Carbamazepine

SKU: orb1310147

Description

Carbamazepine is a tricyclic anticonvulsant and analgesic agent structurally similar to TCAs. It reduces polysynaptic responses and blocks post-tetanic potentiation, underpinning its use in epilepsy and trigeminal neuralgia research. Its mechanisms are studied in vitro and in animal models for neuropathic pain and seizure disorders.

Research Area

Cell Biology, Epigenetics & Chromatin, Metabolism Research, Molecular Biology, Pharmacology & Drug Discovery

Key Properties

• CAS Number: 298-46-4
• MW: 236.2686
• Purity: >99.99% (May vary between batches)
• Formula: C₁₅H₁₂N₂O
• SMILES: NC(=O)N1C2=CC=CC=C2C=CC2=C1C=CC=C2
• Target: Calcium Channel,Sodium Channel,Potassium Channel,Mitophagy,Autophagy,HDAC
• Solubility: DMSO:62 mg/mL (262.41 mM);Ethanol:15 mg/mL (63.49 mM);10% DMSO+40% PEG300+5% Tween 80+45% Saline:2 mg/mL (8.46 mM)

Bioactivity

• Target IC50:
  Na+ channel:131 μM
• In Vivo:
  Treatment with Carbamazepine (25 mg/kg) significantly increases the levels of hippocampal dopamine, dihydroxyphenylalanine (DOPA), striatal homovanillic acid, and 3,4-dihydroxyphenylacetic acid, with these effects being dose-dependent. However, a higher dose of Carbamazepine (50 mg/kg) markedly reduces the overall hippocampal homovanillic acid and striatal DOPA and dopamine levels, while not affecting hippocampal dopamine, DOPA, and DOPAC levels, nor overall striatal DOPAC and homovanillic acid. At a dose of Carbamazepine (100 mg/kg, i.p.), there is a dose-dependent significant increase in the concentrations of neuroactive steroids in rat plasma corticosterone.
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• In Vitro:
  In the presence of batrachotoxin, carbamazepine did not alter the binding of scorpion toxin (125I-labeled) to synaptosomes; however, upon the addition of 1.25 μM batrachotoxin, carbamazepine concentration dependently inhibited the enhancement of batrachotoxin-dependent scorpion toxin binding (IC50: 260 μM) via regulatory sites of the toxin alkaloid. Importantly, carbamazepine had no effect on [3H]saxitoxin binding. When acting on rat brain synaptosomes, carbamazepine impeded the binding of [3H]Batrachotoxinin A 20-α-benzoate to the voltage-sensitive sodium channel site (IC50: 131 μM), thereby reducing the ion flow activity of the sodium channels. As the dissociation rate of the ligand from the receptor-ligand complex increased, carbamazepine, despite decreasing receptor affinity, did not change the maximal binding capacity in Scatchard analyses of [3H]Batrachotoxinin A 20-α-benzoate to synaptosomes, suggesting that binding of [3H]Batrachotoxinin A 20-α-benzoate inhibits conformational changes associated with anticonvulsant effects.
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Storage & Handling

• Storage: -20°C
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

inhibit, NSC 169864, Na channels, Na+ channels, NSC169864, NSC-169864, Mitophagy, Mitochondrial Autophagy, Inhibitor, Autophagy, Carbamazepine, CBZ, SodiumChannel, Sodium Channel

Compound Identifiers

PubChem CID

2554