product name Carbamazepine
Description: Carbamazepine (also known as NSC 169864, Carbatrol) is a sodium channel blocker with IC50 of 131 μM in rat brain synaptosomes. Carbamazepine is a medication used primarily in the treatment of epilepsy and neuropathic pain. For seizures it works as well as phenytoin and valproate. It is not effective for absence seizures or myoclonic seizures. It may be used in schizophrenia along with other medications and as a second line agent in bipolar disorder.
References: Mol Pharmacol. 1982 Nov;22(3):627-35; Epilepsy Res. 1997 Sep;28(2):143-53.
236.27
Formula
C15H12N2O
CAS No.
298-46-4
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 47 mg/mL (198.9 mM)
Water: <1 mg/mL
Ethanol: 18 mg/mL (76.2 mM)
Solubility (In vivo)
1% DMSO+30% polyethylene glycol+1% Tween 80: 5 mg/mL
Synonyms
NSC 169864
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19395628
| In Vitro |
In vitro activity: Carbamazepine inhibits the binding of [3H]batrachotoxinin A 20-α-benzoate (BTX-B) to a receptor site of voltage-sensitive sodium channel with IC50 of 131 μM, to decrease the activation of sodium channel ion flux in rat brain synaptosomes. Carbamazepine reduces receptor affinity due to an increased rate of ligand dissociation from the receptor-ligand complex, without altering maximal binding capacity from the scatchard analysis of BTX-B binding to synaptosome, suggesting an indirect allosteric mechanism for anticonvulsant inhibition of BTX-B binding. Carbamazepine does not alter basal 125I-labeled scorpion toxin binding to synaptosomes in the absence of batrachotoxin, but when batrachotoxin (1.25 μM) added, Carbamazepine inhibits the batrachotoxin-dependent increase in scorpion toxin binding in a concentration-dependent manner with IC50 of 260 μM mediated at the alkaloid toxin binding site, none of which affects [3H]saxitoxin binding. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Carbamazepine at 25 mg/kg significantly increases extracellular levels of striatal and hippocampal dopamine (DA), 3,4-dihydroxyphenylalanine (DOPA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in a dose dependent manner, while Carbamazepine at 50 mg/kg significantly decreases total levels of striatal DA and DOPA as well as hippocampal HVA, but has no effect on total levels of striatal DOPAC and HVA nor on hippocampal DA, DOPA and DOPAC. Intraperitoneal administration of Carbamazepine （~100 mg/kg）to rats produces significant increases in the cerebral cortical concentrations of neuroactive steroids and neuroactive steroids in plasma in a dose and time dependent maner with DHEA formed as a result of side chain cleavage of pregnenolone not affected. |
| Animal model | Male Wistar rats |
| Formulation & Dosage | Dissolved in saline/DMSO (50/50 vol/vol); 100 mg/kg; i.p. injection |
| References | Mol Pharmacol. 1982 Nov;22(3):627-35; Epilepsy Res. 1997 Sep;28(2):143-53. |
Related Posts
product name Carbamazepine
Description: Carbamazepine (also known as NSC 169864, Carbatrol) is a sodium channel blocker with IC50 of 131 μM in rat brain synaptosomes. Carbamazepine is a medication used primarily in the treatment of epilepsy and neuropathic pain. For seizures it works as well as phenytoin and valproate. It is not effective for absence seizures or myoclonic seizures. It may be used in schizophrenia along with other medications and as a second line agent in bipolar disorder.
References: Mol Pharmacol. 1982 Nov;22(3):627-35; Epilepsy Res. 1997 Sep;28(2):143-53.
236.27
Formula
C15H12N2O
CAS No.
298-46-4
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 47 mg/mL (198.9 mM)
Water: <1 mg/mL
Ethanol: 18 mg/mL (76.2 mM)
Solubility (In vivo)
1% DMSO+30% polyethylene glycol+1% Tween 80: 5 mg/mL
Synonyms
NSC 169864
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19395628
| In Vitro |
In vitro activity: Carbamazepine inhibits the binding of [3H]batrachotoxinin A 20-α-benzoate (BTX-B) to a receptor site of voltage-sensitive sodium channel with IC50 of 131 μM, to decrease the activation of sodium channel ion flux in rat brain synaptosomes. Carbamazepine reduces receptor affinity due to an increased rate of ligand dissociation from the receptor-ligand complex, without altering maximal binding capacity from the scatchard analysis of BTX-B binding to synaptosome, suggesting an indirect allosteric mechanism for anticonvulsant inhibition of BTX-B binding. Carbamazepine does not alter basal 125I-labeled scorpion toxin binding to synaptosomes in the absence of batrachotoxin, but when batrachotoxin (1.25 μM) added, Carbamazepine inhibits the batrachotoxin-dependent increase in scorpion toxin binding in a concentration-dependent manner with IC50 of 260 μM mediated at the alkaloid toxin binding site, none of which affects [3H]saxitoxin binding. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Carbamazepine at 25 mg/kg significantly increases extracellular levels of striatal and hippocampal dopamine (DA), 3,4-dihydroxyphenylalanine (DOPA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in a dose dependent manner, while Carbamazepine at 50 mg/kg significantly decreases total levels of striatal DA and DOPA as well as hippocampal HVA, but has no effect on total levels of striatal DOPAC and HVA nor on hippocampal DA, DOPA and DOPAC. Intraperitoneal administration of Carbamazepine （~100 mg/kg）to rats produces significant increases in the cerebral cortical concentrations of neuroactive steroids and neuroactive steroids in plasma in a dose and time dependent maner with DHEA formed as a result of side chain cleavage of pregnenolone not affected. |
| Animal model | Male Wistar rats |
| Formulation & Dosage | Dissolved in saline/DMSO (50/50 vol/vol); 100 mg/kg; i.p. injection |
| References | Mol Pharmacol. 1982 Nov;22(3):627-35; Epilepsy Res. 1997 Sep;28(2):143-53. |