Xaliproden free base

Xaliproden free base extends the average survival time and improves motor function in pmn mice with hereditary axonopathy, and rescues motor neurons from death in mice with transected sciatic nerves^[1].
Xaliproden (0.3-1.5 mg/kg/day; oral administration; once daily; for 4 consecutive weeks) free base exerts renoprotective effects on db/db mice with diabetic nephropathy by significantly improving renal function, reducing proteinuria, alleviating renal tubular injury and fibrosis, as well as blocking inflammatory, apoptotic and fibrotic pathways via inhibition of the JNK/p65/c-Jun signaling axis^[2].
Xaliproden (0.3-3 mg/kg; p.o.; single administration) free base significantly, persistently and dose-dependently inhibits Paclitaxel (HY-B0015)-induced mechanical allodynia^[3].
Xaliproden (0.3-3 mg/kg; p.o.; single administration) free base exerts only a mild, transient 19% inhibition of vincristine (HY-N0488A)-induced mechanical allodynia at the single dose of 3 mg/kg, shows no effect at low doses, and does not alter the tibial nerve firing response in vincristine-treated mice^[3].
Xaliproden (0.63-40 mg/kg; p.o.; single administration) free base produces a dose-dependent inhibitory effect on in vivo 5-HT_1A receptor binding in the frontal cortex and hippocampus of mice, with ID₅₀ values of 3.5 mg/kg and 3.3 mg/kg (p.o.), respectively^[4].
Xaliproden (0.63-10 mg/kg; intraperitoneal injection; single administration) free base dose-dependently increases dopamine levels in the prefrontal cortex of rats (ED₅₀=0.7 mg/kg, i.p.) and decreases 5-HT levels in the rat hippocampus (ED₅₀=1.2 mg/kg, i.p.) via activation of the 5-HT_1A receptor^[4].
Xaliproden (0.63-10 mg/kg; intraperitoneal injection; single administration) free base exerts a dose-dependent, 5-HT_1A receptor-mediated antinociceptive effect in the rat formalin pain test, and completely inhibits paw licking and lifting responses at 10 mg/kg (i.p.)^[4].