- Review, Var, NA
chemoPv↑, AntiCan↑, ROS↑, TumCG↓, ROS↑, MMP↑, Apoptosis↑, TumCCA↑, JNK↑, SOD↓, Catalase↓, GPx↓, other↓, SIRT1↓, NADPH↑, FOXO3↑,
2394- CAP,    Capsaicin acts as a novel NRF2 agonist to suppress ethanol induced gastric mucosa oxidative damage by directly disrupting the KEAP1-NRF2 interaction
- in-vitro, Nor, GES-1
*mtDam↓, *NRF2↑, *HO-1↑, *Trx↑, *GSS↑, *NQO1↑, *Keap1↓, *ROS↓, *PKM2↓, *LDHA↓, *Inflam↓,
2348- CAP,    Recent advances in analysis of capsaicin and its effects on metabolic pathways by mass spectrometry
- Analysis, Nor, NA
Warburg↓, *PKM2↓, *COX2↓, *Inflam↓, *Sepsis↓, *AMPK↑, *PKA↑, *mitResp↑, *FAO↑, *FASN↓, *PGM1?, *ATP↑, *ROS↓,
2020- CAP,    Capsaicinoids and Their Effects on Cancer: The “Double-Edged Sword” Postulate from the Molecular Scale
- Review, Var, NA
AntiTum↑, selectivity↑, TRPV1↑, MMP↓, Ca+2↑, ER Stress↑, angioG↓, Casp3?, cl‑PARP↑, selectivity↑, ROS↑, *ROS∅, selectivity↑,

Showing Research Papers: 1 to 33 of 33

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 33

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↓, 2,   compI↓, 1,   ENOX2↓, 1,   GPx↓, 2,   GSH↓, 1,   GSH/GSSG↓, 1,   HO-1↑, 1,   NADH↓, 2,   NRF2↑, 1,   RNS↑, 1,   ROS↑, 28,   SOD↓, 3,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 3,   compIII↓, 1,   ETC↓, 1,   mitResp↓, 2,   MMP↓, 16,   MMP↑, 2,   MPT↑, 3,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 4,   Glycolysis↓, 1,   HK2↓, 1,   NADPH↑, 1,   PDK1↓, 1,   SIRT1↓, 5,   SIRT1↑, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 3,   Apoptosis↑, 16,   Bak↑, 2,   BAX↑, 4,   Bax:Bcl2↑, 1,   Bcl-2↓, 5,   Bcl-2↑, 1,   BIM↑, 1,   Casp↑, 5,   Casp3?, 1,   Casp3↑, 9,   cl‑Casp3↑, 1,   Casp9↑, 2,   Cyt‑c↑, 8,   Fap1↓, 2,   Fas↑, 1,   iNOS↓, 1,   JNK↑, 5,   p38↑, 1,   survivin↓, 1,   TRPV1↑, 11,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

CaMKII ↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,   tumCV↓, 5,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 3,  

Autophagy & Lysosomes ⓘ

ATG5↑, 2,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   LC3II↑, 2,   p62↓, 1,   p62↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 3,   P53↑, 6,   ac‑P53↑, 1,   cl‑PARP↑, 5,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 2,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,   p‑RB1↓, 1,   TumCCA↑, 9,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   EMT↑, 1,   ERK↓, 1,   FOXO3↑, 2,   mTOR↓, 3,   PI3K↓, 2,   PI3K↑, 1,   STAT3↓, 2,   STAT3↑, 2,   p‑STAT3↑, 1,   TOP1↓, 1,   TOP2↓, 1,   TumCG↓, 5,  

Migration ⓘ

Ca+2↑, 12,   i-Ca+2?, 1,   E-cadherin↑, 2,   p‑FAK↓, 1,   MMP2↓, 3,   MMP2↑, 1,   MMP9↓, 4,   MMP9↑, 1,   N-cadherin↓, 1,   p‑pax↓, 1,   Snail↓, 1,   TRIB3↑, 1,   TumCI↑, 1,   TumCMig↓, 5,   TumCMig↑, 1,   TumCP↓, 6,   TumCP↑, 1,   TumMeta↑, 1,   Twist↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   Hif1a↓, 2,  

Barriers & Transport ⓘ

GLUT1↓, 1,   P-gp↓, 2,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   PD-L1↑, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↑, 1,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 4,   Dose↝, 1,   Dose∅, 2,   eff↓, 4,   eff↑, 8,   Half-Life↓, 1,   selectivity↑, 9,  

Clinical Biomarkers ⓘ

AR↑, 1,   PD-L1↑, 1,   TRIB3↑, 1,  

Functional Outcomes ⓘ

AntiCan↓, 2,   AntiCan↑, 2,   AntiTum↑, 2,   chemoPv↑, 5,   Obesity↓, 2,   Pain↓, 1,   RenoP↑, 1,  
Total Targets: 132

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Catalase↑, 1,   GPx↑, 1,   GSR↑, 1,   GSS↑, 1,   HO-1↑, 2,   Keap1↓, 1,   lipid-P↓, 1,   lipid-P↑, 1,   NQO1↑, 1,   NRF2↑, 2,   ROS?, 1,   ROS↓, 7,   ROS↑, 1,   ROS∅, 2,   SOD↑, 1,   Trx↑, 1,   UCPs↑, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   Insulin↑, 1,   mitResp↑, 1,   MMP↑, 1,   MMP∅, 1,   mtDam↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,   FAO↑, 1,   FASN↓, 1,   glucose↓, 1,   LDHA↓, 1,   NADPH↓, 1,   PGM1?, 1,   PKM2↓, 2,   PPARγ↑, 1,   SIRT1↑, 2,  

Cell Death ⓘ

p‑Akt↑, 1,   Apoptosis↓, 1,   Casp3∅, 1,   Cyt‑c∅, 1,   iNOS↓, 1,   MAPK↓, 1,   TRPV1↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

Wnt/(β-catenin)↓, 1,  

Migration ⓘ

AntiAg↑, 1,   Ca+2↑, 2,   Na+↑, 1,   PKA↑, 1,  

Angiogenesis & Vasculature ⓘ

eNOS↑, 1,  

Barriers & Transport ⓘ

BBB↓, 1,   Na+↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   IL18↓, 1,   IL1β↓, 2,   IL6↓, 1,   Inflam↓, 8,   NF-kB↓, 2,   PGE2↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

tau↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 1,   eff↑, 2,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

BP↓, 1,   GutMicro↑, 2,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   cardioP↑, 1,   cognitive↑, 1,   memory↑, 1,   motorD↓, 1,   neuroP↑, 3,   Pain↓, 2,   RenoP↑, 1,   Risk↓, 2,   toxicity∅, 1,  

Infection & Microbiome ⓘ

Sepsis↓, 1,  
Total Targets: 78

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
33 Capsaicin
1 Magnetic Fields
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#:55  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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