tbResList Print — MAG Magnolol

Filters: qv=121, qv2=%, rfv=%

Product

MAG Magnolol
Description: <b>Lignan</b> found in bark of some magnolia species.<br>
Magnolol (MAG) — a bioactive biphenolic compound from Magnolia officinalis<br>
derived from the bark (roots and branches) of Magnolia species such as M. officinalis, M. obovata, and M. grandiflora<br>
The two main bioactive compounds isolated from these plants are MAG (5,5ʹ-diallyl-2,2ʹ-dihydroxybiphenyl) and <b>Honokiol</b> (3,5ʹ-diallyl-4,2ʹ-dihydroxybiphenyl) (Fig. 1) which are phenolic regioisomers. <br>
In the bark extracts of Magnolia plants, the composition of MAG ranges from 1 to 10%, while Honokiol comprises 1 to 5%<br>
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.<br>
<br>

<p><b>Magnolol</b> — 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.</p>

<p><b>Primary mechanisms (ranked):</b></p>
<ol>
<li>Mitochondrial apoptosis and mitochondrial dysfunction, including ↑ Bax/Bcl-2 ratio, ↑ cytochrome c release, ↑ caspase activation, ↓ mitochondrial membrane potential, and in some models MPTP opening.</li>
<li>PI3K/AKT/mTOR survival signaling suppression, contributing to reduced proliferation, survival, invasion, and treatment resistance.</li>
<li>NF-κB and STAT3 suppression, reducing pro-survival, inflammatory, EMT, and stemness-related transcription.</li>
<li>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.</li>
<li>Cell-cycle arrest through modulation of cyclins, CDKs, p21, p27, and p53.</li>
<li>Inhibition of invasion and EMT through effects on MMPs, E-cadherin, Snail/Slug, TGF-β/Smad, and related pathways.</li>
<li>Suppression of HIF-1α/VEGF-mediated angiogenic signaling in selected tumor models.</li>
<li>Wnt/β-catenin suppression in colorectal and other selected cancer models.</li>
<li>Ca²⁺ dysregulation and mitochondrial signaling in selected cancer models, contributing to cytochrome-c release and apoptosis.</li>
<li>Chemosensitization and radiosensitization in preclinical models, including reported enhancement of 5-FU, cisplatin, and radiation responses.</li>
<li>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.</li>
</ol>

<p><b>Bioavailability / PK relevance:</b> 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.</p>

<p><b>In-vitro vs systemic exposure relevance:</b> 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.</p>

<p><b>Clinical evidence status:</b> 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.</p>


major pathways and molecular targets involved in magnolol’s anticancer actions:<br>
-Apoptosis: ↑ Bax, ↓ Bcl-2, ↑ cytochrome c, ↑ caspase-9, ↑ caspase-3 <br>
-Arrests cell cycle at G0/G1 or G2/M phase:↓ Cyclin D1, CDK4, CDK6, Cyclin B1, CDK1<br>
-Inhibits NF-κB activation: ↓ IκBα, COX-2, TNF-α<br>
-Inhibits PI3K, Akt, and mTOR phosphorylation<br>
-Suppresses angiogenesis: ↓ Bcl-XL, Mcl-1, VEGF, cyclin D1<br>
-Inhibits β-catenin nuclear translocation<br>
-increase ROS production in tumor cells → triggers mitochondrial apoptosis<br>
-Magnolol activates Nrf2 in normal cells → upregulates HO-1, NQO1: Protects normal tissue from oxidative stress during chemotherapy or inflammation.<br>
<br>
Most in-vitro IC50 values fall in the 10–100 µM range, often above typical systemic exposure.<br>
<br>





