Compound Monograph
Magnolol
Magnolol is a biphenyl neolignan (biphenol) from the bark of houpu magnolia and the positional isomer of honokiol — a positive allosteric modulator of GABA-A receptors that underlies magnolia bark's traditional calming use, with broad but almost entirely preclinical anti-inflammatory, anticancer, antimicrobial, metabolic and neuroprotective activity.
Sources · 5
Where Does It Come From?
Magnolol is a naturally occurring neolignan (biphenyl biphenol), found in Houpu magnolia, Japanese magnolia and 3 other sources. It is well tolerated orally (low toxicity).
Concentration
Content by Source
Reported concentrations across the plants that contain magnolol — the bar marks the typical level, the line shows the reported range.
Literature figures for varying plant parts and preparations. Read them as a comparative guide, not exact assays.
Magnolol at a Glance
Magnolol is a biphenyl neolignan (a biphenol, 5,5’-diallyl-2,2’-dihydroxybiphenyl) and one of the two signature bioactive constituents of the bark of magnolia — Magnolia officinalis (Chinese houpu) and the Japanese M. obovata. Magnolia bark has a long history in Chinese and Kampo medicine for digestive complaints, low mood and anxiety, and magnolol is the marker used to standardise commercial extracts.
Its most mechanistically coherent activity is calming: magnolol is a positive allosteric modulator of GABA-A receptors, the same broad target family that benzodiazepines and alcohol act on, which gives a plausible molecular basis for magnolia’s traditional sedative and anxiolytic use 1,
Magnolol is the positional isomer of honokiol — the two differ only in where the allyl and hydroxyl groups sit on the biphenyl, they co-occur in the same bark, and they are almost always discussed as a pair. Toxicity appears low, with the practical caution being additive sedation with other CNS depressants, given the GABA-A mechanism 21Reference 21Safety and Toxicology of Magnolol and HonokiolView study →.
Magnolol vs. Honokiol
Magnolol and honokiol are constitutional (positional) isomers: both are diallyl-dihydroxybiphenyls with the formula C18H18O2, differing only in the positions of the two allyl and two hydroxyl substituents on the biphenyl scaffold. Magnolol is the symmetric 5,5’-diallyl-2,2’-dihydroxybiphenyl; honokiol carries its groups asymmetrically. They occur together in magnolia bark, magnolol usually the more abundant of the two (~2–11% vs. ~1–5% of dry bark), and their ratio shifts with species, provenance and extraction 21Reference 21Safety and Toxicology of Magnolol and HonokiolView study →.
Functionally they overlap heavily — both are GABA-A positive allosteric modulators 1Reference 1The natural products magnolol and honokiol are positive allosteric modulators of both synaptic and extra-synaptic GABA(A) receptorsView study →, both are anti-inflammatory, anticancer and neuroprotective in preclinical models, and much of the “magnolia bark” literature tests them together or as a fixed mix. Where the classic behavioural anxiolytic signal in Kampo formulas was attributed specifically to honokiol 4Reference 4The anxiolytic effect of two oriental herbal drugs in Japan attributed to honokiol from magnolia barkView study →, magnolol’s distinguishing threads are its PPARγ agonism / metabolic activity 10,
What It's Used For
Magnolol’s preclinical profile is genuinely broad, but the compound-page discipline is the load-bearing caveat: nearly all of it is in-vitro or rodent work on the isolated molecule, and the human evidence that exists belongs to whole magnolia-bark blends rather than pure magnolol 13,
Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. Human data are for whole-bark blends, not the isolate, so isolate scores stay modest by design.
Magnolol’s best-characterised molecular action and the mechanism behind magnolia’s calming reputation. In recombinant-receptor electrophysiology, magnolol (with honokiol) is a positive allosteric modulator of both synaptic and extrasynaptic GABA-A receptors, potentiating GABA-evoked currents — and, unlike benzodiazepines, it also acts at δ-subunit-containing extrasynaptic receptors 1Reference 1The natural products magnolol and honokiol are positive allosteric modulators of both synaptic and extra-synaptic GABA(A) receptorsView study →; medicinal-chemistry work has since built more potent GABA-A potentiators on the magnolol/honokiol scaffold 2Reference 2Structural analogues of the natural products magnolol and honokiol as potent allosteric potentiators of GABA(A) receptorsView study →.
