Boldine hydrochloride
Based on 1 publication(s) in Google Scholar
Boldine hydrochloride 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 hydrochloride 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 hydrochloride blocks Panx1, Cx43, Cx26, and Cx30 hemichannels as well as P2X7 receptor-mediated calcium influx. Boldine hydrochloride exhibits antioxidant, anti-inflammatory, antiproliferative, and cytotoxic activities by scavenging ROS, inhibiting NFκB, dephosphorylating SGK1, and reducing TNF-alpha levels. Boldine hydrochloride can be used in research on breast cancer, Alzheimer's disease, glioblastoma, diabetes, and spinal cord injury.
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- CAS 番号: 16625-69-7
- 分子式: C19H22ClNO4
- 分子量:363.84
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
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MedChemExpress（MCE）の使用を引用している文献 Boldine hydrochloride
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生物活性
製品説明
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HEK293 | IC50 |
110 μM
|
Cytotoxicity against human HEK293 embryonic kidney cells assessed as reduction in cell viability after 48 hrs treatment by MTT assay.
Cytotoxicity against human HEK293 embryonic kidney cells assessed as reduction in cell viability after 48 hrs treatment by MTT assay.
|
25746354 |
| MDA-MB-231 | IC50 |
150 μM
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Cytotoxicity against human MDA-MB-231 breast cancer cells assessed as reduction in cell viability after 48 hrs treatment by MTT assay.
Cytotoxicity against human MDA-MB-231 breast cancer cells assessed as reduction in cell viability after 48 hrs treatment by MTT assay.
|
25746354 |
| MCF7 | IC50 |
160 μM
|
Cytotoxicity against human MCF-7 breast cancer cells assessed as reduction in cell viability after 48 hrs treatment by MTT assay.
Cytotoxicity against human MCF-7 breast cancer cells assessed as reduction in cell viability after 48 hrs treatment by MTT assay.
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25746354 |
| HFF | IC50 |
280 μM
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Cytotoxicity against human foreskin fibroblasts (HFF) assessed as reduction in cell viability after 48 hrs treatment by MTT assay.
Cytotoxicity against human foreskin fibroblasts (HFF) assessed as reduction in cell viability after 48 hrs treatment by MTT assay.
|
25746354 |
| MCF7 | IC50 |
60 μM
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Inhibition of telomerase activity in human MCF-7 breast cancer cell lysates incubated for 48 hrs by SYBR Green q-TRAP assay.
Inhibition of telomerase activity in human MCF-7 breast cancer cell lysates incubated for 48 hrs by SYBR Green q-TRAP assay.
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25746354 |
| MDA-MB-231 | IC50 |
29.1 μM
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Inhibition of telomerase activity in human MDA-MB-231 breast cancer cell lysates incubated for 48 hrs by SYBR Green q-TRAP assay.
Inhibition of telomerase activity in human MDA-MB-231 breast cancer cell lysates incubated for 48 hrs by SYBR Green q-TRAP assay.
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25746354 |
| HEK293 | IC50 |
38.8 μM
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Inhibition of telomerase activity in human HEK293 embryonic kidney cell lysates incubated for 48 hrs by SYBR Green q-TRAP assay.
Inhibition of telomerase activity in human HEK293 embryonic kidney cell lysates incubated for 48 hrs by SYBR Green q-TRAP assay.
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25746354 |
| U-87MG ATCC | IC50 |
213.8 μM
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Inhibition of cell growth in human U87-MG glioblastoma cells assessed after 72 hrs of treatment by MTT assay.
Inhibition of cell growth in human U87-MG glioblastoma cells assessed after 72 hrs of treatment by MTT assay.
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37655012 |
| MCF7 | LD50 |
160 μM
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Cytotoxicity against human MCF7 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.
Cytotoxicity against human MCF7 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.
|
29671783 |
| MDA-MB-231 | LD50 |
150 μM
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Cytotoxicity against human MDA-MB-231 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.
Cytotoxicity against human MDA-MB-231 breast cancer cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.
|
29671783 |
体外実験
Boldine (48 h) hydrochloride 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) hydrochloride 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) hydrochloride inhibits hemichannel activity in patient-derived GBM59, GBM96, and U87-MG glioblastoma cells[4].
Boldine (0-160 μM; 48 h) hydrochloride 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) hydrochloride decreases hTERT mRNA levels in MCF-7 cells in a dose-dependent manner[1].
Boldine (0-160 μM; 48 h) hydrochloride 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) hydrochloride inhibits hemichannel activity in LPS-treated cultured mouse cortical astrocytes[3].
Boldine (100 μM) hydrochloride inhibits Panx1 hemichannels in HeLa-Panx1-YPF cells[3].
Boldine (50 μM; 15 min) hydrochloride inhibits hemichannel activity in rat SVZ neurosphere-derived NPCs[4].
Boldine (50-100 μM; 72 h) hydrochloride decreases the diameter of rat SVZ neurosphere-derived NPCs and disrupts the integrity of neurospheres[4].
Boldine hydrochloride (50 μM; 72 h) reduces the proliferation of NPCs derived from rat SVZ neurospheres, as evidenced by decreased BrdU incorporation[4].
Boldine (50 μM) hydrochloride blocks Cx26 and Cx30 hemichannels and blocks P2X7R in transfected HeLa cells[8].
Boldine (10-100 μM; 1 h) hydrochloride 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) hydrochloride prevents inflammatory responses induced by LPS, IFN-γ, and conditioned medium in neonatal Sprague-Dawley rat cardiac fibroblasts[2].
Boldine (100 μM; 1 h) hydrochloride prevents LPS-induced oxidative stress in cardiac fibroblasts isolated from neonatal Sprague-Dawley rats[2].
Boldine hydrochloride directly scavenges superoxide anions and highly reactive hydroxyl radicals[6].
Boldine (1-100 μM; 1 h (STZ); 30 min (iron/ascorbate)) hydrochloride 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.
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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%.
体内実験
Boldine (100 mg/kg; p.o.; daily; 8 weeks) hydrochloride 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.) hydrochloride 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) hydrochloride, 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.
- RNA extraction experimental
- ROS/oxidative-stress fluorescent staining
- Transepithelial/transendothelial electrical resistance assay
- Ca2+ Staining Technique
- Research Protocol for Inflammation-related Diseases
- Breast Cancer Modeling
- Research Protocol for Metabolic Diseases
- CRISPR-Cas9 RNP editing of primary immune cells
- Cell Viability Determination by MTT Colorimetric Assay
- Alzheimer’s Disease Modeling
化学情報
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CAS 番号 16625-69-7
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分子量 363.84
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分子式 C19H22ClNO4
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SMILES
OC1=C(OC)C2=C3C(CCN(C)[C@@]3([H])CC4=CC(O)=C(OC)C=C24)=C1.Cl
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
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
純度とドキュメンテーション
参考文献
[2]. Catalán M, et al. Boldine prevents the inflammatory response of cardiac fibroblasts induced by SGK1-NFκB signaling pathway activation. Cellular signalling. 2024 Aug;120:111241. [Content Brief]
[3]. Yi C, et al. Inhibition of glial hemichannels by boldine treatment reduces neuronal suffering in a murine model of Alzheimer's disease. Glia. 2017 Oct;65(10):1607-1625. [Content Brief]
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
Boldine hydrochloride 関連分類
HY-W683756 関連分類
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