Boldine
Based on 1 publication(s) in Google Scholar
Boldine is an aporphine alkaloid telomerase (telomerase) inhibitor (IC50 of 0.17 μM for TERT) and a pannexin/connexin hemichannel blocker, with oral activity and blood-brain barrier permeability. Boldine inhibits telomerase activity through direct interaction with the telomerase ribonucleoprotein and non-competitive binding near the TERT active site, and downregulates hTERT mRNA while shifting alternative splicing toward non-functional transcripts. Boldine blocks Panx1, Cx43, Cx26, and Cx30 hemichannels as well as P2X7 receptor-mediated calcium influx. Boldine exhibits antioxidant, anti-inflammatory, antiproliferative, and cytotoxic activities by scavenging ROS, inhibiting NFκB, dephosphorylating SGK1, and reducing TNF-alpha levels. Boldine can be used in research on breast cancer, Alzheimer's disease, glioblastoma, diabetes, and spinal cord injury.
For research use only. We do not sell to patients.
- Purity : 99.24%
- CAS No.: 476-70-0
- Formula: C19H21NO4
- Molecular Weight:327.37
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Publications Citing Use of MedChemExpress (MCE) Boldine
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Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| SH-SY5Y | IC50 |
81 μM
Compound: 5
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Displacement of [125I]alpha-bungarotoxin from human alpha-7 nAChR expressed in SH-SY5Y cells
Displacement of [125I]alpha-bungarotoxin from human alpha-7 nAChR expressed in SH-SY5Y cells
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[PMID: 17391965] |
| Vero | CC50 |
250 μM
Compound: 6
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Cytotoxicity against african green monkey Vero cells
Cytotoxicity against african green monkey Vero cells
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[PMID: 9584402] |
| Vero | ED50 |
125 μM
Compound: 6
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Antiviral activity against Poliovirus 2 Sabin 2 infected in african green monkey Vero cells at 0.001 multiplicity of infection assessed as inhibition of virus-induced cytopathogenicity
Antiviral activity against Poliovirus 2 Sabin 2 infected in african green monkey Vero cells at 0.001 multiplicity of infection assessed as inhibition of virus-induced cytopathogenicity
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[PMID: 9584402] |
In Vitro
Boldine (48 h) exhibits dose- and time-dependent cytotoxicity in HEK293, MDA-MB-231, and MCF-7 cells, with IC50 values of 110 μM, 150 μM, and 160 μM, respectively, while showing less toxicity to normal HFF cells[1].
Boldine (0-300 μM; 72 h) inhibits the growth of primary human GBM59, GBM96, and U87-MG glioblastoma cells in a concentration-dependent manner, with IC50 values of 68.6 μM, 141.7 μM, and 213.8 μM, respectively[4].
Boldine (50-300 μM; 15 min) inhibits hemichannel activity in patient-derived GBM59, GBM96, and U87-MG glioblastoma cells[4].
Boldine (0-160 μM; 48 h) significantly inhibits telomerase activity in MCF-7, MDA-MB-231, and HEK293 cells in a dose-dependent manner, with IC50 values of 60 μM, 29.1 μM, and 38.8 μM, respectively[1].
Boldine (0-160 μM; 48 h) decreases hTERT mRNA levels in MCF-7 cells in a dose-dependent manner[1].
Boldine (0-160 μM; 48 h) stimulates nonfunctional splice variants of hTERT, and in MCF-7 cells, the -b variant is the only detectable transcript at 160 μM[1].
Boldine (100-500 μM; 5 min) inhibits hemichannel activity in LPS-treated cultured mouse cortical astrocytes[3].
Boldine (100 μM) inhibits Panx1 hemichannels in HeLa-Panx1-YPF cells[3].
Boldine (50 μM; 15 min) inhibits hemichannel activity in rat SVZ neurosphere-derived NPCs[4].
Boldine (50-100 μM; 72 h) decreases the diameter of rat SVZ neurosphere-derived NPCs and disrupts the integrity of neurospheres[4].
