Art. -Nr.: HY-N0430

Coptisine

(Synonyms: Coptisin)

11 Cited Publications

Kundenbewertung

Based on 11 publication(s) in Google Scholar

Coptisine is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine is a reversible, uncompetitive IDO inhibitor with a K_i of 5.8 μM and an IC₅₀ of 6.3 μM. Coptisine suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine can be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease.

Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.

CAS. Nr.: 3486-66-6
Formel: C₁₉H₁₄NO₄
Molecular Weight:320.32

Speicherung:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (292 KB)

Coptisine Chemical Structure

CAS. Nr.: 3486-66-6

Größe

Preis

Verfügbarkeit

Menge

Amount: USD 0.00

* Bitte wählen Sie Menge, bevor Sie Artikel hinzufügen.

Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Publications (11)
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target^[4]

IDO

6.3 μM (IC₅₀)

IDO

5.8 μM (Ki)

Alle Indoleamine 2,3-Dioxygenase (IDO) Isoform-spezifische Produkte anzeigen :

Alle NF-κB Isoform-spezifische Produkte anzeigen :

Alle p38 MAPK Isoform-spezifische Produkte anzeigen :

Alle PI3K Isoform-spezifische Produkte anzeigen :

Alle Akt Isoform-spezifische Produkte anzeigen :

Alle DNA/RNA Synthesis Isoform-spezifische Produkte anzeigen :

Alle ROCK Isoform-spezifische Produkte anzeigen :

Cellular Effect

Cell Line	Type	Value	Description	References
A2780/Taxol	IC₅₀	>=24.33 μM Compound: 3	Antiproliferative activity against human A2780T cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay Antiproliferative activity against human A2780T cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay	[PMID: 39213483]
A549/TR	IC₅₀	>=24.33 μM Compound: 3	Antiproliferative activity against human A549/Taxol cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay Antiproliferative activity against human A549/Taxol cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay	[PMID: 39213483]
LoVo	IC₅₀	>=24.33 μM Compound: 3	Antiproliferative activity against human LoVo cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay Antiproliferative activity against human LoVo cells assessed as reduction in cell viability incubated for 48 hrs by CCK-8 assay	[PMID: 39213483]
Panel NCI-60 (60 carcinoma cell lines)	GI₅₀	260 nM Compound: Coptisine	Growth inhibitory activity against human cancer cell line in the NCI's anticancer drug screening program Growth inhibitory activity against human cancer cell line in the NCI's anticancer drug screening program	[PMID: 15743190]
PC-3	IC₅₀	>=24.33 μM Compound: 3	Antiproliferative activity against human PC-3 cells assessed as reduction in cell viability incubated for 24 hrs by CCK-8 assay Antiproliferative activity against human PC-3 cells assessed as reduction in cell viability incubated for 24 hrs by CCK-8 assay	[PMID: 39213483]

In Vitro

Coptisine (0.1-100 μM; 48 h) potently inhibits proliferation of human lung adenocarcinoma A5499, H460,
and H2170 cells (IC₅₀ = 18.09, 29.50, and 21.60 μM) and other tested human cancer cell lines, with moderate selectivity relative to normal human umbilical vein endothelial cells^[1].
Coptisine (12.5-50 μM; 48 h) induces concentration-dependent DNA damage in human lung adenocarcinoma A549 cells, as shown by increased γH2AX expression^[1].
Coptisine (12.5-50 μM; 48 h) induces concentration-dependent G2/M phase cell cycle arrest in human lung adenocarcinoma A549 cells, mediated by downregulated cyclin B1, cdc2, and cdc25C expression and upregulated p21 expression^[1].
Coptisine (12.5-50 μM; 48 h) induces concentration-dependent apoptosis in human lung adenocarcinoma A549 cells, inducing concentration-dependent activation of caspase 3/7, caspase 8, caspase 9, and cleavage of PARP^[1].
Coptisine (12.5-50 μM; 0.5-24 h) induces time- and concentration-dependent reactive oxygen species generation in human lung adenocarcinoma A549 cells^[1].
Coptisine (12.5-50 μM; 24 h) induces concentration-dependent mitochondrial dysfunction in human lung adenocarcinoma A549 cells, including loss of mitochondrial membrane potential and altered Bax, Bcl-2, and cytochrome c expression^[1].
Coptisine potently inhibits recombinant human IDO as a reversible, uncompetitive inhibitor with a K_i of 5.8 μM and an IC₅₀ of 6.3 μM^[4].
Coptisine inhibits IDO activity in HEK 293 cells with an IC₅₀ of 7.1 μM^[4].
Coptisine (10 μM; 5 h pre-incubation) reverses amyloid-β peptide 1-42 and interferon-γ-induced IDO activation and restores cell viability in PC12 cells^[4].
Coptisine inhibits LPS (HY-D1056)-stimulated inflammation by blocking NF-κB, MAPK, and PI3K/Akt activation in
macrophages^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis^[1]

