A-582941 dihydrochloride is a potent, selective and brain-penetrant partial agonist ofα7nAChR, withK_is of 10.8 and 16.7 nM in rat brain membranes and human frontal cortex, respectively. A-582941 dihydrochloride also binds to human5-HT₃receptorwith aK_iof 150 nM. A-582941 has the potential for cognitive deficits associated with various neurodegenerative and psychiatric disorders research^[1][2].

A-582941 (0.1-100 μM) protects against cell death induced by NGF withdrawal in PC12 cells^[2].
A‐582941 (100 nM) increases the number of inhibitory postsynaptic potentials (IPSCs) by 260±70%, the sum of amplitudes by 220±30%, and the sum of areas by 210±40%^[2].
A‐582941 increases ERK1/2 phosphorylation with an EC₅₀of 95 nM in PC12 cells^[2].

A‐582941 (3 μM/kg, i.p. once daily for 3 d) induces a moderate increase in ACh release in the medial prefrontal cortex (mPFCx) of freely moving rats^[2].
A‐582941 (0.01-1.00 μM/kg, i.p.) produces a dose‐dependent increase in ERK1/2 phosphorylation in the cingulate cortex and hippocampus, and increases cAMP response element‐inding protein (CREB) phosphorylation in the cingulate cortex in mice^[2].
A‐582941 (0.1-1.0 μM/kg, i.p.) evokes dose‐dependent increases in Ser‐9 GSK‐3β phosphorylation in the mouse cingulate cortex^[2].
A‐582941 shows high oral bioavailability (mouse ~100%, rat 90%, dog 22%, monkey 50%) and C_max(mouse 18, rat 114, dog 79, monkey 39 ng/mL) following oral administration (mouse 1.0, rat 6.2, dog 3.0, monkey 3.0 μM/kg)^[2].
A‐582941 shows terminal elimination half-lives (mouse 1.4, rat 1.5, dog 1.4, monkey 2.0 h), plasma clearance (mouse 7.9, rat 4.7, dog 5.3, monkey 1.6 L/h/kg) and volumes of distribution (mouse 11.4, rat 9.2, dog 7.9, monkey 3.9 L/kg) following intravenous administration (mouse 1.0, rat 6.2, dog 0.5, monkey 0.5 μM/kg)^[2].

353.29

C₁₇H₂₂Cl₂N₄

848591-90-2

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.