Licochalcone A / ROS Cancer Research Results

LCA, Licochalcone A: Click to Expand ⟱
Features:

Licochalcone A - Licorice-Derived Chalcone

Type: Natural chalcone / flavonoid-related phytochemical

Sources: Found primarily in licorice species including Glycyrrhiza inflata and related Glycyrrhiza plants.

Function: Licochalcone A is a bioactive chalcone with anticancer, anti-inflammatory, antioxidant, antimicrobial, and metabolic effects. Reported mechanisms include modulation of PI3K/AKT, MAPK, NF-κB, STAT3, ROS, apoptosis, autophagy, and cell-cycle regulatory pathways.

Cancer: Preclinical studies demonstrate inhibition of cancer-cell proliferation, migration, invasion, and metastasis, together with induction of apoptosis, autophagy, oxidative stress, and cell-cycle arrest. LCA has shown anticancer activity in breast, lung, gastric, colorectal, prostate, liver, ovarian, and other experimental cancer models.

Alzheimer's Disease: Preclinical evidence suggests neuroprotective and anti-inflammatory effects relevant to neurodegeneration, including suppression of oxidative stress and inflammatory signaling, although the Alzheimer's-specific evidence is less developed than the cancer literature.

Licochalcone A — a naturally occurring prenylated chalcone and phenolic phytochemical found principally in licorice species, especially Glycyrrhiza inflata. It is classified as a natural chalcone/flavonoid-related small molecule and is commonly abbreviated LCA, LicA, or Lico A. Its experimental pharmacology is strongly context-dependent: in many cancer models LCA promotes oxidative stress, mitochondrial dysfunction, apoptosis, autophagy, cell-cycle arrest, and suppression of proliferative and inflammatory signaling, whereas in non-malignant injury models it can activate NRF2-dependent antioxidant defenses. Anticancer development remains preclinical.

Primary mechanisms (ranked):

  1. ROS/redox disruption through mitochondrial ROS generation and inhibition of antioxidant systems including TrxR1, promoting oxidative-stress-mediated cancer-cell death.
  2. PI3K/AKT/mTOR suppression, reducing survival signaling and frequently promoting apoptosis and autophagy.
  3. Mitochondrial and endoplasmic-reticulum stress-mediated apoptosis involving mitochondrial membrane depolarization, cytochrome c release, caspase activation, PARP cleavage, and CHOP signaling.
  4. STAT3 suppression, including reduced STAT3 protein/activation and downstream survival and proliferative signaling.
  5. NF-κB and Ras/Raf/MEK pathway suppression, including reduced PD-L1 expression and tumor-cell immune-evasion signaling in experimental models.
  6. Cell-cycle arrest through modulation of cyclins, CDKs, p21/p27, survivin, and related regulatory proteins.
  7. HIF-1α suppression through inhibition of mitochondrial respiration and restoration of intracellular oxygen availability under hypoxic conditions.
  8. Ferroptosis induction in selected models through increased lipid oxidative stress and suppression of the IGF2BP3/MDM2 axis.
  9. Suppression of migration, invasion, angiogenic signaling, and EMT-associated pathways including MAPK/AKT, VEGF, ICAM-1, and related regulators.
  10. NRF2 modulation (context-dependent): NRF2 can be suppressed in some cancer cells, increasing ROS susceptibility, while NRF2 is activated in non-malignant cells and tissues, producing antioxidant and cytoprotective effects.

Bioavailability / PK relevance: Free oral LCA has poor systemic exposure; a rat pharmacokinetic study reported absolute oral bioavailability of approximately 3.3%. Poor aqueous solubility, limited permeability, intestinal first-pass metabolism, glucuronidation, and other metabolic pathways constrain exposure. Formulation materially changes PK: a self-microemulsifying drug-delivery system increased oral bioavailability approximately 2.36-fold in rats, while nanoparticle approaches have produced still larger increases experimentally. LCA also inhibits P-glycoprotein and several CYP enzymes, particularly CYP3A and CYP2C9 in experimental systems, creating a potential drug-interaction concern.

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 μM LCA, with several reported IC50 values in the tens of micromolar range. These concentrations are difficult to reconcile with the low systemic exposure of unformulated oral LCA, so direct translation of conventional cell-culture concentrations to achievable human systemic exposure is uncertain. Delivery systems, local exposure, metabolites, and combination strategies may alter this limitation.

