p-F-Deprenyl (racemic), ≥98%

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MAO-B inhibitor, neuroprotective agent, and putative NGF, BDNF, and GDNF synthesis promoter. 

Chemical Name(±)-1-(4-fluorophenyl)-N-methyl-N-prop-2-ynylpropan-2-amine hydrochloride
Synonyms(±)-p-Fluorodeprenyl hydrochloride, (±)-4-fluorodeprenyl hydrochloride; (±)-4-fluoro-N,α-dimethyl-N-2-propyn-1-yl-benzeneethanamine hydrochloride (1:1)
CAS #103596-31-2
FormOff white powder
Molecular FormulaC13H16FN.HCl
Molecular Weight241.73 g/mol
Solubility Soluble in H2O, Soluble in EtOH.

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Precaution and Disclaimer:

This Material is Sold For Research Use Only. Terms of Sale Apply. Not for Human Consumption, nor Medical, Veterinary, or Household Uses.

Chemical Information:

CAS Number:103596-31-2
Purity:≥98% (racemate)
Molecular Weight:241.73 g/mol
Melting Point:142-145 °C [1]
Molecular Formula:C13H16FN.HCl
Synonyms: (±)-1-(4-fluorophenyl)-N-methyl-N-prop-2-ynylpropan-2-amine hydrochloride, (±)-p-Fluorodeprenyl hydrochloride, (±)-4-fluorodeprenyl hydrochloride; (±)-4-fluoro-N,α-dimethyl-N-2-propyn-1-yl-benzeneethanamine hydrochloride (1:1)
PubChem CID:198695


Technical Information:

Application:MAO-B inhibitor, neuroprotective agent, and putative NGF, BDNF, and GDNF synthesis promoter. A derivative of deprenyl used in research for Parkinson’s disease and major depressive disorder
Appearance:Off white powder
Physical State:Solid
Solubility:Soluble in H2O, Soluble in EtOH
Storage:Store at room temperature or cooler, in a sealed airtight container, protected from heat, light and humidity.  



This compound, racemic p-F-deprenyl (also known as (±)-p-Fluorodeprenyl or (±)-4-Fluorodeprenyl) is halogenated derivative of Deprenyl, with similar chemical properties and pharmacological effects.[2] It was first studied by Simon et al., and was later shown by Magyar to be a potential substitute for (-)-deprenyl, who concluded that p-F-deprenyl was the most effective (-)-deprenyl analogue.[3] The compound was developed to have similar pharmacological effects as deprenyl, with improved ability at inhibiting the uptake of indirectly acting amines into catecholamine nerve terminals.[4]

(-)-Deprenyl (selegiline), the parent compound, is a selective and irreversible inhibitor of monoamine oxidase type B (MAO-B) enzymes, used in the treatment of Parkinson’s disease and major depressive disorder (MDD).[5] By blocking the action of MAO-B enzymes, selegiline allows the accumulation of PEA and dopamine in the brain.[6] Extensive research and clinical trials have elucidated selegiline’s beneficial effects on symptoms of MDD and Parkinson’s disease, while animal studies have hinted at its additional neuroprotective and longevity-enhancing effects.


Modes of action:

Acts as a selective irreversible inhibitor of MAO-B enzymes by forming a covalent bond at the active site. PET studies have shown that this compound is metabolized at MAO-B enzyme sites.[7] As with selegiline, this mechanism of action prevents the breakdown of endogenous phenylethylamine and catecholamines such as dopamine in the brain.

(-)-Deprenyl has neuroprotective properties and acts as an inhibitor of MAO-A enzymes at high dosages.[8] P-F-deprenyl has confirmed neuroprotective effects in some studies, but does not appear to act as an MAO-A substrate, even at high dosages.[9]

In 1991, Plenevaux, et al., reported the synthesis of ‘no-carrier-added’ DL-4-[18F]Fluorodeprenyl via nucleophilic substitution reaction, and quantitative analysis of distribution in rat tissue, 1, 10, and 60 minutes after administration. They found that clearance from the brain was faster than previously reported with the racemic mixture and recommended use of the pure L-enantiomer for optimal use.[6] Since then, many similar experiments have been conducted. In 2015, Swedish researchers determined the distribution of radio-labeled 18F-fluorodeprenyl-D2 in the primate brain and in human brain sections. Results showed effective crossing of the blood-brain barrier and binding to MAO-B sites within 4 minutes. Binding was almost 100% blocked by L-deprenyl (MAO-B selective) and 10-12% blocked by pirlindole (MAO-A selective). [10]

In human brain sections, binding occurred primarily in the caudatus, putamen, globus pallidum and thalamus, while lower radioactivity was measured in the cortex and cerebellum. The highly effective binding to MAO-B enzymes has prompted many researchers to suggest using radio-labeled enantiomers of the compound to study the density of astrocytes in the brain, as well as to visualize MAO-B activity.[9]

Furthermore, a 1994 study on rat brain tissue using HPCL measured the release of biogenic amines after 21 days of subcutaneous administration. The effects were studied at a dosage of 0.05 mg/kg for p-fluorodeprenyl. Results showed that, like (-)deprenyl, treatment of the compound enhanced the release of dopamine from striatum, substantia nigra and tuberculum olfactorium, as well as noradrenaline from the locus coeruleus.[11]


Human studies:

No studies have been conducted to-date using human volunteers.


Clinical reviews:

Due to the relative lack of data on the compound, there are no literature reviews or meta-analyses available at this time.