<h3>Magnolol Cancer Mechanisms</h3>
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer Cells</th>
<th>Normal Cells</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
<tr>
<td>1</td>
<td>Mitochondrial apoptosis and MPTP</td>
<td>Apoptosis ↑; Bax/Bcl-2 ↑; cytochrome c ↑; caspase-3/9 ↑; ΔΨm ↓; MPTP opening ↑</td>
<td>↔ (model-dependent)</td>
<td>R, G</td>
<td>Mitochondrial cell-death execution</td>
<td>One of the most reproducible anticancer phenotypes. Mitochondrial depolarization, fragmentation, ROS generation, and permeability transition have been reported in several cancer models.</td>
</tr>
<tr>
<td>2</td>
<td>PI3K AKT mTOR survival signaling</td>
<td>PI3K ↓; p-AKT ↓; AKT ↓; mTOR ↓; p70S6K ↓ (model-dependent)</td>
<td>↔ or protective AKT signaling (context-dependent)</td>
<td>R, G</td>
<td>Growth and survival suppression</td>
<td>Repeatedly implicated across prostate, gastric, cervical, bladder, and other tumor models.</td>
</tr>
<tr>
<td>3</td>
<td>NF-κB and STAT3 transcription</td>
<td>NF-κB ↓; p-STAT3 ↓; survival and inflammatory targets ↓</td>
<td>NF-κB inflammatory signaling ↓</td>
<td>R, G</td>
<td>Pro-survival transcription suppression</td>
<td>NF-κB evidence is broad. Direct STAT3 evidence is more model-specific but important in NSCLC and oral cancer stemness models.</td>
</tr>
<tr>
<td>4</td>
<td>Mitochondrial ROS and oxidative stress</td>
<td>ROS ↑; mtROS ↑; mitochondrial damage ↑; antioxidant capacity ↓ (model-dependent)</td>
<td>ROS ↓; oxidative damage ↓ in many non-cancer models</td>
<td>P, R</td>
<td>Pro-oxidant tumor stress</td>
<td>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.</td>
</tr>
<tr>
<td>5</td>
<td>Cell-cycle checkpoints</td>
<td>Cell-cycle arrest ↑; Cyclin D1/B1 ↓; CDK1/2/4 ↓; p21 ↑; p27 ↑; p53 ↑</td>
<td>↔ (generally)</td>
<td>G</td>
<td>Cytostasis</td>
<td>G0/G1 or G2/M arrest occurs depending on tumor type and experimental conditions.</td>
</tr>
<tr>
<td>6</td>
<td>EMT invasion and metastasis</td>
<td>Migration ↓; invasion ↓; MMP2/7/9 ↓; E-cadherin ↑; Snail/Slug ↓; EMT ↓</td>
<td>↔</td>
<td>G</td>
<td>Anti-invasive phenotype</td>
<td>Multiple upstream mechanisms contribute, including PI3K/AKT/mTOR, NF-κB/STAT3, TGF-β/Smad, and Wnt signaling.</td>
</tr>
<tr>
<td>7</td>
<td>HIF-1α VEGF angiogenesis</td>
<td>HIF-1α ↓; VEGF ↓; VEGFR2 signaling ↓; angiogenesis ↓</td>
<td>↔ (context-dependent)</td>
<td>R, G</td>
<td>Hypoxia and angiogenesis suppression</td>
<td>Particularly well characterized in hypoxic bladder cancer models; should not be generalized to every tumor type.</td>
</tr>
<tr>
<td>8</td>
<td>Wnt β-catenin signaling</td>
<td>β-catenin nuclear translocation ↓; β-catenin/TCF transcription ↓; c-Myc ↓; MMP7 ↓; uPA ↓</td>
<td>↔</td>
<td>R, G</td>
<td>Proliferation and invasion suppression</td>
<td>Strong mechanistic evidence exists in colorectal cancer cells and xenografts, but this is not a universal magnolol mechanism across all cancers.</td>
</tr>
<tr>
<td>9</td>
<td>Ca²⁺ mitochondrial signaling</td>
<td>Intracellular Ca²⁺ ↑ (model-dependent); mitochondrial dysfunction ↑; cytochrome c release ↑</td>
<td>↔</td>
<td>P, R</td>
<td>Apoptotic signal amplification</td>
<td>Reported in colon and liver cancer models. Mechanistically meaningful but less universally demonstrated than mitochondrial apoptosis or PI3K/AKT inhibition.</td>
</tr>
<tr>
<td>10</td>
<td>MAPK stress signaling</td>
<td>ERK/JNK/p38 modulation (model-dependent)</td>
<td>Inflammatory MAPK activation ↓ in several non-cancer models</td>
<td>P, R</td>
<td>Stress and proliferation signaling</td>
<td>Direction varies substantially with cell type, concentration, and endpoint; individual MAPKs should be entered separately where primary studies establish direction.</td>
</tr>
<tr>
<td>11</td>
<td>NRF2 antioxidant response</td>
<td>↔ or context-dependent</td>
<td>NRF2 ↑; HO-1 ↑; antioxidant defense ↑</td>
<td>R, G</td>
<td>Secondary cytoprotection</td>
<td>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.</td>
</tr>
<tr>
<td>12</td>
<td>Chemosensitization and radiosensitization</td>
<td>Chemosensitivity ↑; radiosensitivity ↑ (model-dependent)</td>
<td>Potential normal-tissue protection reported in selected chemotherapy injury models</td>
<td>G</td>
<td>Treatment response modulation</td>
<td>Reported with 5-FU and cisplatin and in radiation experiments, but evidence remains preclinical and combination-specific.</td>
</tr>
<tr>
<td>13</td>
<td>Clinical Translation Constraint</td>
<td>Effective experimental concentrations commonly in the tens of µM</td>
<td>Systemic exposure limited by solubility and rapid conjugation</td>
<td>G</td>
<td>Exposure limitation</td>
<td>Poor aqueous solubility, extensive glucuronidation/sulfation, uncertain human tumor exposure, and absence of oncology trials limit direct translation of in-vitro findings.</td>
</tr>
</table>
<p><b>TSF:</b> P: 0–30 min &nbsp;&nbsp; R: 30 min–3 hr &nbsp;&nbsp; G: &gt;3 hr</p>






