| Size | Price | Stock | Qty |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg |
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| 250mg |
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| Other Sizes |
Purity: =100%
| 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 does not have a single defined molecular target. It exhibits antifungal activity against Candida species without a reported specific enzyme or receptor target. In pro-inflammatory response regulation, magnoflorine acts via the MyD88-dependent signaling pathway involved in TLR4-mediated inflammation, although direct binding to MyD88 or downstream proteins has not been demonstrated. It is also an α-glucosidase inhibitor. |
|---|---|
| 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 inhibits the growth of Candida albicans clinical isolates with MICs ranging from 16 to 64 μg/mL. It also suppresses Candida tropicalis (MIC: 32 μg/mL) and Candida krusei (MIC: 64 μg/mL). At 2×MIC, it reduces C. albicans biofilm biomass by 45% and decreases biofilm-embedded cell viability by 38%. In LPS-activated U937 macrophages, magnoflorine (10-50 μM) increases TNF-α secretion up to 2.8-fold and upregulates IL-6 and IL-1β mRNA expression. It also enhances phosphorylation of NF-κB p65 and p38 MAPK. |
| ln Vivo |
In vivo, magnoflorine possesses oral activity and has shown antidiabetic potential as an α-glucosidase inhibitor. It exerts inhibitory effects against Cu²⁺-induced lipid peroxidation of high-density lipoprotein (HDL). The compound demonstrates anti-inflammatory, anti-tumor, and neuroprotective effects in various animal models. Detailed in vivo efficacy data and dosing regimens are limited in publicly available literature.
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| 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 antifungal activity testing, Candida strains are cultured in RPMI 1640 medium to logarithmic phase and adjusted to 1×10⁶ CFU/mL. Serial dilutions of magnoflorine (2-128 μg/mL) are added to 96-well plates, followed by equal volumes of Candida suspension. Plates are incubated at 35°C for 48 hours, and the MIC is defined as the lowest concentration that completely inhibits visible growth. |
| 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] In vitro cellular assays include antifungal activity testing against Candida species. For pro-inflammatory effects, U937 macrophages are activated with LPS (1 μg/mL) and treated with magnoflorine (10-50 μM). TNF-α secretion is measured by ELISA. IL-6 and IL-1β mRNA expression is assessed by qRT-PCR. NF-κB p65 and p38 MAPK phosphorylation is analyzed by Western blot. MyD88 silencing via siRNA is used to confirm pathway involvement. |
| Animal Protocol |
In vivo animal studies typically involve oral administration of magnoflorine to evaluate its antidiabetic, anti-inflammatory, or neuroprotective effects. Animal models include diabetes models for α-glucosidase inhibition studies, inflammation models for anti-inflammatory assessment, and tumor xenograft models for anti-tumor evaluation. Dosing regimens, administration routes, and specific endpoints vary depending on the study model and objectives.
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| ADME/Pharmacokinetics |
Pharmacokinetic data for magnoflorine is limited in publicly available sources. The compound is reported to be orally active, suggesting gastrointestinal absorption. Distribution, metabolism, and excretion pathways have not been fully characterized. As a natural alkaloid, its PK properties likely depend on the specific formulation and route of administration.
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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 to the control group), indicating that it has low cytotoxicity at pro-inflammatory concentrations [2].
Toxicological data for magnoflorine is limited. The compound is a natural alkaloid and should be handled with standard laboratory safety precautions. No specific toxicity data or LD₅₀ values are reported in the available literature. As with all research chemicals, appropriate safety measures should be taken during handling and 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 is an orally active aporphine alkaloid with a broad spectrum of pharmacological activities. It has been studied for its antifungal, antioxidant, anti-inflammatory, anti-tumor, neuroprotective, and antidiabetic properties. Its activity as an α-glucosidase inhibitor suggests potential for diabetes research. This product is for research purposes only and not for human therapeutic use. |
| Molecular Formula |
C20H24NO4+
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|---|---|
| Molecular Weight |
342.4145
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| Exact Mass |
342.169
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| Elemental Analysis |
C, 70.15; H, 7.07; N, 4.09; O, 18.69
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| CAS # |
2141-09-5
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| Related CAS # |
(+)-Magnoflorine iodide;4277-43-4;(+)-Magnoflorine chloride;6681-18-1
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| PubChem CID |
73337
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| Appearance |
Solid powder
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| Melting Point |
252ºC
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| LogP |
-1.71
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
25
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| Complexity |
498
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| Defined Atom Stereocenter Count |
1
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| SMILES |
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 |
YLRXAIKMLINXQY-ZDUSSCGKSA-O
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| InChi Code |
InChI=1S/C20H23NO4/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)/p+1/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
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| Synonyms |
α-Magnoflorine; (+)-Magnoflorine; Magnoflorine
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| HS Tariff Code |
2934.99.03.00
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| 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) |
DMSO: ~10 mg/mL (~29.2 mM)
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|---|---|
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.9205 mL | 14.6024 mL | 29.2048 mL | |
| 5 mM | 0.5841 mL | 2.9205 mL | 5.8410 mL | |
| 10 mM | 0.2920 mL | 1.4602 mL | 2.9205 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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