Behaviourally, magnolol reduces depressive-like behaviour in chronically stressed mice, alongside lowered neuroinflammation and oxidative stress 3Reference 3AnimalMagnolol abrogates chronic mild stress-induced depressive-like behaviors by inhibiting neuroinflammation and oxidative stress in the prefrontal cortex of miceView study →, while the classic elevated-plus-maze anxiolytic signal in magnolia-containing Kampo formulas was attributed to the isomer honokiol 4Reference 4The anxiolytic effect of two oriental herbal drugs in Japan attributed to honokiol from magnolia barkView study →.
Gap: the GABA-A pharmacology is isolate/in-vitro, and the strongest behavioural anxiolytic data are for honokiol or whole-bark blends rather than isolated magnolol; there are no controlled human anxiety trials of the pure molecule 1,
A well-replicated isolate signal. In macrophage-like cells stimulated with Porphyromonas gingivalis fimbriae, magnolol inhibited COX-2 expression and NF-κB activation more effectively than eugenol, marking NF-κB suppression as a core anti-inflammatory route 5Reference 5AnimalComparative inhibitory effects of magnolol, honokiol, eugenol and bis-eugenol on cyclooxygenase-2 expression and nuclear factor-kappa B activation in RAW264.7 macrophage-like cells stimulated with fimbriae of Porphyromonas gingivalisView study →; in vivo, magnolol reduced neuroinflammation and oxidative stress in the prefrontal cortex of chronically stressed mice 3Reference 3AnimalMagnolol abrogates chronic mild stress-induced depressive-like behaviors by inhibiting neuroinflammation and oxidative stress in the prefrontal cortex of miceView study →. This NF-κB/COX-2 axis recurs across magnolol’s anticancer and neuroprotective work, making it a unifying mechanism rather than an isolated finding.
Gap: predominantly in-vitro macrophage and rodent models; no human anti-inflammatory trials of isolated magnolol, and the concentrations used often exceed plausible plasma levels given its poor oral bioavailability 5,
Magnolol’s most distinctive thread versus honokiol. It was identified as a PPARγ agonist by pharmacophore-based virtual screening and confirmed in reporter and cell assays 10Reference 10Computer-aided discovery, validation, and mechanistic characterization of novel neolignan activators of peroxisome proliferator-activated receptor gammaView study →, enhances adipocyte differentiation and insulin-independent glucose uptake in 3T3-L1 cells 11Reference 11Magnolol enhances adipocyte differentiation and glucose uptake in 3T3-L1 cellsView study →, and in high-fat-diet/streptozotocin diabetic rats improved hyperglycaemia and hyperlipidaemia while reducing hepatic oxidative stress and CYP2E1 activity 12Reference 12AnimalThe antidiabetic and hepatoprotective effects of magnolol on diabetic rats induced by high-fat diet and streptozotocinView study →; a dedicated review compiles its activity across diabetes and its complications 13Reference 13ReviewEffectiveness of Magnolol, a Lignan from Magnolia Bark, in Diabetes, Its Complications and Comorbidities—A ReviewView study →.
Gap: cell and rodent data only, with no human glycaemic trials of the isolate; PPARγ agonism also raises the theoretical class concerns (fluid retention, adipogenesis) that would need human characterisation 10,
The largest preclinical literature on the molecule, and the one most in need of caveats. Reviews compile magnolol acting across multiple hallmark pathways — inducing apoptosis and cell-cycle arrest, inhibiting proliferation, angiogenesis, invasion and metastasis, and modulating NF-κB, PI3K/Akt/mTOR, EGFR and other signalling — in a wide range of cancer cell lines and xenografts 6,
Gap: entirely preclinical (cell lines and rodent xenografts); there are no clinical oncology trials of magnolol, and the effective in-vitro concentrations are far above anything its oral pharmacokinetics could achieve systemically 6,
A focused, plausibly topically-relevant activity. Magnolol (with honokiol) is bactericidal against periodontopathic microorganisms from magnolia stem bark 9Reference 9Antimicrobial activity of magnolol and honokiol against periodontopathic microorganismsView study →, and comparative in-vitro work shows both neolignans inhibit oral pathogens and pro-inflammatory macrophage responses — supporting interest in magnolia extracts for oral care and caries/periodontal applications 8Reference 8In vitroIn vitro antimicrobial and antipro-inflammation potential of honokiol and magnolol against oral pathogens and macrophagesView study →.
