Magnolol Cancer Research Results

MAG, Magnolol: Click to Expand ⟱
Features:
Lignan found in bark of some magnolia species.
Magnolol (MAG) — a bioactive biphenolic compound from Magnolia officinalis
derived from the bark (roots and branches) of Magnolia species such as M. officinalis, M. obovata, and M. grandiflora
The two main bioactive compounds isolated from these plants are MAG (5,5ʹ-diallyl-2,2ʹ-dihydroxybiphenyl) and Honokiol (3,5ʹ-diallyl-4,2ʹ-dihydroxybiphenyl) (Fig. 1) which are phenolic regioisomers.
In the bark extracts of Magnolia plants, the composition of MAG ranges from 1 to 10%, while Honokiol comprises 1 to 5%
Magnolol is a biphenolic neolignan isolated from the bark of Magnolia officinalis. It is structurally related to honokiol and is studied for anti-inflammatory, antioxidant, antimicrobial, and neuroactive effects. In preclinical oncology models, magnolol is reported to modulate NF-κB, STAT3, PI3K/AKT, MAPK, Wnt/β-catenin, and redox pathways, with downstream effects on cell-cycle arrest, apoptosis, invasion/EMT, and angiogenesis. Oral bioavailability is limited and many cytotoxic concentrations reported in vitro are in the tens of µM range, often above typical systemic levels from standard supplementation.

Magnolol — a naturally occurring biphenolic neolignan and polyphenolic small molecule found primarily in the bark of Magnolia officinalis and related Magnolia species, including M. obovata. It is commonly abbreviated MAG or MG and is a structural regioisomer of honokiol. Magnolol has anti-inflammatory, redox-modulating, neuroprotective, and preclinical antineoplastic activity. Its cancer pharmacology is pleiotropic rather than attributable to a single molecular target, with prominent effects on mitochondrial apoptosis, PI3K/AKT/mTOR, NF-κB/STAT3, ROS, cell-cycle regulation, invasion/EMT, and angiogenesis.

Primary mechanisms (ranked):

  1. Mitochondrial apoptosis and mitochondrial dysfunction, including ↑ Bax/Bcl-2 ratio, ↑ cytochrome c release, ↑ caspase activation, ↓ mitochondrial membrane potential, and in some models MPTP opening.
  2. PI3K/AKT/mTOR survival signaling suppression, contributing to reduced proliferation, survival, invasion, and treatment resistance.
  3. NF-κB and STAT3 suppression, reducing pro-survival, inflammatory, EMT, and stemness-related transcription.
  4. ROS elevation in multiple cancer models, particularly mitochondrial ROS, which can drive mitochondrial injury and apoptosis; magnolol can instead act as an antioxidant in non-malignant tissues.
  5. Cell-cycle arrest through modulation of cyclins, CDKs, p21, p27, and p53.
  6. Inhibition of invasion and EMT through effects on MMPs, E-cadherin, Snail/Slug, TGF-β/Smad, and related pathways.
  7. Suppression of HIF-1α/VEGF-mediated angiogenic signaling in selected tumor models.
  8. Wnt/β-catenin suppression in colorectal and other selected cancer models.
  9. Ca²⁺ dysregulation and mitochondrial signaling in selected cancer models, contributing to cytochrome-c release and apoptosis.
  10. Chemosensitization and radiosensitization in preclinical models, including reported enhancement of 5-FU, cisplatin, and radiation responses.
  11. NRF2-mediated antioxidant protection is primarily relevant to normal/non-malignant cells and should be considered a secondary, context-dependent mechanism rather than a universal anticancer mechanism.

Bioavailability / PK relevance: Magnolol is lipophilic and poorly water soluble, with substantial first-pass phase-II metabolism. After oral administration, glucuronide and sulfate conjugates predominate in circulation, whereas unconjugated magnolol can accumulate more substantially in tissues. Rapid glucuronidation and sulfation materially limit systemic free-magnolol exposure. Nanoparticles, micelles, nanosuspensions, lipid-based delivery systems, and structural derivatives have therefore been investigated to improve exposure.

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 µM magnolol, commonly tens of micromolar. These concentrations should not be assumed to be achievable as sustained free-magnolol plasma concentrations following conventional oral supplementation. Tissue exposure may exceed circulating unconjugated concentrations, but the exposure gap remains a major translational limitation.

