Carvacrol / ROS Cancer Research Results

CAR, Carvacrol: Click to Expand ⟱

Features:

Carvacrol monoterpenoid phenol with odor of oregano. Found in essential oils and plants, has antimicorbial and antioxidant properties. Carvacrol is present abundantly in the essential oils of many medicinal plants and well known for its numerous biological activities.

Carvacrol — Carvacrol is a small lipophilic monoterpenoid phenol that occurs naturally in oregano, thyme, and related essential oils. It is best classified as a natural product phytochemical and food-flavoring constituent rather than an approved anticancer drug. Standard abbreviations include CAR and CARV. In translational oncology, carvacrol is mainly a preclinical multitarget stress-response modulator with recurring signals around mitochondrial apoptosis, PI3K/Akt suppression, TRPM7-linked Ca²⁺ handling, and anti-migratory/anti-inflammatory effects.

Primary mechanisms (ranked):

Mitochondria-linked intrinsic apoptosis induction with BAX↑, Bcl-2↓, cytochrome c release, and caspase-3 activation
PI3K/Akt survival signaling suppression with associated cell-cycle arrest and reduced proliferation
TRPM7-associated ion signaling disruption with downstream effects on Ca²⁺-dependent growth, migration, and survival
Anti-migratory and anti-invasive remodeling with reduced extracellular matrix and mesenchymal programs in some models
COX-2 and inflammatory signaling suppression
PPARα and PPARγ activation, which is mechanistically relevant but probably context-dependent and not the dominant antitumor axis
ROS modulation is model-dependent rather than uniformly pro-oxidant; it can contribute to tumor cell stress in some systems but also show antioxidant/cytoprotective behavior in non-cancer contexts

Bioavailability / PK relevance: Carvacrol is orally absorbable but has clear translational PK constraints: it is volatile, highly lipophilic, rapidly metabolized, and cleared mainly as glucuronide and sulfate conjugates. Reported plasma half-life in animal PK work is short, around 1.5 hours, which supports frequent dosing or formulation strategies if systemic antitumor exposure is desired.

In-vitro vs systemic exposure relevance: Many mechanistic cancer studies use micromolar concentrations that may exceed sustained free systemic exposure achievable with simple oral dosing. Accordingly, positive cell-culture findings should be treated as exposure-sensitive unless supported by in-vivo efficacy or delivery enhancement. The mechanism is concentration-driven, not field-based.

Clinical evidence status: Preclinical anticancer evidence with some in-vivo support, but no established oncology RCTs or approved cancer use. Human evidence is limited mainly to early safety/tolerability rather than efficacy, so current oncology relevance is investigational and adjunct-conceptual rather than clinically validated.

Mechanistic pathway table

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	Mitochondrial apoptosis program	BAX ↑; Bcl-2 ↓; Cyt-c ↑; caspase-3 ↑; apoptosis ↑	↔ or cytoprotection in some non-cancer injury models	R/G	Cell death induction	Most reproducible antitumor signal across models; aligns with the strongest Nestronics-supported entries
2	PI3K Akt survival signaling	PI3K ↓; Akt ↓	↔ or protective depending on tissue/injury context	R/G	Reduced survival and proliferation	Mechanistically central and repeatedly linked to apoptosis, cell-cycle arrest, and reduced motility
3	TRPM7 and Ca²⁺ signaling	TRPM7 activity ↓; Ca²⁺-linked growth signaling ↓	Context-dependent	P/R	Growth and migration restraint	Especially relevant in breast cancer and glioblastoma models; likely one of the better-defined proximal targets
4	Cell-cycle control	G0/G1 arrest ↑; cyclin-driven progression ↓	↔	R/G	Antiproliferative effect	Often downstream of PI3K/Akt and TRPM7 disruption rather than fully independent
5	Migration invasion EMT ECM axis	Fibronectin ↓; collagen programs ↓; migration/invasion ↓; epithelial state ↑	Context-dependent	G	Anti-invasive remodeling	Relevant but heterogeneous; some EMT-marker directionality in source listings appears inconsistent across models
6	COX-2 inflammatory signaling	COX-2 ↓	Inflammatory tone ↓	R/G	Anti-inflammatory support	Likely supportive rather than sufficient alone for anticancer activity
7	PPARα PPARγ axis	PPARα ↑; PPARγ ↑	Metabolic and anti-inflammatory modulation ↑	R/G	Contextual metabolic reprogramming	Biochemically credible and documented, but probably not the dominant explanation for direct tumor kill
8	ROS redox modulation	↑ or ↓ (context-dependent)	Often oxidative stress buffering ↑	P/R/G	Stress modulation	Should not be treated as a uniformly pro-oxidant cancer mechanism; direction varies by model, dose, and timing
9	Clinical Translation Constraint	Short half-life; conjugative metabolism; exposure heterogeneity	Tolerability appears acceptable at early human doses	G	Limits direct translation	Many in-vitro concentrations likely exceed sustained free systemic exposure without optimized formulations