Clinical evidence status: Cancer: preclinical only, with cell-culture and animal xenograft evidence but no established anticancer efficacy in humans. Human exposure evidence is substantially stronger for topical dermatologic/cosmetic use: randomized or prospective studies have evaluated LCA-containing formulations for acne, dermatitis, erythema, and rosacea. LCA is not an established systemic oncology drug. Current translational priorities are exposure optimization, human PK, dose-limiting safety characterization, and controlled oncology trials.

Licochalcone A Cancer Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 ROS and TrxR1 redox disruption ROS ↑; TrxR1 ↓; GSH ↓ ROS ↓ in oxidative-injury models (context-dependent) P/R Oxidative-stress-mediated cancer-cell death ROS generation is mechanistically central in gastric, colorectal, bladder, ovarian, and other models. ROS scavenging with NAC can substantially attenuate LCA-induced apoptosis.
2 PI3K AKT mTOR survival signaling PI3K ↓; AKT ↓; mTOR ↓ AKT ↑ can contribute to NRF2 protection (context-dependent) R/G Survival inhibition, apoptosis, autophagy Strong recurring cancer mechanism, but signaling direction differs in cytoprotective non-cancer models.
3 Mitochondrial apoptosis Mitochondrial membrane potential ↓; cytochrome c ↑; caspase-9/3 ↑; PARP cleavage ↑ Apoptosis ↓ in several oxidative-injury models R/G Intrinsic apoptotic cell death Often downstream of ROS generation; supported across multiple cancer types.
4 Endoplasmic reticulum stress CHOP GRP78 ↑; CHOP ↑; ER stress ↑; caspase signaling ↑ ER-stress injury ↓ in neuroprotective models R/G ER-stress-mediated apoptosis Reported in bladder, lung, and endometrial cancer; cellular context determines whether ER stress is promoted or suppressed.
5 STAT3 signaling STAT3 ↓; p-STAT3 ↓ Not established R/G Reduced survival and proliferation Demonstrated in ovarian and cholangiocarcinoma models; downstream effects include altered mTOR-associated translation and survival proteins.
6 NF-κB and inflammatory survival signaling NF-κB p65 ↓ NF-κB inflammatory activation ↓ R/G Reduced proliferation, inflammation, migration, and immune-evasion signaling Unlike ROS and NRF2, NF-κB suppression is directionally similar in many malignant and non-malignant inflammatory models.
7 PD-L1 and Ras Raf MEK immune-evasion axis PD-L1 ↓; Ras ↓; NF-κB interaction ↓ Cytotoxic T-cell activity ↑ in co-culture G Reduced tumor immune evasion Colon-cancer experiments showed enhanced T-cell-mediated tumor-cell killing after LCA pretreatment; remains preclinical.
8 Cell-cycle regulation G0/G1 or G2/M arrest ↑; cyclin/CDK signaling ↓ Variable G Cytostatic growth inhibition The arrest point is cell-type-dependent. Cyclin D1, cyclin B1, CDK1, survivin, p21, and related regulators have been implicated.
9 Autophagy and LC3 signaling LC3-II ↑; autophagic flux ↑ Context-dependent G Autophagic response accompanying growth inhibition Prominent in breast and NSCLC models. Autophagy is not consistently required for LCA-induced apoptosis.
10 HIF-1α and mitochondrial respiration Mitochondrial respiration ↓; intracellular O2 ↑; HIF-1α ↓; GLUT1 ↓; PDK1 ↓ Not established P/R Suppression of hypoxic tumor adaptation LCA directly suppresses mitochondrial oxygen consumption, promoting oxygen-dependent HIF-1α degradation under hypoxia.
11 Energy metabolism Mitochondrial ATP production ↓; total ATP ↓ Not established P/R Energetic stress Observed with HIF-1α inhibition. The major demonstrated effect is inhibition of mitochondrial respiration rather than direct blockade of glycolysis.
12 Ferroptosis IGF2BP3 MDM2 IGF2BP3 ↓; MDM2 ↓; lipid ROS ↑; MDA ↑; GSH ↓; ferroptosis ↑ Not established R/G Ferroptotic cell death Demonstrated particularly in acute myeloid leukemia; currently less broadly established than apoptotic mechanisms.
13 MAPK JNK p38 ERK signaling JNK/p38/ERK modulation (model-dependent) ERK ↑ can support NRF2 activation (context-dependent) R/G Apoptosis and stress-response regulation In several cancer models JNK/p38 activation contributes to apoptosis, whereas inhibition of MAPK-associated motility signaling has also been reported.
14 Migration invasion and EMT Migration ↓; invasion ↓; vimentin ↓; EMT signaling ↓ Not established G Reduced metastatic phenotype Includes modulation of MAPK/AKT, adhesion proteins, VEGF, and ICAM-1; evidence is preclinical.
15 NRF2 antioxidant response NRF2 ↓ in selected tumors (context-dependent) NRF2 ↑; HO-1 ↑; GCLC/GCLM ↑ R/G Opposing redox effects according to cellular context Particularly important for interpretation: LCA can suppress NRF2 and increase ROS in some cancers while activating NRF2 and protecting normal tissues from oxidative injury.
16 Chemosensitization Drug-induced apoptosis ↑ (model-dependent) Not established R/G Enhanced anticancer drug response LCA enhanced geldanamycin-induced ROS generation, mitochondrial apoptosis, and caspase activation in ovarian cancer cells; no established clinical combination regimen.
17 Clinical Translation Constraint Systemic exposure limited CYP and transporter interactions possible G Limits translation of high-concentration in-vitro effects Free oral bioavailability in rats has been reported at approximately 3.3%. Poor solubility and first-pass metabolism are important constraints. LCA inhibits CYP3A4, CYP2C9, and P-gp experimentally; formulation can substantially increase exposure.