Clinical evidence status: Preclinical for cancer treatment. Evidence includes extensive cell studies and multiple animal/xenograft models, but magnolol is not an established or approved anticancer therapy and there is no convincing human oncology efficacy evidence. Human experience is mainly with Magnolia officinalis extracts or multi-ingredient natural-health products for non-oncologic indications. Magnolia-containing natural health products are licensed in Canada, but this does not constitute approval of purified magnolol for cancer treatment.

major pathways and molecular targets involved in magnolol’s anticancer actions:
-Apoptosis: ↑ Bax, ↓ Bcl-2, ↑ cytochrome c, ↑ caspase-9, ↑ caspase-3
-Arrests cell cycle at G0/G1 or G2/M phase:↓ Cyclin D1, CDK4, CDK6, Cyclin B1, CDK1
-Inhibits NF-κB activation: ↓ IκBα, COX-2, TNF-α
-Inhibits PI3K, Akt, and mTOR phosphorylation
-Suppresses angiogenesis: ↓ Bcl-XL, Mcl-1, VEGF, cyclin D1
-Inhibits β-catenin nuclear translocation
-increase ROS production in tumor cells → triggers mitochondrial apoptosis
-Magnolol activates Nrf2 in normal cells → upregulates HO-1, NQO1: Protects normal tissue from oxidative stress during chemotherapy or inflammation.

Most in-vitro IC50 values fall in the 10–100 µM range, often above typical systemic exposure.

Magnolol Cancer Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial apoptosis and MPTP Apoptosis ↑; Bax/Bcl-2 ↑; cytochrome c ↑; caspase-3/9 ↑; ΔΨm ↓; MPTP opening ↑ ↔ (model-dependent) R, G Mitochondrial cell-death execution One of the most reproducible anticancer phenotypes. Mitochondrial depolarization, fragmentation, ROS generation, and permeability transition have been reported in several cancer models.
2 PI3K AKT mTOR survival signaling PI3K ↓; p-AKT ↓; AKT ↓; mTOR ↓; p70S6K ↓ (model-dependent) ↔ or protective AKT signaling (context-dependent) R, G Growth and survival suppression Repeatedly implicated across prostate, gastric, cervical, bladder, and other tumor models.
3 NF-κB and STAT3 transcription NF-κB ↓; p-STAT3 ↓; survival and inflammatory targets ↓ NF-κB inflammatory signaling ↓ R, G Pro-survival transcription suppression NF-κB evidence is broad. Direct STAT3 evidence is more model-specific but important in NSCLC and oral cancer stemness models.
4 Mitochondrial ROS and oxidative stress ROS ↑; mtROS ↑; mitochondrial damage ↑; antioxidant capacity ↓ (model-dependent) ROS ↓; oxidative damage ↓ in many non-cancer models P, R Pro-oxidant tumor stress Magnolol is not uniformly pro-oxidant. Cancer-cell ROS elevation is well demonstrated in selected breast, renal, lung, and mitochondrial models, whereas antioxidant activity predominates in many normal-tissue studies.
5 Cell-cycle checkpoints Cell-cycle arrest ↑; Cyclin D1/B1 ↓; CDK1/2/4 ↓; p21 ↑; p27 ↑; p53 ↑ ↔ (generally) G Cytostasis G0/G1 or G2/M arrest occurs depending on tumor type and experimental conditions.
6 EMT invasion and metastasis Migration ↓; invasion ↓; MMP2/7/9 ↓; E-cadherin ↑; Snail/Slug ↓; EMT ↓ ↔ G Anti-invasive phenotype Multiple upstream mechanisms contribute, including PI3K/AKT/mTOR, NF-κB/STAT3, TGF-β/Smad, and Wnt signaling.
7 HIF-1α VEGF angiogenesis HIF-1α ↓; VEGF ↓; VEGFR2 signaling ↓; angiogenesis ↓ ↔ (context-dependent) R, G Hypoxia and angiogenesis suppression Particularly well characterized in hypoxic bladder cancer models; should not be generalized to every tumor type.
8 Wnt β-catenin signaling β-catenin nuclear translocation ↓; β-catenin/TCF transcription ↓; c-Myc ↓; MMP7 ↓; uPA ↓ ↔ R, G Proliferation and invasion suppression Strong mechanistic evidence exists in colorectal cancer cells and xenografts, but this is not a universal magnolol mechanism across all cancers.
9 Ca²⁺ mitochondrial signaling Intracellular Ca²⁺ ↑ (model-dependent); mitochondrial dysfunction ↑; cytochrome c release ↑ ↔ P, R Apoptotic signal amplification Reported in colon and liver cancer models. Mechanistically meaningful but less universally demonstrated than mitochondrial apoptosis or PI3K/AKT inhibition.
10 MAPK stress signaling ERK/JNK/p38 modulation (model-dependent) Inflammatory MAPK activation ↓ in several non-cancer models P, R Stress and proliferation signaling Direction varies substantially with cell type, concentration, and endpoint; individual MAPKs should be entered separately where primary studies establish direction.
11 NRF2 antioxidant response ↔ or context-dependent NRF2 ↑; HO-1 ↑; antioxidant defense ↑ R, G Secondary cytoprotection Best supported as a normal-tissue antioxidant mechanism. It should not be listed as a uniformly activated anticancer pathway because tumor NRF2 activation could theoretically protect malignant cells in some contexts.
12 Chemosensitization and radiosensitization Chemosensitivity ↑; radiosensitivity ↑ (model-dependent) Potential normal-tissue protection reported in selected chemotherapy injury models G Treatment response modulation Reported with 5-FU and cisplatin and in radiation experiments, but evidence remains preclinical and combination-specific.
13 Clinical Translation Constraint Effective experimental concentrations commonly in the tens of µM Systemic exposure limited by solubility and rapid conjugation G Exposure limitation Poor aqueous solubility, extensive glucuronidation/sulfation, uncertain human tumor exposure, and absence of oncology trials limit direct translation of in-vitro findings.

