Declopramide
Declopramide (3-Chloroprocainamide) is an orally active, blood-brain barrier-permeable IκBβ/NF-κB inhibitor and chemosensitizer. Declopramide exhibits affinity for rabbit 5-HT3 receptors (5-HT3R) with a Ki value of 3.2 μM. Declopramide inhibits IκBβ degradation, blocks NFκB activation, and induces rapid apoptosis and DNA strand breaks in cancer cells. Declopramide enhances the cytotoxicity induced by Cisplatin (HY-17394) and is also metabolically converted to N-acetyl declopramide. Declopramide can be used in the research of tumors such as brain astrocytoma.
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- CAS No.: 891-60-1
- Formule: C13H20ClN3O
- Masse moléculaire:269.77
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Pureté et documentation
- Références
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Activité biologique
Declopramide (250-1000 µM; 20 h) induces dose-dependent caspase-mediated early apoptosis in 70Z/3 mouse pre-B cells[1].
Declopramide (250-1000 µM; 24 h) inhibits LPS-induced activation of NF-κB in 70Z/3 mouse pre-B cells[1].
Declopramide inhibits the growth of HL60 and K562 leukemia cells in vitro, but its activity is weaker than that of its metabolite N-acetyl-declopramide[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:murine pre-B-cell line 70Z/3
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Concentration:250 µM; 500 µM; 1000 µM; 500 µM (with 1 h ZVADfmk pretreatment)
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Incubation Time:20 h; 17 h (with 1 h ZVADfmk pretreatment)
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Result:Induced a dose-dependent increase in early apoptosis (Annexin V-positive/7AAD-negative cells) and corresponding decrease in viable (7AAD-negative) cells in 70Z/3 cells.
Reduced viable cell percentage and increased early apoptotic cell percentage relative to untreated cells at 500 µM.
Significantly reduced declopramide-induced apoptosis when caspase inhibitor ZVADfmk was used, measured via both 7AAD and Annexin V staining.
| Species | Dose | Route | T1/2 (Absorption) | T1/2β | Tmax | Cmax | Vd | CL | AUC | Bioavailability |
|---|---|---|---|---|---|---|---|---|---|---|
| Rat[3] | 25 mg/kg | i.v. | / | 36.6 min | / | 33.6 nM | 2.4 L/kg | 45 nM/mL | 30.25 nM·h | / |
| Rat[3] | 25 mg/kg | i.m. | 2.8 min | 43.3 min | 11.8 min | 11.3 nM | 5.3 L/kg | 85 nM/mL | 15.62 nM·h | 52 % |
| Rat[3] | 25 mg/kg | p.o. | 5.85 min | 8.8 min | 10.3 min | 9.0 nM | 3.9 L/kg | 308 nM/mL | 4.3 nM·h | 14.2 % |
Declopramide (25-200 mg/kg; i.m., p.o.; single dose) does not induce central nervous system-related sedative side effects in female Wistar-Furth rats[3].
Declopramide (25 mg/kg; i.m., p.o.; single dose) distributes to the brain, spleen and tumor tissues in scid mice bearing H2981 xenografts[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:SCID mice (xenografted with human T24 brain astrocytoma cells)[2]
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Dosage:40 mg/kg
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Administration:p.o.; 3 doses at 0, 24, and 48 hours
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Result:Exhibited equivalent in vivo tumor growth inhibitory efficacy to intramuscularly administered 40 mg/kg declopramide.
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Animal Model:Wistar-Furth (female, 2 months old, ~200 g)[3]
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Dosage:25 mg/kg; 200 mg/kg
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Administration:i.m.; single dose; p.o.; single dose
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Result:Showed no observable sedative side effects or notable symptoms across all tested doses and observation periods.
Detected no significant differences in tunnel travel time between declopramide-treated rats and control rats at any dosage, administration route, or time point.
Chemical Information
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CAS No. 891-60-1
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Masse moléculaire 269.77
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Formule C13H20ClN3O
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SMILES
O=C(NCCN(CC)CC)C1=CC=C(N)C(Cl)=C1
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Synonyms
3-Chloroprocainamide
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
[1]. Liberg D, et al. N-substituted benzamides inhibit NFkappaB activation and induce apoptosis by separate mechanisms. British journal of cancer. 1999 Nov;81(6):981-8. [Content Brief]
[2]. Hua J, et al. Comparison of antitumor activity of declopramide (3-chloroprocainamide) and N-acetyl-declopramide. Anticancer research. 1999;19(1A):285-90. [Content Brief]
[3]. Hua J, et al. Pharmacokinetics and central nervous system toxicity of declopramide (3-chloroprocainamide) in rats and mice. Anti-cancer drugs. 1999 Jan;10(1):79-88. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Declopramide Related Classifications
HY-111193 Related Classifications
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