PF-3845

Animal models

Male C57BL/6 mice with TBI-induced deficits, CFA rat model with inflammatory pain

Preparation method

The solubility of this compound in DMSO is > 10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months.

Dosage form

Intraperitoneal injection, 30 min after TBI, and then once daily for 3 or 14 days; oral administration, 1–30 mg/kg;

Application

Treatment with PF3845 (5 mg/kg, i.p.) completely restored the ability of TBI mice to successfully alternate arms during maze exploration. PF3845 (5 mg/kg, 10 mg/kg, i.p.) significantly attenuated TBI-induced anxiogenic behavior. Treatment with PF3845 (5 mg/kg, 10 mg/kg, i.p.) significantly reduced TBI-induced deficits in fine motor movement. In a rat model of inflammatory pain, PF-3845 (1–30 mg/kg, oral administration) caused a dose-dependent inhibition of mechanical allodynia. In FAAH (-/-) mice and wild-type mice, treatment with PF-3845 (1–10 mg/kg i.p.) induced an anti-allodynic phenotype. PF-3845 (0.1–10 μg intraplantar) increased AEA levels in the brain and spinal cord. Intraplantar PF-3845 produced a partial reduction in allodynia.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1]. Tchantchou F, Tucker L B, Fu A H, et al. The fatty acid amide hydrolase inhibitor PF-3845 promotes neuronal survival, attenuates inflammation and improves functional recovery in mice with traumatic brain injury[J]. Neuropharmacology, 2014, 85: 427-439.

[2]. Ahn K, Johnson D S, Mileni M, et al. Discovery and characterization of a highly selective FAAH inhibitor that reduces inflammatory pain[J]. Chemistry & biology, 2009, 16(4): 411-420.

[3]. Booker L, Kinsey S G, Abdullah R A, et al. The fatty acid amide hydrolase (FAAH) inhibitor PF‐3845 acts in the nervous system to reverse LPS‐induced tactile allodynia in mice[J]. British journal of pharmacology, 2012, 165(8): 2485-2496.