Cell Line:

human lung adenocarcinoma A549
Concentration:

12.5, 25, 50 μM
Incubation Time:

48 h
Result:

Caused a concentration-dependent upregulation of pH2AX, a marker of DNA double-strand breaks, relative to untreated control cells.

Cell Cycle Analysis^[1]

Cell Line:

human lung adenocarcinoma A549
Concentration:

12.5, 25, 50 μM
Incubation Time:

48 h
Result:

Caused concentration-dependent G2/M phase arrest, with 26.5%, 29.9%, and 36.8% of cells in G2/M phase after treatment with 12.5, 25, and 50 μM, respectively, compared to 16.95% in control cells.
Accompanied this arrest by concentration-dependent downregulation of cyclin B1, cdc2, and cdc25C, and upregulation of p21.

Apoptosis Analysis^[1]

Cell Line:

human lung adenocarcinoma A549
Concentration:

12.5, 25, 50 μM
Incubation Time:

48 h
Result:

Caused concentration-dependent induction of apoptosis: treatment with 50 μM resulted in 58.5% early apoptotic cells and 24.2% late apoptotic cells; treatment with 25 μM resulted in 26.4% early apoptotic cells; treatment with 12.5 μM resulted in 10.8% early apoptotic cells, compared to 8.6% early and 4.6% late apoptotic cells in control cultures.
Caused concentration-dependent activation of caspase 3/7, with a 19-fold increase in activity at 50 μM relative to control.
Induced concentration-dependent upregulation of active caspase 8, active caspase 9, and cleaved PARP.

Cell Viability Assay^[4]

Cell Line:

PC12
Concentration:

10 μM (pre-incubation)
Incubation Time:

5 h (pre-incubation); 24 h (amyloid-β peptide 1-42 treatment); 24 h (interferon-γ treatment)
Result:

Down-regulated the enhanced IDO activity induced by combined 25 μM amyloid-β peptide 1-42 and 1000 U/mL interferon-γ treatment.
Restored the reduced cell viability caused by these stimuli to levels comparable to untreated control cells.

In Vivo

Coptisine (10-30 mg/kg; p.o.; single dose 10 min before ischemia or plus additional dose 4 h after reperfusion) exerts pronounced cardioprotective effects against rat myocardial ischemia/reperfusion injury by reducing arrhythmias, infarct size, cardiac enzyme release, and left ventricular dysfunction, while suppressing myocardial apoptosis, inflammation, and Rho/ROCK pathway activation^[2].
Coptisine (23.35-70.05 mg/kg/day; i.g.; daily; 4 weeks) dose-dependently improves hypercholesterolemia in HFHC-fed Syrian golden hamsters^[3].
Coptisine (482.5-1728 mg/kg; p.o.; single dose) has low acute toxicity in Kunming mice, with an LD₅₀ of 880.18 mg/kg following a single oral dose^[3].
Coptisine (154 mg/kg/day; p.o.; daily; 90 days) is well-tolerated in SD rats with no observable toxicity via daily oral administration for 90 days^[3].
Coptisine (50 mg/kg; p.o.; once daily; 1 month) normalizes serum IDO activity, suppresses neuroinflammation, reduces Aβ plaque burden, restores neuronal integrity, and completely reverses cognitive impairment in A-PPswe/PS1ΔE9 transgenic Alzheimer's disease mice^[4].
Coptisine attenuates obesity-related inflammation through LPS/TLR-4-mediated signaling pathway in Syrian golden hamsters^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

Sprague-Dawley (male, 280±20 g, left anterior descending coronary artery occlusion for 30 min followed by reperfusion)^[2]
Dosage:

3 mg/kg; 10 mg/kg; 30 mg/kg
Administration:

p.o.; single dose 10 min before ischemia, plus an additional dose 4 h after reperfusion (24 h reperfusion studies); single dose 10 min before ischemia (3 h reperfusion studies)
Result:

Significantly decreased I/R-induced arrhythmia score and reduced incidence of premature ventricular complexes and ventricular tachycardia.
Significantly reduced infarct size compared with I/R controls.
Significantly reduced serum levels of aspartate transaminase, lactate dehydrogenase, and creatine kinase-MB compared with I/R controls.
Significantly attenuated I/R-induced reductions in left ventricular ejection fraction and fractional shortening at 24 h post-reperfusion.
Significantly reduced the percentage of TUNEL-positive apoptotic cardiomyocytes, dose-dependently decreased cleaved caspase-3 expression, and upregulated Bcl-2 protein expression compared with I/R controls.
Reduced DNA fragmentation indicative of apoptosis.
Significantly decreased heart tissue levels of proinflammatory cytokines IL-1β, IL-6, and TNF-α, inhibited NF-κB p65 translocation from cytoplasm to nucleus, reduced Rho, ROCK1, and ROCK2 protein expression, and attenuated phosphorylation of myosin phosphatase targeting subunit-1 compared with I/R controls.

Animal Model:

Syrian golden hamsters (male, 4-week-old, 100±5 g, HFHC diet-induced hypercholesterolemia)^[3]
Dosage:

23.35 mg/kg/day; 46.7 mg/kg/day; 70.05 mg/kg/day
Administration:

I.g.; daily; 4 weeks
Result:

Reduced serum total cholesterol (TC) by 10.9% and increased fecal cholesterol by 29% at 23.35 mg/kg.
Reduced serum TC by 24.3% and low-density lipoprotein cholesterol (LDL-c) by 20.0%, increased high-density lipoprotein cholesterol (HDL-c) by 24.8%, increased fecal cholesterol by 44% and fecal total bile acids (TBA) by 31.6% at 46.7 mg/kg.
Reduced serum TC by 26.7%, LDL-c by 22.2%, and triglycerides (TG) by 15.4%, increased HDL-c by 41.7%, increased fecal cholesterol by 51.5% and fecal TBA by 61.4% at 70.05 mg/kg.
Reduced body weight by 9.2% at 70.05 mg/kg/day after 33 days of treatment versus HFHC group.
Suppressed liver Hmgcr mRNA expression, increased liver Ldlr mRNA expression by 8.5-fold, 9.78-fold, and 11-fold, increased liver Cyp7a1 mRNA expression (21% increase at 70.05 mg/kg), and increased liver Srebp-2 mRNA expression across all doses versus HFHC group.
Reduced liver HMGCR protein expression by 16.4%, increased liver SREBP-2, LDLR, and CYP7A1 protein expression by 46.0%, 51.9%, and 107% at 70.05 mg/kg versus HFHC group.
Increased liver LDLR protein expression by 30.7% and CYP7A1 protein expression at 46.7 mg/kg versus HFHC group.

Animal Model:

B6C3-Tg (APPswe, PSEN1dE9)85Dbo/J (A-PPswe/PS1ΔE9) (8-month-old male)^[4]
Dosage:

50 mg/kg
Administration:

p.o.; once daily; 1 month
Result:

Reduced escape latency to levels indistinguishable from wild-type mice.
Showed significantly shorter latency to first target crossing, increased number of target platform crossings, and increased time spent in the target quadrant, with performance matching wild-type mice.
Normalized serum IDO activity (measured by kynurenine/tryptophan ratio) to wild-type levels, without altering IDO mRNA or protein expression in brain tissue.
Reduced brain expression of GFAP (astrocytic activation marker) and CD11b (microglial activation marker) to wild-type levels.
Restored hippocampal MAP2 (neuronal marker) immunoreactivity in the CA1 region, which was reduced in AD control mice.
Significantly reduced hippocampal Aβ_1-42 plaque burden to near wild-type levels.

