Honokiol / NF-kB Cancer Research Results

HNK, Honokiol: Click to Expand ⟱
Features:
Honokiol is a Lignan isolated from bark, seed cones and leaves of trees of Magnolia species. Honokiol was traditionally used for anxiety and stroke treatment, as well as the alleviation of flu symptoms.
-considered to have antioxidant properties
-low oral bioavailability and difficulty in intravenous administration
-the development of various formulations of honokiol, including microemulsion, liposomes, nanoparticles and micelle copolymers have successfully solved the problem of low water solubility.

Pathways:
-Inhibit NF-κB activation
-Downregulate STAT3 signalin
-Inhibiting the PI3K/Akt pathway,
-Inhibition of mTOR
-Influences various MAPK cascades—including ERK, JNK, and p38
-Inhibition of EGFR
-Inhibiting Notch pathway (CSCs)
-GPx4 inhibit
-Can induce ER stress in cancer cells, which contributes to the activation of unfolded protein response (UPR) pathways
-Disrupt the mitochondrial membrane potential in cancer cells.
-Reported to increase ROS production in cancer cells
-Can exhibit antioxidant properties in normal cells. - has some inhibitor activity but Not classified as HDAC inhibitor as weaker and may work more indirectly.
- is well-known in the research community for its role in activating SIRT3

-Note half-life 40–60 minutes
BioAv
Pathways:
- induce ROS production in cancer cells, and typically lowers ROS in normal cells
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓ Prx
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓">NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, VEGF↓, ROCK1↓, RhoA↓, NF-κB↓, CXCR4↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, EZH2↓, P53↑, HSP↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, EGFR↓,
- inhibits Cancer Stem Cells : CSC↓, CD133↓, β-catenin↓, sox2↓, nestin↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, TrxR**, - Shown to modulate the nuclear translocation of SREBP-2 (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Honokiol — a small, lipophilic biphenolic neolignan isolated principally from the bark, seed cones, and leaves of Magnolia species, especially Magnolia officinalis. It is a natural-product small molecule rather than a standardized Magnolia extract; the standard abbreviation is HNK. Honokiol crosses biological membranes readily and has documented CNS penetration, but its pharmaceutical development is constrained by extremely poor aqueous solubility, rapid metabolism, and low/variable oral systemic exposure. Cancer research is dominated by cell and animal studies, although an oral Phase I window-of-opportunity study in patients with resectable early-stage non-small-cell lung cancer is now enrolling.

Primary mechanisms (ranked):

  1. Mitochondrial targeting and respiratory Complex I inhibition, producing mitochondrial dysfunction, loss of membrane potential, energetic stress, and intrinsic apoptosis in susceptible cancer cells.
  2. Suppression of oncogenic survival signaling, particularly STAT3 and PI3K/AKT/mTOR, with additional inhibition of EGFR and context-dependent MAPK signaling.
  3. Induction of mitochondrial ROS and oxidative stress in cancer cells as a major stress-amplifying mechanism; in nonmalignant tissues honokiol can instead activate antioxidant and mitochondrial-protective programs including SIRT3 and NRF2.
  4. Suppression of NF-κB-dependent inflammatory and prosurvival transcription, contributing to apoptosis, reduced inflammatory signaling, and treatment sensitization.
  5. Suppression of EMT, migration, invasion, cancer-stem-cell phenotypes, and angiogenic signaling through STAT3, Wnt/β-catenin, EGFR, HIF-1α, VEGF, Snail/Slug, MMPs, and related networks.
  6. Metabolic inhibition, including suppression of HIF-1α-driven glycolysis, GLUT1, HK2, LDHA and PDK signaling, with reduced glycolytic flux and ATP availability in several tumor models.
  7. Induction of ER stress, autophagy, cell-cycle arrest and, in selected tumor contexts, ferroptosis; these effects appear downstream or context-dependent rather than universal initiating mechanisms.
  8. Chemosensitization, radiosensitization and immune-modulatory effects have been demonstrated preclinically, including enhancement of selected targeted therapies and PD-1/PD-L1-directed approaches.

Bioavailability / PK relevance: Native honokiol is highly lipophilic and poorly water-soluble, limiting conventional oral and intravenous delivery. It undergoes extensive metabolic clearance, including conjugation, and systemic exposure after ordinary oral formulations may be substantially lower than concentrations commonly used experimentally. Liposomes, nanoemulsions, micelles, nanoparticles and other delivery systems can substantially improve solubility and exposure. A validated pharmacokinetic study of injectable liposomal honokiol has been reported, but clinically established human anticancer PK targets have not yet been defined.

In-vitro vs systemic exposure relevance: Many anticancer studies use approximately 10–60 µM honokiol, with some models requiring still higher concentrations. These concentrations should not automatically be considered achievable following conventional oral supplementation because oral bioavailability is limited and human tumor exposure has not been established. The current Phase I lung-cancer study is therefore important for defining human tolerability, systemic exposure and pharmacodynamic effects rather than demonstrating established therapeutic efficacy.

Clinical evidence status: Predominantly preclinical. Extensive in-vitro and animal anticancer evidence exists across multiple tumor types. Human anticancer efficacy has not been established. A Phase I oral honokiol study in approximately 15 patients with early-stage resectable NSCLC is currently listed by Houston Methodist as enrolling; treatment is given before surgery primarily to determine safety and maximum tolerated dose. Honokiol is not an FDA-approved anticancer drug.

Safety / translation: Preclinical toxicology has generally suggested a comparatively broad therapeutic window, but concentrated honokiol should not be assumed equivalent to historical consumption of Magnolia bark preparations. Potential pharmacokinetic interactions, formulation-dependent exposure, and insufficient controlled human safety data remain major translational limitations. FDA records identify Magnolia cortex extract containing honokiol as having been submitted through the New Dietary Ingredient notification process, but this does not constitute approval of honokiol for cancer treatment.