P: 0–30 min
R: 30 min–3 hr
G: >3 hr

Carvacrol in Alzheimer’s disease

Carvacrol in Alzheimer’s disease — Carvacrol is a small lipophilic monoterpenoid phenol found in oregano and thyme oils. In the AD context it is best classified as a preclinical neuroprotective natural product rather than a validated anti-dementia drug. The main recurring signals are anti-neuroinflammatory activity, oxidative-stress attenuation, partial cholinesterase inhibition, and protection against amyloid-β-associated synaptic and cognitive impairment. It is brain-active, but current AD evidence remains largely limited to cell and rodent models, with no established clinical efficacy.

Primary mechanisms (ranked):

Neuroinflammation suppression, including TNF-α and related inflammatory signaling reduction
Oxidative stress buffering with restoration of thiol and lipid-peroxidation balance
Protection against amyloid-β-induced synaptic dysfunction and memory impairment
Acetylcholinesterase and butyrylcholinesterase inhibition, likely symptomatic/supportive rather than disease-modifying alone
Anti-apoptotic neuronal protection with caspase-3 reduction in injury models
Barrier and ion-channel related neuroprotection, including TRPM7-linked and BBB-stabilizing effects in non-AD CNS injury models that may be mechanistically relevant but are not yet AD-specific

Bioavailability / PK relevance: Carvacrol is lipophilic and appears capable of CNS activity, but it is also rapidly metabolized and conjugated, which likely limits sustained free brain exposure with simple oral dosing. This makes formulation and exposure profile important for translation.

In-vitro vs systemic exposure relevance: Several mechanistic studies use exposure conditions that may not map cleanly onto sustained human brain concentrations. The AD signal is still concentration-dependent and preclinical, so mechanistic plausibility is stronger than translational certainty.

Clinical evidence status: Preclinical only for AD. There are rodent and cell-model signals for cognitive and biochemical benefit, but no established AD randomized clinical trials demonstrating efficacy.

AD mechanistic pathway table

Rank	Pathway / Axis	Modulation	Primary Effect	Notes / Interpretation
1	Neuroinflammatory cytokine axis	TNF-α ↓; inflammatory tone ↓	Microenvironment stabilization	One of the more reproducible in-vivo findings; linked to improved learning and memory in inflammatory rodent models
2	Oxidative stress and thiol balance	Lipid peroxidation ↓; total thiols ↑; oxidative injury ↓	Neuronal stress reduction	Probably a core mechanism in AD-relevant models, though this is protective redox buffering rather than a disease-specific hallmark target
3	Amyloid-β neurotoxicity	Aβ-induced synaptic dysfunction ↓ (model-dependent)	Memory and LTP preservation	Supported by Aβ rodent and cell studies; promising but still model-bound
4	Cholinergic enzyme axis	AChE ↓; BuChE ↓	Potential symptomatic cognitive support	Mechanistically relevant to AD, but likely supportive rather than sufficient for disease modification
5	Neuronal apoptosis signaling	Caspase-3 ↓; apoptosis ↓	Cell survival support	Seen in cell stress paradigms and fits the broader neuroprotection profile
6	Blood-brain barrier and TRPM7-related injury signaling	BBB leakage ↓; TRPM7-related injury signaling ↓	Barrier and excitotoxic injury restraint	Not AD-specific evidence, but mechanistically relevant to CNS resilience and worth noting as secondary
7	Clinical Translation Constraint	Rapid metabolism; exposure uncertainty; no AD trials	Limits translation	Current evidence supports a lead compound or adjunct concept, not a clinically established AD therapy

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⟱

5901-

CAR,

Neuroprotective role of carvacrol in ischemic brain injury: a systematic review of preclinical evidence and proposed TRPM7 involvement

Review,

Stroke,

*neuroP↑, *ROS↓, *MDA↓, *4-HNE↓, *SOD↑, *Catalase↑, *GPx↑, *Apoptosis↓, *cl‑Casp3↓, *TRPM7⇅, *BBB↓, *TRPM7↓,

5902-

CAR,

A novel antagonist of TRPM2 and TRPV4 channels: Carvacrol

in-vitro,

Nor,

HEK293

*other↓, *GSH↑, *GPx↑, *ROS↓, *Apoptosis↓,

5925-

CAR,

Neuroprotective effects of carvacrol against Alzheimer’s disease and other neurodegenerative diseases: A review

