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    4-Fluorodeprenyl molecular structure

    4-Fluorodeprenyl Stats & Data

    Fludepryl Sr-96516-a Chinoin-175 P-f-deprenyl P-fluoro-l-deprenyl
    Chemical Class Amphetamine
    Psychoactive Class Stimulant
    Half-Life Approx. 10–14 h (parent, presumed by analogy to selegiline); functional MAO‑B inhibition 24–48 h.

    Pharmacology

    DrugBank

    Description

    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. 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. 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. (-)-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). By blocking the action of MAO-B enzymes, selegiline allows the accumulation of PEA and dopamine in the brain. 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.

    Mechanism 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. As with selegiline, this mechanism of action prevents the breakdown of endogenous phenylethylamine and catecholamines such as dopamine in the brain.\n\n(-)-Deprenyl has neuroprotective properties and acts as an inhibitor of MAO-A enzymes at high dosages. 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.\n\nIn 1991, Plenevaux, et al., reported the synthesis of ‘no-carrier-added’ DL-4-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. 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).

    Toxicity

    No toxicity cases have been reported for this compound.

    Effect Profile

    Curated
    Stimulant 5.4

    Moderate focus and anxiety/jitters with mild stimulation and euphoria

    Stimulation / Energy×3
    5
    Euphoria / Mood Lift×2
    5
    Focus / Productivity×2
    7
    Anxiety / Jitters×1
    6

    Tolerance & Pharmacokinetics

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    Half-Life
    Approx. 10–14 h (parent, presumed by analogy to selegiline); functional MAO‑B inhibition 24–48 h.
    Addiction Potential
    Low to moderate; psychological habituation possible with frequent or productivity‑linked use; physical dependence unlikely.

    Tolerance Decay

    Full tolerance 0h Half tolerance 14d Baseline ~28d

    Irreversible MAO‑B inhibition recovers via enzyme resynthesis over days to weeks, not by drug clearance; subjective stimulant tolerance appears limited, but functional interactions persist for 24–48 h post‑dose. Values are heuristic, based on MAOI pharmacology rather than direct human datasets for this analog.

    Cross-Tolerances

    Selegiline
    100% ●●○
    Rasagiline
    60% ●○○
    Amphetamines (subjective stimulant effects only)
    30% ●○○

    Harm Reduction

    drugs.wiki

    4‑Fluorodeprenyl is presumed to act as an irreversible, selective MAO‑B inhibitor at low doses by close analogy to selegiline; selectivity can diminish at higher doses, increasing tyramine sensitivity and hypertensive risk. Evidence from selegiline shows loss of strict MAO‑B selectivity with dose escalation and standard 14‑day washouts when switching to serotonergic agents; similar caution is prudent here. The functional duration of MAO‑B inhibition (24–48 h) outlasts the subjective stimulation, so redosing within this window can stack enzyme inhibition and unpredictably amplify interactions. Selegiline is metabolized via CYP2B6 (major) and CYP3A4/2A6 (minor) to active amphetamine/methamphetamine metabolites; 4‑fluorodeprenyl likely follows a similar CYP pattern, so strong inducers/inhibitors may alter exposure. By structure analogy to selegiline, para‑fluoro substitution implies possible formation of 4‑fluoromethamphetamine and 4‑fluoroamphetamine as metabolites; this is plausible but not directly confirmed in humans—treat as a risk that could add serotonergic/stimulant load. Avoid combining with serotonergic drugs (SSRIs/SNRIs/TCAs/MDMA/DXM/tramadol) or certain antibiotics (linezolid) and dyes (methylene blue) due to serotonin‑toxicity risk established for MAO inhibitors. At higher doses, counsel on tyramine control (aged cheeses, cured meats, soy products, certain beers/wines) because irreversible MAO inhibition can precipitate hypertensive crises, especially as MAO‑A inhibition emerges. Monitor for insomnia, anxiety, headache, orthostatic hypotension, and BP elevation; these are documented with selegiline and are possible here. If used more than once weekly, consider spacing doses by at least 48 h (preferably longer) to avoid accumulation of irreversible MAO‑B inhibition. Because RC markets are error‑prone, get samples analyzed by a trusted drug‑checking service; mislabeling and batch variability are common, and ‘lab screenshots’ from sellers can be misleading or outdated. If switching to or from serotonergic prescription meds, use conservative washouts (often 14 days for irreversible MAOIs) unless a clinician directs otherwise.

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