<br><br>
<hr>
<br><br>



<p><b>Alzheimer’s disease relevance:</b> 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.</p>

<p><b>Primary AD mechanisms:</b> 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.</p>


<h3>Magnolol Alzheimer’s Disease Mechanisms</h3>
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Modulation</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
<tr>
<td>1</td>
<td>AMPK mTOR ULK1 autophagy</td>
<td>p-AMPK ↑; p-ULK1 ↑; p-mTOR ↓; LC3-II ↑; Beclin-1 ↑; p62 ↓</td>
<td>Autophagic clearance ↑</td>
<td>Mechanistically supported in APP/PS1 mice and Aβ oligomer cell models; pathway inhibition weakened magnolol protection.</td>
</tr>
<tr>
<td>2</td>
<td>Amyloid pathology</td>
<td>Aβ burden ↓; Aβ40 ↓; Aβ42 ↓; APP processing modulation</td>
<td>Amyloid pathology ↓</td>
<td>Demonstrated in transgenic mouse models; not established clinically.</td>
</tr>
<tr>
<td>3</td>
<td>Neuroinflammation</td>
<td>Microglial activation ↓; astrocyte activation ↓; TNF-α ↓; IL-1β ↓; IL-6 ↓; IL-10 ↑</td>
<td>Neuroinflammatory signaling ↓</td>
<td>Observed in AD mouse models and consistent with magnolol's broader anti-inflammatory pharmacology.</td>
</tr>
<tr>
<td>4</td>
<td>CHRM1 cAMP PKA CREB and tau</td>
<td>CHRM1 ↑; cAMP/PKA/CREB ↑; tau hyperphosphorylation ↓</td>
<td>Neuronal protection</td>
<td>Primarily cell-model evidence; useful mechanistic target but lower translational weight than the animal AD data.</td>
</tr>
<tr>
<td>5</td>
<td>Synaptic integrity</td>
<td>PSD93 ↑; PSD95 ↑; synapsin-1 ↑; synaptophysin ↑</td>
<td>Synaptic function preservation</td>
<td>Associated with improved cognition in transgenic AD mice.</td>
</tr>
<tr>
<td>6</td>
<td>Neuronal apoptosis</td>
<td>Bax ↓; cleaved caspase-9 ↓; Bcl-2 ↑</td>
<td>Apoptosis ↓</td>
<td>Direction contrasts appropriately with the pro-apoptotic effect observed in many cancer-cell models.</td>
</tr>
</table>