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





Alzheimer’s disease relevance: Magnolol has significant preclinical AD relevance but no established clinical efficacy. In transgenic AD mouse models it improved cognitive performance and reduced amyloid pathology, while mechanistic studies implicate AMPK/mTOR/ULK1-dependent autophagy, reduced neuroinflammation, modulation of APP/Aβ processing, improved synaptic-protein expression, and protection against Aβ-induced tau hyperphosphorylation and neuronal apoptosis. These findings remain preclinical.

Primary AD mechanisms: Promotion of autophagic clearance through AMPK/mTOR/ULK1 signaling currently has particularly direct mechanistic support. Additional mechanisms include ↓ Aβ burden, ↓ neuroinflammation, preservation of synaptic proteins, and CHRM1/cAMP/PKA/CREB-mediated reduction of Aβ-associated tau hyperphosphorylation and neuronal apoptosis.

Magnolol Alzheimer’s Disease Mechanisms

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 AMPK mTOR ULK1 autophagy p-AMPK ↑; p-ULK1 ↑; p-mTOR ↓; LC3-II ↑; Beclin-1 ↑; p62 ↓ Autophagic clearance ↑ Mechanistically supported in APP/PS1 mice and Aβ oligomer cell models; pathway inhibition weakened magnolol protection.
2 Amyloid pathology Aβ burden ↓; Aβ40 ↓; Aβ42 ↓; APP processing modulation Amyloid pathology ↓ Demonstrated in transgenic mouse models; not established clinically.
3 Neuroinflammation Microglial activation ↓; astrocyte activation ↓; TNF-α ↓; IL-1β ↓; IL-6 ↓; IL-10 ↑ Neuroinflammatory signaling ↓ Observed in AD mouse models and consistent with magnolol's broader anti-inflammatory pharmacology.
4 CHRM1 cAMP PKA CREB and tau CHRM1 ↑; cAMP/PKA/CREB ↑; tau hyperphosphorylation ↓ Neuronal protection Primarily cell-model evidence; useful mechanistic target but lower translational weight than the animal AD data.
5 Synaptic integrity PSD93 ↑; PSD95 ↑; synapsin-1 ↑; synaptophysin ↑ Synaptic function preservation Associated with improved cognition in transgenic AD mice.
6 Neuronal apoptosis Bax ↓; cleaved caspase-9 ↓; Bcl-2 ↑ Apoptosis ↓ Direction contrasts appropriately with the pro-apoptotic effect observed in many cancer-cell models.


