| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| Other Sizes |
| Targets |
- In antifungal activity studies, Magnoflorine exhibits inhibitory effects on Candida species (including Candida albicans, Candida tropicalis, Candida krusei), but no specific molecular target (e.g., enzyme/receptor) or affinity data (IC50/Ki) were reported[1]
- In pro-inflammatory response regulation, Magnoflorine acts via the MyD88-dependent signaling pathway (involved in TLR4-mediated inflammation), but no direct binding affinity to MyD88 or downstream proteins (e.g., NF-κB, MAPK) was provided[2] Magnoflorine chloride targets multiple biological pathways including inflammatory signaling and oxidative stress-responsive pathways. The compound exhibits anti-inflammatory effects through inhibition of pro-inflammatory cytokine production and modulation of NF-κB signaling. Its antioxidant activity involves free radical scavenging mechanisms. The compound also demonstrates neuroprotective effects and may modulate neurotransmitter systems. |
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| ln Vitro |
- Antifungal activity against Candida strains:
- Magnoflorine inhibited the growth of 8 clinical isolates of Candida albicans, with minimum inhibitory concentrations (MICs) ranging from 16 to 64 μg/mL; it also suppressed Candida tropicalis (MIC: 32 μg/mL) and Candida krusei (MIC: 64 μg/mL) growth[1]
- At 2×MIC concentration, Magnoflorine reduced the biomass of Candida albicans biofilms by 45% (measured via crystal violet staining) and decreased the viability of biofilm-embedded cells by 38% (XTT reduction assay)[1] - Pro-inflammatory effects in U937 macrophages: - In LPS (1 μg/mL)-activated U937 macrophages, Magnoflorine (10-50 μM) increased TNF-α secretion in a dose-dependent manner: 50 μM Magnoflorine elevated TNF-α levels by 2.8-fold compared to LPS alone (ELISA)[2] - It also upregulated IL-6 (2.1-fold) and IL-1β (1.9-fold) mRNA expression at 50 μM (qRT-PCR) and enhanced the phosphorylation of p65 (NF-κB subunit) and p38 (MAPK) by 2.3-fold and 1.7-fold, respectively (Western blot)[2] - Silencing MyD88 via siRNA abolished the pro-inflammatory effects of Magnoflorine: TNF-α secretion was reduced by 65% compared to non-silenced cells[2] In vitro, magnoflorine chloride exhibits anti-inflammatory effects by inhibiting the production of pro-inflammatory cytokines. It demonstrates antioxidant activity through free radical scavenging. The compound may also show neuroprotective effects in neuronal cell models. Its effects on cell signaling pathways have been characterized in cellular models, with modulation of inflammatory and oxidative stress pathways observed. |
| ln Vivo |
In vivo studies on magnoflorine chloride are limited. Based on its mechanism of action, the compound may have potential in inflammatory disorders and neurodegenerative diseases. Its anti-inflammatory and neuroprotective properties suggest potential therapeutic applications. Further in vivo studies are needed to fully characterize its pharmacological effects and therapeutic potential.
|
| Enzyme Assay |
- Candida growth inhibition assay (MIC determination):
- Candida strains were cultured in RPMI 1640 medium to logarithmic phase, then adjusted to 1×10⁶ CFU/mL.
- Serial dilutions of Magnoflorine (2-128 μg/mL) were added to 96-well plates, followed by equal volumes of Candida suspension.
- Plates were incubated at 35°C for 48 hours, and MIC was defined as the lowest Magnoflorine concentration that completely inhibited visible fungal growth[1]
- MyD88-dependent signaling activation assay (Western blot for phosphorylated proteins): - U937 macrophages were pretreated with Magnoflorine (10-50 μM) for 1 hour, then stimulated with LPS (1 μg/mL) for 30 minutes. - Cells were lysed, and proteins were separated by SDS-PAGE, transferred to PVDF membranes, and probed with antibodies against phospho-p65, phospho-p38, and total p65/p38. GAPDH was used as a loading control[2] For in vitro antioxidant assays, magnoflorine chloride can be evaluated using DPPH or ABTS radical scavenging assays. The compound is incubated with radical solutions, and the decrease in absorbance is measured. Scavenging activity is calculated as a percentage. Anti-inflammatory activity can be assessed by measuring inhibition of pro-inflammatory cytokine production in stimulated cells using ELISA. |
| Cell Assay |
- Candida biofilm inhibition assay:
- Candida albicans was inoculated into 96-well plates and cultured at 35°C for 24 hours to form biofilms.
- Biofilms were treated with Magnoflorine (2×MIC, 32 μg/mL) for 24 hours, then stained with crystal violet (0.1%) for 15 minutes.
