Hermetica Superfood Encyclopedia
The Short Answer
Morusin is a prenylated flavonoid derived from the root bark of Morus alba (white mulberry) that exerts its primary biological effects through inhibition of the NF-κB signaling pathway and induction of mitochondria-dependent apoptosis. Current research is limited to preclinical and in vitro models, with no established human clinical trials confirming its efficacy or safe dosing range.
CategoryNamed Bioactive Compounds
GroupCompound
Evidence LevelModerate
Primary Keywordmorusin benefits
Synergy Pairings3
Morusin — botanical close-up
Health Benefits
Origin & History
Natural habitat
Morusin is a prenylated flavonoid primarily extracted from the root bark of mulberry trees (Morus alba and related species) using organic solvents. The compound's prenyl groups enhance its lipophilicity and cellular membrane interaction compared to non-prenylated flavonoids.
“The research sources do not specify any historical or traditional medicinal uses of isolated morusin. The compound is referenced only as a modern phytochemical discovery from mulberry species.”Traditional Medicine
Scientific Research
No human clinical trials, RCTs, or meta-analyses have been conducted on morusin. All available evidence comes from preclinical studies including cell lines (breast cancer MCF-7/MDA-MB-231, PMID: 28599457; prostate DU145/PC3, PMID: 25628938) and animal models, with significant pharmacokinetic barriers preventing human translation.
Preparation & Dosage
Traditional preparation
No clinically studied human dosages exist. Preclinical studies used 0.1-10 mM for in vitro assays, 20 mg/kg in animal seizure models, and 6.72-13.45 μg/ml for antimicrobial effects. Consult a healthcare provider before starting any new supplement.
Nutritional Profile
Morusin is a prenylated flavonoid (molecular formula C₂₀H₁₈O₅, MW 338.35 g/mol) isolated primarily from the root bark of Morus alba (white mulberry). It is not a conventional nutritional compound and contains no meaningful macronutrient, vitamin, mineral, or fiber content as an isolated bioactive. As a pure compound, it is typically studied at microgram-to-milligram dosages (effective preclinical doses range from 5–20 mg/kg in animal models). Its primary bioactive identity lies in its prenylated flavone scaffold, which confers lipophilicity (LogP approximately 3.8), contributing to moderate membrane permeability but poor aqueous solubility (~0.5 μg/mL in water). Oral bioavailability is substantially limited due to rapid hepatic metabolism, low water solubility, and P-glycoprotein efflux; nanoparticle formulations and lipid-based delivery systems have been explored preclinically to improve absorption. No established dietary reference intake or therapeutic dosage exists for human use. Concentrations in Morus alba root bark extracts typically range from 0.02–0.15% dry weight depending on extraction method.
How It Works
Mechanism of Action
Morusin suppresses inflammatory signaling by blocking IκB kinase (IKK) phosphorylation, thereby preventing nuclear translocation of NF-κB p65 and reducing downstream cytokine production including TNF-α and IL-6. In cancer cell lines, morusin activates the intrinsic apoptotic pathway by upregulating pro-apoptotic proteins Bax and cleaved caspase-3 while downregulating anti-apoptotic Bcl-2, and induces G2/M cell cycle arrest through inhibition of cyclin B1 and CDK1 expression. Its antimicrobial activity against Mycobacterium tuberculosis strains is attributed to disruption of mycobacterial cell wall biosynthesis, with recorded minimum inhibitory concentration (MIC) values of 6.72–13.45 μg/ml in vitro.
Clinical Evidence
All current evidence for morusin derives from in vitro cell culture studies and rodent animal models, with zero published randomized controlled trials or human pharmacokinetic studies as of 2024. In vitro studies across multiple cancer cell lines, including HeLa, MCF-7, and HepG2, have demonstrated IC50 values in the low micromolar range (typically 5–20 μM) for cytotoxic activity, but these concentrations have not been validated in human plasma. Anti-inflammatory rodent models using lipopolysaccharide (LPS)-induced inflammation showed reduced serum TNF-α and IL-1β following morusin administration, though doses, bioavailability, and metabolic conversion were not standardized across studies. The overall evidence is preliminary and insufficient to support any therapeutic claims in humans.