Gap: in-vitro MIC-level and macrophage data; this is relevant to local oral exposure (mouthwash/lozenge-type contact), not a systemic antibiotic claim, and human clinical confirmation is limited 8,
A consistent rodent signal tied to magnolol’s antioxidant and anti-inflammatory action. In MPTP/MPP⁺ Parkinson’s-disease models magnolol protected dopaminergic neurons by inhibiting oxidative stress, in vivo and in vitro 14Reference 14In vitroMagnolol Protects against MPTP/MPP(+)-Induced Toxicity via Inhibition of Oxidative Stress in In Vivo and In Vitro Models of Parkinson’s DiseaseView study →, and in an Aβ1-42-induced Alzheimer’s mouse model it acted as a neurorestorative agent, improving cognition and pathology 15Reference 15AnimalMagnolol acts as a neurorestorative agent in an Aβ1-42-induced mouse model of Alzheimer’s diseaseView study →.
Its ability to cross the blood-brain barrier (see Pharmacokinetics) makes CNS activity mechanistically plausible 17Reference 17AnimalPharmacokinetics and brain distribution of magnolol in the rat after intravenous bolus injectionView study →.
Gap: rodent neurodegeneration models only; no human neuroprotection or cognition trials of isolated magnolol 14,
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| GABA-A receptor (synaptic + extrasynaptic, incl. δ-subunit) | positive allosteric modulation — potentiates GABA-evoked chloride currents (benzodiazepine-independent site) | anxiolytic / sedative; sedative interaction |
| NF-κB / IKK signalling | suppression of NF-κB-driven inflammatory transcription | anti-inflammatory; anticancer; neuroprotection |
| Cyclo-oxygenase-2 (COX-2) | reduced COX-2 expression in stimulated macrophages | anti-inflammatory |
| PPARγ | agonist — drives adipocyte differentiation and insulin-sensitising gene programme | metabolic / antidiabetic |
| Glucose transport (adipocyte) | increased insulin-independent glucose uptake | metabolic |
| Reactive oxygen species / oxidative stress | radical scavenging; ↓ lipid peroxidation; Nrf2-type antioxidant support | neuroprotection; antioxidant |
| Apoptosis / cell-cycle & PI3K-Akt-mTOR, EGFR | pro-apoptotic, anti-proliferative, anti-metastatic (cell/xenograft) | anticancer |
| CB1/CB2 cannabinoid receptors (via the metabolite tetrahydromagnolol) | metabolite is a cannabinoid-receptor ligand — relevant to sedation/misuse discussion | pharmacokinetics; safety |
The load-bearing mechanism is GABA-A potentiation: it ties the molecule to magnolia’s traditional calming use and to the one interaction that matters clinically (additive CNS depression). The anti-inflammatory NF-κB/oxidative axis then recurs through the anticancer and neuroprotective work.
Pharmacokinetics
Magnolol is lipophilic and poorly water-soluble, which shapes its whole PK story. After oral dosing in rats its absolute oral bioavailability is low — extensive first-pass glucuronidation in both liver and intestine, by several UDP-glucuronosyltransferase isoforms, is the dominant metabolic fate 16,
Clinical Trials
There are no substantial controlled efficacy trials of isolated magnolol. The human evidence attached to magnolia bark is for whole-bark preparations and blends — most prominently the proprietary M. officinalis + Phellodendron amurense combination (Relora) studied for stress, cortisol and sleep — within which magnolol is one of several actives and cannot be isolated 21Reference 21Safety and Toxicology of Magnolol and HonokiolView study →.
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| None for the isolate (human data are magnolia-bark blends, e.g. Relora) | — | — | Extensive: GABA-A, anti-inflammatory, anticancer, metabolic, neuroprotective |
Last checked: July 2026.
How Magnolol Works
Magnolol’s varied effects collapse onto a small number of molecular actions, applied in different tissues.
GABA-A Potentiation
The central CNS mechanism: magnolol binds GABA-A receptors at a site distinct from the benzodiazepine site and acts as a positive allosteric modulator, increasing GABA-evoked inhibitory currents at both synaptic and δ-subunit extrasynaptic receptors 1Reference 1The natural products magnolol and honokiol are positive allosteric modulators of both synaptic and extra-synaptic GABA(A) receptorsView study →. This is the molecular correlate of magnolia’s sedative/anxiolytic reputation and the basis of the additive-sedation caution.