Scientific Papers found: Click to Expand⟱
4523- HNK,  MAG,  BA,    Honokiol-Magnolol-Baicalin Possesses Synergistic Anticancer Potential and Enhances the Efficacy of Anti-PD-1 Immunotherapy in Colorectal Cancer by Triggering GSDME-Dependent Pyroptosis
- in-vitro, CRC, HCT116 - in-vitro, CRC, LoVo - in-vivo, CRC, HCT116
AntiCan↑, eff↑, TumCP↓, TumCCA↓, cycD1/CCND1↓, Pyro↑, Apoptosis↑, cl‑GSDME↑, Bcl-2↓, Cyt‑c↑, Casp9↑, TumCG↓,
4522- HNK,  MAG,    Honokiol Is More Potent than Magnolol in Reducing Head and Neck Cancer Cell Growth
- in-vitro, HNSCC, FaDu
AntiCan↑, tumCV↓, eff↑, survivin↓, RadioS↑,
8517- HNK,  MAG,    Modulation of Rat Hepatic CYP1A and 2C Activity by Honokiol and Magnolol: Differential Effects on Phenacetin and Diclofenac Pharmacokinetics In Vivo
- in-vivo, Nor, NA
Ingr↝, CYP1A1↓, *antiAll↑, *Stress↓, *Inf↓,
8509- MAG,  Rad,    The In Vivo Radiosensitizing Effect of Magnolol on Tumor Growth of Hepatocellular Carcinoma
- in-vivo, HCC, NA
TumVol↓, TumW↓, *ERK↓, *NF-kB↓, Casp3↑, Casp9↑, RadioS↑, *toxicity↓, Ki-67↓, IL1β↓, TNF-α↓,
8512- MAG,    Enhanced Oral Bioavailability of the Pharmacologically Active Lignin Magnolol via Zr-Based Metal Organic Framework Impregnation
- in-vivo, Nor, NA
*other↝, *toxicity↓, *Half-Life↑, *BioAv↑,
8507- MAG,    Magnolol acts as a neurorestorative agent in an Aβ1‑42‑induced mouse model of Alzheimer's disease
- in-vivo, AD, NA
*Dose?, *cognitive↑, *Aβ↓, *NeuroI↓, *neuroP↑, *tau↓, *GFAP↓, *AIF1/Iba-1↓, *GSK‐3β↑, *SYP↑, *BDNF↑,
8506- MAG,    Magnolia officinalis Lignans induce apoptosis and epigenetic reprogramming via the miR-148a-3p/DNMT-1/UTF-1 axis in pancreatic cancer cells
- in-vitro, PC, Panc02 - in-vitro, PC, MIA PaCa-2
*Inflam↓, *antiOx↑, Ingr↝, tumCV↓, Apoptosis↑, ROS↑, MMP↓, Casp↑, selectivity↑, DNMT1↓, JAK2↓, STAT3↓, miR-148a↑, UTF1↑, IL6↓, survivin↓,
8505- MAG,    Role of magnolol in gastrointestinal cancers: Recent trends and future perspectives
- Review, GC, NA
TumCP↓, TumCI↓, TumCMig↓, angioG↓, EMT↓, TumCCA↑, Apoptosis↑, PI3K↝, Akt↝, NF-kB↝, MAPK↝, JNK↝, ERK↝, TGF-β↝, Smad1↝,
8504- MAG,    Magnolol nanoparticles combat MRSA by disrupting TCA cycle and arginine metabolism to induce oxidative stress
- in-vitro, Var, NA
*BioAv↓, *CompStab↑, *Bacteria↓, *eff↑, TCA↝, ROS↑, SOD↓,
8503- MAG,    Magnolol mitigates neuroinflammation via NF-κB/IL-6/IL-1β pathways in AlCl₃-induced Alzheimer's disease: insights from in-vivo and in-silico investigations
- in-vivo, AD, NA
*Dose↝, *LDH↓, *NO↓, *cognitive↑, *GSH↑, *Catalase↑, *SOD↑, *neuroP↑, *NF-kB↓, *IL6↓, *IL1β↓, *neuroP↑, *ROS↓, *Inflam↓,
8502- MAG,    Magnolol as a promising multitarget agent for Alzheimer's disease: Evidence from a systematic evidence synthesis, network pharmacology, and molecular dynamics simulations
- Review, AD, NA
*cognitive↑, *antiOx↑, *Inflam↓, *AChE↓, *HER2/EBBR2↓,
8501- MAG,    Synergistic effects of autophagy/mitophagy inhibitors and magnolol promote apoptosis and antitumor efficacy
- vitro+vivo, neuroblastoma, NA
MMP↓, mtDam↑, ROS↑, PINK1↑, TumCG↓, OS↑, TumAuto↑, MitoP↑,
8500- MAG,    Magnolol Induces Apoptosis Through Extrinsic/intrinsic Pathways and Attenuates NF-κB/STAT3 Signaling in Non-small-cell Lung Cancer Cells
- in-vitro, NSCLC, A549
NF-kB↓, STAT3↓, EMT↓,
8499- MAG,    Wnt/β-catenin signaling mediates the antitumor activity of magnolol in colorectal cancer cells
- vitro+vivo, CRC, SW480 - in-vitro, CRC, HCT116
β-catenin/ZEB1↓, TCF↓, TOPflash↓, cMyc↓, MMP7↓, UroPA↓, TumCI↓,
8498- MAG,    Induction of apoptosis by magnolol via the mitochondrial pathway and cell cycle arrest in renal carcinoma cells
- in-vitro, Kidney, 786-O - in-vitro, RCC, OS-RC-2 - in-vitro, Nor, HK-2
Apoptosis↑, TumCCA↑, selectivity↑, TumCMig↓, TumCI↓, MPT↑, ROS↓, MMP↓, mtDam↑,
8497- MAG,    Magnolol induces apoptosis in MCF-7 human breast cancer cells through G2/M phase arrest and caspase-independent pathway
- in-vitro, BC, MCF7