Boldine (50 μM; 72 h) reduces the proliferation of NPCs derived from rat SVZ neurospheres, as evidenced by decreased BrdU incorporation[4].
Boldine (50 μM) blocks Cx26 and Cx30 hemichannels and blocks P2X7R in transfected HeLa cells[8].
Boldine (10-100 μM; 1 h) prevents LPS (HY-D1056)-induced activation of SGK1 and NFκB in cardiac fibroblasts isolated from neonatal Sprague-Dawley rats[2].
Boldine (100 μM; 1 h) prevents inflammatory responses induced by LPS, IFN-γ, and conditioned medium in neonatal Sprague-Dawley rat cardiac fibroblasts[2].
Boldine (100 μM; 1 h) prevents LPS-induced oxidative stress in cardiac fibroblasts isolated from neonatal Sprague-Dawley rats[2].
Boldine directly scavenges superoxide anions and highly reactive hydroxyl radicals[6].
Boldine (1-100 μM; 1 h (STZ); 30 min (iron/ascorbate)) attenuates lipid peroxidation, protein oxidation, and thiol oxidation induced by STZ (HY-13753) and iron/ascorbate in rat pancreatic homogenates in a dose-dependent manner[6].
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:MCF-7
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Concentration:0, 10, 100, 160 μM
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Incubation Time:48 h
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Result:Caused a dose-dependent repression of transcripts of the hTERT gene.
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Cell Line:MCF-7
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Concentration:0, 10, 100, 160 μM
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Incubation Time:48 h
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Result:Decreased the full-length variant while the three shorter transcripts were still visible.
At 10 μM, the full-length transcript exhibited a marked decrease while all non-functional variants remained unchanged.
At 160 μM, the -b spliced form was the only detectable variant.
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Cell Line:Cardiac fibroblasts (CF) isolated from neonatal Sprague-Dawley rats
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Concentration:10, 50, 100 μM (NFκB phosphorylation); 100 μM (NFκB nuclear localization, SGK1/NDRG1 phosphorylation, SGK1 mRNA)
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Incubation Time:1 h pretreatment followed by 1 μg/mL LPS for 6 h (NFκB phosphorylation, NFκB nuclear localization, SGK1/NDRG1 phosphorylation); 1 h pretreatment followed by 1 μg/mL LPS for 8 h (SGK1 mRNA)
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Result:Prevented NFκB phosphorylation induced by LPS at 100 μM.
Reduced NFκB nuclear localization induced by LPS at 100 μM.
Inhibited LPS-induced activation of SGK1 at 100 μM, evidenced by reduced phosphorylation of SGK1 and its downstream target NDRG after 6 h of LPS treatment.
Decreased SGK1 mRNA expression after 8 h of LPS treatment at 100 μM.
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Cell Line:Cardiac fibroblasts (CF) isolated from neonatal Sprague-Dawley rats and monocytes derived from rat spleen (SMC)
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Concentration:100 μM (boldine); 1 μg/mL (LPS); 10 ng/mL (IFN-γ); conditioned medium (CM)
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Incubation Time:1 h pretreatment (boldine); 6 h (LPS for protein); 24 h (LPS for adhesion); 4 h (co-incubation with SMC)
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Result:Prevented the LPS-induced increase in pro-inflammatory cytokines IL-1β and TNF-α mRNA expression at 100 μM.
Inhibited the upregulation of ICAM1 and VCAM1 at both protein and mRNA levels at 100 μM.
Reduced monocyte adhesion on LPS-stimulated CFs at 100 μM.
Blocked the increase in ICAM1 and VCAM1 protein levels induced by IFN-γ and CM at 100 μM.
Reduced monocyte adhesion to CFs stimulated by IFN-γ and CM at 100 μM.
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Cell Line:Rat subventricular zone (SVZ) neural progenitor cells (NPCs)
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Concentration:50 μM
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Incubation Time:72 h
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Result:Reduced BrdU incorporation from 29.3% to 12.7%.