Pathway results for Effect on Cancer / Diseased Cells

NA, unassigned(tgid=0) ⓘ

CES1↓, 1,   Ingr↝, 2,   Ingr?, 2,   NA⇅, 1,   UTF1↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   compI↓, 1,   CYP1A1↓, 2,   H2O2↓, 1,   MDA↓, 1,   OXPHOS↓, 1,   ox-PrxI↑, 1,   ROS↑, 7,   ROS↓, 1,   SOD↓, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 1,   CDC2↓, 1,   CDC25↓, 1,   ETC↓, 1,   mitResp↓, 1,   MMP↓, 8,   MPT↑, 1,   mtDam↑, 3,   PINK1↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

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

Cell Death(tgid=5) ⓘ

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,   p‑JNK↓, 1,   JNK↑, 2,   JNK↝, 1,   MAPK↓, 2,   MAPK↝, 1,   Mcl-1↓, 1,   p27/CDKN1B↑, 1,   p‑p38↓, 1,   p38↑, 1,   Pyro↑, 1,   survivin↓, 3,   TumCD↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 9,   Akt↝, 1,   Akt?, 1,   p‑Akt↓, 4,  

Transcription & Epigenetics(tgid=7) ⓘ

H3K4↓, 1,   other↝, 1,   tumCV↓, 4,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

MitoP↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 4,   DNMT1↓, 1,   P53↑, 4,   cl‑PARP↑, 5,   PARP↑, 1,   PCNA↓, 3,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 3,   CDK4↓, 3,   cycA1/CCNA1↓, 2,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 7,   cycE/CCNE↓, 1,   P21↑, 6,   TumCCA↑, 16,   TumCCA↓, 1,  

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

4E-BP1↓, 1,   CSCs↓, 1,   EMT↓, 3,   p‑ERK↓, 1,   ERK↝, 1,   ERK↓, 1,   FOXO3↓, 1,   HDAC↓, 1,   mTOR↓, 4,   P70S6K↓, 1,   p‑PI3K↓, 3,   PI3K↓, 6,   PI3K↝, 1,   PTEN↓, 1,   PTEN↑, 1,   p‑PTEN↓, 1,   STAT3↓, 5,   TCF↓, 1,   TOPflash↓, 1,   TumCG↓, 10,   TumCG?, 2,  

Migration(tgid=13) ⓘ

CA↓, 1,   Ca+2↑, 3,   CD31/PECAM-1↓, 1,   E-cadherin↑, 3,   Ki-67↓, 5,   miR-148a↑, 1,   MMP2↓, 4,   MMP7↓, 5,   MMP9↑, 1,   MMP9↓, 6,   N-cadherin↓, 1,   p‑PKCδ↓, 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,   TumCP↓, 13,   TumMeta↓, 2,   uPA↓, 1,   UroPA↓, 1,   Vim↓, 1,   vinculin↓, 1,   β-catenin/ZEB1↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 3,   p‑EGFR↓, 1,   Hif1a↓, 2,   VEGF↓, 2,   VEGFR2/KDR/Flk1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   FOXP3↓, 1,   IL1β↓, 1,   IL6↓, 1,   p‑IκB↓, 2,   JAK2↓, 1,   NF-kB↓, 10,   NF-kB↝, 1,   p‑NF-kB↓, 1,   p‑p65↓, 1,   Th17↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

p‑EGFR↓, 1,   IL6↓, 1,   Ki-67↓, 5,   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,  
Total Targets: 190