P: 0–30 min    R: 30 min–3 hr    G: >3 hr



Alzheimer's disease relevance: Licochalcone A now has meaningful disease-specific preclinical evidence rather than only general neuroprotective plausibility. Studies in transgenic AD mouse models report improved cognition together with reduced Aβ burden, reduced neuroinflammation, improved insulin/glucose signaling, inhibition of ER-stress-mediated neuronal apoptosis, and NRF2-associated protection. A 2026 APP/PS1 study reported improved memory, increased synaptic markers, reduced Aβ42 and plaque burden, improved glucose handling, and reduced glial activation after 15 mg/kg/day intraperitoneal LCA for four weeks. A separate transgenic mouse study found inhibition of PERK/eIF2α/ATF4/CHOP ER-stress signaling and neuronal apoptosis. Evidence remains preclinical; there is no established human AD efficacy.

Primary AD mechanisms (ranked):

  1. Reduction of Aβ accumulation and plaque burden.
  2. Suppression of ER-stress-mediated neuronal apoptosis through PERK/eIF2α/ATF4/CHOP inhibition.
  3. Reduction of neuroinflammation and glial activation.
  4. Improvement of brain insulin/glucose signaling and GLUT1-associated metabolic function.
  5. NRF2-dependent antioxidant and neuronal stress protection.
  6. Preservation of synaptic structure and plasticity.
  7. Reduction of tau misfolding and tau-associated oxidative stress in cellular models.

Clinical evidence status: Preclinical. Evidence includes cell studies and multiple transgenic mouse AD models, including disease-specific studies published in 2025 and 2026. Human efficacy, optimal systemic dose, CNS pharmacokinetics, and long-term safety have not been established.

Licochalcone A Alzheimer Mechanisms

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Amyloid beta burden Aβ42 ↓; plaque burden ↓ Reduced amyloid pathology Demonstrated in transgenic mouse AD models; earlier cellular and biochemical work also supports interference with Aβ aggregation.
2 PERK eIF2α ATF4 CHOP ER stress ER stress ↓; CHOP signaling ↓ Reduced neuronal apoptosis Mechanistically supported in triple-transgenic AD mice and primary hippocampal neurons.
3 Neuroinflammation and glial activation Glial reactivity ↓; inflammatory signaling ↓; TREM2 ↓ (model-dependent) Reduced chronic neuroinflammatory burden Consistent with broader LCA suppression of TLR4, NF-κB, and MAPK inflammatory signaling.
4 Brain insulin and glucose signaling Insulin response ↑; Insr ↑; GLUT1 ↑ Improved cerebral metabolic function Reported in APP/PS1 mice together with improved systemic glucose tolerance.
5 NRF2 antioxidant signaling NRF2 ↑; antioxidant defense ↑ Reduced oxidative and ER stress NRF2 inhibition reduces LCA neuroprotective effects in experimental systems, supporting a causal contribution.
6 Synaptic plasticity PSD95 ↑; spinophilin ↑; dendritic spine density ↑ Improved neuronal connectivity and memory-associated plasticity Observed in the 2026 APP/PS1 mouse study together with improvement in behavioral memory tests.
7 Tau proteostasis Tau misfolding ↓; tau-associated ROS ↓ Reduced tau-associated cellular toxicity Supported principally by cellular tau-misfolding models; less developed in vivo than the amyloid and ER-stress evidence.
8 Clinical Translation Constraint Human efficacy not established Limits clinical interpretation Animal studies support CNS activity, but human brain exposure, oral dosing requirements, chronic safety, and disease-modifying efficacy remain unknown.


ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






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






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






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






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






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






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
8242- LCA,    Nrf2 signaling and autophagy are complementary in protecting lipopolysaccharide/d-galactosamine-induced acute liver injury by licochalcone A
- in-vivo, LiverDam, NA
*ALAT↓, *AST↓, *Inflam↓, *ROS↓, *TLR4↓, *MAPK↓, *NF-kB↓, *TXNIP↓, *NLRP3↓, *NRF2↑, *p62↑, *hepatoP↑, *autophagy↑,
8245- LCA,    Licochalcone A Upregulates Nrf2 Antioxidant Pathway and Thereby Alleviates Acetaminophen-Induced Hepatotoxicity
- in-vivo, LiverDam, NA
*hepatoP↑, *Apoptosis↓, *mtDam↓, *ROS↓, *NRF2↑, *Keap1↓, *ARE↑, *ALAT↓, *AST↓, *MDA↓, *MPO↓, *SOD↑, *GSH/GSSG↑, *Bcl-2↑, *BAX↓, *cl‑Casp3↓, *p‑cJun↓, *AIF↓, *Cyt‑c↓,
8223- LCA,    Lico A Enhances Nrf2-Mediated Defense Mechanisms against t-BHP-Induced Oxidative Stress and Cell Death via Akt and ERK Activation in RAW 264.7 Cells
- in-vitro, Nor, RAW264.7
*Apoptosis↓, *ROS↓, *GSH↑, *GCLM↑, *GCLC↑, *HO-1↑, *NRF2↑, *Keap1↓, *ARE↑, *Akt↑, *ERK↑, *PI3K↑,
8224- LCA,    3,3',4,4'-Tetrahydroxy-2-methoxychalcone from Glycyrrhiza uralensis roots inhibits HIF-1α and Nrf2, suppressing hypoxia-induced angiogenesis
- in-vitro, CRC, HCT116
Hif1a↓, NRF2↓, VEGF↓, HO-1↓, ROS↓,
8225- LCA,  Cisplatin,    Licochalcone A protects against cisplatin-induced acute kidney injury via the modulation of Nrf2/Keap1-mediated ferroptosis and apoptosis
- in-vivo, Nor, NA
*RenoP↑, *Urea↓, *BUN↓, *creat↓, *Apoptosis↓, *Ferroptosis↓, *Iron↓, *ROS↓, *lipid-P↓, *mtDam↓, *NRF2↑,
8230- LCA,    The Ameliorative Role of Lico A on Aflatoxin B1-Triggered Hepatotoxicity Partially by Activating Nrf2 Signal Pathway
- vitro+vivo, Nor, NA
*hepatoP↑, *ROS↓, *TLR4↓, *NF-kB↓, *MAPK↓, *NLRP3↓, *NRF2↑, *Inflam↓, *Pyro↓,

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:


Redox & Oxidative Stress(tgid=1) ⓘ

HO-1↓, 1,   NRF2↓, 1,   ROS↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,   VEGF↓, 1,  
Total Targets: 5

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

autophagy↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ARE↑, 2,   Ferroptosis↓, 1,   GCLC↑, 1,   GCLM↑, 1,   GSH↑, 1,   GSH/GSSG↑, 1,   HO-1↑, 1,   Iron↓, 1,   Keap1↓, 2,   lipid-P↓, 1,   MDA↓, 1,   MPO↓, 1,   NRF2↑, 5,   ROS↓, 5,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↓, 1,   mtDam↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 2,   BUN↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   Apoptosis↓, 3,   BAX↓, 1,   Bcl-2↑, 1,   cl‑Casp3↓, 1,   Cyt‑c↓, 1,   Ferroptosis↓, 1,   MAPK↓, 2,   Pyro↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

p‑cJun↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

p62↑, 1,  

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

ERK↑, 1,   PI3K↑, 1,  

Migration(tgid=13) ⓘ

TXNIP↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 2,   NF-kB↓, 2,   TLR4↓, 2,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 2,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   AST↓, 2,   creat↓, 1,   Urea↓, 1,  

Functional Outcomes(tgid=23) ⓘ

hepatoP↑, 3,   RenoP↑, 1,  
Total Targets: 44

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
6 Licochalcone A
1 Cisplatin
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#:447  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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