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 iodide

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

Cat. No.: HY-N0334A Purity: 99.74%
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(+)-Magnoflorine (α-Magnoflorine) iodide is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine iodide 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 iodide 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 iodide also has significant antifungal activity.

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(+)-Magnoflorine iodide

(+)-Magnoflorine iodide Chemical Structure

CAS No. : 4277-43-4

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Based on 1 publication(s) in Google Scholar

Other Forms of (+)-Magnoflorine iodide:

(+)-Magnoflorine iodide Related Antibodies

Top Publications Citing Use of Products

1 Publications Citing Use of MCE (+)-Magnoflorine iodide

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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

  • Biological Activity

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  • Customer Review

Description

(+)-Magnoflorine (α-Magnoflorine) iodide is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine iodide 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 iodide 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 iodide also has significant antifungal activity[1][2][3][4][5][6][7].

Cellular Effect
Cell Line Type Value Description References
KB IC50
> 533 μM
Compound: magnoflorine iodide
Cytotoxicity against human KB cells after 72 hrs
Cytotoxicity against human KB cells after 72 hrs
[PMID: 11141105]
In Vitro

(+)-Magnoflorine iodide 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) iodide inhibit the proliferation, invasion and epithelial-mesenchymal transition process of MG-63 and U-2 OS cells[3].
(+)-Magnoflorine (10-40 μM, 24 h) iodide upregulates miR-410-3p and thereby inhibits the HMGB1/NF-κB pathway[3].
(+)-Magnoflorine (10 μM, 27 h) iodide significantly reverses the decline in PC12 cell viability caused by Aβ1-42and reduces the apoptosis rate[4].
(+)-Magnoflorine (10 μM, 27 h) iodide 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) iodide 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 iodide 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 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 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) iodide 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) iodide has a protective effect on cerebral ischemia-reperfusion injury in rats[5].
(+)-Magnoflorine (10 mg/kg, i.g., once daily for 10 days) iodide 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) iodide 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

469.31

Formula

C20H24INO4
CAS No.
Appearance

Solid

Color

White to light yellow

SMILES

C[N+]1(C)CCC2=CC(OC)=C(O)C3=C2[C@]1([H])CC4=CC=C(OC)C(O)=C34.[I-]
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, sealed storage, away from moisture and light

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

Solvent & Solubility
In Vitro: 

DMSO : 62.5 mg/mL (133.17 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.1308 mL 10.6539 mL 21.3079 mL
5 mM 0.4262 mL 2.1308 mL 4.2616 mL
View the Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

  • Protocol 1

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

    Solubility: ≥ 2.08 mg/mL (4.43 mM); Clear solution

    This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

    Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
  • Protocol 2

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

    Solubility: ≥ 2.08 mg/mL (4.43 mM); Clear solution

    This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

    Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.

For the following dissolution methods, please prepare the working solution directly. It is recommended to prepare fresh solutions and use them promptly within a short period of time.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

  • Protocol 1

    Add each solvent one by one:  50% PEG300    50% Saline

    Solubility: 10 mg/mL (21.31 mM); Clear solution; Need ultrasonic and warming and heat to 60°C

In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:

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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration: mg/mL
Method for preparing stock solution: mg drug dissolved in μL  DMSO (Stock solution concentration: mg/mL).

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
 If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation

Purity: 99.74%

SDS (420 KB)

COA (255 KB) HNMR (289 KB) LCMS (101 KB)

Handling Instructions (2659 KB)
References

Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 2.1308 mL 10.6539 mL 21.3079 mL 53.2697 mL
5 mM 0.4262 mL 2.1308 mL 4.2616 mL 10.6539 mL
10 mM 0.2131 mL 1.0654 mL 2.1308 mL 5.3270 mL
15 mM 0.1421 mL 0.7103 mL 1.4205 mL 3.5513 mL
20 mM 0.1065 mL 0.5327 mL 1.0654 mL 2.6635 mL
25 mM 0.0852 mL 0.4262 mL 0.8523 mL 2.1308 mL
30 mM 0.0710 mL 0.3551 mL 0.7103 mL 1.7757 mL
40 mM 0.0533 mL 0.2663 mL 0.5327 mL 1.3317 mL
50 mM 0.0426 mL 0.2131 mL 0.4262 mL 1.0654 mL
60 mM 0.0355 mL 0.1776 mL 0.3551 mL 0.8878 mL
80 mM 0.0266 mL 0.1332 mL 0.2663 mL 0.6659 mL
100 mM 0.0213 mL 0.1065 mL 0.2131 mL 0.5327 mL
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Keywords:

(+)-Magnoflorine4277-43-4Magnoflorineα-MagnoflorineThalictrineFungalAutophagyApoptosisPINK1/ParkinNOD-like Receptor (NLR)CaspaseJNKNF-κBSirtuinAMPKReactive Oxygen Species (ROS)PTEN-induced kinase 1/Parkinc-Jun N-terminal kinaseNuclear factor-κBNuclear factor-kappaBAMP-activated protein kinaseAporphinealkaloidAcoruscalamusC.albicansbiofilm anti-fungalanti-antidiabeticanti-oxidativeInhibitorinhibitorinhibit

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