In Vivo
Boldine (100 mg/kg; p.o.; daily; 8 weeks) attenuates the development of STZ-induced diabetes in rats by preventing the increase in blood glucose levels, reducing body weight loss, and alleviating oxidative mitochondrial damage in multiple organs[6].
Boldine (2.5-40 mg/kg; i.p.) significantly inhibits Apomorphine (HY-12723)-induced yawning and penile erection in rats, with an inhibition rate exceeding 50%[7].
Boldine (50 mg/kg; p.o.; daily; starting from 3 dpi), administered starting 3 days after contusive SCI, significantly improves motor function, preserves white matter, and reduces glial reactivity in mice[8].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley rats (male, 250-260 g, streptozotocin-induced diabetes)[6]
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Dosage:100 mg/kg
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Administration:p.o.; daily; 8 weeks
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Result:Attenuated the development of hyperglycemia and weight loss induced by STZ injection.
Reduced plasma glucose levels to 330.6 mg/dl at 4 weeks and 311.4 mg/dl at 8 weeks, compared to 505.2 mg/dl and 538.4 mg/dl in the STZ group.
Attenuated STZ-induced weight loss, with body weight at 8 weeks of 298 g versus 221 g in the STZ group.
Significantly lowered MDA levels in pancreas and liver mitochondria.
Significantly lowered carbonyl contents in pancreas and kidney mitochondria.
Decreased increased MnSOD activities in the pancreas and kidney.
Restored altered GSH-Px enzyme activities in the liver and pancreas.
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Animal Model:Wistar (Charles River, France; male; 220 ± 40 g)[7]
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Dosage:2.5 mg/kg; 10 mg/kg; 20 mg/kg; 40 mg/kg
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Administration:i.p.; single dose
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Result:Inhibited Apomorphine-induced yawning by more than 50% at 40 mg/kg.
Inhibited Apomorphine-induced penile erections by more than 50% at 40 mg/kg.
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Animal Model:C57Bl6 (male and female, 4 months of age)[8]
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Dosage:50 mg/kg
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Administration:p.o.; daily; starting at 3 dpi
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Result:Improved locomotor function as assessed by BMS scores in males at 7 dpi (3.41 vs. 2.29), 14 dpi (6.56 vs. 4.61), 21 dpi (7.44 vs. 5.57), and 28 dpi (7.94 vs. 6.11).
Improved locomotor function as assessed by BMS scores in females at 14 dpi (4.84 vs. 3.53), 21 dpi (5.89 vs. 4.88), and 28 dpi (6.46 vs. 5.00).
Showed a lower percentage of foot placement errors in the LRWT at 14 dpi (14.7% vs. 37.4% for males; 21.6% vs. 38.0% for females), 21 dpi (12.0% vs. 30.2% for males; 16.0% vs. 30.1% for females), and 28 dpi (8.9% vs. 23.3% for males; 11.2% vs. 22.0% for females).
Significantly increased spared white matter at 28 dpi and reduced lesion volume.
Reduced immunofluorescence for GFAP and Iba1 while increasing GAP43 fluorescence in sections rostral to the injury site at 14 dpi.
Reduced mRNA levels of Ccl2, IL-6, S100a, Cd68, Iba1, Gfap, and Mmp9, and increased mRNA levels of Snap25 and Gap43 at 14 dpi.
Showed significantly lower levels of Gfap and S100a8 mRNA in RNAscope in-situ hybridization at 14 dpi.
Identified 426 upregulated and 913 downregulated genes in the spinal cord segment caudal to the lesion at 14 dpi.
Chemical Information
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CAS No. 476-70-0
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Appearance Solid
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Molecular Weight 327.37
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Formula C19H21NO4
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Color Off-white to light yellow
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SMILES
OC1=C(OC)C2=C3C(CCN(C)[C@@]3([H])CC4=CC(O)=C(OC)C=C24)=C1
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Publications (1)
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Journal Impact Factor
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Most Recent
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Phytother Res
Total glucosides of white paeony capsule alleviate articular cartilage degeneration and aberrant subchondral bone remodeling in knee osteoarthritis. [Abstract]2025 Apr;39(4):1758-1775. PMID: 38649260
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (305.46 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL (7.64 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 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.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (7.64 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 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.