TumCP↓, Apoptosis↑, *TumCCA↑, *ROS↑, *MMP↓, *Cyt‑c↑, *AIF↑, *BAX↑, *P21↑, *P53↑, *Bcl-2↓, *CycB/CCNB1↓, *CDK1↓,
8496- MAG,    Metabolic interactions of magnolol with cytochrome P450 enzymes: uncompetitive inhibition of CYP1A and competitive inhibition of CYP2C
- in-vitro, Nor, NA
*CYP1A1↓, *CYP2C6↓,
8495- MAG,    Pharmacokinetics, bioavailability, and tissue distribution of magnolol following single and repeated dosing of magnolol to rats
- in-vivo, Nor, NA
*Dose↝, *other?, *BioAv↝,
8510- MAG,    Pharmacokinetic and Metabolic Profiling of Key Active Components of Dietary Supplement Magnolia officinalis Extract for Prevention against Oral Carcinoma
- in-vitro, Oral, CAL27 - in-vitro, Tong, SCC9 - in-vitro, SCC, SCC4
Ingr?, BioAv↓, other↝, BioAv↓, Half-Life↓,
8511- MAG,    Suppression of PKCδ/NF-κB Signaling and Apoptosis Induction through Extrinsic/Intrinsic Pathways Are Associated Magnolol-Inhibited Tumor Progression in Colorectal Cancer In Vitro and In Vivo
- vitro+vivo, CRC, HT-29 - in-vitro, Colon, CT26
p‑PKCδ↓, p‑NF-kB↓, TumCI↓, Fas↓, FasL↓, TumCG?, toxicity↓, cl‑Casp8↑, MMP↓, Casp9↑, ChemoSen↑,
8493- MAG,    Magnolol upregulates CHRM1 to attenuate Amyloid-β-triggered neuronal injury through regulating the cAMP/PKA/CREB pathway
- in-vitro, AD, SH-SY5Y
*neuroP↑, *Aβ↓, *p‑tau↓, *Apoptosis↓, *CHRM1↑, *cAMP↑, *PKA↑, *CREB↑,
8513- MAG,    Magnolia extract is effective for the chemoprevention of oral cancer through its ability to inhibit mitochondrial respiration at complex I
- vitro+vivo, Oral, SCC4 - in-vitro, Tong, SCC9 - in-vitro, SCC, CAL27
TumCG↓, TumMeta↓, *toxicity↓, Ingr?, chemoPv↑, compI↓, mitResp↓, ETC↓, AMPK↑, STAT3↓, ox-PrxI↑, Dose↝, Ki-67↓, STAT3↓, P70S6K↓, HK2↓, survivin↓, BioAv↝, Half-Life↝, ROS↑,
8514- MAG,    Magnolol alleviates Alzheimer's disease-like pathology in transgenic C. elegans by promoting microglia phagocytosis and the degradation of beta-amyloid through activation of PPAR-γ
- in-vivo, AD, NA
*PPARγ↑, *NF-kB↓, *NRF2↑, *ARE↑, *ROS↓,
8515- MAG,    Inhibition of human carboxylesterases by magnolol: Kinetic analyses and mechanism
- in-vitro, Liver, HepG2
CES1↓,
8516- MAG,    Magnolol induces cell death through PI3K/Akt-mediated epigenetic modifications boosting treatment of BRAF- and NRAS-mutant melanoma
- in-vitro, Melanoma, NA
TumCCA↑, Apoptosis↑, TumCD↑, PI3K↓, Akt↓, H3K4↓, ChemoSen↑,
8518- MAG,    Magnolol suppresses the proliferation and invasion of cholangiocarcinoma cells via inhibiting the NF-κB signaling pathway
- in-vitro, CCA, NA
TumCG↓, TumCMig↓, TumCI↓, PCNA↓, Ki-67↓, MMP2↓, MMP7↓, MMP9↓, TumCCA↑, cycD1/CCND1↓, p‑IκB↓, p‑p65↓, NF-kB↓,
8519- MAG,    Magnolol inhibits growth of gallbladder cancer cells through the p53 pathway
- vitro+vivo, Gall, NA
TumCG?, TumCCA↑, mt-Apoptosis↑, P53↑, P21↑, cycD1/CCND1↓, CDC25↓, CDK2↓, MMP↓, Bax:Bcl2↑, Casp9↑, Casp3↑, cl‑PARP↑,
8520- MAG,    The natural compound magnolol inhibits invasion and exhibits potential in human breast cancer therapy
- in-vitro, BC, MDA-MB-231
TumCI↓, MMP9↓, NF-kB↓, *toxicity↓,
8521- MAG,    Magnolol induces apoptosis via caspase-independent pathways in non-small cell lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Lung, H520 - in-vitro, Lung, NCI-H441
TumCP↓, DNAdam↑, MMP↓, selectivity↑, BID↑, BAX↑, Cyt‑c↑, AIF↑, Endon↑, cl‑PARP↑, PI3K↓, Akt↓, ERK↓, p38↑, JNK↑,
8522- MAG,    Effects of magnolol on impairment of learning and memory abilities induced by scopolamine in mice
- in-vivo, AD, NA
*Learn↑, *memory↑, AChE↓, NOS2↑, SOD↑, MDA↓,
8523- MAG,    Anticancer potential of magnolol for lung cancer treatment
- in-vitro, Lung, A549
TumCG↓, LDH↑, TumCCA↑, Casp3↑, cl‑PARP↑, NF-kB↓,
8524- MAG,    Magnolol induces apoptosis via inhibiting the EGFR/PI3K/Akt signaling pathway in human prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, CRC, HCT116
Apoptosis↑, Akt?, BAD↑, Cyt‑c↑, cl‑Casp8↑, cl‑Casp9↑, cl‑Casp3↑, cl‑PARP↑, NA⇅, selectivity↑, p‑EGFR↓, p‑PI3K↓, p‑Akt↓,
8525- MAG,    Mechanisms for the magnolol-induced cell death of CGTH W-2 thyroid carcinoma cells
