4-Fluoroamphetamine

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4-Fluoroamphetamine
4-fluoroamphetamine.svg
Systematic (IUPAC) name
(RS)-1-(4-Fluorophenyl)propan-2-amine
Clinical data
Pregnancy cat. N
Legal status Unscheduled
Routes oral
Identifiers
CAS number 459-02-9 N
ATC code ?
PubChem CID 9986
ChemSpider 9592 YesY
Chemical data
Formula C9H12FN 
Mol. mass 153.20 g/mol
 N (what is this?)  (verify)

4-Fluoroamphetamine (4-FA; PAL-303; "Flux"), also known as para-fluoroamphetamine (PFA) is a psychoactive drug and research chemical of the phenethylamine and substituted amphetamine chemical classes. It produces stimulant and possibly entactogenic effects. 4-FA is sometimes sold as a designer drug along with related compounds such as 2-fluoroamphetamine and 4-fluoromethamphetamine.[1][2]

Effects[edit]

The subjective effects of 4-Fluoroamphetamine include euphoria which some find similar to the effects of MDMA, increased energy (stimulation), mood elevation, excessive talking, bruxism, and suppressed appetite (anorexic).

The dopamine reuptake inhibition produced by 4-FA is stronger than that of either 4-CA or 4-IA.[3] 4-FA also produces less hyperthermia than similar compounds such as PMA, 3-MTA and 4-methylamphetamine.

Effects begin within an hour after ingestion and typically last anywhere between 4–12 hours. Common dose range is 75–150 mg, usually taken orally.

Common acute side effects are nausea, headaches, increased heart rate and insomnia.[citation needed]

Neurotoxicity[edit]

4-FA does not cause long-lasting depletion of brain serotonin, unlike its analogues 4-CA and 4-BA.[4] This is thought to "reflect the inability of the fluoro-compound to be metabolized in the same way as the other haloamphetamines."[5]

Contrary to popular belief, neurotoxicity does not increase down the series of para-halogenated amphetamine derivatives, even though serotonin releasing potency does follow this trend. For example, 4-iodoamphetamine is less toxic than is 4-chloroamphetamine.[3][6] Hence, this property is not related to serotonin releasing potency as such, since PAL-287 was reported to be not at all neurotoxic even though it is a powerful 5-HT releasing agent.[7]

Bearing in mind the above statements, it is unclear where 4-methylamphetamine fits in on the neurotoxicity scale. 4-MTA is an example of a para-substituted, non-neurotoxic amphetamine.[8][9][10]

Pharmacology[edit]

4-fluoroamphetamine is a releasing agent and reuptake inhibitor of dopamine, serotonin, and norepinephrine.[citation needed] The respective EC50 values are 2.0 x 10−7 M, 7.3 x 10−7 M, and 0.37 x 10−7 M, while the IC50 values are 7.7 x 10−7 M, 68 x 10−7 M, and 4.2 x 10−7 M.[11]

Regarding the metabolic fate of 4-FA, the C-F bond at the 4-position on the phenyl ring likely resists deactivation in the liver by cytochrome P450 oxidase.[12]

Toxicology[edit]

LD50 (mouse; i.p.) = 46 mg/kg.[13]

See also[edit]

References[edit]

  1. ^ Rösner, P; Quednow, B; Girreser, U; Junge, T (2005). "Isomeric fluoro-methoxy-phenylalkylamines: a new series of controlled-substance analogues (designer drugs)". Forensic Science International 148 (2–3): 143–56. doi:10.1016/j.forsciint.2004.05.003. PMID 15639609. 
  2. ^ Nagai, F; Nonaka, R; Satoh Hisashi Kamimura, K (2007). "The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain". European Journal of Pharmacology 559 (2–3): 132–7. doi:10.1016/j.ejphar.2006.11.075. PMID 17223101. 
  3. ^ a b Marona-Lewicka, D; Rhee, GS; Sprague, JE; Nichols, DE (1995). "Psychostimulant-like effects of p-fluoroamphetamine in the rat". European Journal of Pharmacology 287 (2): 105–13. doi:10.1016/0014-2999(95)00478-5. PMID 8749023.  edit
  4. ^ Harvey, J. A. (1978). "Neurotoxic Action of Halogenated Amphetamines". Annals of the New York Academy of Sciences 305: 289–304. doi:10.1111/j.1749-6632.1978.tb31530.x. PMID 81648.  edit
  5. ^ Fuller, R. W.; Baker, J. C.; Perry, K. W.; Molloy, B. B. (1975). "Comparison of 4-chloro-, 4-bromo- and 4-fluoroamphetamine in rats: Drug levels in brain and effects on brain serotonin metabolism". Neuropharmacology 14 (10): 739–746. doi:10.1016/0028-3908(75)90099-4. PMID 1196472.  edit
  6. ^ Nichols, DE; Johnson, MP; Oberlender, R (1991). "5-Iodo-2-aminoindan, a nonneurotoxic analogue of p-iodoamphetamine". Pharmacology, Biochemistry, and Behavior 38 (1): 135–9. doi:10.1016/0091-3057(91)90601-W. PMID 1826785.  edit
  7. ^ Rothman, R. B.; Blough, BE; Woolverton, WL; Anderson, KG; Negus, SS; Mello, NK; Roth, BL; Baumann, MH (2005). "Development of a Rationally Designed, Low Abuse Potential, Biogenic Amine Releaser That Suppresses Cocaine Self-Administration". Journal of Pharmacology and Experimental Therapeutics 313 (3): 1361–1369. doi:10.1124/jpet.104.082503. PMID 15761112.  edit
  8. ^ Huang, X.; Marona-Lewicka, D.; Nichols, D. E. (1992). "P-methylthioamphetamine is a potent new non-neurotoxic serotonin-releasing agent". European journal of pharmacology 229 (1): 31–38. doi:10.1016/0014-2999(92)90282-9. PMID 1473561.  edit
  9. ^ Li, Q; Murakami, I; Stall, S; Levy, AD; Brownfield, MS; Nichols, DE; Van De Kar, LD (1996). "Neuroendocrine pharmacology of three serotonin releasers: 1-(1,3-benzodioxol-5-yl)-2-(methylamino)butane (MBDB), 5-methoxy-6-methyl-2-aminoindan (MMAi) and p-methylthioamphetamine (MTA).". The Journal of Pharmacology and Experimental Therapeutics 279 (3): 1261–7. PMID 8968349. 
  10. ^ Murphy, J; Flynn, JJ; Cannon, DM; Guiry, PJ; McCormack, P; Baird, AW; McBean, GJ; Keenan, AK (2002). "In vitro neuronal and vascular responses to 5-hydroxytryptamine: modulation by 4-methylthioamphetamine, 4-methylthiomethamphetamine and 3,4-methylenedioxymethamphetamine.". European Journal of Pharmacology 444 (1–2): 61–7. doi:10.1016/S0014-2999(02)01586-8. PMID 12191583. 
  11. ^ Nagai, Fumiko; Ryouichi Nonaka, Kanako Satoh, Hisashi Kamimura (29 November 2006). "The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain". European Journal of Pharmacology. Retrieved 22 September 2012. 
  12. ^ Fisher MB, Henne KR, Boer J (2006). "The complexities inherent in attempts to decrease drug clearance by blocking sites of CYP-mediated metabolism". Current Opinion in Drug Discovery & Development 9 (1): 101–9. PMID 16445122. 
  13. ^ E. Costa and S. Garattini (1970) Amphetamines and Related Compounds, p.28, New York: Raven Press.