Pathway results for Effect on Normal Cells

NA, unassigned(tgid=0) ⓘ

AIF1/Iba-1↓, 1,   Aβ42↓, 1,   CHRM1↑, 1,   GFAP↓, 2,   Learn↑, 1,   NeuroI↓, 2,   SYN1↑, 1,   SYP↑, 1,   SYT1↑, 1,   ULK1/ATG1↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 8,   ARE↑, 1,   Catalase↑, 2,   CYP1A1↓, 1,   CYP2E1↓, 1,   GPx↑, 1,   GSH↑, 1,   MDA↓, 1,   NRF2↑, 2,   ROS↓, 4,   ROS↑, 1,   SOD↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   cAMP↑, 1,   CREB↑, 1,   CYP2C6↓, 1,   glucose↓, 1,   LDH↓, 1,   PPARγ↓, 1,   PPARγ↑, 2,  

Cell Death(tgid=5) ⓘ

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

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

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

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1/ATG6↑, 1,   LC3II↑, 1,   p62↓, 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) ⓘ

ERK↓, 1,   GSK‐3β↓, 1,   GSK‐3β↑, 1,   IGF-1↑, 1,   mTOR↑, 1,  

Migration(tgid=13) ⓘ

AntiAg↑, 2,   PKA↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   NO↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

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

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↑, 1,   AChE↓, 1,   BDNF↑, 2,   PSD95?, 1,   p‑tau↓, 1,   tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,   Aβ↓, 3,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,   BioAv↝, 3,   BioAv↑, 2,   Dose↝, 2,   Dose?, 1,   eff↑, 2,   Half-Life↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

