BRF110

BRF110 (10-14 mg/kg; i.p., p.o.; daily; 4-5 days) does not increase triglyceride levels after repeated i.p. or p.o. administration in mice, and moderately reduces triglyceride levels by approximately 25% following 5 days of i.p. administration^[1].
BRF110 (15 mg/kg; p.o.; single administration) increases the level of BDNF mRNA in mouse brains by approximately 25%^[1].
BRF110 (10 mg/kg; i.p.; once every 12 hours; for 6 consecutive days) exerts neuroprotective effects against acute MPTP (HY-W114750)-induced Parkinson's disease in C57BL/6 mice, increasing the survival rate of TH (+) midbrain neurons by 31%, doubling the retention rate of striatal axon terminals, and improving motor coordination by more than 100%^[2].
The neuroprotective effect of BRF110 (10 mg/kg, i.p., once every 12 hours for 6 days) against MPTP-induced Parkinson's disease in 129SV mice depends on functional Nurr1: it increases the survival rate of TH (+) midbrain neurons in wild-type mice, but shows no effect in Nurr1⁺⁻ mice^[2].
BRF110 (10 mg/kg; i.p.; once every 12 hours for 14 consecutive days) exerts potent neuroprotective effects in a unilateral 6-OHDA (HY-B1081)-induced Parkinson's disease model in C57BL/6 mice, increasing the survival rate of TH (+) midbrain neurons by 47%, restoring motor coordination, reducing contralateral rotation counts by 8-fold, and increasing the retention rate of striatal axonal projections by 10-fold^[2].
BRF110 (10 mg/kg; i.p.; once every 12 hours; for 14 consecutive days) exerts neuroprotective effects in the AAV-ASYN hereditary Parkinson's disease model of C57BL/6 mice, increasing the survival rate of TH (⁺) midbrain neurons by approximately 47% and enhancing the retention rate of striatal axonal projections by more than 5-fold^[2].
BRF110 (10 mg/kg; i.p.; single administration) increases the expression level of TH in the midbrain, as well as the levels of DA and its metabolites in the striatum, in both wild-type and ASYN transgenic mice, without altering the norepinephrine level^[2].