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Fladrafinil

Emerging

Lafon-era research compound (CRL-40,941) — the bisfluoro analog of adrafinil that never made it past 1970s-80s animal pharmacology and has… | Pharmaceutical · Oral

Aliases (6)
CRL-40 · 941 · CRL-40941 · Fluorafinil · bis(p-fluoro)adrafinil · (±)-2-[[Bis(4-fluorophenyl)methyl]sulfinyl]-N-hydroxyacetamide
TYPICAL DOSE
30 mg
ROUTE
Oral (tablet)
CYCLE
Don't
STORAGE
Room temp; original container
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Brand options3 known
CRL-40CRL-40941Fluorafinil

StatusUnscheduled in US; not approved in any jurisdiction (research-chem only)

Overview TL;DR

Lafon-era research compound (CRL-40,941) — the bisfluoro analog of adrafinil that never made it past 1970s-80s animal pharmacology and has zero published human trials. Marketed in 2010s-2020s nootropic forums on a "calmer modafinil with anti-aggression effects" pitch derived almost entirely from a single mouse study and structural extrapolation. SKIP-FOR-NOW for Dylan and every other archetype — modafinil itself is cheap, well-studied, and strictly dominant.

Mechanism of action

Presumed mechanism (none of this is verified in humans):

Fladrafinil is the bis(p-fluoro) analog of adrafinil — adrafinil's diphenylmethyl group has both phenyl rings substituted with para-fluorine. Like adrafinil, it is theorized to be a hepatic prodrug that converts to a modafinil-class active metabolite — specifically, the bisfluoro analog of modafinil (sometimes called "lauflumide" or "fluoromodafinil" in research-chem channels, but this nomenclature is not standardized).

Once converted, the assumed downstream pharmacology mirrors modafinil:

  • Weak DAT inhibition with downstream dopamine elevation in striatum
  • Orexin → histamine → cortical wakefulness cascade
  • Glutamate up, GABA down in hypothalamus/thalamus/hippocampus
  • Mild norepinephrine + serotonin contribution

The bisfluoro modification's theoretical effect:

  • Increased lipophilicity → potentially better blood-brain barrier penetration → potentially lower required dose
  • Slower hepatic clearance of the active metabolite → potentially longer duration
  • Different P450 substrate profile from racemic modafinil

Critical caveat — none of this has been demonstrated in humans. The mechanism section above is structural inference from adrafinil/modafinil pharmacology plus animal data from a small handful of 1970s-80s Lafon papers. There are no published clinical pharmacokinetic studies, no DAT-occupancy imaging, no controlled wakefulness trials. Fladrafinil is a structure that should behave like a slightly tweaked modafinil based on chemistry — but "should" is doing a lot of work in that sentence.

Pharmacokinetics No data
Pharmacokinetics data not available for this compound.
No half-life mentions found in the source notes.
Research protocols1 protocols
GoalDoseFrequencySoloCycle
Cycled use only

Auto-extracted from dosing notes. For full context including caveats and Dylan-specific protocols, see the Dosing protocols section.

Quality indicators4 checks
FDA-approved manufacturer
NDC code on the bottle matches FDA registration. Generic OK; backyard not OK.
Brand vs generic listed
Pharmacy fills should disclose substitution. AB-rated generics are bioequivalent.
Tamper-evident packaging
Pharmacy seal intact, lot number + expiry visible on the bottle and the box.
!
Schedule labeling correct
C-II / C-IV warnings on label match the medication; report any mismatch to the pharmacist.
What to expect Generic
  1. 1
    Day 1
    PK-driven acute peak per administration. Verify dose tolerated.
  2. 2
    Week 1
    Steady-state reached for most daily-dosed pharma.
  3. 3
    Week 2-4
    Therapeutic effect established; titration window if needed.
  4. 4
    Long-term
    Periodic monitoring per drug class (labs, BP, ECG as applicable).
Side effects + safety Tabbed view

The fundamental problem: Almost everything in this section is inferred from modafinil + adrafinil. Fladrafinil's actual human safety profile has never been characterized. The "this is probably safe because it looks like modafinil" reasoning is exactly how compounds with novel toxicities slip through — modafinil itself didn't surface its SJS/TEN signal until thousands of patients had taken it.

Common (>10% users, presumed by class)

  • Headache — reported by users; assumed modafinil-class.
  • Reduced appetite — reported.
  • Insomnia / shifted sleep onset if dosed late.
  • Anxiety / nervousness — reported less frequently than with modafinil per anecdote, though this is unreliable.

Less common (1-10%, presumed by class)

  • Nausea, GI upset
  • Dry mouth, increased thirst
  • Mild HR / BP elevation
  • Dizziness
  • Skin irritation
Interactions6 compounds
  • N/ASynergistic
    once converted (assuming the prodrug hypothesis is correct), the synergy profile would be modafinil's (l-theanine, citicoline, rhodiola, bromantane, selegili…
  • Other hepatotoxic compoundsAvoid
    alcohol, high-dose acetaminophen, statins, methotrexate, isoniazid, kava, comfrey, high-dose niacin. The presumed adrafinil-class hepatic load makes additive…
  • CYP3A4 inducers/inhibitorsAvoid
    would unpredictably alter conversion to active metabolite. With no human PK data, the direction of the interaction is unpredictable.
  • Hormonal contraceptivesAvoid
    assumed CYP3A4 induction (modafinil-class) reduces efficacy; same partner-relevant caveat.
  • Other research-chem eugeroicsAvoid
    (hydrafinil, flmodafinil, etc.) — combining undocumented compounds compounds the unknown safety surface.
  • Cannot reliably define.Compatible
    Without characterized drug-interaction profile, "neutral" is inference, not knowledge.
References8 sources
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