Honokiol Cancer-Relevant Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial Complex I and intrinsic apoptosis ↓ Complex I; ↓ ΔΨm; ↓ respiration; ↑ cytochrome-c; ↑ caspases ↔ or mitochondrial protection (context-dependent) P/R Mitochondria-directed cytotoxicity A particularly strong mechanistic feature of honokiol; mitochondrial accumulation and respiratory inhibition can precede downstream apoptotic signaling.
2 STAT3 survival and stemness signaling ↓ STAT3; ↓ p-STAT3; ↓ mitochondrial STAT3 ↔ (context-dependent) R/G Loss of survival, proliferation and stemness signaling Relevant across several cancer models and linked to reduced CSC phenotype, EMT and resistance.
3 PI3K AKT mTOR signaling ↓ PI3K; ↓ AKT; ↓ mTOR ↔ or adaptive modulation R/G Growth and anabolic suppression Frequently observed and contributes to apoptosis, metabolic stress and treatment sensitization.
4 Mitochondrial ROS increase ↑ ROS; ↑ mt-ROS (secondary) ↓ ROS or ↔ (context-dependent) P/R Oxidative stress amplification Cancer-cell ROS elevation often accompanies mitochondrial respiratory disruption. Honokiol can instead act antioxidatively in nonmalignant tissues.
5 NF-κB inflammatory and survival signaling ↓ NF-κB; ↓ COX-2; ↓ inflammatory survival signaling ↓ pathological inflammatory signaling R/G Reduced inflammatory and prosurvival transcription Provides both anticancer and tissue-protective effects depending on cellular context.
6 EMT invasion and metastasis ↓ EMT; ↓ Snail; ↓ Slug; ↓ MMP2; ↓ MMP9; ↑ E-cadherin ↔ G Reduced migration, invasion and metastasis Supported across breast, lung, renal, pancreatic and other tumor models.
7 Cancer stem cell signaling ↓ CSCs; ↓ CD133; ↓ SOX2; ↓ OCT4; ↓ Nestin; ↓ Wnt/β-catenin ↔ G Reduced tumor-initiating and resistant cell phenotype Closely overlaps STAT3, EGFR, Notch and Wnt pathway inhibition.
8 HIF-1α glycolytic metabolism ↓ HIF-1α; ↓ GLUT1; ↓ HK2; ↓ LDHA; ↓ PDK1; ↓ ECAR; ↓ glycolysis ↔ (context-dependent) G Reduced glycolytic flux and ATP production Especially relevant in glycolysis-dependent and hypoxic tumors.
9 EGFR and receptor tyrosine kinase signaling ↓ EGFR; ↓ downstream AKT and ERK ↔ R/G Growth-factor signal suppression Honokiol can also impair EGFR stability through HDAC6/HSP90-associated mechanisms.
10 Angiogenesis and hypoxia response ↓ VEGF; ↓ HIF-1α; ↓ angiogenesis ↔ G Reduced tumor vascular support Largely downstream of HIF-1α, NF-κB and growth-factor suppression.
11 ER stress and calcium signaling ↑ ER stress; ↑ GRP78; ↑ CHOP; ↑ Ca²⁺ (model-dependent) ↔ or protective stress response R/G Proteotoxic stress and apoptosis Prominent in selected osteosarcoma and other experimental models rather than universal across cancers.
12 Cell cycle regulation ↑ G0/G1 or G2/M arrest; ↓ cyclin D1; ↓ CDK2; ↓ CDK4; ↓ CDK6 ↔ G Cytostatic growth suppression Checkpoint phenotype depends on tumor type and upstream signaling context.
13 Ferroptosis and lipid peroxidation ↑ ferroptosis; ↑ lipid peroxidation; GPX4 modulation (model-dependent) ↔ G Alternative regulated cell death GPX4 direction is not uniform across studies; HMOX1-associated and GPX4-associated ferroptosis have both been reported.
14 NRF2 antioxidant response ↔ or ↑ (model-dependent) ↑ NRF2; ↑ antioxidant defenses R/G Secondary tissue-protective redox response NRF2 activation is more compelling as a normal-cell or neuroprotective mechanism than as a core anticancer mechanism.
15 SIRT3 mitochondrial protection ↑ SIRT3 (context-dependent) ↑ SIRT3; ↑ mitochondrial resilience; ↓ oxidative injury R/G Context-dependent mitochondrial regulation Important for cardioprotective and neuroprotective effects; its cancer role can vary with tumor context because SIRT3 itself has context-dependent tumor biology.
16 Chemosensitization and targeted-therapy sensitization ↑ treatment sensitivity (drug-dependent) ↔ or tissue protection G Combination-treatment enhancement Preclinical evidence includes chemotherapy, cetuximab, mTOR inhibitors and immune-checkpoint strategies.
17 Radiosensitization ↑ radiosensitivity (model-dependent) ↔ or radioprotection (context-dependent) G Greater radiation response This apparent duality emphasizes cell type, dose, redox state and treatment timing.
18 Clinical Translation Constraint ↓ achievable exposure with conventional formulations Systemic safety incompletely characterized in humans G Bioavailability and evidence limitation Poor aqueous solubility, extensive metabolism, uncertain human tumor exposure and lack of efficacy trials remain central constraints; Phase I investigation is underway.

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



Honokiol and Alzheimer’s disease: Honokiol has meaningful but entirely preclinical relevance to Alzheimer’s disease and related neurodegeneration. Its lipophilicity permits CNS penetration, and experimental studies indicate reductions in oxidative stress, neuroinflammation, excitotoxicity and Aβ-associated toxicity together with preservation of mitochondrial function. SIRT3, NRF2, PPAR/PGC-1α signaling and restoration of microglial metabolic competence are among the more plausible mechanistic axes. No convincing clinical evidence currently establishes honokiol as an AD treatment.

Evidence level: Preclinical only. Cell and animal studies support neuroprotective and cognition-related effects, but human AD efficacy, dose-response relationships and long-term neurological safety have not been demonstrated.

