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

Pharmacology & Drug Discovery

Key Properties

• CAS Number: 298-46-4
• MW: 236.27
• Purity: >99.99% (May vary between batches)
• Formula: C₁₅H₁₂N₂O
• SMILES: NC(=O)N1C2=CC=CC=C2C=CC2=C1C=CC=C2
• Target: HDAC,Calcium Channel,Sodium Channel,Mitophagy,Autophagy,Potassium Channel
• 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.
• 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.

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• 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