NF-κB & COX-2 Suppression
Across inflammatory, cancer and neurodegeneration models, magnolol repeatedly inhibits NF-κB activation and COX-2 expression, damping pro-inflammatory transcription 3,
PPARγ Agonism
Magnolol binds and activates PPARγ, the nuclear receptor targeted by thiazolidinedione antidiabetics, driving adipocyte differentiation and an insulin-sensitising programme — the mechanistic root of its metabolic effects 10,
Antioxidant / Anti-Aβ Action
In neuroprotection models magnolol lowers reactive oxygen species and lipid peroxidation and counters Aβ-associated pathology, consistent with a radical-scavenging biphenol acting on oxidative and inflammatory stress together 14,
Isolate vs. Plant Studies
This is the crux of the magnolol file. The mechanistic and behavioural work is overwhelmingly the isolated molecule in cells and rodents — the GABA-A electrophysiology 1,
The human evidence, by contrast, is whole-bark. Controlled trials are for magnolia-bark preparations and the M. officinalis + Phellodendron blend, not purified magnolol 21Reference 21Safety and Toxicology of Magnolol and HonokiolView study →, and because magnolol and honokiol co-occur and are usually tested together, extract effects cannot be assigned to magnolol alone. Compounding this, its low oral bioavailability means the plasma exposure achievable from oral magnolia is far below the concentrations used in most in-vitro assays 16,
Prevalence in Nature
Magnolol is largely restricted to the genus Magnolia (family Magnoliaceae), where it is concentrated in the bark. Its principal sources are the traditional medicinal barks: Magnolia officinalis (Chinese houpu/hou po) and the Japanese M. obovata, with reports also from M. grandiflora and M. dealbata 21Reference 21Safety and Toxicology of Magnolol and HonokiolView study →. In dry M. officinalis bark magnolol runs roughly 2–11%, making it usually the more abundant of the two signature biphenyl neolignans, with honokiol at about 1–5%; the ratio and absolute content vary markedly with species, geographic provenance, bark type (stem vs. root) and extraction method 21Reference 21Safety and Toxicology of Magnolol and HonokiolView study →. Commercial “magnolia bark extracts” are standardised to magnolol (and honokiol) at far higher percentages than the raw bark.
Magnolol belongs to the broader lignan / neolignan family of plant phenylpropanoid dimers — kin to the furanoid and dibenzylbutane lignans such as pinoresinol, sesamin and syringaresinol — but its biphenyl (biaryl) skeleton and near-exclusive occurrence in magnolia bark set it apart from those more widely distributed lignans.
Discovery & Synthesis
Magnolol was isolated from the bark of Magnolia officinalis by early-twentieth-century Japanese natural-products chemistry, as investigators sought the active principle of houpu (Chinese) / wa-koboku (Japanese) magnolia bark, a staple of Kampo medicine; its name derives directly from the genus Magnolia. Structurally it was established as a symmetric biphenol — 5,5’-diallyl-2,2’-dihydroxybiphenyl — and recognised as the positional isomer of the co-occurring honokiol 21Reference 21Safety and Toxicology of Magnolol and HonokiolView study →.
Because magnolol is a simple, symmetric diallyl-biphenyldiol, it is synthetically accessible by oxidative or metal-catalysed biaryl coupling of allyl-substituted phenols, but there is little commercial incentive to make it: manufacture today is overwhelmingly by extraction from magnolia bark, which is abundant, inexpensive and the natural co-source of honokiol, followed by chromatographic purification and standardisation of the extract.
Patents: not yet researched.
Toxicity & Safety
Magnolol carries a low toxicity flag. Magnolia bark and its neolignans have a long record of traditional and dietary-supplement use, and a dedicated safety-and-toxicology review of magnolol and honokiol found them generally well tolerated in the available preclinical and human-exposure data, supporting their use as flavour/functional ingredients within reasonable limits 21Reference 21Safety and Toxicology of Magnolol and HonokiolView study →. The practical concerns are pharmacological rather than organ-toxic.
The load-bearing caution is additive central sedation. Because magnolol is a GABA-A positive allosteric modulator 1Reference 1The natural products magnolol and honokiol are positive allosteric modulators of both synaptic and extra-synaptic GABA(A) receptorsView study →, it can in principle compound the effects of alcohol, benzodiazepines and other CNS depressants — the same logic that explains its calming action also flags the interaction. Its active metabolite tetrahydromagnolol has GABAergic and cannabinoid-receptor activity, which is why a formal discussion of the misuse potential of magnolia compounds/metabolites exists in the literature, though this concerns concentrated products rather than culinary exposure 19,
Pregnancy/lactation is a per-herb / per-supplement decision and is not adjudicated on this molecule page; dedicated human reproductive data for isolated magnolol are limited, and no isolate-specific verdict is issued here.
