N-Methylcoclaurine
N-Methylcoclaurine is an orally active anticancer agent and PDI inhibitor with an IC50 of 3.91 μM for the bovine-derived target. N-Methylcoclaurine selectively binds to κ opioid receptors with a Ki value of 0.9 μM. N-Methylcoclaurine inhibits tumor cell proliferation, migration, and invasion, and suppresses tumor growth in vivo. N-Methylcoclaurine inhibits iNOS expression and scavenges NO and DPPH radicals. N-Methylcoclaurine is a substrate of CyNMCH and an important branch intermediate in the biosynthesis of benzylisoquinoline alkaloids. N-Methylcoclaurine can be used in research related to hepatocellular carcinoma and neurological diseases.
For research use only. We do not sell to patients.
- CAS No.: 3423-07-2
- Formula: C18H21NO3
- Molecular Weight:299.36
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
All Opioid Receptor Isoforms
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Biological Activity
Description
IC50 & Target
[2]|
human κ-opioid receptor (hKOR) 0.9 μM (Ki) |
δ Opioid Receptor/DOR 20.1 μM (Ki) |
human μ-opioid receptor 4.0 μM (Ki) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| HepG2 | CC50 |
5.44 μM
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Cytotoxicity against human HepG2 cells assessed as viability reduction after 24 hrs incubation with N-Methylcoclaurine by MTT assay.
Cytotoxicity against human HepG2 cells assessed as viability reduction after 24 hrs incubation with N-Methylcoclaurine by MTT assay.
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ijp.2025.464.474 |
In Vitro
N-Methylcoclaurine (1-10 μM; 24 h) reduces the number of HepG2 cells in crystal violet staining[1].
N-Methylcoclaurine (1-10 μM; 24-48 h) inhibits HepG2 cell migration in the scratch assay[1].
N-Methylcoclaurine (1-10 μM; 24 h) inhibits HepG2 cell invasion in the transwell assay[1].
N-methylcoclaurine (6.25-12.5 μM; 16 h) inhibits iNOS expression in LPS-induced RAW 264.7 macrophages[5].
N-Methylcoclaurine (1.7 nM-300 μM; 60-90 min) binds to κ opioid receptors expressed in HEK293 cell membranes with a Ki of 0.9 μM and shows weaker affinity for δ and μ opioid receptors, with Ki values of 20.1 and 4.0 μM, respectively[2].
N-methylcoclaurine is an alkaloid among the TAs in lotus leaves, accounting for 275 mg/g (27.5%) as determined by HPLC[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HepG2 human hepatocellular carcinoma cells
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Concentration:1, 2, 3, 5 and 10 μM
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Incubation Time:24 and 48 h
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Result:Suppressed HepG2 proliferation, with survival rates of 79.46%, 60.32% and 17.06% for 1, 3 and 10 μM N-Methylcoclaurine, respectively.
CC50 = 5.44 μM.
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Cell Line:HepG2 cells
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Concentration:1 and 10 μM
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Incubation Time:24 h
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Result:Reduced the cell number index to 0.76 and 0.22 at 1 and 10 μM, respectively.
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Cell Line:HepG2 cells
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Concentration:1, 3, 5, 10 μM
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Incubation Time:24 and 48 h
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Result:Control migration rates were 65.15% at 24 h and 86.93% at 48 h.
N-Methylcoclaurine-exposed low-, medium- and high-dose groups had migration rates of 47.76%, 42.02% and 34.45% at 24 h, and 53.97%, 46.57% and 35.96% at 48 h, respectively, showing reduced migration versus control.
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Cell Line:HepG2 cells
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Concentration:1, 5, 10 μM
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Incubation Time:24 h
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Result:Effectively inhibited HepG2 cell invasion at 1-10 μM in a concentration-dependent manner.
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Cell Line:RAW 264.7 murine macrophages
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Concentration:6.25 and 12.5 μM
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Incubation Time:16 h (with 1 μg/mL LPS)
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Result:The results illustrated that compound 5 significantly inhibited iNOS expression in a concentration-dependent manner.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ICR (6 weeks old, 18-22 g)[1]
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Dosage:10 mg/kg/day, 20 mg/kg/day, and 40 mg/kg/day
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Administration:intragastrically; daily; 2 weeks
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Result:Compared with the saline group, N-Methylcoclaurine dose-dependently inhibited H22 tumor growth, with tumor inhibition rates of 42.27%, 54.63%, and 63.67% at 10, 20, and 40 mg/kg/day, respectively.
H&E staining showed various degrees of cell loss and white vacuoles in tumors from N-Methylcoclaurine groups, and the remaining cell number index decreased in all N-Methylcoclaurine groups.
- RNA extraction experimental
- BrdU Incorporation Assay
- Cell migration
- Somatic Cell Culture
- CFSE Dye Dilution Proliferation Assay
- Dye-dilution cell tracking and proliferation staining
- Patient-Derived Orthotopic Xenograft (PDOX)
- CCK-8/WST-8 Cell Proliferation Assay
- Protocol for Cell Cycle
- Cell Counting-Based Growth Curve Assay
- Liver Cancer Modeling
- Colony Formation (Clonogenic) Assay
- Cell Viability Determination by MTT Colorimetric Assay
- EdU Incorporation Assay (Click Chemistry-Based DNA Synthesis Measurement)
- Ki-67 Immunostaining Proliferation Assay
- PCNA Immunodetection Proliferation Assay
- Protocol for Cell Counting and Cell Density Analysis
- Patient-Derived Xenograft (PDX)
- Cell invasion
- MTT Cell Proliferation Assay
- Subcutaneous Cell-Line-Derived Xenograft
- Orthotopic Cell-Line Xenograft
Chemical Information
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CAS No. 3423-07-2
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Molecular Weight 299.36
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Formula C18H21NO3
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SMILES
OC1=CC2=C(C=C1OC)CCN(C)[C@H]2CC3=CC=C(O)C=C3
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
N-Methylcoclaurine Related Classifications
HY-W705415A Related Classifications
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Keywords
- N-Methylcoclaurine
- 3423-07-2
- PDI
- Opioid Receptor
- Free Radical Scavengers
- Drug Intermediate
- endoplasmic reticulum chaperone
- hepatocellular carcinoma
- iNOS expression
- nitric oxide scavenging
- opioid receptors
- protein disulfide isomerase inhibitor
- protein folding
- tumor cell invasion
- tumor cell migration
- tumor cell proliferation
- Inhibitor
- inhibitor
- inhibit