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

Functional Outcomes(tgid=23) ⓘ

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

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 6,  
Total Targets: 103

Research papers

Year Title Authors PMID Link Flag
2025Honokiol-Magnolol-Baicalin Possesses Synergistic Anticancer Potential and Enhances the Efficacy of Anti-PD-1 Immunotherapy in Colorectal Cancer by Triggering GSDME-Dependent PyroptosisQuan GaoPMC11967828https://pmc.ncbi.nlm.nih.gov/articles/PMC11967828/0
2024Honokiol Is More Potent than Magnolol in Reducing Head and Neck Cancer Cell GrowthRobert Kleszcz—https://www.mdpi.com/1467-3045/46/10/6370
2018Modulation of Rat Hepatic CYP1A and 2C Activity by Honokiol and Magnolol: Differential Effects on Phenacetin and Diclofenac Pharmacokinetics In VivoSang-Bum KimPMC6100004https://pmc.ncbi.nlm.nih.gov/articles/PMC6100004/0
2026Magnolia officinalis Lignans induce apoptosis and epigenetic reprogramming via the miR-148a-3p/DNMT-1/UTF-1 axis in pancreatic cancer cellsJinwon Choi41628692https://pubmed.ncbi.nlm.nih.gov/41628692/0
2026Role of magnolol in gastrointestinal cancers: Recent trends and future perspectivesHardeep Singh Tuli42054835https://pubmed.ncbi.nlm.nih.gov/42054835/0
2026Magnolol nanoparticles combat MRSA by disrupting TCA cycle and arginine metabolism to induce oxidative stress4228496142284961https://pubmed.ncbi.nlm.nih.gov/42284961/0
2026Magnolol as a promising multitarget agent for Alzheimer's disease: Evidence from a systematic evidence synthesis, network pharmacology, and molecular dynamics simulationsYiying Qin42497520https://pubmed.ncbi.nlm.nih.gov/42497520/0
2026Magnolol mitigates neuroinflammation via NF-κB/IL-6/IL-1β pathways in AlCl₃-induced Alzheimer's disease: insights from in-vivo and in-silico investigationsFangyu LinPMC13346411https://pubmed.ncbi.nlm.nih.gov/42427890/0
2025Magnolol and its semi-synthetic derivatives: a comprehensive review of anti-cancer mechanisms, pharmacokinetics, and future therapeutic potentialAsmita RayamajhiPMC12058641https://pmc.ncbi.nlm.nih.gov/articles/PMC12058641/0
2025Mitochondrion-targeted magnolol derivatives exert synergistic anticancer activity by modulating energy metabolism and tumor microenvironmentYing Wang41145083https://pubmed.ncbi.nlm.nih.gov/41145083/0
2025Magnolol facilitates mitochondrial-peroxisome dysfunction and induces oxeiptosis in lung cancer cells following transfer via tunneling nanotubesMeng-Hsuan Cheng40347844https://pubmed.ncbi.nlm.nih.gov/40347844/0
2024Magnolol acts as a neurorestorative agent in an Aβ1‑42‑induced mouse model of Alzheimer's diseaseQian YuPMC11609612https://pmc.ncbi.nlm.nih.gov/articles/PMC11609612/0
2024Magnolol Induces Apoptosis and Suppresses Immune Evasion in Non-small Cell Lung Cancer Xenograft ModelsPo-Ju Lin39348964https://pubmed.ncbi.nlm.nih.gov/39348964/0
2023Magnolol and 5-fluorouracil synergy inhibition of metastasis of cervical cancer cells by targeting PI3K/AKT/mTOR and EMT pathwaysYuanyuan ChenPMC10874772https://pmc.ncbi.nlm.nih.gov/articles/PMC10874772/0
2023Magnolol improves Alzheimer's disease-like pathologies and cognitive decline by promoting autophagy through activation of the AMPK/mTOR/ULK1 pathwayXuechu Wang36889111https://pubmed.ncbi.nlm.nih.gov/36889111/0
2023Evaluating the Magnolol Anticancer Potential in MKN-45 Gastric Cancer CellsMahsa NaghashpourPMC9963572https://pmc.ncbi.nlm.nih.gov/articles/PMC9963572/0
2023Magnolol as STAT3 inhibitor for treating multiple sclerosis by restricting Th17 cellsJian-Yu Chen37301184https://pubmed.ncbi.nlm.nih.gov/37301184/0
2022Magnolol upregulates CHRM1 to attenuate Amyloid-β-triggered neuronal injury through regulating the cAMP/PKA/CREB pathwayGemin Zhu34705126https://pubmed.ncbi.nlm.nih.gov/34705126/0
2022Magnolol as a Potential Anticancer Agent: A Proposed Mechanistic InsightXiaofeng WangPMC9570903https://pmc.ncbi.nlm.nih.gov/articles/PMC9570903/0
2022Magnolol inhibits cancer stemness and IL-6/Stat3 signaling in oral carcinomasChih-Yu Peng33551310https://pubmed.ncbi.nlm.nih.gov/33551310/0
