Licochalcone A / AntiBio 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.


AntiBio, Antibiotic/Antimicrobial activity: Click to Expand ⟱
Source:
Type:

Antibiotic / antimicrobial activity: The ability of a substance to suppress or kill microorganisms, especially bacteria, by disrupting microbial survival, growth, biofilm formation, cell-wall integrity, membrane function, protein synthesis, nucleic-acid synthesis, quorum sensing, or virulence.

Natural Products that might have antimicrobial properties

Natural supplement or product Principal constituents Potential antimicrobial activity Evidence assessment Reference
Garlic
Allium sativum		 Allicin, ajoene and diallyl sulfides Antibacterial and antifungal activity, with some antiviral and antiparasitic effects reported in laboratory studies. Extensive laboratory evidence, but insufficient clinical evidence to use garlic as a treatment for established infections. Tesfaye A. Revealing the therapeutic uses of garlic and its potential for drug discovery. Scientific review.
Berberine Berberine isoquinoline alkaloid May damage bacterial membranes, inhibit efflux pumps, interfere with nucleic-acid and protein synthesis, and inhibit biofilm formation. Strong preclinical evidence and limited indication-specific clinical evidence. Poor oral bioavailability and drug interactions limit its use as a general antimicrobial. Berberine as a therapeutic alkaloid against ESKAPE and multidrug-resistant bacteria: a comprehensive review.
Cranberry extract
Vaccinium macrocarpon		 A-type proanthocyanidins Primarily reduces adhesion of uropathogenic bacteria, particularly Escherichia coli, to urinary epithelial cells. May reduce recurrent urinary tract infections in selected populations. It is preventive rather than a reliable treatment for an active UTI. National Center for Complementary and Integrative Health: Cranberry—Usefulness and Safety.
Probiotics
Lactobacillus, Bifidobacterium and Saccharomyces boulardii 		Live microorganisms; effects are strain-specific Competitive exclusion of pathogens, production of bacteriocins, inhibition of pathogen adhesion and restoration of microbiome function. Some human evidence for antibiotic-associated diarrhea and selected gastrointestinal or vaginal indications. Results cannot be generalized from one strain to another. NIH Office of Dietary Supplements: Probiotics—Health Professional Fact Sheet.
Medical-grade honey / Manuka honey Methylglyoxal, hydrogen peroxide, defensin-1, organic acids and high osmolarity Broad topical antibacterial and antibiofilm activity; also supports autolytic debridement and wound healing. Clinically relevant primarily as a standardized, medical-grade topical wound product. Ordinary food honey is not equivalent. Jull AB et al. Honey as a topical treatment for wounds. Cochrane systematic review.
Oregano oil
Origanum vulgare		 Carvacrol and thymol Antibacterial, antifungal and antibiofilm activity, largely through disruption of microbial membranes. Strong laboratory activity, but inadequate human evidence for oral treatment of infections. Concentrated oil can cause irritation. Chemical composition, biological activity and potential uses of oregano and oregano essential oil: a review.
Thyme
Thymus vulgaris		 Thymol and carvacrol Antibacterial, antifungal and antibiofilm activity through membrane damage and altered microbial permeability. Better established as a constituent of topical antiseptic and oral-care formulations than as an oral treatment for systemic infection. PubMed literature: thyme, thymol and antimicrobial activity.
Tea tree oil
Melaleuca alternifolia		 Terpinen-4-ol and related monoterpenes Topical antibacterial and antifungal activity with some antiviral laboratory activity. Some clinical evidence for topical acne and fungal skin conditions. Tea tree oil is toxic when swallowed and may cause contact dermatitis. Carson CF et al. Melaleuca alternifolia oil: a review of antimicrobial and other medicinal properties.
Echinacea
Echinacea species		 Alkamides, caffeic-acid derivatives, polysaccharides and glycoproteins Primarily immunomodulatory; relatively weak and inconsistent direct antimicrobial activity. Evidence for preventing or shortening respiratory infections is inconsistent and preparation-dependent. National Center for Complementary and Integrative Health: Echinacea—Usefulness and Safety.
Elderberry
Sambucus nigra		 Anthocyanins, flavonols and phenolic acids Antiviral effects have been reported in cell-culture and preclinical studies, including interference with viral entry or replication. Small human trials have examined respiratory symptoms, but evidence remains insufficient to establish treatment of influenza or other viral infections. National Center for Complementary and Integrative Health: Elderberry.
Curcumin / turmeric
Curcuma longa		 Curcumin and related curcuminoids Antibacterial, antifungal, antiviral and antibiofilm activity through multiple membrane, enzyme and signalling effects. Predominantly laboratory evidence. Poor aqueous solubility and low systemic bioavailability are major clinical limitations. Moghadamtousi SZ et al. A review on antibacterial, antiviral and antifungal activity of curcumin.
Ginger
Zingiber officinale		 Gingerols, shogaols and zingerone Antibacterial and antifungal activity, including possible inhibition of microbial adhesion and biofilm formation. Primarily laboratory evidence; there is little direct clinical evidence that ginger supplements treat infections. PubMed literature: ginger, gingerols and antimicrobial activity.
Clove
Syzygium aromaticum		 Eugenol and eugenyl acetate Antibacterial, antifungal and local antiseptic activity, principally through membrane and protein disruption. Relevant mainly to topical, food-preservation and dental applications. Evidence for systemic infection treatment is insufficient. PubMed literature: clove, eugenol and antimicrobial activity.
Cinnamon
Cinnamomum species		 Cinnamaldehyde, eugenol and cinnamic acid derivatives Antibacterial, antifungal and antibiofilm activity; may alter microbial membranes and quorum-sensing pathways. Predominantly laboratory evidence. Cassia cinnamon can contribute substantial coumarin exposure when consumed in concentrated amounts. PubMed literature: cinnamon, cinnamaldehyde and antimicrobial activity.
Neem
Azadirachta indica		 Nimbidin, nimbin, nimbolide, azadirachtin and other limonoids Antibacterial, antifungal, antiparasitic and antibiofilm effects have been reported. Some topical and dental research exists, but systemic clinical evidence is inadequate. Oral neem preparations have important safety concerns. PubMed literature: Azadirachta indica and antimicrobial activity.
Black seed
Nigella sativa		 Thymoquinone, thymohydroquinone and related volatile compounds Antibacterial, antifungal, antiparasitic and possible antiviral activity. Considerable laboratory research but limited, heterogeneous clinical evidence for infectious diseases. PubMed literature: Nigella sativa, thymoquinone and antimicrobial activity.
Green tea extract
Camellia sinensis		 Epigallocatechin gallate (EGCG) and other catechins Antibacterial, antiviral and antibiofilm activity; may damage membranes, inhibit microbial enzymes and enhance some antibiotics. Some localized oral-health evidence, but limited evidence for treating systemic infections. Concentrated extracts may cause liver injury in susceptible individuals. PubMed literature: EGCG, green tea and antimicrobial activity.
Licorice root
Glycyrrhiza species		 Glycyrrhizin, glycyrrhetinic acid, liquiritigenin and other flavonoids Antiviral, antibacterial and antifungal effects have been reported in laboratory and preclinical studies. Limited clinical antimicrobial evidence. Glycyrrhizin can cause hypertension, hypokalemia, fluid retention and clinically important drug interactions. National Center for Complementary and Integrative Health: Licorice Root.
Andrographis
Andrographis paniculata		 Andrographolide and related diterpenoid lactones Immunomodulatory, anti-inflammatory and possible antiviral or antibacterial activity. Some evidence for modest symptom reduction in uncomplicated respiratory infections, but this does not establish direct pathogen eradication. PubMed literature: Andrographis and respiratory infections.
Pelargonium sidoides Proanthocyanidins, phenolic acids and oxygenated coumarin derivatives Possible antiviral, antibacterial anti-adhesive and immunomodulatory activity. Some human evidence for modest symptom improvement in acute bronchitis and selected respiratory infections. It is not a substitute for antibiotics when bacterial treatment is indicated. Timmer A et al. Pelargonium sidoides extract for acute respiratory tract infections. Cochrane systematic review.
Monolaurin
Glycerol monolaurate		 Monolaurin, a monoester derived from lauric acid May disrupt lipid membranes and interfere with signalling or virulence in certain bacteria and enveloped viruses. Predominantly laboratory and animal evidence. There is insufficient clinical evidence to recommend oral monolaurin for infections. PubMed literature: glycerol monolaurate and antimicrobial activity.
Caprylic acid Octanoic acid, an eight-carbon medium-chain fatty acid Antifungal and membrane-disrupting activity, particularly against Candida species, has been reported in vitro. Insufficient human evidence for treating candidiasis or systemic fungal infection. Marketing claims commonly exceed the evidence. PubMed literature: caprylic acid and Candida.
Olive leaf extract
Olea europaea		 Oleuropein, hydroxytyrosol and elenolic-acid derivatives Antibacterial, antiviral and antifungal activity has been observed in laboratory studies. Preliminary evidence only; clinical trials have not established it as a treatment for infectious disease. PubMed literature: olive leaf, oleuropein and antimicrobial activity.
Goldenseal
Hydrastis canadensis		 Hydrastine, canadine and berberine Extracts and individual alkaloids show antibacterial activity in laboratory studies. There is no good clinical evidence that goldenseal treats human infections. Product composition, absorption and drug interactions are important limitations. National Center for Complementary and Integrative Health: Goldenseal.
Sweet wormwood / artemisinin
Artemisia annua 		Artemisinin and related sesquiterpene lactones Artemisinin derivatives are potent antimalarial agents. Additional antibacterial, antiviral and antiparasitic effects are being studied. Artemisinin-based combination therapies are established medicines, not ordinary supplements. Herbal preparations should not replace standardized malaria treatment because dose variability can promote treatment failure and resistance. World Health Organization: Guidelines for malaria.