- in-vitro, Thyroid, NA
Casp3↑, Casp7↑, PARP↑, Akt↓, p‑PTEN↓, p‑Akt↓,
4526- MAG,  HNK,    Targeting apoptosis pathways in cancer with magnolol and honokiol, bioactive constituents of the bark of Magnolia officinalis
- Review, Var, NA
*antiOx↑, *Inflam↓, *Bacteria↓, *toxicity↓, AntiTum↑, Apoptosis↑, DR5↝,
1089- MAG,    Magnolol potently suppressed lipopolysaccharide-induced iNOS and COX-2 expression via downregulating MAPK and NF-κB signaling pathways
- in-vitro, AML, RAW264.7
p‑IκB↓, NF-kB↓, p‑ERK↓, p‑JNK↓, p‑PI3K↓, p‑Akt↓, iNOS↓, COX2/PTGS2↓,
1196- MAG,    2-O-Methylmagnolol, a Magnolol Derivative, Suppresses Hepatocellular Carcinoma Progression via Inhibiting Class I Histone Deacetylase Expression
- in-vitro, HCC, NA
TumCG↓, TumCMig↓, TumCI↓, TumCCA↑, HDAC↓,
1197- MAG,    Magnolol as STAT3 inhibitor for treating multiple sclerosis by restricting Th17 cells
- in-vivo, MS, NA
Weight↑, Th17↓, STAT3↓,
1198- MAG,    Mitochondria-targeted magnolol inhibits OXPHOS, proliferation, and tumor growth via modulation of energetics and autophagy in melanoma cells
- in-vivo, Melanoma, NA
OXPHOS↓, TumCP↓,
1314- MAG,    Magnolol induces apoptosis via activation of both mitochondrial and death receptor pathways in A375-S2 cells
- in-vitro, Melanoma, A375
TumCP↓, Casp3↑, Casp8↑, Casp9↑, Bcl-2↓, BAX↑,
4514- MAG,    Magnolol and its semi-synthetic derivatives: a comprehensive review of anti-cancer mechanisms, pharmacokinetics, and future therapeutic potential
- Review, Var, NA
AntiCan↑, TumCP↓, TumCCA↑, TumMeta↓, angioG↓, NF-kB↓, MAPK↓, PI3K↓, Akt↓, mTOR↓, BioAv↓, *antiOx↑, *Inflam↓, *AntiAg↑, ChemoSen↑, cycD1/CCND1↓, CycB/CCNB1↓, cycE/CCNE↓, CDK2↓, CDK4↓, p27/CDKN1B↑, P21↑, P53↑, PTEN↓, XIAP↓, Mcl-1↓, Casp3↑, Casp9↑, MMP9↑,
4515- MAG,    Magnolol as a Potential Anticancer Agent: A Proposed Mechanistic Insight
- Review, Var, NA
AntiCan↑, TumCP↓, TumCCA↑, Apoptosis↑, TumCMig↑, angioG↓, PI3K↓, Akt↓, mTOR↓, MAPK↓, NF-kB↓,
4516- MAG,    Magnolol Induces Apoptosis and Suppresses Immune Evasion in Non-small Cell Lung Cancer Xenograft Models
- in-vivo, NSCLC, NA
selectivity↑, Apoptosis↑, TumCCA↑, Casp3↑, cycD1/CCND1↓, CDK4↓, VEGF↓, FOXP3↓, IDO1↓,
4517- MAG,    Mitochondrion-targeted magnolol derivatives exert synergistic anticancer activity by modulating energy metabolism and tumor microenvironment
- vitro+vivo, Var, NA
eff↑, AntiCan↑, ROS↑, ER Stress↑, Apoptosis↑,
4518- MAG,  Cisplatin,    Evaluating the Magnolol Anticancer Potential in MKN-45 Gastric Cancer Cells
- in-vitro, GC, MKN45
ChemoSen↑, tumCV↓, BAX↑, Bcl-2↓, P21↑, P53↑, MMP9↓,
4519- MAG,    Magnolol: A Neolignan from the Magnolia Family for the Prevention and Treatment of Cancer
- Review, Var, NA
*antiOx↑, *Inflam↓, *Bacteria↓, *AntiAg↑, *BBB↑, *BioAv↓, BAD↑, Casp3↑, Casp6↑, Casp9↑, JNK↑, Bcl-xL↓, PTEN↑, Akt↓, NF-kB↓, MMP7↓, MMP9↓, uPA↓, Hif1a↓, VEGF↓, FOXO3↓, Ca+2↑, TumCCA↑, ROS↑, Cyt‑c↑,
4520- MAG,    Magnolol Suppresses Pancreatic Cancer Development In Vivo and In Vitro via Negatively Regulating TGF-β/Smad Signaling
- vitro+vivo, PC, PANC1
Vim↓, E-cadherin↑, EMT↓, N-cadherin↓, p‑SMAD2↓, p‑SMAD3↓, TumCP↓, TumCMig↓, TumCI↓, TGF-β↓,
4521- MAG,  HNK,    Safety and Toxicology of Magnolol and Honokiol
- Review, Nor, NA
*antiOx↑, *Inflam↓, *Bacteria↓, *toxicity↓,
4524- MAG,    Magnolol facilitates mitochondrial-peroxisome dysfunction and induces oxeiptosis in lung cancer cells following transfer via tunneling nanotubes
- vitro+vivo, Lung, NA
ROS↑, antiOx↓, mtDam↑,
4525- MAG,  HNK,    Magnolol and Honokiol: Two Natural Compounds with Similar Chemical Structure but Different Physicochemical and Stability Properties
- Study, Nor, NA
*BioAv↝, *CompStab↑,
8494- MAG,    Magnolol Ameliorates Behavioral Impairments and Neuropathology in a Transgenic Mouse Model of Alzheimer's Disease
- in-vivo, AD, NA
*cognitive↑, *PSD95?, *SYN1↑, *SYT1↑, *IL10↑, *TNF-α↓, *IL6↓, *Aβ42↓, *GFAP↓, *other↑, *cognitive↑, *NeuroI↓, *Aβ↓, *GSK‐3β↓, *NF-kB↓,

