CDPPB

CDPPB is a selective, orally active and brain-penetrant mGluR5 allosteric modulator. CDPPB increases AKT and ERK1/2 activation and augments the BDNF mRNA. CDPPB inhibits caspase-3 activation and mitochondrial dysfunction. CDPPB improves cognitive impairment, depression, and Huntington's disease^{[1][2][3][4][5][6][7][8][9]}. In Vitro:CDPPB (above 1 μM) exhibits agonist-like activity on CHO cells expressing mGluR5^[1].
CDPPB (0.1 mM, 30 min) inhibits SO₂-induced protein radical formation and mitochondrial dysfunction through activation of Akt in mouse hippocampal HT22 cells^[2].
CDPPB (0.02-0.2 mM, 2 h before traumatic neuronal injury) suppresses the increase of LDH release and caspase-3 activation induced by traumatic neuronal injury in a dose-dependent manner^[3].
In Vivo:CDPPB (1-30 mg/kg, s.c., 20 min prior to Amphetamine injection (locomotor test) or 20 min after Amphetamine injection (PPI test)) suppresses Amphetamine-induced locomotor activity without affecting spontaneous locomotor activity and reverses Amphetamine-induced deficits in PPI in rats^[1].
CDPPB (10 mg/kg/day, i.p., 14 days) improves Phencyclidine-induced cognitive deficits in mice^[4].
CDPPB (5 mg/kg, i.p., 14 days) improves cognitive impairment and partially reverses the lesion-induced changes in eNOS and nNOS expressions in olfactory bulbectomized rats^[5].
CDPPB (1.5 mg/kg, s.c., 18 weeks) ameliorates pathology and phenotypic signs of Huntington's disease mice^[6].
CDPPB (20 mg/kg, p.o., single) attenuates depressive-like behavior induced by repeated social defeat stress in mice^[7].
CDPPB (10 mg/kg, i.p., adolescence) reverses MK-801 (HY-15084B)-induced locomotor hyperactivity and anhedonia in mice^[8].
CDPPB (1-5 mg/kg, i.p., 8 days) improves neuronal survival and prevents memory deficits in C57BL/6 mice injected intrahippocampally with Aβ. ^[9].