Evidence interpretation

  • Clinical evidence: Effects have been studied in human participants, but usually for a specific preparation, route, dose and indication.
  • Preclinical evidence: Activity has mainly been demonstrated in cell culture, microbial cultures or animal models.
  • Anti-adhesive or probiotic activity: The product may reduce colonization or pathogen attachment without directly killing the microorganism.
  • Topical evidence: Results from topical use cannot be assumed to apply to an orally administered supplement.


Scientific Papers found: Click to Expand⟱
8246- LCA,    Licochalcone A activates Keap1-Nrf2 signaling to suppress arthritis via phosphorylation of p62 at serine 349
- in-vivo, Arthritis, NA
*AntiBio↑, *AntiTum↑, *Inflam↓, *AntiArt↑, *p62↑, *NRF2↑,
8221- LCA,    Anti-inflammatory efficacy of Licochalcone A: correlation of clinical potency and in vitro effects
- in-vitro, Nor, NA
*Inflam↓, *AntiBio↑, *PGE2↓, *IL6↓, *TNF-α↓,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1,   AntiBio↑, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

NRF2↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

p62↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL6↓, 1,   Inflam↓, 2,   PGE2↓, 1,   TNF-α↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 1,  
Total Targets: 10

Scientific Paper Hit Count for: AntiBio, Antibiotic/Antimicrobial activity
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#:1483  State#:%  Dir#:%
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