Honokiol Alzheimer’s-Relevant Mechanisms

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Mitochondrial function and SIRT3 ↑ SIRT3; ↑ mitochondrial function; ↑ ΔΨm Mitochondrial resilience One of the strongest mechanistic links between honokiol and neuronal protection.
2 Oxidative stress and NRF2 ↓ ROS; ↑ NRF2; ↑ antioxidant defenses Reduced oxidative injury Direction differs from the pro-oxidant stress frequently induced by honokiol in cancer cells.
3 Microglial metabolism and phagocytosis ↑ PPARα; ↑ PGC-1α; ↑ OXPHOS; ↑ phagocytosis Improved microglial metabolic function Experimental evidence suggests reversal of dysfunctional metabolic programming can restore microglial clearance capacity.
4 Amyloid beta toxicity ↓ Aβ-associated toxicity Neuroprotection Supported primarily by experimental models; evidence for modifying human amyloid pathology is absent.
5 Neuroinflammation ↓ NF-κB; ↓ TNF-α; ↓ IL-1β Reduced inflammatory injury Likely overlaps the general anti-inflammatory pharmacology of honokiol.
6 Excitotoxic calcium signaling ↓ pathological Ca²⁺ signaling Reduced excitotoxic neuronal injury Reported neuroprotective actions include modulation of glutamatergic signaling and intracellular calcium overload.
7 Clinical Translation Constraint No demonstrated human AD efficacy Preclinical evidence only BBB penetration is pharmacologically favorable but does not establish an effective or safe human CNS dose.


NF-kB, Nuclear factor kappa B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
NF-kB signaling
Nuclear factor kappa B (NF-κB) is a transcription factor that plays a crucial role in regulating immune response, inflammation, cell proliferation, and survival.
NF-κB is often found to be constitutively active in many types of cancer cells. This persistent activation can promote tumorigenesis by enhancing cell survival, proliferation, and metastasis.
Scientific Papers found: Click to Expand⟱
2897- HNK,    Honokiol Inhibits Proliferation, Invasion and Induces Apoptosis Through Targeting Lyn Kinase in Human Lung Adenocarcinoma Cells
- in-vitro, Lung, PC9 - in-vitro, Lung, A549
TumCP↓, Honokiol Inhibits Cell Proliferation in Both A549 Cells and PC-9 Cells
Apoptosis↑, Honokiol Induces Apoptosis in PC-9 Cells
EGFR↓, Honokiol Suppresses Lyn Kinase and EGFR Signaling Pathway in PC-9 Cells
PI3K↓, led to a reduction of EGFR/PI3K/AKT and STAT3, and their phosphorylation status.
Akt↓,
STAT3↓,
TumCI↓, honokiol inhibits PC-9 cell proliferation, invasion and induces apoptosis through targeting Lyn kinase and Lyn-mediated EGFR signaling pathway.
TNF-α↑, Honokiol has efficacy to enhance the activation of TNF-α, in this way, honokiol inhibits activation of NF-κB and Akt. As a result, honokiol dramatically decreases expression level of NF-κB target genes, such as VEGF, MMP-9, and COX-2.
NF-kB↓,
VEGF↓,
MMP9↓,
COX2/PTGS2↓,

2894- HNK,    Pharmacological features, health benefits and clinical implications of honokiol
- Review, Var, NA - Review, AD, NA
*BioAv↓, HNK showed poor aqueous solubility due to phenolic hydroxyl groups forming intramolecular hydrogen bonds and poor solubility in water (
*neuroP↑, HNK has the accessibility to reach the neuronal tissue by crossing the BBB and showing neuroprotective effects
*BBB↑,
*ROS↓, fig 2
*Keap1↑,
*NRF2↑,
*Casp3↓,
*SIRT3↑,
*Rho↓,
*ERK↓,
*NF-kB↓,
angioG↓,
RAS↓,
PI3K↓,
Akt↓,
mTOR↓,
*memory↑, oral administration of HNK (1 mg/kg) in senescence-accelerated mice prevents age-related memory and learning deficits
*Aβ↓, in Alzheimer’s disease, HNK significantly reduces neurotoxicity of aggregated Ab
*PPARγ↑, Furthermore, the expression of PPARc and PGC1a was increased by HNK, suggesting its beneficial impact on energy metabolism
*PGC-1α↑,
NF-kB↓, activation of NFjB was suppressed by HNK via suppression of nuclear translocation and phosphorylation of the p65 subunit and further instigated apoptosis by enhancing TNF-a
Hif1a↓, HNK has anti-oxidative properties and can downregulate the HIF-1a protein, inhibiting hypoxia- related signaling pathways
VEGF↓, renal cancer, via decreasing the vascular endothelial growth factor (VEGF) and heme-oxygenase-1 (HO-1)
HO-1↓,
FOXM1↓, HNK interaction with the FOXM1 oncogenic transcription factor inhibits cancer cells
p27/CDKN1B↑, HNK treatment upregulates the expression of CDK inhibitor p27 and p21, whereas it downregulates the expression of CDK2/4/6 and cyclin D1/2
P21↑,
CDK2↓,
CDK4↓,
CDK6↓,
cycD1/CCND1↓,
Twist↓, HNK averted the invasion of urinary bladder cancer cells by downregulating the steroid receptor coactivator, Twist1 and Matrix metalloproteinase-2
MMP2↓,
Rho↑, By activating the RhoA, ROCK and MLC signaling, HNK inhibits the migration of highly metastatic renal cell carcinoma
ROCK1↑,
TumCMig↓,
cFLIP↓, HNK can be used to suppress c-FLIP, the apoptosis inhibitor.
BMPs↑, HNK treatment increases the expression of BMP7 protein
OCR↑, HNK might increase the oxygen consumption rate while decreasing the extracellular acidification rate in breast cancer cells.
ECAR↓,
*AntiAg↑, It also suppresses the platelet aggregation
*cardioP↑, HNK is an attractive cardioprotective agent because of its strong antioxidative properties
*antiOx↑,
*ROS↓, HNK treatment reduced cellular ROS production and decreased mitochondrial damage in neonatal rat cardiomyocytes exposed to hypoxia/reoxygenation
P-gp/ABCB1↓, The expres- sion of P-gp at mRNA and protein levels is reduced in HNK treatment on human MDR and MCF-7/ADR breast cancer cell lines