Showing Research Papers: 1 to 50 of 64
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 64

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

NA⇅, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   H2O2↓, 2,   MDA↓, 1,   ox-PrxI↑, 1,   ROS↓, 1,   ROS↑, 7,   SOD↓, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC2↓, 1,   CDC25↓, 1,   compI↓, 1,   ETC↓, 1,   mitResp↓, 1,   mtDam↑, 3,   OXPHOS↓, 1,   PINK1↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   p‑AMPK↑, 1,   HK2↓, 1,   IDO1↓, 1,   TCA↝, 1,  

Cell Death(tgid=5) ⓘ

AIF↑, 1,   Apoptosis↑, 19,   mt-Apoptosis↑, 1,   BAD↑, 2,   BAX↑, 5,   Bax:Bcl2↑, 2,   Bcl-2↓, 6,   Bcl-xL↓, 1,   BID↑, 1,   Casp↑, 1,   Casp3↑, 12,   cl‑Casp3↑, 2,   Casp6↑, 1,   Casp7↑, 1,   Casp8↑, 2,   cl‑Casp8↑, 2,   Casp9↑, 8,   cl‑Casp9↑, 2,   Cyt‑c↑, 6,   DR5↝, 1,   Endon↑, 1,   Fas↓, 1,   FasL↓, 1,   cl‑GSDME↑, 1,   iNOS↓, 1,   Mcl-1↓, 1,   p38↑, 1,   p‑p38↓, 1,   Pyro↑, 1,   survivin↓, 3,   TumCD↑, 1,   XIAP↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt?, 1,   Akt↓, 10,   Akt↝, 1,   p‑Akt↓, 4,   p‑EGFR↓, 1,   ERK↓, 1,   ERK↝, 1,   p‑ERK↓, 1,   p‑IκB↓, 2,   JAK2↓, 1,   JNK↑, 2,   JNK↝, 1,   p‑JNK↓, 1,   MAPK↓, 2,   MAPK↝, 1,   mTOR↓, 5,   P70S6K↓, 2,   PI3K↓, 6,   PI3K↝, 1,   p‑PI3K↓, 3,   p‑PKCδ↓, 1,   PTEN↓, 1,   PTEN↑, 1,   p‑PTEN↓, 1,   STAT3↓, 5,  

Transcription & Epigenetics(tgid=7) ⓘ

cMyc↓, 1,   DNMT1↓, 1,   FOXO3↓, 1,   H3K4↓, 1,   HDAC↓, 1,   miR-148a↑, 1,   other↝, 1,   tumCV↓, 4,   UTF1↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

MitoP↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 4,   P53↑, 4,   PARP↑, 1,   cl‑PARP↑, 5,   PCNA↓, 3,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 3,   CDK4↓, 3,   cycA1/CCNA1↓, 2,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 7,   cycE/CCNE↓, 1,   Ki-67↓, 5,   P21↑, 6,   p27/CDKN1B↑, 1,   TumCCA↓, 1,   TumCCA↑, 16,  