Safety & Interactions
No human safety data, maximum tolerated dose, or established adverse event profile exists for morusin supplementation due to the complete absence of human clinical trials. In vitro data suggests morusin may inhibit cytochrome P450 enzymes, particularly CYP3A4 and CYP2C9, which could theoretically alter the metabolism of co-administered drugs such as statins, anticoagulants, and immunosuppressants, though this has not been confirmed in vivo. Morusin's potent pro-apoptotic activity in proliferating cells raises theoretical concern for use during pregnancy, and it should be avoided by pregnant or breastfeeding individuals until safety is established. Individuals taking anticoagulants, chemotherapy agents, or immunosuppressive drugs should consult a physician before use due to uncharacterized interaction risks.
Synergy Stack
Hermetica Formulation Heuristic
Also Known As
prenylated flavonoid from Morus albamulberry root bark flavonoidMorus alba prenylated compoundmorusin flavonoidmulberry prenylated flavonoid
Frequently Asked Questions
What plant does morusin come from?
Morusin is isolated primarily from the root bark of Morus alba, commonly called white mulberry, a plant used extensively in traditional Chinese medicine. It belongs to the prenylated flavonoid subclass and is also found in smaller concentrations in other Morus species such as Morus nigra and Morus rubra.
Does morusin have anticancer properties?
Preclinical in vitro studies demonstrate that morusin induces apoptosis in multiple cancer cell lines, including breast (MCF-7), cervical (HeLa), and liver (HepG2) cells, with IC50 values typically in the 5–20 μM range. The mechanism involves upregulation of Bax, activation of caspase-3, and downregulation of Bcl-2, alongside G2/M cell cycle arrest via CDK1 and cyclin B1 suppression. No human clinical trials have been conducted, so these findings cannot be extrapolated to cancer treatment in people.
Can morusin fight tuberculosis?
In vitro studies have shown morusin exhibits antimycobacterial activity against Mycobacterium tuberculosis strains with minimum inhibitory concentration (MIC) values ranging from 6.72 to 13.45 μg/ml, which is considered moderate activity in laboratory settings. These results have not been replicated in animal infection models or human trials, and morusin should not be considered an alternative or adjunct to established tuberculosis antibiotics such as rifampicin or isoniazid.
What is the recommended dosage of morusin?
There is currently no established or clinically validated dosage for morusin in humans, as no pharmacokinetic or dose-escalation studies have been conducted in human subjects. Animal studies have used widely varying doses without standardization, and commercially available supplements listing morusin have not undergone regulatory review for dosing guidance. Until human trials are completed, any dosage recommendation would be speculative and potentially unsafe.
How does morusin reduce inflammation?
Morusin inhibits inflammation primarily by blocking phosphorylation of IκB kinase (IKK), which prevents the release and nuclear translocation of transcription factor NF-κB p65. This suppression reduces transcription of pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6, as demonstrated in LPS-stimulated macrophage cell lines and rodent inflammatory models. These effects are preclinical only, and no human data confirm this mechanism translates to a measurable anti-inflammatory benefit in clinical settings.
What does the current research evidence tell us about morusin's safety and effectiveness in humans?
Most research on morusin remains in preclinical stages, consisting of laboratory and animal studies rather than human clinical trials. While animal models show promise for neuroprotective effects (at 20 mg/kg in seizure studies) and antimicrobial activity in vitro, these results cannot be directly translated to human dosing or efficacy. Human safety data and clinical efficacy data are currently lacking, making it premature to make definitive health claims based on existing evidence.
Are there any known drug interactions or safety concerns with morusin supplementation?
No well-documented drug interactions with morusin have been established in the scientific literature, primarily because human clinical studies are limited. However, given its mechanism of action through NF-κB pathway inhibition, theoretical interactions with anti-inflammatory medications or immunosuppressants are possible and warrant caution. Anyone considering morusin supplementation, especially those on medications, should consult with a healthcare provider before use.
Which supplement forms of morusin are available, and how does the form affect absorption?
Morusin is typically available as an isolated compound in powder or capsule form, though standardized extracts from its source plant may also contain it in combination with other bioactives. Information on the comparative bioavailability of different morusin forms in humans is not currently available in published research. Absorption may be influenced by factors such as fat intake and individual digestive variation, but specific pharmacokinetic data in humans remains lacking.
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