2891- HNK,    Honokiol, an Active Compound of Magnolia Plant, Inhibits Growth, and Progression of Cancers of Different Organs
- Review, Var, NA
AntiCan↑, honokiol possesses anti-carcinogenic, anti-inflammatory, anti-oxidative, anti-angiogenic as well as inhibitory effect on malignant transformation of papillomas to carcinomas in vitro and in vivo animal models without any appreciable toxicity.
Inflam↓,
antiOx↑,
selectivity↑,
*toxicity↓,
cycD1/CCND1↓, honokiol resulted in inhibition of UVB-induced expression levels of cyclins (cyclins D1, D2, and E) and CDKs in skin tumors
cycE/CCNE↓,
CDK2↓,
CDK4↓,
TumMeta↓, Honokiol Inhibits Metastatic Potential of Melanoma Cells
NADPH↓, Honokiol not only reduces the NADPH oxidase activity
MMP2↓, honokiol treatment reduces the expression of MMP-2 and MMP-9
MMP9↓,
p‑mTOR↓, honokiol caused significant downregulation of mTOR phosphorylation
EGFR↓, honokiol decreases the expression levels of total EGFR
EMT↓, honokiol effectively inhibits EMT in breast cancer cells
SIRT1↑, onokiol increases the expressions of SIRT1 and SIRT3,
SIRT3↑,
EZH2↓, depletion of EZH2 by honokiol treatment inhibited cell proliferation
Snail↓, significantly down regulates Snail, vimentin, N-cadherin expression, and upregulates cytokeratin-18 and E-cadherin expression
Vim↓,
N-cadherin↓,
E-cadherin↑,
COX2/PTGS2↓, honokiol as an inhibitor of COX-2 expression
NF-kB↓, inhibited transcriptional activity of NF-jB,
*ROS↓, Inhibition of UVR-induced inflammatory mediators as well as ROS by honokiol treatment contributes to the prevention of UVR-induced skin tumor development
Ca+2↑, excessive influx of cytosolic calcium ion into the mitochondria triggers dysfunction of the mitochon- drial membrane permeabilization with mitochondrial ROS induction
ROS↑,

7468- HNK,    Honokiol and Its Emerging Role in Breast Cancer Therapy
- Review, BC, NA
*ROS↓, HNK inhibits essential oncogenic pathways and reduces oxidative stress, inflammation, metabolic reprogramming, and cancer stemness.
*Inflam↓,
CSCs↓,
ChemoSen↑, HNK demonstrates synergistic activity with chemotherapy, endocrine therapy, targeted therapy, and immune checkpoint inhibitors, increasing sensitivity to treatment across models of ER+, PR+, and HER2+ BrCas, as well as triple-negative breast cancers
BioAv↑, Nanotechnological delivery systems enhance the solubility, bioavailability, and intratumoral accumulation of HNK, increasing its translational capacity.
ROS↑, HNK increases intracellular reactive oxygen species (ROS) levels in cancer cells, coinciding with a time-dependent loss of mitochondrial membrane potential (ΔΨm), indicating that ROS production is closely linked to mitochondrial damage
MMP↓,
mtDam↑,
TumCCA↑, HNK causes G0/G1 cell cycle arrest by downregulating cyclin D1 and CDK4, as well as promoting intrinsic apoptosis-like pathways marked by increases in caspase-3 and caspase-9 activities
cycD1/CCND1↓,
CDK4↓,
Casp3↑,
Casp9↑,
Bcl-2↓, reducing the anti-apoptotic Bcl-2 and Bcl-xL, and increasing the pro-apoptotic Bax
Bcl-xL↓,
BAX↑,
p‑STAT3↓, HNK suppresses the phosphorylation of STAT3 in MDA-MB-231
AMPK↑, HNK was found to activate the LKB1–AMPK axis and induce miR-34a expression in MCF7, SKBR3, and SUM149 cells, thereby inhibiting EMT, stemness, and oncogenic leptin signaling in an LKB1-dependent manner
miR-34a↑,
EMT↓,
HH↓, HNK can induce apoptosis by suppressing essential components of the Hh pathway, including SHH [28], Gli1, and Ptch1 [26], as well as downregulating NF-κB
Shh↓,
Gli1↓,
PTCH1↓,
NF-kB↓,
TNF-α↓, reduces the production of inflammatory cytokines, including TNF-α and IL-6
IL6↓,
Glycolysis↓, HNK suppresses HIF-1α-controlled glycolysis by downregulating glycolytic metabolic enzymes, disrupting glucose uptake, and inhibiting tumor growth.
GlucoseCon↓,
BioAv↓, This limitation is primarily attributed to pharmacokinetic challenges, including poor aqueous solubility, low oral bioavailability, rapid metabolism, and the lack of standardized dosing regimens,
BioAv↓, Preclinical studies demonstrate that following oral administration at 40 mg/kg, HNK is rapidly absorbed (Tmax ≈ 20 min) but exhibits low systemic exposure [75], due to extensive first-pass metabolism and high hepatic extraction
Half-Life↝, While the plasma elimination half-life is moderately prolonged (t½ ≈ 290 min),

