Glaucine hydrobromide
Glaucine hydrobromide (O,O-Dimethylisoboldine hydrobromide) is an alkaloid extracted from Glaucium flavum that possesses various activities, including cough relief, bronchodilation, anti-inflammatory effects, analgesia, antipyretic properties, and anticancer effects. Glaucine hydrobromide acts as a selective and orally active inhibitor of phosphodiesterase 4 (PDE4), with a Ki of 3.4 µM in human bronchial tissues and polymorphonuclear leukocytes. Glaucine hydrobromide induces relaxation of human isolated bronchi by antagonizing calcium channels. Additionally, Glaucine hydrobromide inhibits the activation of NF-κB, leading to a reduction in the expression of the MMP-9 gene, thereby suppressing the migration and invasion of breast cancer cells. Therefore, Glaucine hydrobromide holds potential for research in asthma and breast cancer.
For research use only. We do not sell to patients.
- CAS No.: 5996-06-5
- Formula: C21H26BrNO4
- Molecular Weight:436.34
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Calcium Channel Isoforms
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Biological Activity
Description
IC50 & Target
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PDE4 |
In Vitro
Glaucine (0.1 μM-1 mM; 30 min) hydrobromide produces a concentration-dependent inhibition of both spontaneous tension and histamine (HY-B1204)-induced tension in isolated human bronchial tissues[1]. Glaucine (10 μM-1 mM; 30 min) hydrobromide concentration-dependently inhibits the concentration of calcium ions in isolated human bronchial tissues induced by potassium depolarization[1]. Glaucine (0.1-3 mM; 120 min) hydrobromide concentration-dependently inhibits the release of peroxidase from human eosinophils[1]. Glaucine (0-50 μM; 24 and 48 h) hydrobromide inhibits the proliferation of MCF-7 cells induced by Phorbol 12-myristate 13-acetate (HY-18739) in a concentration-dependent manner[4]. Glaucine (0-30 μM; 36 h) hydrobromide significantly blocks the expression and activity of MMP-9 in MCF-7 cells induced by Phorbol 12-myristate 13-acetate (HY-18739) in a dose-dependent manner[4]. Glaucine (0-30 μM; 24 h) hydrobromide significantly inhibits the invasion of MDA-MB-231 cells in a dose-dependent manner[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:PMA-induced MCF-7 cells
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Concentration:0, 1, 3, 15, 30 and 50 µM
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Incubation Time:24 and 48 h
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Result:Inhibited PMA-induced colony formation by 48 and 63 % at a dose of 15 and 30 µM.
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Cell Line:PMA-induced MCF-7 cells
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Concentration:0, 15 and 30 µM
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Incubation Time:36 h
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Result:Inhibited PMA-induced phosphorylation of IκBα in a dose-dependent manner and decreased nuclear NF-κB p65 subunit levels.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Ovalbumins (HY-W250978) sensitized guinea pigs to inhaled aerosol antigens[5]
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Dosage:10 mg/mL
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Administration:inhale; 10 min
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Result:Reduced airway hyperresponsiveness to histamine and lung eosinophil accumulation 30 minutes and 3 hours after inhalation of the antigen. Increased eosinophil peroxidase activity in bronchoalveolar lavage fluid 24 hours after inhalation of aerosol antigen.
Chemical Information
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CAS No. 5996-06-5
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Molecular Weight 436.34
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Formula C21H26BrNO4
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SMILES
CN1CCC2=CC(OC)=C(OC)C3=C2[C@]1([H])CC4=CC(OC)=C(OC)C=C34.Br
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Synonyms
O,O-Dimethylisoboldine hydrobromide; S-(+)-Glaucine hydrobromide; NSC 34396 hydrobromide
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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.
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Mitochondrial membrane-potential fluorescent assay
Mitochondrial membrane potential fluorescent assays estimate ΔΨm in living cells using lipophilic cationic dyes such as TMRM, TMRE, rhodamine 123, and JC-1, which accumulate in mitochondria according to membrane polarization; loss of signal after FCCP or CCCP treatment is interpreted as mitochondrial depolarization. TMRM/TMRE and rhodamine 123 are commonly used for semi-quantitative live-cell microscopy or flow cytometry, while JC-1 can report a shift from red aggregate fluorescence to green monomer fluorescence during depolarization; interpretation requires controls because dye concentration, quenching mode, cell type, dye efflux, and mitochondrial mass can affect fluorescence independently of ΔΨm.
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Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
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Mitochondrial membrane-potential and mitochondrial mass staining
Mitochondrial membrane potential staining measures the electrochemical polarization across the mitochondrial inner membrane in live cells using lipophilic cationic fluorescent probes; early rhodamine-based work showed that selective mitochondrial dye accumulation is lost when the mitochondrial transmembrane potential is dissipated. JC-1 reports mitochondrial polarization by shifting from green monomer fluorescence to red J-aggregate fluorescence as dye concentration increases within energized mitochondria; therefore, the red/green fluorescence ratio is used as a relative readout of mitochondrial membrane potential. TMRE or TMRM staining provides a single-channel relative readout because these cationic rhodamine esters accumulate in polarized mitochondria, and lower fluorescence indicates reduced mitochondrial polarization when acquisition and dye-loading conditions are controlled. Mitochondrial mass staining is commonly performed with MitoTracker Green FM or related MitoTracker dyes as
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Cell invasion
Cell invasion is the ability of cells to migrate from one area to another via the extracellular matrix. Cell invasion is the response of normal and cancer cells to chemical and mechanical stimuli. Before migrating to a new region, the extracellular matrix is degraded by proteases within the cell. Cell invasion often occurs during wound repair, vascularization and inflammation, abnormal tissue invasion, and tumor cell metastasis.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
Purity & Documentation
References
[1]. J Cortijo, et al. Bronchodilator and Anti-Inflammatory Activities of Glaucine: In Vitro Studies in Human Airway Smooth Muscle and Polymorphonuclear Leukocytes. Br J Pharmacol. 1999 Aug;127(7):1641-51. [Content Brief]
[2]. Golo M J Meyer, et al. Studies on the in Vivo Contribution of Human Cytochrome P450s to the Hepatic Metabolism of Glaucine, a New Drug of Abuse. Biochem Pharmacol. 2013 Nov 15;86(10):1497-506. [Content Brief]
[3]. Maya Spasova, et al. Cinnamoyl- And Hydroxycinnamoyl Amides of Glaucine and Their Antioxidative and Antiviral Activities. Bioorg Med Chem. 2008 Aug 1;16(15):7457-61. [Content Brief]
[4]. Hyereen Kang, et al. "Glaucine inhibits breast cancer cell migration and invasion by inhibiting MMP-9 gene expression through the suppression of NF-κB activation." Molecular and cellular biochemistry 403 (2015): 85-94. [Content Brief]
[5]. Pons, et al. "Effects of inhaled glaucine on pulmonary responses to antigen in sensitized guinea pigs." European journal of pharmacology 397.1 (2000): 187-195. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)