2022Magnolol Induces Apoptosis Through Extrinsic/intrinsic Pathways and Attenuates NF-κB/STAT3 Signaling in Non-small-cell Lung Cancer CellsYang-Cheng Lee35896265https://pubmed.ncbi.nlm.nih.gov/35896265/0
2021Magnolol and Honokiol: Two Natural Compounds with Similar Chemical Structure but Different Physicochemical and Stability PropertiesIris UsachPMC7915353https://pmc.ncbi.nlm.nih.gov/articles/PMC7915353/0
2021Pharmacology, Toxicity, Bioavailability, and Formulation of Magnolol: An UpdateYiping Lin—https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2021.632767/full0
2021Effectiveness of Magnolol, a Lignan from Magnolia Bark, in Diabetes, Its Complications and Comorbidities—A ReviewKatarzyna Szałabska-RąpałaPMC8467064https://pmc.ncbi.nlm.nih.gov/articles/PMC8467064/0
2021Mitochondria-targeted magnolol inhibits OXPHOS, proliferation, and tumor growth via modulation of energetics and autophagy in melanoma cellsGang ChengPMC7883397https://pmc.ncbi.nlm.nih.gov/articles/PMC7883397/0
2021Synergistic effects of autophagy/mitophagy inhibitors and magnolol promote apoptosis and antitumor efficacyYancheng TangPMC8727919https://pmc.ncbi.nlm.nih.gov/articles/PMC8727919/0
2020Magnolol Ameliorates Behavioral Impairments and Neuropathology in a Transgenic Mouse Model of Alzheimer's DiseaseYan-Fang XianPMC7354664https://pmc.ncbi.nlm.nih.gov/articles/PMC7354664/0
2020Pharmacokinetic and Metabolic Profiling of Key Active Components of Dietary Supplement Magnolia officinalis Extract for Prevention against Oral CarcinomaDinh BuiPMC7604171https://pmc.ncbi.nlm.nih.gov/articles/PMC7604171/0
2020Magnolol Attenuates Cisplatin-Induced Muscle Wasting by M2c Macrophage ActivationChanju LeePMC7018987https://pmc.ncbi.nlm.nih.gov/articles/PMC7018987/0
2020The In Vivo Radiosensitizing Effect of Magnolol on Tumor Growth of Hepatocellular CarcinomaYU-SHAN CHENPMC7439903https://pmc.ncbi.nlm.nih.gov/articles/PMC7439903/0
2020Suppression 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 VivoChun-Min SuPMC7278962https://pmc.ncbi.nlm.nih.gov/articles/PMC7278962/0
2020Enhanced Oral Bioavailability of the Pharmacologically Active Lignin Magnolol via Zr-Based Metal Organic Framework ImpregnationJoshua H SantosPMC7285002https://pmc.ncbi.nlm.nih.gov/articles/PMC7285002/0
2020Magnolol Suppresses Pancreatic Cancer Development In Vivo and In Vitro via Negatively Regulating TGF-β/Smad SignalingShuo ChenPMC7738609https://pmc.ncbi.nlm.nih.gov/articles/PMC7738609/0
2020Magnolia extract is effective for the chemoprevention of oral cancer through its ability to inhibit mitochondrial respiration at complex IQi ZhangPMC7140380https://pmc.ncbi.nlm.nih.gov/articles/PMC7140380/0
2020Magnolol alleviates Alzheimer's disease-like pathology in transgenic C. elegans by promoting microglia phagocytosis and the degradation of beta-amyloid through activation of PPAR-γZhishen Xie32000045https://pubmed.ncbi.nlm.nih.gov/32000045/0
20202-O-Methylmagnolol, a Magnolol Derivative, Suppresses Hepatocellular Carcinoma Progression via Inhibiting Class I Histone Deacetylase ExpressionChi-Yuan ChenPMC7431949https://pmc.ncbi.nlm.nih.gov/articles/PMC7431949/0
2019Magnolol induces cell death through PI3K/Akt-mediated epigenetic modifications boosting treatment of BRAF- and NRAS-mutant melanomaAbdullah Al EmranPMC6434221https://pmc.ncbi.nlm.nih.gov/articles/PMC6434221/0
2019Inhibition of human carboxylesterases by magnolol: Kinetic analyses and mechanismYun-Qing Song31170387https://pubmed.ncbi.nlm.nih.gov/31170387/0
2019Induction of apoptosis by magnolol via the mitochondrial pathway and cell cycle arrest in renal carcinoma cellsHaiyan Wen30573364https://pubmed.ncbi.nlm.nih.gov/30573364/0
2019Insights on the Multifunctional Activities of MagnololJianhong Zhang—https://www.researchgate.net/publication/333332570_Insights_on_the_Multifunctional_Activities_of_Magnolol0
2019Magnolol inhibits growth and induces apoptosis in esophagus cancer KYSE-150 cell lines via the MAP kinase pathwayYu ChenPMC6688004https://pmc.ncbi.nlm.nih.gov/articles/PMC6688004/0