- Excess stain was washed off, and absorbance at 570 nm was measured to quantify biomass; XTT reagent was added to assess viable cells via absorbance at 490 nm[1]
- U937 macrophage pro-inflammatory factor detection (ELISA/qRT-PCR): - U937 cells were differentiated into macrophages with PMA (100 nM) for 48 hours, then pretreated with Magnoflorine (10-50 μM) for 1 hour, followed by LPS (1 μg/mL) stimulation for 24 hours. - Cell supernatants were collected for TNF-α/IL-6 detection via ELISA; total RNA was extracted, reverse-transcribed to cDNA, and IL-1β mRNA expression was measured via qRT-PCR (GAPDH as internal control)[2] - MyD88 siRNA transfection assay in U937 cells: - U937 macrophages were transfected with MyD88 siRNA or negative control siRNA using transfection reagent for 48 hours. - Transfected cells were treated with Magnoflorine (50 μM) and LPS (1 μg/mL) for 24 hours, then TNF-α secretion was detected via ELISA to verify MyD88 dependence[2] For in vitro cell-based assays, magnoflorine chloride is typically tested on immune cells or neuronal cells. Cells are treated with the compound at various concentrations (typically 1-100 μM) for 24-72 hours. Cell viability is assessed using MTT or CCK-8 assays. Cytokine production is measured by ELISA. Neuroprotective effects are assessed in models of oxidative stress. Signaling pathway modulation is assessed by Western blotting. |
| Animal Protocol |
In vivo animal experiments for magnoflorine chloride have not been extensively reported. Based on its anti-inflammatory and neuroprotective activities, potential experimental models include inflammation models and neurodegeneration models in mice or rats. The compound could be administered orally or intraperitoneally, with relevant biomarkers assessed as pharmacodynamic endpoints.
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| ADME/Pharmacokinetics |
Pharmacokinetic data for magnoflorine chloride are limited. As an alkaloid, it is expected to have moderate oral bioavailability. The chloride salt form may influence its absorption properties. Standard pharmacokinetic studies would be required to determine its absorption, distribution, metabolism, and excretion profile.
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| Toxicity/Toxicokinetics |
In U937 macrophages, concentrations up to 50 μM of magnoflorine did not affect cell viability (MTT assay: cell viability >90%, compared with the control group), indicating that it had low cytotoxicity at pro-inflammatory concentrations [2]. In vivo toxicity data (e.g., LD50, liver and kidney function indicators, plasma protein binding rate) were not described in either literature [1][2].
Toxicological data for magnoflorine chloride are limited. As a natural product isolate, it is generally considered to have low toxicity at pharmacological doses. However, comprehensive toxicological studies have not been extensively reported. The compound is classified as a research-grade reagent and is not for human use. |
| References | |
| Additional Infomation |
Magnoliaine is a natural apophene alkaloid, primarily isolated from plants of the Magnoliaceae family (e.g., Magnolia officinalis), and possesses potential natural antifungal and immunomodulatory activities [1][2]. The antifungal mechanism of magnoliaine may involve disruption of the integrity of Candida cell membranes (increased membrane permeability in preliminary tests suggests this), but direct evidence has not yet been provided (e.g., ergosterol content assays) [1]. In LPS-activated macrophages, the pro-inflammatory effect of magnoliaine is TLR4/MyD88 dependent, as it does not enhance the inflammatory response in cells treated with the TLR4 inhibitor (TAK-242) [2].
Magnoflorine chloride is a research-use only compound and has not been approved for clinical applications. It is an aporphine alkaloid. Its molecular weight and formula are well-characterized. It is available from various research chemical suppliers. Further research is needed to fully elucidate its pharmacological profile and therapeutic potential. |
| Molecular Formula |
C20H24CLNO4
|
|---|---|
| Molecular Weight |
377.8619
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| Exact Mass |
377.139
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| CAS # |
6681-18-1
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| Related CAS # |
(+)-Magnoflorine iodide; 4277-43-4; (+)-Magnoflorine; 2141-09-5
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| PubChem CID |
23149
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| Appearance |
Yellow to brown solid
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
5
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
26
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| Complexity |
498
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| Defined Atom Stereocenter Count |
1
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| SMILES |
[Cl-].O([H])C1=C(C([H])=C2C([H])([H])C([H])([H])[N+](C([H])([H])[H])(C([H])([H])[H])[C@@]3([H])C([H])([H])C4C([H])=C([H])C(=C(C=4C1=C32)O[H])OC([H])([H])[H])OC([H])([H])[H]
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| InChi Key |
STVJLBTYWBXDBP-ZOWNYOTGSA-N
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| InChi Code |
InChI=1S/C20H23NO4.ClH/c1-21(2)8-7-12-10-15(25-4)20(23)18-16(12)13(21)9-11-5-6-14(24-3)19(22)17(11)18;/h5-6,10,13H,7-9H2,1-4H3,(H-,22,23);1H/t13-;/m0./s1
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| Chemical Name |
(6aS)-2,10-dimethoxy-6,6-dimethyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinolin-6-ium-1,11-diol;chloride
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| Synonyms |
α-Magnoflorine chloride; Magnoflorine chloride; Thalictrine chloride
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O : ~41.67 mg/mL (~110.28 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: 100 mg/mL (264.65 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.6465 mL | 13.2324 mL | 26.4648 mL | |
| 5 mM | 0.5293 mL | 2.6465 mL | 5.2930 mL | |
| 10 mM | 0.2646 mL | 1.3232 mL | 2.6465 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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