(+)-Magnoflorine
Based on 1 publication(s) in Google Scholar
(+)-Magnoflorine (α-Magnoflorine) is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine promotes Parkin/PINK1 -mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine also has significant antifungal activity.
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- CAS. Nr.: 2141-09-5
- Formel: C20H24NO4+
- Molecular Weight:342.41
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Publications Citing Use of MedChemExpress (MCE) (+)-Magnoflorine
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Biologische Aktivität
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HepG2 2.2.15 | CC50 |
>4.114 mM
Compound: 12
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Cytotoxicity against human Hep G2.2.15 cells
Cytotoxicity against human Hep G2.2.15 cells
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[PMID: 17723297] |
| HepG2 2.2.15 | IC50 |
>4.114 mM
Compound: 12
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Antiviral activity against HBV transfected Hep G2.2.15 cells assessed as inhibition of e antigen HBsAg secretion
Antiviral activity against HBV transfected Hep G2.2.15 cells assessed as inhibition of e antigen HBsAg secretion
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[PMID: 17723297] |
| HepG2 2.2.15 | IC50 |
>4.114 mM
Compound: 12
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Antiviral activity against HBV transfected Hep G2.2.15 cells assessed as inhibition of surface antigen HBsAg secretion
Antiviral activity against HBV transfected Hep G2.2.15 cells assessed as inhibition of surface antigen HBsAg secretion
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[PMID: 17723297] |
(+)-Magnoflorine has significant antifungal activities against Penicillium avellaneum UC-4376, T. rubrum and T. mentagrophyte with MIC values of 5 μg/disc, 62.5 μg/mL and 62.5 μg/mL, respectively[1][2].
(+)-Magnoflorine (5-80 μM, 24 h) inhibit the proliferation, invasion and epithelial-mesenchymal transition process of MG-63 and U-2 OS cells[3].
(+)-Magnoflorine (10-40 μM, 24 h) upregulates miR-410-3p and thereby inhibits the HMGB1/NF-κB pathway[3].
(+)-Magnoflorine (10 μM, 27 h) significantly reverses the decline in PC12 cell viability caused by Aβ1-42and reduces the apoptosis rate[4].
(+)-Magnoflorine (10 μM, 27 h) significantly reduces the increase in intracellular ROS levels caused by Aβ1-42, and restores the damaged mitochondrial membrane potential[4].
(+)-Magnoflorine (0-50 μM, 24 h) inhibits the activation of the NLRP3 inflammasome in HK-2 cells by promoting Parkin-dependent mitochondrial autophagy[7].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MG-63 and U-2 OS cells
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Concentration:10, 20 and 40 μM
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Incubation Time:24 h
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Result:Significantly reduced the number of MG-63 and U-2 OS cells passing through the matrix gel.
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Cell Line:MG-63 and U-2 OS cells
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Concentration:10, 20 and 40 μM
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Incubation Time:24 h
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Result:Upregulated the mRNA expression of E-cadherin in a dose-dependent manner, and downregulate the expressions of N-cadherin and Vimentin.
Dose-dependently down-regulates the mRNA expression of HMGB1.
Inhibited the activation of the NF-κB pathway resulting in a decrease in the levels of phosphorylated-p65 and phosphorylated-IκBα.
Significantly upregulated the expression of miR-410-3p in osteosarcoma cells.
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Cell Line:MG-63 and U-2 OS cells
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Concentration:10, 20 and 40 μM
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Incubation Time:24 h
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Result:Upregulated the protein expression of E-cadherin in a dose-dependent manner, and downregulate the expressions of N-cadherin and Vimentin.
Dose-dependently down-regulates the protein expression of HMGB1.
Inhibited the activation of the NF-κB pathway resulting in a decrease in the levels of phosphorylated-p65 and phosphorylated-IκBα.
Significantly upregulated the expression of miR-410-3p in osteosarcoma cells.
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Cell Line:PC12 cells
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Concentration:10 μM
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Incubation Time:pre-treated for 3 h, and then add Aβ1-42 for co-culture for 24 h
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Result:Significantly reduced the apoptosis rate caused by Aβ1-42.
Reduced the expression of pro-apoptotic proteins Bax and Cleaved Caspase-3, and increased the expression of anti-apoptotic protein Bcl-2.
(+)-Magnoflorine (10-20 mg/kg, i.g., once daily for 15 days) has a protective effect on cerebral ischemia-reperfusion injury in rats[5].
(+)-Magnoflorine (10 mg/kg, i.g., once daily for 10 days) relieves colitis induced by DDS (HY-116282C) in mice and the concurrent anxiety-like behaviors[6].
(+)-Magnoflorine (5-10 mg/kg, i.g., once daily for 12 weeks) exhibits renal protective effects in a mouse model of chronic kidney disease induced by a high-fat and high-fructose diet[7].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:AD model established in APP/PS1 (APPswe/PSEN1dE9) double-transgenic mice (8 months, 30-32 g, female)[4]
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Dosage:1 and 10 mg/kg
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Administration:Intraperitoneal injection (i.p.), once daily for a month
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Result:Improved the learning and memory abilities of mice. Reduced the core pathological changes in the brain, including Aβ deposition, excessive phosphorylation of Tau protein, neuroinflammation and neuronal loss.