2864- HNK,    Honokiol: A Review of Its Anticancer Potential and Mechanisms
- Review, Var, NA
TumCCA↑, induction of G0/G1 and G2/M cell cycle arrest
CDK2↓, (via the regulation of cyclin-dependent kinase (CDK) and cyclin proteins),
EMT↓, epithelial–mesenchymal transition inhibition via the downregulation of mesenchymal markers
MMPs↓, honokiol possesses the capability to supress cell migration and invasion via the downregulation of several matrix-metalloproteinases
AMPK↑, (activation of 5′ AMP-activated protein kinase (AMPK) and KISS1/KISS1R signalling)
TumCI↓, inhibiting cell migration, invasion, and metastasis, as well as inducing anti-angiogenesis activity (via the down-regulation of vascular endothelial growth factor (VEGFR) and vascular endothelial growth factor (VEGF)
TumCMig↓,
TumMeta↓,
VEGFR2/KDR/Flk1↓,
*antiOx↑, diverse biological activities, including anti-arrhythmic, anti-inflammatory, anti-oxidative, anti-depressant, anti-thrombocytic, and anxiolytic activities
*Inflam↓,
*BBB↑, Due to its ability to cross the blood–brain barrier
*neuroP↑, beneficial towards neuronal protection through various mechanism, such as the preservation of Na+/K+ ATPase, phosphorylation of pro-survival factors, preservation of mitochondria, prevention of glucose, reactive oxgen species (ROS), and inflammatory
*ROS↓,
Dose↝, Generally, the concentrations used for the in vitro studies are between 0–150 μM
selectivity↑, Interestingly, honokiol has been shown to exhibit minimal cytotoxicity against on normal cell lines, including human fibroblast FB-1, FB-2, Hs68, and NIH-3T3 cells
Casp3↑, ↑ Caspase-3 & caspase-9
Casp9↑,
NOTCH1↓, Inhibition of Notch signalling: ↓ Notch1 & Jagged-1;
cycD1/CCND1↓, ↓ cyclin D1 & c-Myc;
cMyc↓,
P21?, ↑ p21WAF1 protein
DR5↑, ↑ DR5 & cleaved PARP
cl‑PARP↑,
P53↑, ↑ phosphorylated p53 & p53
Mcl-1↑, ↓ Mcl-1 protein
p65↓, ↓ p65; ↓ NF-κB
NF-kB↓,
ROS↑, ↑ JNK activation ,Increase ROS activity:
JNK↑,
NRF2↑, ↑ Nrf2 & c-Jun protein activation
cJun↑,
EF-1α↓, ↓ EFGR; ↓ MAPK/PI3K pathway activity
MAPK↓,
PI3K↓,
mTORC1↓, ↓ mTORC1 function; ↑ LKB1 & cytosolic localisation
CSCs↓, Inhibit stem-like characteristics: ↓ Oct4, Nanog & Sox4 protein; ↓ STAT3;
OCT4↓,
Nanog↓,
SOX4↓,
STAT3↓,
CDK4↓, ↓ Cdk2, Cdk4 & p-pRbSer780;
p‑RB1↓,
PGE2↓, ↓ PGE2 production ↓ COX-2 ↑ β-catenin
COX2/PTGS2↓,
β-catenin/ZEB1↑,
IKKα↓, ↓ IKKα
HDAC↓, ↓ class I HDAC proteins; ↓ HDAC activity;
HATs↑, ↑ histone acetyltransferase (HAT) activity; ↑ histone H3 & H4
H3↑,
H4↑,
LC3II↑, ↑ LC3-II
c-Raf↓, ↓ c-RAF
SIRT3↑, ↑ Sirt3 mRNA & protein; ↓ Hif-1α protein
Hif1a↓,
ER Stress↑, ↑ ER stress signalling pathway activation; ↑ GRP78,
GRP78/BiP↑,
cl‑CHOP/DDIT3↑, ↑ cleaved caspase-9 & CHOP;
MMP↓, mitochondrial depolarization
PCNA↓, ↓ cyclin B1, cyclin D1, cyclin D2 & PCNA;
Zeb1↓, ↓ ZEB2 Inhibit
NOTCH3↓, ↓ Notch3/Hes1 pathway
CD133↓, ↓ CD133 & Nestin protein
Nestin↓,
ATG5↑, ↑ Atg7 protein activation; ↑ Atg5;
ATG7↑,
survivin↓, ↓ Mcl-1 & survivin protein
ChemoSen↑, honokiol potentiated the apoptotic effect of both doxorubicin and paclitaxel against human liver cancer HepG2 cells.
SOX2↓, Honokiol was shown to downregulate the expression of Oct4, Nanog, and Sox2 which were known to be expressed in osteosarcoma, breast carcinoma and germ cell tumours
OS↑, Lipo-HNK was also shown to prolong survival and induce intra-tumoral apoptosis in vivo.
P-gp/ABCB1↓, Honokiol was shown to downregulate the expression of P-gp at mRNA and protein levels in MCF-7/ADR, a human breast MDR cancer cell line
Half-Life↓, For i.v. administration, it has been found that there was a rapid rate of distribution followed by a slower rate of elimination (elimination half-life t1/2 = 49.22 min and 56.2 min for 5 mg or 10 mg of honokiol, respectively
Half-Life↝, male and female dogs was assessed. The elimination half-life (t1/2 in hours) was found to be 20.13 (female), 9.27 (female), 7.06 (male), 4.70 (male), and 1.89 (male) after administration of doses of 8.8, 19.8, 3.9, 44.4, and 66.7 mg/kg, respectively.
eff↑, Apart from that, epigallocatechin-3-gallate functionalized chitin loaded with honokiol nanoparticles (CE-HK NP), developed by Tang et al. [224], inhibit HepG2
BioAv↓, extensive biotransformation of honokiol may contribute to its low bioavailability.

2082- HNK,    Revealing the role of honokiol in human glioma cells by RNA-seq analysis
- in-vitro, GBM, U87MG - in-vitro, GBM, U251
AntiCan↑, In summary, studies have demonstrated that honokiol has multiple anticancer effects
TumCP↑, honokiol suppresses cell proliferation, and promotes autophagy and apoptosis
TumAuto↑,
Apoptosis↑,
*BioAv↑, honokiol could improve bioavailability in nerve tissue through passing the blood-brain barrie
*neuroP↑, honokiol has neuroprotective effects.
*NF-kB↑, honokiol could reduce cytokine production and stimulate glial nuclear factor kappa B (NFκB) to eliminate the inflammatory response during cerebral ischemia-reperfusion activity
MAPK↑, honokiol activated cells MAPK signaling pathway in human glioma cells
GPx4↑, The results showed that the ferroptosis-associated protein GPX4 was suppressed in honokiol-treated cells compared to control cells.
Tf↑, Ferroptosis-associated protein TF was upregulated in both honokiol-treated cell lines compared to the control
BAX↑, BAX was increased, and the expression of Bcl-2 was suppressed in both honokiol-treated cells, indicating that honokiol induced apoptosis in the human glioma cell lines U87-MG and U251-MG.
Bcl-2↓,
antiOx↑, Researchers have found that the antioxidant capacity of honokiol is 1000 times greater than that of vitamin E
Hif1a↓, reduce HIF-1α protein levels and suppress hypoxia-related signaling pathways
Ferroptosis↑, Honokiol activated ferroptosis in human glioma cells