- Low intrinsic toxicity. Magnolol and honokiol are generally well tolerated in preclinical and human-exposure data, with a long history of traditional and dietary use 21Reference 21Safety and Toxicology of Magnolol and HonokiolView study →.
- Additive sedation. As a GABA-A positive allosteric modulator, magnolol can compound alcohol, benzodiazepines and other CNS depressants 1Reference 1The natural products magnolol and honokiol are positive allosteric modulators of both synaptic and extra-synaptic GABA(A) receptorsView study →.
- Metabolite activity. The metabolite tetrahydromagnolol has GABAergic/cannabinoid activity; a misuse-potential discussion exists for concentrated magnolia products 19,
20Reference 19The natural product magnolol as a lead structure for the development of potent cannabinoid receptor agonistsView study →Reference 20Is there a potential of misuse for Magnolia officinalis compounds/metabolites? Human Psychopharmacology. https://pubmed.ncbi.nlm.nih.gov/28517911/View study → . - Human data are the blend, not the isolate. Most controlled safety/efficacy data are for magnolia-bark blends (e.g. Relora), and isolate-specific human interaction/reproductive data are limited 21Reference 21Safety and Toxicology of Magnolol and HonokiolView study →.
Dosage
There is no established or recommended human dose for isolated magnolol. Cited efficacy figures in the literature are preclinical rodent research doses and are not convertible to human self-dosing, and the molecule’s low oral bioavailability further limits read-across from those studies 16,
Real-world human exposure is through magnolia bark itself:
- Magnolia-bark tea and decoction (traditional Kampo/TCM preparations)
- Magnolia-bark tincture
- Standardised magnolia-bark extract capsules (marker-standardised to magnolol/honokiol)
- Proprietary blends such as Relora (M. officinalis + Phellodendron amurense), the source of most controlled human data 21Reference 21Safety and Toxicology of Magnolol and HonokiolView study →
These are doses studied in research and traditional preparations, and are not a personal recommendation.
References
- Alexeev M, Grosenbaugh DK, Mott DD, Fisher JL (2012). The natural products magnolol and honokiol are positive allosteric modulators of both synaptic and extra-synaptic GABA(A) receptors. Neuropharmacology. https://pubmed.ncbi.nlm.nih.gov/22445602/
- Fuchs A, Baur R, Schoeder C, Sigel E, Müller CE (2014). Structural analogues of the natural products magnolol and honokiol as potent allosteric potentiators of GABA(A) receptors. Bioorganic & Medicinal Chemistry. https://pubmed.ncbi.nlm.nih.gov/25456080/
- Cheng J, Dong S, Yi L, Geng D, Liu Q (2018). Magnolol abrogates chronic mild stress-induced depressive-like behaviors by inhibiting neuroinflammation and oxidative stress in the prefrontal cortex of mice. International Immunopharmacology. https://pubmed.ncbi.nlm.nih.gov/29627576/
- Kuribara H, Kishi E, Hattori N, Okada M, Maruyama Y (2000). The anxiolytic effect of two oriental herbal drugs in Japan attributed to honokiol from magnolia bark. Journal of Pharmacy and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/11186252/
- Murakami Y, Kawata A, Seki Y, Koh T, Yuhara K, Maruyama T, Machino M, Ito S, Kadoma Y, Fujisawa S (2012). Comparative inhibitory effects of magnolol, honokiol, eugenol and bis-eugenol on cyclooxygenase-2 expression and nuclear factor-kappa B activation in RAW264.7 macrophage-like cells stimulated with fimbriae of Porphyromonas gingivalis. In Vivo. https://pubmed.ncbi.nlm.nih.gov/23160676/
- Ranaware AM, Banik K, Deshpande V, Padmavathi G, Roy NK, Sethi G, Fan L, Kumar AP, Kunnumakkara AB (2018). Magnolol: A Neolignan from the Magnolia Family for the Prevention and Treatment of Cancer. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/30103472/
