PFPP. (p-Fluorophenylpiperazine. Aka Flipiperazine). Works mainly on the serotonine system and creates changes in sensory perceptions. Effective dose is 20 mg and effects last for around 3 hours. A significant portion of users experience migraines and naussea. Especially when taking over the reccomended dose. The research done on this compound seems to be very limited: Prog Neuropsychopharmacol Biol Psychiatry. 1988;12(6):989-1001. [SIZE=+1]Molecular pharmacology of niaprazine. Institut de Biologie Physico-Chimique, Paris, France. 1. The pharmacological profile of niaprazine was investigated using in vitro ligand binding techniques. 2. Niaprazine exhibits a low affinity for the vesicular monoamine transporter and for D2, alpha 2, beta, H1 and muscarinic cholinergic receptors. Niaprazine, particularly the (+)stereoisomer, has a higher affinity for alpha 1 (Ki = 77 nM) and 5-HT2 (Ki = 25 nM) binding sites, but is poorly recognized by 5-HT1A and 5-HT1B binding sites (Ki sigma mciroM). In contrast, p-fluoro-phenylpiperazine, a major metabolite of niaprazine, exhibits a higher affinity for the 5-HT1 subclasses than for the 5HT2 class. 3. These results suggest that the pharmacological properties of niaprazine reflect both its non-reserpinic catecholamine depletor effect and its action on alpha 1 and 5-HT2 receptors. A role of p-fluoro-phenylpiperazine via 5-HT1 sites cannot be excluded. Neuropharmacology. 1982 Feb;21(2):163-9. [SIZE=+1]The effect of niaprazine on the turnover of 5-hydroxytryptamine in the rat brain. Niaprazine (60 mg/kg i.p.) increased rat brain 5-hydroxyindole acetic acid (5-HIAA) concentrations 30 min after treatment, and reduced them at 3-8 hr after treatment. Rat brain 5-hydroxytryptamine (5-HT) levels were unchanged. Niaprazine also produced a short-lasting depletion of rat brain noradrenaline (NA) and dopamine (DA). Pretreatment with alpha-phenyl-alpha-propyl-benzeneacetic acid, 2-(diethylamino) ethyl ester hydrochloride (SKF 525A) (75 mg/kg i.p.) potentiated the increase in 5-HIAA and depletion of catecholamines produced 1 hr after niaprazine, but abolished the reduction in 5-HIAA produced 8 hr after the drug. This suggested that a metabolite might be responsible for the delayed reduction in 5-HIAA levels. A potential metabolite, p-fluoro-phenylpiperazine (FPP) (5-40 mg/kg i.p.) reduced rat brain 5-HIAA and 3,4-dihydroxyphenyl acetic acid (DOPAC), and inhibited 5-HT and NA uptake in vitro. Unlike niaprazine, FPP produced no behavioural sedation, but in large doses produced a behavioural syndrome indicative of serotonergic stimulation. Studies of the metabolism of 14C-niaprazine in rats indicated the presence of a urinary metabolite with the same chromatographic characteristics as FPP. These results suggest that niaprazine itself depletes brain catecholamines and increases 5-HT turnover, while a metabolite, FPP, subsequently reduces the turnover of 5-HT and DA.