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

4E-BP1↓, 1,   CSCs↓, 1,   Ki-67↓, 5,   TOPflash↓, 1,   TumCG?, 2,   TumCG↓, 11,   TumCP↓, 13,  

Migration(tgid=13) ⓘ

CA↓, 1,   Ca+2↑, 3,   E-cadherin↑, 3,   EMT↓, 3,   MMP2↓, 4,   MMP7↓, 5,   MMP9↓, 6,   MMP9↑, 1,   N-cadherin↓, 1,   Slug↓, 1,   Smad1↝, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   Snail↓, 1,   TGF-β↓, 1,   TGF-β↝, 1,   TumCA↓, 1,   TumCI↓, 12,   TumCMig↓, 10,   TumCMig↑, 1,   TumMeta↓, 2,   uPA↓, 1,   UroPA↓, 1,   Vim↓, 1,   vinculin↓, 1,   β-catenin/ZEB1↓, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 4,   CD31/PECAM-1↓, 1,   Hif1a↓, 3,   VEGF↓, 3,   VEGFR2/KDR/Flk1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

MMP↓, 8,   MPT↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   FOXP3↓, 1,   IL1β↓, 1,   IL6↓, 1,   NF-kB↓, 10,   NF-kB↝, 1,   p‑NF-kB↓, 1,   p‑p65↓, 1,   TCF↓, 1,   Th17↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4,   BioAv↝, 1,   CES1↓, 1,   ChemoSen↑, 6,   CYP1A1↓, 2,   Dose↝, 1,   eff↑, 3,   Half-Life↓, 1,   Half-Life↝, 1,   RadioS↑, 2,   selectivity↑, 8,   Synergy↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

p‑EGFR↓, 1,   IL6↓, 1,   LDH↓, 1,   LDH↑, 1,   NOS2↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 8,   AntiTum↑, 2,   cachexia↓, 1,   chemoP↑, 1,   chemoPv↑, 1,   OS↑, 1,   toxicity↓, 1,   TumVol↓, 1,   TumW↓, 1,   Weight↑, 1,  

Ingredients & Constituents(tgid=25) ⓘ

Ingr?, 2,   Ingr↝, 2,  
Total Targets: 189

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 8,   ARE↑, 1,   Catalase↑, 2,   GPx↑, 1,   GSH↑, 1,   MDA↓, 1,   NRF2↑, 2,   ROS↓, 4,   ROS↑, 1,   SOD↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   cAMP↑, 1,   glucose↓, 1,   GSK‐3β↓, 1,   GSK‐3β↑, 1,  

Cell Death(tgid=5) ⓘ

AIF↑, 1,   Apoptosis↓, 1,   Apoptosis↑, 1,   BAX↓, 1,   BAX↑, 1,   Bcl-2↓, 2,   cl‑Casp8↑, 1,   cl‑Casp9↓, 1,   Cyt‑c↑, 1,   iNOS↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

CREB↑, 1,   ERK↓, 1,   HER2/EBBR2↓, 1,   MAPK↓, 1,   mTOR↑, 1,   PKA↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other?, 1,   other↑, 1,   other↝, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1/ATG6↑, 1,   LC3II↑, 1,   p62↓, 1,   ULK1/ATG1↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CycB/CCNB1↓, 1,   P21↑, 2,   TumCCA↑, 1,  

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

IGF-1↑, 1,  

Migration(tgid=13) ⓘ

AntiAg↑, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   NO↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   MMP↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

AIF1/Iba-1↓, 1,   COX2/PTGS2↓, 1,   IL10↑, 2,   IL1β↓, 1,   IL6↓, 2,   Inflam↓, 8,   Inflam↑, 1,   M2 MC↑, 1,   NeuroI↓, 2,   NF-kB↓, 5,   PGE2↓, 1,   TLR2↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

GFAP↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   AChE↑, 1,   BDNF↑, 2,   CHRM1↑, 1,   PSD95?, 1,   SYN1↑, 1,   SYP↑, 1,   SYT1↑, 1,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,   Aβ↓, 3,   Aβ42↓, 1,   tau↓, 1,   p‑tau↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

PPARγ↓, 1,   PPARγ↑, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,   BioAv↑, 1,   BioAv↝, 3,   CompStab↑, 2,   CYP1A1↓, 1,   CYP2C6↓, 1,   CYP2E1↓, 1,   Dose?, 1,   Dose↝, 2,   eff↑, 1,   Half-Life↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

HER2/EBBR2↓, 1,   IL6↓, 2,   LDH↓, 1,  

Functional Outcomes(tgid=23) ⓘ

antiAll↑, 1,   AntiDiabetic↑, 1,   cardioP↑, 2,   cognitive↑, 5,   Learn↑, 1,   memory↑, 1,   neuroP↑, 7,   Stress↓, 1,   toxicity↓, 7,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 6,   GutMicro↑, 1,   Inf↓, 1,  
Total Targets: 106

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#:121  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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