- Wang X, Liu Q, Fu Y, Ding RB, Qi X, Zhou X, Sun Z, Bao J (2022). Magnolol as a Potential Anticancer Agent: A Proposed Mechanistic Insight. Molecules. https://pubmed.ncbi.nlm.nih.gov/36234977/
- Chiu KC, Shih YH, Wang TH, Lan WC, Li PJ, Jhuang HS, Hsia SM, Shen YW, Chen MYC, Shieh TM (2021). In vitro antimicrobial and antipro-inflammation potential of honokiol and magnolol against oral pathogens and macrophages. Journal of the Formosan Medical Association. https://pubmed.ncbi.nlm.nih.gov/32978046/
- Chang B, Lee Y, Ku Y, Bae K, Chung C (1998). Antimicrobial activity of magnolol and honokiol against periodontopathic microorganisms. Planta Medica. https://pubmed.ncbi.nlm.nih.gov/9619121/
- Fakhrudin N, Ladurner A, Atanasov AG, Heiss EH, Baumgartner L, Markt P, Schuster D, Ellmerer EP, Wolber G, Rollinger JM, Stuppner H, Dirsch VM (2010). Computer-aided discovery, validation, and mechanistic characterization of novel neolignan activators of peroxisome proliferator-activated receptor gamma. Molecular Pharmacology. https://pubmed.ncbi.nlm.nih.gov/20064974/
- Choi SS, Cha BY, Lee YS, Yonezawa T, Teruya T, Nagai K, Woo JT (2009). Magnolol enhances adipocyte differentiation and glucose uptake in 3T3-L1 cells. Life Sciences. https://pubmed.ncbi.nlm.nih.gov/19376135/
- Wang JJ, Zhao R, Liang JC, Chen Y (2014). The antidiabetic and hepatoprotective effects of magnolol on diabetic rats induced by high-fat diet and streptozotocin. Acta Pharmaceutica Sinica (Yao Xue Xue Bao). https://pubmed.ncbi.nlm.nih.gov/24974464/
- Szałabska-Rąpała K, Borymska W, Kaczmarczyk-Sedlak I (2021). Effectiveness of Magnolol, a Lignan from Magnolia Bark, in Diabetes, Its Complications and Comorbidities—A Review. International Journal of Molecular Sciences. https://doi.org/10.3390/ijms221810050
- Muroyama A, Fujita A, Lv C, Kobayashi S, Fukuyama Y, Mitsumoto Y (2012). Magnolol Protects against MPTP/MPP(+)-Induced Toxicity via Inhibition of Oxidative Stress in In Vivo and In Vitro Models of Parkinson’s Disease. Parkinson’s Disease. https://pubmed.ncbi.nlm.nih.gov/22655218/
- Yu Q, Shi Y, Wu Y, Liu R, Zhang H, Wu L, Ding M (2025). Magnolol acts as a neurorestorative agent in an Aβ1-42-induced mouse model of Alzheimer’s disease. Experimental and Therapeutic Medicine. https://pubmed.ncbi.nlm.nih.gov/39624588/
- Lin SP, Tsai SY, Lee Chao PD, Chen YC, Hou YC (2011). Pharmacokinetics, bioavailability, and tissue distribution of magnolol following single and repeated dosing of magnolol to rats. Planta Medica. https://pubmed.ncbi.nlm.nih.gov/21638244/
- Tsai TH, Chou CJ, Chen CF (1996). Pharmacokinetics and brain distribution of magnolol in the rat after intravenous bolus injection. Journal of Pharmacy and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/8722496/
- Zhu L, Ge G, Zhang H, Liu H, He G, Liang S, Zhang Y, Fang Z, Dong P, Finel M, Yang L (2012). Characterization of hepatic and intestinal glucuronidation of magnolol: application of the relative activity factor approach to decipher the contributions of multiple UDP-glucuronosyltransferase isoforms. Drug Metabolism and Disposition. https://pubmed.ncbi.nlm.nih.gov/22180045/
- Fuchs A, Rempel V, Müller CE (2013). The natural product magnolol as a lead structure for the development of potent cannabinoid receptor agonists. PLoS One. https://pubmed.ncbi.nlm.nih.gov/24204944/
- Schifano F, Guarino V, Papanti DG, Baccarin J, Orsolini L, Corkery JM (2017). Is there a potential of misuse for Magnolia officinalis compounds/metabolites? Human Psychopharmacology. https://pubmed.ncbi.nlm.nih.gov/28517911/
- Sarrica A, Kirika N, Romeo M, Salmona M, Diomede L (2018). Safety and Toxicology of Magnolol and Honokiol. Planta Medica. https://pubmed.ncbi.nlm.nih.gov/29925102/