2018Magnolol: A Neolignan from the Magnolia Family for the Prevention and Treatment of CancerAbhishek Manoj RanawarePMC6121321https://pmc.ncbi.nlm.nih.gov/articles/PMC6121321/0
2018Safety and Toxicology of Magnolol and HonokiolAndrea Sarrica29925102https://pubmed.ncbi.nlm.nih.gov/29925102/0
2017Magnolol suppresses the proliferation and invasion of cholangiocarcinoma cells via inhibiting the NF-κB signaling pathwayFu-Hui Zhang28779709https://pubmed.ncbi.nlm.nih.gov/28779709/0
2016Metabolic interactions of magnolol with cytochrome P450 enzymes: uncompetitive inhibition of CYP1A and competitive inhibition of CYP2CSang-Bum Kim26133083https://pubmed.ncbi.nlm.nih.gov/26133083/0
2015Magnolol inhibits growth of gallbladder cancer cells through the p53 pathwayMaolan LiPMC4638010https://pmc.ncbi.nlm.nih.gov/articles/PMC4638010/0
2014Magnolol induces apoptosis via caspase-independent pathways in non-small cell lung cancer cellsJong-Rung Tsai23943503https://pubmed.ncbi.nlm.nih.gov/23943503/0
2013Effects of magnolol on impairment of learning and memory abilities induced by scopolamine in miceYang-si Li23445942https://pubmed.ncbi.nlm.nih.gov/23445942/0
2013The natural compound magnolol inhibits invasion and exhibits potential in human breast cancer therapyYing LiuPMC3827615https://pmc.ncbi.nlm.nih.gov/articles/PMC3827615/0
2013Magnolol induces apoptosis in MCF-7 human breast cancer cells through G2/M phase arrest and caspase-independent pathwayYongfeng Zhou24147344https://pubmed.ncbi.nlm.nih.gov/24147344/0
2013Magnolol suppresses hypoxia-induced angiogenesis via inhibition of HIF-1α/VEGF signaling pathway in human bladder cancer cellsMeng-Chuan Chen23416116https://pubmed.ncbi.nlm.nih.gov/23416116/0
2012Magnolol-induced apoptosis in HCT-116 colon cancer cells is associated with the AMP-activated protein kinase signaling pathwayJun Beom Park22975518https://pubmed.ncbi.nlm.nih.gov/22975518/0
2012Wnt/β-catenin signaling mediates the antitumor activity of magnolol in colorectal cancer cellsYou-Jin Kang22550094https://pubmed.ncbi.nlm.nih.gov/22550094/0
2011Anticancer potential of magnolol for lung cancer treatmentJae-Uk Seo21544728https://pubmed.ncbi.nlm.nih.gov/21544728/0
2011Magnolol potently suppressed lipopolysaccharide-induced iNOS and COX-2 expression via downregulating MAPK and NF-κB signaling pathwaysChing-Shu Lai—https://www.sciencedirect.com/science/article/pii/S17564646110004910
2011Pharmacokinetics, bioavailability, and tissue distribution of magnolol following single and repeated dosing of magnolol to ratsShiuan-Pey Lin21638244https://pubmed.ncbi.nlm.nih.gov/21638244/0
2011Effects of magnolol on UVB-induced skin cancer development in mice and its possible mechanism of actionChandeshwari ChilampalliPMC3234292https://pmc.ncbi.nlm.nih.gov/articles/PMC3234292/0
2011Magnolol, a natural compound, induces apoptosis of SGC-7901 human gastric adenocarcinoma cells via the mitochondrial and PI3K/Akt signaling pathwaysAzhar RasulPMC3584565https://pmc.ncbi.nlm.nih.gov/articles/PMC3584565/0
2011Targeting apoptosis pathways in cancer with magnolol and honokiol, bioactive constituents of the bark of Magnolia officinalisH L Xu22466367https://pubmed.ncbi.nlm.nih.gov/22466367/0
2009Magnolol induces apoptosis via activation of both mitochondrial and death receptor pathways in A375-S2 cellsQingjun You20162409https://pubmed.ncbi.nlm.nih.gov/20162409/0
2009Magnolol induces apoptosis via inhibiting the EGFR/PI3K/Akt signaling pathway in human prostate cancer cellsDae-Hee Lee19229860https://pubmed.ncbi.nlm.nih.gov/19229860/0
2007Mechanisms for the magnolol-induced cell death of CGTH W-2 thyroid carcinoma cellsShih-Horng Huang17390340https://pubmed.ncbi.nlm.nih.gov/17390340/0
2002Magnolol suppresses proliferation of cultured human colon and liver cancer cells by inhibiting DNA synthesis and activating apoptosisShyr-Yi Lin11813258https://pubmed.ncbi.nlm.nih.gov/11813258/0
2001Molecular mechanisms of apoptosis induced by magnolol in colon and liver cancer cellsS Y Lin11746819https://pubmed.ncbi.nlm.nih.gov/11746819/0