Review,

AD,

Review,

Park,

Review,

Stroke,

*Inflam↓, *antiOx↑, *AChE↓, *BBB↑, *cardioP↑, *neuroP↑, *memory↑, *TAC↑, *ROS↓, *lipid-P↓, *MDA↓, *SOD↑, *Catalase↑, *NRF2↑, *cognitive↑, *IL1β↓, *COX2↓, *TNF-α↓, *TLR4↓, *BDNF↑, *PKCδ↑, *5LO↓, *TRPM7↓, *GSH↑, *other↑, *Ferroptosis↓, *GPx4↑,

5927-

CAR,

Neuroprotective Potential and Underlying Pharmacological Mechanism of Carvacrol for Alzheimer’s and Parkinson’s Diseases

Review,

AD,

Review,

Park,

*memory↑, *cognitive↑, *ROS↓, *Inflam↓, *motorD↑, *toxicity↓, *TRPV3↑, *other↓, *antiOx↑, *LDL↓, *COX2↓, *PPARα↑, *NO↓, *AChE↓, *eff↑, *SOD↑, *Catalase↑, *neuroP↑, *BioAv↝, *BBB↑, *BioAv↑,

5888-

CAR,

Therapeutic application of carvacrol: A comprehensive review

Review,

Var,

Review,

Stroke,

Review,

Diabetic,

Review,

Park,

*antiOx↑, *AntiCan↑, *AntiDiabetic↑, *cardioP↑, *Obesity↓, *hepatoP↑, *AntiAg↑, *Bacteria↓, *Imm↑, MMP2↓, MMP9↓, Apoptosis↓, MMP↓, ERK↓, PI3K↓, ALAT↓, *ROS↓, *Catalase↑, *SOD↑, *GPx↑, *AST↓, *LDH↓, *necrosis↓, ROS↑, TumCCA↑, CDK4↓, cycD1/CCND1↓, NOTCH↓, IL6↓, chemoP↑, *Pain↓, *neuroP↑, *TRPM7↓, *motorD↑, *NF-kB↓, *COX2↓, *MDA↓,

5895-

CAR,

Carvacrol as a Therapeutic Candidate in Breast Cancer: Insights into Subtype-Specific Cellular Modulation

in-vitro,

BC,

MCF-7

in-vitro,

BC,

MDA-MB-231

TumCG↓, TumCMig↓, Apoptosis↑, Bax:Bcl2↑, ROS↓, CD44↓, CSCs↓,

Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

chemoP↑, 1,
Total Targets: 23

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

4-HNE↓, 1, antiOx↑, 3, Catalase↑, 4, Ferroptosis↓, 1, GPx↑, 3, GPx4↑, 1, GSH↑, 2, lipid-P↓, 1, MDA↓, 3, NRF2↑, 1, ROS↓, 5, SOD↑, 4, TAC↑, 1,

Core Metabolism/Glycolysis ⓘ

LDH↓, 1, LDL↓, 1, PPARα↑, 1,

Cell Death ⓘ

Apoptosis↓, 2, cl‑Casp3↓, 1, Ferroptosis↓, 1, necrosis↓, 1,

Kinase & Signal Transduction ⓘ

TRPV3↑, 1,

Transcription & Epigenetics ⓘ

other↓, 2, other↑, 1,

Proliferation, Differentiation & Cell State ⓘ

TRPM7↓, 3, TRPM7⇅, 1,

Migration ⓘ

5LO↓, 1, AntiAg↑, 1, PKCδ↑, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 1,

Barriers & Transport ⓘ

BBB↓, 1, BBB↑, 2,

Immune & Inflammatory Signaling ⓘ

COX2↓, 3, IL1β↓, 1, Imm↑, 1, Inflam↓, 2, NF-kB↓, 1, TLR4↓, 1, TNF-α↓, 1,

Synaptic & Neurotransmission ⓘ

AChE↓, 2, BDNF↑, 1,

Drug Metabolism & Resistance ⓘ

BioAv↑, 1, BioAv↝, 1, eff↑, 1,

Clinical Biomarkers ⓘ

AST↓, 1, LDH↓, 1,

Functional Outcomes ⓘ

AntiCan↑, 1, AntiDiabetic↑, 1, cardioP↑, 2, cognitive↑, 2, hepatoP↑, 1, memory↑, 2, motorD↑, 2, neuroP↑, 4, Obesity↓, 1, Pain↓, 1, toxicity↓, 1,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 57

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

6 Carvacrol

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#:57  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

Carvacrol / ROS Cancer Research Results

Mechanistic pathway table

Carvacrol in Alzheimer’s disease

AD mechanistic pathway table

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Immune & Inflammatory Signaling ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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