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Animal Model:Middle cerebral artery occlusion (MCAO) models model established in male Sprague-Dawley rats (weighing 220 g)[5]
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Dosage:10 and 20 mg/kg
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Administration:Intragastric administration (i.g.), once daily for 15 days
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Result:Significantly reduced the neurological deficit score, indicating that it improved motor, balance and sensory functions.
Significantly reduced the volume of cerebral infarction and decreased the brain water content. Reduced the number of damaged neurons shown by Nissl staining and increased the density of NeuN-positive neurons.
Reduced the upregulation of LC3 fluorescence intensity and the LC3-II/LC3-I ratio caused by cerebral ischemia, and increased the expression of p62, Sirt1 and p-AMPK proteins.
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Animal Model:Colitis models model established in female C57BL/6 J mice (6-8 weeks old)[6]
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Dosage:10 mg/kg
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Administration:Intragastric administration (i.g.), once daily for 10 days
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Result:Reduced the disease activity index, the length of the colon, the tissue pathological damage, and decreased the mRNA levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in the colon tissue.
Significantly improved the anxiety-like behaviors induced by DSS. Inhibited the activation of microglia (IBA1+) in the hippocampus caused by DSS.
Reduced the mRNA levels of TNF-α, IL-1β, and IL-6 in the hippocampal tissue, and upregulated the expression of tight junction proteins ZO-1 and PV1 in the choroid plexus and blood-brain barrier.
Promoted the production of secondary bile acid HDCA by the microbiota.
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Animal Model:Chronic kidney disease model established in male C57BL/6 J mice (20 g)[6]
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Dosage:5 and 10 mg/kg
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Administration:Intragastric administration (i.g.), once daily for 12 weeks
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Result:Significantly reduced the levels of serum creatinine, urea nitrogen, uric acid and elevated urine protein.
Reduced the fatty degeneration of renal tubules, lipid deposition and tubular dilation. Reduced the collagen deposition in the kidneys, and downregulated the mRNA and protein expressions of fibrosis-related markers (TGF-β, α-SMA, COL-I, COL-III).
Reduced the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in the kidneys, and increased the activity of total superoxide dismutase (T-SOD).
Inhibited the activation of the NLRP3 inflammasome (reduced the expression of NLRP3, ASC, Cleaved Caspase-1, GSDMD-N and IL-1β).
Chemical Information
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CAS. Nr. 2141-09-5
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Molecular Weight 342.41
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Formel C20H24NO4+
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SMILES
C[N+]1(C)CCC2=CC(OC)=C(O)C3=C2[C@]1([H])CC4=CC=C(OC)C(O)=C34
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Synonyms
Magnoflorine; α-Magnoflorine; Thalictrine
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Structure Classification
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Initial Source
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
Reinheit & Dokumentation
Verweise
[1]. Chen JH, et al. Aporphine alkaloids from Clematis parviloba and their antifungal activity. Arch Pharm Res. 2009 Jan;32(1):3-5. [Content Brief]
[2]. Luo N, et al. Antifungal activity and potential mechanism of magnoflorine against Trichophyton rubrum. J Antibiot (Tokyo). 2021 Mar;74(3):206-214. [Content Brief]
[3]. Wang Y, et al. Magnoflorine inhibits the malignant phenotypes and increases cisplatin sensitivity of osteosarcoma cells via regulating miR-410-3p/HMGB1/NF-κB pathway. Life Sci. 2020 Sep 1;256:117967. [Content Brief]
[4]. Zhong L, et al. Magnoflorine improves cognitive deficits and pathology of Alzheimer's disease via inhibiting of JNK signaling pathway. Phytomedicine. 2023 Apr;112:154714. [Content Brief]
[5]. Liang H, et al. Magnoflorine Attenuates Cerebral Ischemia-Induced Neuronal Injury via Autophagy/Sirt1/AMPK Signaling Pathway. Evid Based Complement Alternat Med. 2022 Sep 10;2022:2131561. [Content Brief]
[6]. Wang L, et al. Magnoflorine alleviates colitis-induced anxiety-like behaviors by regulating gut microbiota and microglia-mediated neuroinflammation. Microbiome. 2025 Jul 26;13(1):172. [Content Brief]
[7]. Cheng Y, et al. Magnoflorine Ameliorates Chronic Kidney Disease in High-Fat and High-Fructose-Fed Mice by Promoting Parkin/PINK1-Dependent Mitophagy to Inhibit NLRP3/Caspase-1-Mediated Pyroptosis. J Agric Food Chem. 2024 Jun 5;72(22):12775-12787. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
(+)-Magnoflorine Related Classifications
HY-N0334 Related Classifications
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