Toxicity cases:

No toxicity cases have been reported for this compound.


Animal studies:

In a 2014 study, researchers developed a method for determining distribution of the compound in rat serum, CSF, testis, eyes, lacrimal gland and liver, after 5 - 15 minutes following administration. The researchers observed moderately slow offtake into other tissues.  They showed the successful use of HPLC/UV method for quantitative analysis of p-F-deprenyl in animal tissue.[12]

In 1990, both (R)-(-) and (S)-(+) enantiomers were synthesized via a four-part chemical sequence and the distribution of labeled compounds was determined in baboon tissue. The results showed a slightly faster metabolism in the stratium for the (S)-(+) enantiomer than for the (R)-(-) enantiomer.[1]

In 1995, the effects and distribution of deprenyl analogues, including p-F-deprenyl, was studied in the rat brain after subcutaneous administration. The half-life of all compounds was around 4.5 hours. P-F-Amphetamine and p-F-methamphetamine metabolites were 2-4 times higher in for p-F-deprenyl than L-deprenyl. Further experiments with compounds administered intracerebrally yielded similar results, albeit with a shorter duration of effects and little diffusion of the parent compound from the site of administration.

Importantly, the authors stressed that the amounts of metabolites produced through cerebral metabolism were very small and of little concern. They postulated that the pharmacological effects of the compound are not related to the metabolites. However, the neuroprotective effects of the compound, which have been shown to be unrelated to the MAO-B inhibition, may be related to the metabolites produced in the brain.[8]

In 1992, the effects of p-F-deprenyl on copulation and survival was studied in rats. In the experimental group, a dosage of 0.25 mg/kg (-)p-fluoro-deprenyl was administered subcutaneously, three times a week, for 25 months. In the control group, saline solution was administered. The survival rate was slightly greater for the experimental group, and the sexual activity was markedly improved.[13]



  • [1] Plenevaux, A., Dewey, S.L., Fowler, J.S., Guillaume, M., Wolf, A.P. (1990). Synthesis of (R)-(-)- and (S)-(+)-4-fluorodeprenyl and (R)-(-)- and (S)-(+)-[N-11C-methyl]-4-fluorodeprenyl and positron emission tomography studies in baboon brain. J Med Chem, 33(7):2015-9.
  • [2] 4-Fluorodeprenyl. (2018). PubChem. Open Chemistry Database, US National Library of Medicine, available online from:  https://pubchem.ncbi.nlm.nih.gov/compound/4-Fluorodeprenyl [Accessed 19 September 2018]
  • [3] Magyar, K. (1994). Behaviour of (-)-deprenyl and its analogues. J Neural Transm Suppl, 41:167-75.
  • [4] Knoll, J., Tóth, V., Kummert, M., Sugár J. (1992). (-)deprenyl and (-)parafluorodeprenyl-treatment prevents age-related pigment changes in the substantia nigra. A TV-image analysis of neuromelanin. Mech Ageing Dev, 63(2):157-63.
  • [5] Selegiline. (2018). PubChem. Open Chemistry Database, US National Library of Medicine, available online from: https://pubchem.ncbi.nlm.nih.gov/compound/selegiline [Accessed 19 September 2018]
  • [6] Gaszner, P. & Miklya, I. (2004). The use of the synthetic enhancer substances (-)-deprenyl and (-)-BPAP in major depression. Neuropsychopharmacol Hung, 6(4):210-20.
  • [7] Plenevaux, A., Fowler, J.S., Dewey, S.L., Wolf, A.P., Guillaume, M. (1991). The synthesis of no-carrier-added DL-4-[18F]fluorodeprenyl via the nucleophilic aromatic substitution reaction. Int J Rad Appl Instrum A, 42(2):121-7.
  • [8] Selegiline. (2018). Drugs.com. Available online from https://www.drugs.com/international/selegiline.html [Accessed 19 September 2018].
  • [9] Lajtha, A., Sershen, H., Cooper, T., Hashim, A., Gaál, J. (1996). Metabolism of (-)-deprenyl and PF-(-)-deprenyl in brain after central and peripheral administration. Neurochem Res, 21(10):1155-60.
  • [10] Nag, S., Fazio, P., Lehmann, L., et al. (2016). In Vivo and In Vitro Characterization of a Novel MAO-B Inhibitor Radioligand, 18F-Labeled Deuterated Fluorodeprenyl. J Nucl Med, 57(2):315-20.
  • [11] Knoll, J. & Miklya, I. (1994). Multiple, small dose administration of (-)deprenyl enhances catecholaminergic activity and diminishes serotoninergic activity in the brain and these effects are unrelated to MAO-B inhibition. Arch Int Pharmacodyn Ther, 328(1):1-15.
  • [12] Pöstényi, Z., Tekes, K., Tóth-Molnár, E., Kalász, H. (2015). HPLC analysis of blood–brain barrier penetration of 4-fluorodeprenyl. Journal of Pharmaceutical and Biomedical Analysis, 102, 529–534.
  • [13] Dalló, J. & Knoll, J. (1992). Effect of (-)-para-fluoro-deprenyl on survival and copulation in male rats. Acta Physiol Hung, 79(2):125-9.

Precaution and Disclaimer:

This Material is Sold For Research Use Only. Terms of Sale Apply. Not for Human Consumption, nor Medical, Veterinary, or Household Uses.

[p-F-Deprenyl Q2 2018]  p-F-Deprenyl.20180420.pdf