1. Membrane Transporter/Ion Channel Neuronal Signaling
  2. GABA Receptor
  3. Abecarnil

Abecarnil (ZK 112119) is a ligand or a partial agonist for benzodiazepine (BZ) receptor. Abecarnil possesses anxiolytic and anticonvulsant properties. Abecarnil can act as a positive allosteric modulator of GABAA receptor. Abecarnil inhibits the binding of the BZ [3H]lormetazepam to rat cerebral cortex membranes, with an IC50 of 0.82 nM. Abecarnil can be used for epilepsy research.

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Abecarnil Chemical Structure

Abecarnil Chemical Structure

CAS No. : 111841-85-1

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Description

Abecarnil (ZK 112119) is a ligand or a partial agonist for benzodiazepine (BZ) receptor. Abecarnil possesses anxiolytic and anticonvulsant properties. Abecarnil can act as a positive allosteric modulator of GABAA receptor. Abecarnil inhibits the binding of the BZ [3H]lormetazepam to rat cerebral cortex membranes, with an IC50 of 0.82 nM. Abecarnil can be used for epilepsy research[1][2][3][4].

In Vitro

Abecarnil enhances the binding of t-[35S]butylbicyclophosphorothionate to rat cortical membranes[1].
Abecarnil exhibits a 3- to 6-fold higher affinity to forebrain BZ receptors than Diazepam (DZP)[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Abecarnil (0.3 mg/kg, IP, once) antagonizes the brain neuroactive steroid increase induced by foot shock[2].
Abecarnil (0-2.5 mg/kg, IP, once) dose dependently reduces epileptic activity[3].
Abecarnil is effective against sound-induced convulsions in DBA/2 mice, against air blast-induced generalized seizures in gerbils and against myoclonus in baboons Papio papio[4].
Abecarnil is 2-10 times more potent than DZP in most rodent tests of anxiolytic activity, and in reducing locomotor activity in mice and rats thoroughly habituated to the test chamber[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male Sprague-Dawley CD rats (200-250 g)[2]
Dosage: 0.3 mg/kg
Administration: IP, once, given 30 min before sacrifice
Result: Failed to change the basal pregnenolone and progesterone, while only slightly decreased THDOC levels, but antagonized the brain neuroactive steroid increase induced by foot shock.
Animal Model: WAG/Rij rats (male and female, 190-380 g, age 13-19 weeks, 8 rats each group)[3]
Dosage: 0, 0.16, 0.4, 1.0, and 2.5 mg/kg; 1 mL/400 g
Administration: IP, once
Result: Reduced the duration of spike-wave discharges and increased immobile behavior. Dose dependently reduced epileptic activity, whether measured as number, mean duration, or total duration of spike-wave discharges. The ED50 for reducing the number of spike-wave discharges in the second hour was 0.4 mg/kg.
Molecular Weight

404.46

Formula

C24H24N2O4

CAS No.
SMILES

O=C(C1=NC=C2NC3=C(C2=C1COC)C=C(OCC4=CC=CC=C4)C=C3)OC(C)C

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Purity & Documentation
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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Abecarnil
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HY-105115
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