1087- HNK,    Honokiol Inhibits Non-Small Cell Lung Cancer Cell Migration by Targeting PGE2-Mediated Activation of β-Catenin Signaling
- in-vitro, Lung, A549 - in-vitro, Lung, H1299 - in-vitro, Lung, H460 - in-vitro, Lung, H226
TumCMig↓,
COX2/PTGS2↓,
PGE2↓,
NF-kB↓,
p65↓,
β-catenin/ZEB1↓,
MMP2↓,
MMP9↓,

2885- HNK,    Honokiol: a novel natural agent for cancer prevention and therapy
NF-kB↓, Honokiol targets multiple signaling pathways including nuclear factor kappa B (NF-κB), signal transducers and activator of transcription 3 (STAT3), epidermal growth factor receptor (EGFR) and mammalian target of rapamycin (m-TOR)
STAT3↓,
EGFR↓,
mTOR↓,
BioAv↝, honokiol has revealed a desirable spectrum of bioavailability after intravenous administration in animal models, thus making it a suitable agent for clinical trials
Inflam↓, inflammation, proliferation, angiogenesis, invasion and metastasis.
TumCP↓,
angioG↓,
TumCI↓,
TumMeta↓,
cSrc↓, STAT3 inhibition by honokiol has also been correlated with the repression of upstream protein tyrosine kinases c-Src, JAK1 and JAK2
JAK1↓,
JAK2↓,
ERK↓, by inhibiting ERK and Akt pathways (31) or by upregulation of PTEN
Akt↓,
PTEN↑,
ChemoSen↑, Chemopreventive/ chemotherapeutic effects of honokiol in various malignancies: preclinical studies
chemoP↑,
COX2/PTGS2↓, honokiol was found to inhibit UVB-induced expression of cyclooxygenase-2, prostaglandin E2, proliferating cell nuclear antigen and pro-inflammatory cytokines, such as TNF-α, interleukin (IL)-1β and IL-6 in the skin
PGE2↓,
TNF-α↓,
IL1β↓,
IL6↓,
Casp3↑, release of caspases-3, -8 and -9as well as poly (ADP-ribose) polymerase (PARP) cleavage and p53 activation upon honokiol treatment that led to DNA fragmentation
Casp8↑,
Casp9↑,
cl‑PARP↑,
DNAdam↑,
Cyt‑c↑, translocation of cytochrome c to cytosol in human melanoma cell lines
RadioS↑, liposomal honokiol for 24 h showed a higher radiation enhancement ratio (~ two-fold) as compared to the radiation alone,
RAS↓, Honokiol also caused suppression of Ras activation
BBB↑, honokiol could effectively cross BBB and BCSFB and inhibit brain tumor growth
BioAv↓, Due to the concerns about poor aqueous solubility, liposomal formulations of honokiol have been developed and tested for their pharmacokinetics
Half-Life↝, In another comparative study, plasma honokiol concentrations was maintained above 30 and 10 μg/mL for 24 and 48 hours, respectively, in liposomal honokiol-treated mice, whereas it fell quickly (less than 5 μg/mL) by 12 hours in free honokiol-treated
Half-Life↝, free honokiol has poor GIT absorption, bio-transformed in liver to mono-glucuronide honokiol and sulphated mono-hydroxyhonokiol, ~ 50% is secreted in bile, ~ 60-65% plasma protein bound with elimination half life of (t1/2) of 49.05 – 56.24 minutes.
toxicity↓, These studies suggest that honokiol either alone or as a part of magnolia bark extract does not induce toxicity in animal models and thus could be clinically safe

2883- HNK,    Honokiol targets mitochondria to halt cancer progression and metastasis
- Review, Var, NA
ChemoSen↑, Combination of HNK with many traditional chemotherapeutic drugs as well as radiation sensitizes cancer cells to apoptotic death
BBB↓, HNK is also capable of crossing the BBB
Ca+2↑, HNK promotes human glioblastoma cancer cell apoptosis via regulation of Ca(2+) channels
Cyt‑c↑, release of mitochondrial cytochrome c and activation of caspase-3
Casp3↑,
chemoPv↑, potent chemopreventive agent against lung SCC development in a carcinogen-induced lung SCC murine model
OCR↓, HNK treatment results in a decreased oxygen consumption rate (OCR) in whole intact cells, rapidly, and persistently inhibiting mitochondrial respiration, which leads to the induction of apoptosis
mitResp↓,
Apoptosis↑,
RadioS↑, Honokiol as a chemo- and radiosensitizer
NF-kB↓, HNK as an anticancer drug is its potential to inhibit multiple important survival pathways, such as NF-B and Akt
Akt↓,
TNF-α↓, by inhibiting TNF-induced nerve growth factor IB expression in breast cancer cells
PGE2↓, reduced prostaglandin E2 (PGE2) and vascular endothelial growth factor (VEGF) secretion levels
VEGF↓,
NO↝, HNK inhibits cancer cell migration by targeting nitric oxide and cyclooxygenase-2 or Ras GTPase-activating-like protein (IQGAP1) [
COX2/PTGS2↓,
RAS↓,
EMT↓, HNK can reverse the epithelial-mesenchymal-transition (EMT) process, which is a key step during embryogenesis, cancer invasion, and metastasis,
Snail↓, HNK reduced the expression levels of Snail, N-cadherin and -catenin, which are mesenchymal markers, but increased E-cadherin,
N-cadherin↓,
β-catenin/ZEB1↓,
E-cadherin↑,
ER Stress↑, induction of ER stress
p‑STAT3↓, HNK inhibited STAT3 phosphorylation
EGFR↓, inhibiting EGFR phosphorylation and its downstream signaling pathways such as the mTOR signaling pathway
mTOR↓,
mt-ROS↑, We demonstrated that HNK treatment suppresses mitochondrial respiration and increases generation of ROS in the mitochondria, leading to the induction of apoptosis in lung cancer cells
PI3K↓, inhibition of PI3K/Akt/ mTOR, EMT, and Wnt signaling pathways.
Wnt↓,

2877- HNK,    Targeting histone deacetylase-3 blocked epithelial-mesenchymal plasticity and metastatic dissemination in gastric cancer
- in-vitro, GC, AGS
HDAC3↓, Honokiol significantly abolished HDAC3 activity (Y298) via inhibition of NFκBp65/CEBPβ signaling,
NF-kB↓,
CEBPB↓,
ER Stress↑, Honokiol increased ER stress markers and inhibited EMT-associated epithelial markers, but decreased Wnt/β-catenin activity
EMT↓,
Wnt↓,
β-catenin/ZEB1↓,

