2. Anti-infection Autophagy Apoptosis Neuronal Signaling Immunology/Inflammation MAPK/ERK Pathway NF-κB Epigenetics Cell Cycle/DNA Damage PI3K/Akt/mTOR Metabolic Enzyme/Protease
  3. Fungal Autophagy Apoptosis PINK1/Parkin NOD-like Receptor (NLR) Caspase JNK NF-κB Sirtuin AMPK Reactive Oxygen Species (ROS)
  4. (+)-Magnoflorine

(+)-Magnoflorine  (Synonyms: Magnoflorine; α-Magnoflorine; Thalictrine)

Cat. No.: HY-N0334
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(+)-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.

Ionic compounds are often challenging to exist independently, it is advisable to opt for a more stable salt form ((+)-Magnoflorine chloride and (+)-Magnoflorine iodide).

For research use only. We do not sell to patients.

(+)-Magnoflorine

(+)-Magnoflorine Chemical Structure

CAS No. : 2141-09-5

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(+)-Magnoflorine Related Antibodies

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NLRP3 NLRP1 NOD1 NOD2

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Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

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JNK1 JNK2 JNK3 JNK

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NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

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Sirtuin SIRT1 SIRT2 SIRT3 SIRT6 SIRT5 SIRT7 SIRT4

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NUAK1 NUAK2 AMPK AMPK α1β1γ1 AMPK α2β1γ1 AMPK α1β2γ1 AMPK α2β2γ1 BRSK1 BRSK2 HUNK AMPKα

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Description

(+)-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[1][2][3][4][5][6][7].

Cellular Effect
Cell Line Type Value Description References
HepG2 2.2.15 CC50
> 4.114 mM
Compound: 12
Cytotoxicity against human Hep G2.2.15 cells
Cytotoxicity against human Hep G2.2.15 cells
[PMID: 17723297]
HepG2 2.2.15 IC50
> 4.114 mM
Compound: 12
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
[PMID: 17723297]
HepG2 2.2.15 IC50
> 4.114 mM
Compound: 12
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
[PMID: 17723297]
In Vitro

(+)-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.

(+)-Magnoflorine Related Antibodies

Cell Invasion Assay[3]

Cell Line: MG-63 and U-2 OS cells
Concentration: 10, 20 and 40 μM
Incubation Time: 24 h
Result: Significantly reduced the number of MG-63 and U-2 OS cells passing through the matrix gel.

RT-PCR[3]

Cell Line: MG-63 and U-2 OS cells
Concentration: 10, 20 and 40 μM
Incubation Time: 24 h
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.

Western Blot Analysis[3]

Cell Line: MG-63 and U-2 OS cells
Concentration: 10, 20 and 40 μM
Incubation Time: 24 h
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.

Apoptosis Analysis[4]

Cell Line: PC12 cells
Concentration: 10 μM
Incubation Time: pre-treated for 3 h, and then add Aβ1-42 for co-culture for 24 h
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.
In Vivo

(+)-Magnoflorine (1-10 mg/kg, i.p., once daily for a month) significantly improves the cognitive dysfunction of Alzheimer’s disease (AD) model mice[4].
(+)-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.

Animal Model: AD model established in APP/PS1 (APPswe/PSEN1dE9) double-transgenic mice (8 months, 30-32 g, female)[4]
Dosage: 1 and 10 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily for a month
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.
Animal Model: Middle cerebral artery occlusion (MCAO) models model established in male Sprague-Dawley rats (weighing 220 g)[5]
Dosage: 10 and 20 mg/kg
Administration: Intragastric administration (i.g.), once daily for 15 days
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.
Animal Model: Colitis models model established in female C57BL/6 J mice (6-8 weeks old)[6]
Dosage: 10 mg/kg
Administration: Intragastric administration (i.g.), once daily for 10 days
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.
Animal Model: Chronic kidney disease model established in male C57BL/6 J mice (20 g)[6]
Dosage: 5 and 10 mg/kg
Administration: Intragastric administration (i.g.), once daily for 12 weeks
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).
Molecular Weight

342.41

Formula

C20H24NO4+
CAS No.
SMILES

C[N+]1(C)CCC2=CC(OC)=C(O)C3=C2[C@]1([H])CC4=CC=C(OC)C(O)=C34
Structure Classification
Initial Source
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Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
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(+)-Magnoflorine Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

(+)-Magnoflorine2141-09-5Magnoflorine α-Magnoflorine ThalictrineFungalAutophagyApoptosisPINK1/ParkinNOD-like Receptor (NLR)CaspaseJNKNF-κBSirtuinAMPKReactive Oxygen Species (ROS)PTEN-induced kinase 1/Parkinc-Jun N-terminal kinaseNuclear factor-κBNuclear factor-kappaBAMP-activated protein kinaseantifungalPenicillium avellaneumT. rubrumT. mentagrophyteaporphine alkaloidInhibitorinhibitorinhibit

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