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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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
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).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
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.
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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Transepithelial/transendothelial electrical resistance assay
TEER measures electrical resistance across epithelial or endothelial monolayers cultured on permeable supports, and the readout reflects ionic conductance through the cell barrier, especially the paracellular pathway regulated by junctional integrity. TEER can be measured without destroying the monolayer and is commonly used before or during transport, permeability, barrier-disruption, and barrier-maturation experiments. TEER values are influenced by biological maturation and technical conditions; reported factors include temperature, medium formulation, passage number, electrode geometry, membrane properties, and junctional length during early monolayer maturation. Therefore, TEER should be interpreted with blank-insert subtraction, area normalization, repeated readings, and, when possible, orthogonal barrier readouts such as FITC-dextran flux or tight-junction staining.
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Ca2+ Staining Technique
Ca2+ staining is an experimental technique that utilizes specific fluorescent probes (such as Fluo-4 AM, Fura-2, etc.) to qualitatively or quantitatively detect dynamic changes in intracellular Ca2+ concentrations; this is achieved by monitoring the changes in fluorescent signals generated when these probes bind to free intracellular calcium ions. The underlying principle relies primarily on the presence of chelating groups within the probe's molecular structure that possess high affinity for calcium ions.
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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.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
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CRISPR-Cas9 RNP editing of primary immune cells
CRISPR-Cas9 RNP editing uses preassembled Cas9 protein and guide RNA to direct sequence-specific DNA cleavage at a genomic target, after which cellular DNA repair generates insertions/deletions for knockout or uses an added donor template for knock-in. In primary immune cells, published protocols deliver Cas9 RNPs mainly by electroporation or nucleofection because these methods can introduce protein-RNA complexes into difficult-to-transfect T cells, B cells, NK cells, monocytes, myeloid cells, and innate lymphoid cells without viral Cas9 expression.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
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Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
Purity & Documentation
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Data Sheet (309 KB)
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SDS (396 KB)
- English - EN (396 KB)
- Français - FR (396 KB)
- Deutsch - DE (396 KB)
- Norwegian - NO (396 KB)
- Español - ES (396 KB)
- Swedish - SV (396 KB)
- Italian - IT (396 KB)
- Korean - KR (396 KB)
- Portuguese - PT (396 KB)
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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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 3.0546 mL | 15.2732 mL | 30.5465 mL | 76.3662 mL |
| 5 mM | 0.6109 mL | 3.0546 mL | 6.1093 mL | 15.2732 mL | |
| 10 mM | 0.3055 mL | 1.5273 mL | 3.0546 mL | 7.6366 mL | |
| 15 mM | 0.2036 mL | 1.0182 mL | 2.0364 mL | 5.0911 mL | |
| 20 mM | 0.1527 mL | 0.7637 mL | 1.5273 mL | 3.8183 mL | |
| 25 mM | 0.1222 mL | 0.6109 mL | 1.2219 mL | 3.0546 mL | |
| 30 mM | 0.1018 mL | 0.5091 mL | 1.0182 mL | 2.5455 mL | |
| 40 mM | 0.0764 mL | 0.3818 mL | 0.7637 mL | 1.9092 mL | |
| 50 mM | 0.0611 mL | 0.3055 mL | 0.6109 mL | 1.5273 mL | |
| 60 mM | 0.0509 mL | 0.2546 mL | 0.5091 mL | 1.2728 mL | |
| 80 mM | 0.0382 mL | 0.1909 mL | 0.3818 mL | 0.9546 mL | |
| 100 mM | 0.0305 mL | 0.1527 mL | 0.3055 mL | 0.7637 mL |
Boldine Related Classifications
HY-N6973 Related Classifications
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