Chemical Information

CAS. Nr. 3486-66-6
Molecular Weight 320.32
Formel C₁₉H₁₄NO₄
SMILES

C1(C(CC[N+]2=C1C=C(C=C3)C(C4=C3OCO4)=C2)=C5)=CC6=C5OCO6
Synonyms

Coptisin
Structure Classification
- Alkaloids
- Quinoline Alkaloids
Initial Source
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Publications (11)

All

Sort by:

Journal Impact Factor

Phytomedicine

Jiao-tai-wan and its component coptisine attenuate PCOS by regulating mitochondrial cholesterol import through suppression of SIRT1 ubiquitination. [Abstract]

2025 Oct 21:148:157446. PMID: 41145090
Int Immunopharmacol

Coptisine inhibits aggressive and proliferative actions of fibroblast like synoviocytes and exerts a therapeutic potential for rheumatoid arthritis. [Abstract]

2024 Feb 15:128:111433. PMID: 38181676
Molecules

Discovery of Nine Dipeptidyl Peptidase-4 Inhibitors from Coptis chinensis Using Virtual Screening, Bioactivity Evaluation, and Binding Studies. [Abstract]

2024 May 14;29(10):2304. PMID: 38792165
Mater Technol (N Y N Y)

2026 Jan 27;41.
Naunyn Schmiedebergs Arch Pharmacol

Coptisine inhibits lipid accumulation in high glucose- and palmitic acid-induced HK-2 cells by regulating the AMPK/ACC/CPT-1 signaling pathway. [Abstract]

2025 May;398(5):5465-5474. PMID: 39560754
Vet Microbiol

The Chinese medicine monomer Schisandrin C inhibits PRRSV infection by regulating the OGT-PI3K/AKT/mTOR signaling pathway. [Abstract]

2026 May:316:110992. PMID: 41865607
DNA Cell Biol

Coptisine Blocks Secretion of Exosomal circCCT3 from Cancer-Associated Fibroblasts to Reprogram Glucose Metabolism in Hepatocellular Carcinoma. [Abstract]

2020 Oct 2. PMID: 33001706
Biochem Biophys Res Commun

Coptisine alleviates insulin resistance by suppressing SMARCE1-mediated glycolysis. [Abstract]

2026 Mar 26:806:153415. PMID: 41662796
Planta Med

Novel Approaches for the Analysis and Isolation of Benzylisoquinoline Alkaloids in Chelidonium majus. [Abstract]

2024 Jun;90(7-08):523-533. PMID: 38843792
SSRN

2024 Apr 1.
J Oncol

Pseudogene MSTO2P Interacts with miR-128-3p to Regulate Coptisine Sensitivity of Non-Small-Cell Lung Cancer (NSCLC) through TGF- β Signaling and VEGFC. [Abstract]

2022 Jun 26:2022:9864411. PMID: 35794983

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (292 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[1]. Rao PC, et al. Coptisine-induced cell cycle arrest at G2/M phase and reactive oxygen species-dependent mitochondria-mediated apoptosis in non-small-cell lung cancer A549 cells. Tumour Biol. 2017;39(3):1010428317694565. [Content Brief]

[2]. Guo J, et al. Coptisine protects rat heart against myocardial ischemia/reperfusion injury by suppressing myocardial apoptosis and inflammation. Atherosclerosis. 2013;231(2):384-391. [Content Brief]

[3]. He K, et al. The safety and anti-hypercholesterolemic effect of coptisine in Syrian golden hamsters. Lipids. 2015;50(2):185-194. [Content Brief]

[4]. Yu D, et al. The IDO inhibitor coptisine ameliorates cognitive impairment in a mouse model of Alzheimer's disease. J Alzheimers Dis. 2015;43(1):291-302. [Content Brief]

[5]. Chen HB, et al. Anti-inflammatory activity of coptisine free base in mice through inhibition of NF-κB and MAPK signaling pathways. Eur J Pharmacol. 2017;811:222-231. [Content Brief]

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Coptisine

11 Cited Publications

100 mg Angebot einholen

Subscribe to the

MedChemExpress

Newsletter

Produktname:
Art. -Nr.:
Menge:
MCE Japan Authorized Agent:

Produktname:
CAS. Nr.:
Species:
Reinheit:
Menge:

Coptisine

Publications Citing Use of MedChemExpress (MCE) Coptisine

Alle Indoleamine 2,3-Dioxygenase (IDO) Isoform-spezifische Produkte anzeigen

Alle NF-κB Isoform-spezifische Produkte anzeigen

Alle p38 MAPK Isoform-spezifische Produkte anzeigen

Alle PI3K Isoform-spezifische Produkte anzeigen

Alle Akt Isoform-spezifische Produkte anzeigen

Alle DNA/RNA Synthesis Isoform-spezifische Produkte anzeigen

Alle ROCK Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Chemical Information

Publications (11)

Reinheit & Dokumentation

Verweise

Calculators

Help & FAQs

Coptisine Related Classifications

HY-N0430 Related Classifications