2869- HNK,    Nature's neuroprotector: Honokiol and its promise for Alzheimer's and Parkinson's
- Review, AD, NA - Review, Park, NA
*neuroP↑, neuroprotective, anti-oxidant, anti-apoptotic, neuromodulating, anti-inflammatory, and many more qualities, honokiol,
*Inflam↓,
*motorD↑, degradation of dopaminergic neurons in Parkinson's disease and improving motor function.
*Aβ↓, Alzheimer's disease, honokiol showed promise in lowering the production of amyloid-beta (Aβ) plaques, phosphorylating tau, and enhancing cognitive performance
*p‑tau↓,
*cognitive↑,
*memory↑, prevented Acetylcholinesterase activity from elevation as well as improved acetylcholine levels, and improved learning, and memory deficits via increased ERK1/2 and Akt phosphorylation
*ERK↑,
*p‑Akt↑,
*PPARγ↑, honokiol has been reported to elevate PPARγ levels in APPswe/PS1dE9 mice as PPARγ is related to ani-inflammatory
*PGC-1α↑, honokiol boosted the expression of PGC1α and PPARγ
*MMP↑, as well as reduced elevated mitochondrial membrane potential and mitochondrial ROS
*mt-ROS↓,
*SIRT3↑, Honokiol has been found as a dual SIRT-3 activator and PPAR-γ agonist that reduced oxidative stress markers within cells and changed the AMPK pathway
*IL1β↓, honokiol prevented restraint stress-induced cognitive dysfunction by reducing the hippocampus's production of IL-1β, TNF-α, glucose-regulated protein (GRP78), and C/EBP homologous protein (CHOP)
*TNF-α↓,
*GRP78/BiP↓,
*CHOP/DDIT3↓,
*NF-kB↓, Additionally, the neuroprotective benefits of honokiol in mice with Aβ-induced learning and memory impairment have been attributed to the inactivation of NF-κB
*GSK‐3β↓, Treatment of honokiol in PC12 cells resulted in reduced GSK-3β and induced β-catenin which effectively showed the neuroprotective and anti-oxidant effect in AD therapy
*β-catenin/ZEB1↑,
*Ca+2↓, , anti-apoptotic effect via reduced caspase 3 levels, and protected membrane injury by reduced calcium level has been investigated in PC12 cells of AD models
*AChE↓, protective effects by serving as an antioxidant, reduced AchE levels, repaired neurofibrillary tangles, reduced NF-kB which downregulates Aβ plaque
*SOD↑, fig1
*Catalase↑,
*GPx↑,

2868- HNK,    Honokiol: A review of its pharmacological potential and therapeutic insights
- Review, Var, NA - Review, Sepsis, NA
*P-gp/ABCB1↓, reduction in the expression of defective proteins like P-glycoproteins, inhibition of oxidative stress, suppression of pro-inflammatory cytokines (TNF-α, IL-10 and IL-6),
*ROS↓,
*TNF-α↓,
*IL10↓,
*IL6↓,
eIF2α↑, Bcl-2, phosphorylated eIF2α, CHOP,GRP78, Bax, cleaved caspase-9 and phosphorylated PERK
CHOP/DDIT3↑,
GRP78/BiP↑,
BAX↑,
cl‑Casp9↑,
p‑PERK↑,
ER Stress↑, endoplasmic reticulum stress and proteins in apoptosis in 95-D and A549 cells
Apoptosis↑,
MMPs↓, decrease in levels of matrix metal-mloproteinases, P-glycoprotein expression, the formation of mammosphere, H3K27 methyltransferase, c-FLIP, level of CXCR4 receptor,pluripotency-factors, Twist-1, class I histone deacetylases, steroid receptor co
cFLIP↓,
CXCR4↓,
Twist↓,
HDAC↓,
BMPs↑, enhancement in Bax protein, and (BMP7), as well as interference with an activator of transcription 3 (STAT3), (mTOR), (EGFR), (NF-kB) and Shh
p‑STAT3↓, secreased the phosphorylation of STAT3
mTOR↓,
EGFR↓,
NF-kB↓,
Shh↓,
VEGF↓, induce apoptosis, and regulate the vascular endothelial growth factor-A expression (VEGF-A)
tumCV↓, human glioma cell lines (U251 and U-87 MG) through inhibition of colony formation, glioma cell viability, cell migration, invasion, suppression of ERK and AKT signalling cascades, apoptosis induction, and reduction of Bcl-2 expression.
TumCMig↓,
TumCI↓,
ERK↓,
Akt↓,
Bcl-2↓,
Nestin↓, increased the Bax expression, lowered the CD133, EGFR, and Nesti
CD133↓,
p‑cMET↑, HKL through the downregulating the phosphorylation of c-Met phosphorylation and stimulation of Ras,
RAS↑,
chemoP↑, Cheng and coworker determined the chemopreventive role of HKL against the proliferation of renal cell carcinoma (RCC) 786‑0 cells through multiple mechanism
*NRF2↑, , HKL also effectively activate the Nrf2/ARE pathway and reverse this pancreatic dysfunction in in vivo and in vitro model
*NADPH↓, (HUVECs) such as inhibition of NADPH oxidase activity, suppression of p22 (phox) protein expression, Rac-1 phosphorylation, reactive oxygen species production, inhibition of degradation of Ikappa-B-alpha, and suppression of activity of of NF-kB
*p‑Rac1↓,
*ROS↓,
*IKKα↑,
*NF-kB↓,
*COX2/PTGS2↓, Furthermore, HKL treatment the inhibited cyclooxygenase (COX-2) upregulation, reduces prostaglandin E2 production, enhanced caspase-3 activity reduction
*PGE2↓,
*Casp3↓,
*hepatoP↑, compound also displayed hepatoprotective action against oxidative injury in tert-butyl hydroperoxide (t-BHP)-injured AML12 liver cells in in vitro model
*antiOx↑, compound reduces the level of acetylation on SOD2 to stimulate its antioxidative action, which results in reduced reactive oxygen species aggregation in AML12 cells
*GSH↑, HKL prevents oxidative damage induced by H2O2 via elevating antioxidant enzymes levels which includes glutathione and catalase and promotes translocation and activation transcription factor Nrf2
*Catalase↑,
*RenoP↑, imilarly, the compound protects renal reperfusion/i-schemia injury (IRI) in adult male albino Wistar rats via reducing theactivities of serum alkaline phosphatase (ALP), aspartate aminotrans- ferase (AST) and alanine aminotransferase (ALT)
*ALP↓,
*AST↓,
*ALAT↓,
*neuroP↑, Several reports and works have shown that HKL displays some neuroprotective properties
*cardioP↑, Cardioprotection
*HO-1↑, the expression level of heme oxygenase-1 (HO-1)was remarkably up-regulated and miR-218-5p was significantly down-regulated in septic mice treated with HKL
*Inflam↓, anti-inflammatory action of HKL at dose of 10 mg/kg in the muscle layer of mice


Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Ferroptosis↑, 1,   GPx4↑, 1,   HO-1↓, 1,   NRF2↑, 1,   ROS↑, 3,   mt-ROS↑, 1,   SIRT3↑, 2,  

Metal & Cofactor Biology(tgid=2) ⓘ

Tf↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mitResp↓, 1,   MMP↓, 2,   mtDam↑, 1,   OCR↓, 1,   OCR↑, 1,   c-Raf↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   ATG7↑, 1,   cMyc↓, 1,   ECAR↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   NADPH↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 5,   Apoptosis↑, 4,   BAX↑, 3,   Bcl-2↓, 3,   Bcl-xL↓, 1,   Casp3↑, 4,   Casp8↑, 1,   Casp9↑, 3,   cl‑Casp9↑, 1,   cFLIP↓, 2,   Cyt‑c↑, 2,   DR5↑, 1,   Ferroptosis↑, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↑, 1,   p27/CDKN1B↑, 1,   survivin↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

cSrc↓, 1,   EF-1α↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↑, 1,   EZH2↓, 1,   H3↑, 1,   H4↑, 1,   HATs↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   cl‑CHOP/DDIT3↑, 1,   eIF2α↑, 1,   ER Stress↑, 4,   GRP78/BiP↑, 2,   p‑PERK↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   P53↑, 1,   cl‑PARP↑, 2,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 3,   CDK4↓, 4,   cycD1/CCND1↓, 4,   cycE/CCNE↓, 1,   P21?, 1,   P21↑, 1,   p‑RB1↓, 1,   TumCCA↑, 2,  

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

CD133↓, 2,   CEBPB↓, 1,   p‑cMET↑, 1,   CSCs↓, 2,   EMT↓, 5,   ERK↓, 2,   FOXM1↓, 1,   Gli1↓, 1,   HDAC↓, 2,   HDAC3↓, 1,   HH↓, 1,   miR-34a↑, 1,   mTOR↓, 4,   p‑mTOR↓, 1,   mTORC1↓, 1,   Nanog↓, 1,   Nestin↓, 2,   NOTCH1↓, 1,   NOTCH3↓, 1,   OCT4↓, 1,   PI3K↓, 4,   PTCH1↓, 1,   PTEN↑, 1,   RAS↓, 3,   RAS↑, 1,   Shh↓, 2,   SOX2↓, 1,   STAT3↓, 3,   p‑STAT3↓, 3,   Wnt↓, 2,  

Migration(tgid=13) ⓘ

Ca+2↑, 2,   E-cadherin↑, 2,   MMP2↓, 3,   MMP9↓, 3,   MMPs↓, 2,   N-cadherin↓, 2,   Rho↑, 1,   ROCK1↑, 1,   Snail↓, 2,   SOX4↓, 1,   TumCI↓, 4,   TumCMig↓, 4,   TumCP↓, 2,   TumCP↑, 1,   TumMeta↓, 3,   Twist↓, 2,   Vim↓, 1,   Zeb1↓, 1,   β-catenin/ZEB1↓, 3,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   EGFR↓, 5,   Hif1a↓, 3,   NO↝, 1,   VEGF↓, 4,   VEGFR2/KDR/Flk1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↓, 1,   BBB↑, 1,   P-gp/ABCB1↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 6,   CXCR4↓, 1,   IKKα↓, 1,   IL1β↓, 1,   IL6↓, 2,   Inflam↓, 2,   JAK1↓, 1,   JAK2↓, 1,   NF-kB↓, 10,   p65↓, 2,   PGE2↓, 4,   TNF-α↓, 3,   TNF-α↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4,   BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 4,   Dose↝, 1,   eff↑, 1,   Half-Life↓, 1,   Half-Life↝, 4,   RadioS↑, 2,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

BMPs↑, 2,   EGFR↓, 5,   EZH2↓, 1,   FOXM1↓, 1,   IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   chemoP↑, 2,   chemoPv↑, 1,   OS↑, 1,   toxicity↓, 1,  
Total Targets: 164

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Catalase↑, 2,   GPx↑, 1,   GSH↑, 1,   HO-1↑, 1,   Keap1↑, 1,   NRF2↑, 2,   ROS↓, 7,   mt-ROS↓, 1,   SIRT3↑, 2,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↑, 1,   PGC-1α↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   NADPH↓, 1,   PPARγ↑, 2,  

Cell Death(tgid=5) ⓘ

p‑Akt↑, 1,   Casp3↓, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1,   GRP78/BiP↓, 1,  

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

ERK↓, 1,   ERK↑, 1,   GSK‐3β↓, 1,  

Migration(tgid=13) ⓘ

AntiAg↑, 1,   Ca+2↓, 1,   p‑Rac1↓, 1,   Rho↓, 1,   β-catenin/ZEB1↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,   P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IKKα↑, 1,   IL10↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 4,   NF-kB↓, 3,   NF-kB↑, 1,   PGE2↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 2,   cognitive↑, 1,   hepatoP↑, 1,   memory↑, 2,   motorD↑, 1,   neuroP↑, 5,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 57

Scientific Paper Hit Count for: NF-kB, Nuclear factor kappa B
12 Honokiol
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#:94  Target#:214  State#:%  Dir#:%
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