DiEt-Fencamfamin HCl (racemic), ≥95%

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N,N-diethylfencamfamin ("DiEt-Fencamfamin") is a lesser known compound discovered as part of a series of mildly stimulating norcamphane derivatives developed in Germany the 1960s by researchers at Merck AG. Fencamfamin, the bettter known, singly N-ethyl substituted member of the series, has been well regarded as a mild eugeroic / psychostimulant compound with a favorable safety profile and relatively low ratio of adverse peripheral effects (compared to stronger catecholamine releasers such as amphetamine). 

The pharmacology of Fencamfamin has not been fully elucidated, but appears somewhat distinctive in its relative absence of adrenergic activity, in conjunction with dopamine reuptake inhibition / relatively weak releaser properties, and potential mild direct dopamine receptor agonist activity.  There have also been speculations about Fencamfamin related compounds possessing weak NMDA antagonist and/or weak MOR agonist properties. N,N-diethylfencamfamin ("DiEt-Fencamfamin"), the N,N-diethyl substituted compound in the series, was found to have similar properties, potency and therapeutic index to those of Fencamfamin.


Chemical Name:N,N-diethyl-3-phenylbicyclo[2.2.1]heptan-2-amine hydrochloride
CAS Number:7177-30-2 
Purity:≥95% (across both enantiomeric pairs)
Form:White or off-white microcrystalline powder
Molecular Weight:243.39 g/mol • 36.46 g/mol
Melting Point:222 °C
Molecular Formula:C17H25N•HCl

DiEt-Fencamfamine HCl; N-Ethylfencamfamine HCl; N,N-diethyl-3-phenyl-2-norbornanamine hydrochloride; CAS 792123-66-1

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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:7177-30-2
Molecular Weight:243.39 g/mol • 36.458 g/mol
Melting Point:222 °C
Molecular Formula:C17H25N•HCl
Synonyms: "DiEt-Fencamfamin"; "DiEt-FCF"; N-Ethylfencamfamine HCl; N,N-diethyl-3-phenyl-2-norbornanamine hydrochloride; N,N-diethyl-3-phenyl-bicyclo[2.2.1]heptan-2-amine hydrochloride; CAS 792123-66-1 (as hydrochloride)
PubChem CID:154102704


Technical Information:


Fencamfamin derivative, non-sympathomimetic dopamine reuptake inhibitor with likely eugeroic / mild psychostimuant effects.

Appearance:White to pale cream crystalline powder
Physical State:Solid
Storage:Store at room temperature or cooler, in a sealed airtight container, protected from heat, light and humidity.
Stability:Stable for at least two years when stored as above.



N,N-diethylfencamfamine (N,N-diethyl-3-phenyl-bicyclo[2.2.1]heptan-2-amine hydrochloride, "DiEt-Fencamfamin"; "DiEt-FCF") is a little-known psychoanaleptic monoterpenoid (norbornane) derivative, first patented in the early 1960s, as one of a series of psychanaleptic norcamphane derivatives by a German medicinal chemistry research team working at Merck AG.  The patents also cover the better-known N-monoethyl compound from the series, Fencamfamine (also known as Fencamfamin, or "FCF").[1] According to the original patents, preliminary investigation suggested that the N,N-diethyl compound, "DiEt-FCF" appeared to share many favorable properties in common with FCF.

FCF was developed by Merck as a pharmaceutical, and was government approved for medical use as an appetite suppressant and gentle psychostimulant, under the brand names Glucoenergan and Reactivan.[2],[3] FCF had been prescribed over prior decades for treating narcolepsy, depressive fatigue in convalescence and other debilitated states as well as in the treatment of general day-time fatigue, lack of concentration and lethargy - but was discontinued in most countries and is now very uncommonly available, due to concerns about possible dependence and misuse potential.[4] Nonetheless, Fencamfamin had been noted as potentially preferable to conventional psychostimulants such as amphetamine for treatment of individuals suffering from chronic medical conditions, due to its relatively favorable physical safety profile, relatively lesser abuse potential, and relative absence of sympathomimetic side effects.[2],[3],[4]

In common with the eugeroic compound Modafinil, Fencamfamin is classified in the United States as a Schedule IV substance, indicating a low potential for abuse relative to the drugs or substances in Schedule III; limited physical dependence / psychological dependence potential relative to the drugs or substances in Schedule III; and an accepted medical use in treatment.[2]  The N,N-diethyl compound DiEt-FCF is not known to be regulated as a controlled substance. 


Modes of action:

The modes of action of DiEt-Fencamfamin have not yet been adequately researched. However, considering its connection to Fencafamamin, we can explore the mechanisms of action for the better known compound.

Research indicates that Fencafamin acts as an dopaminergic agent via dopamine reuptake inhibition, with much weaker norepinephrine reuptake inhibitory activity - and can also weakly induce the release of dopamine at an efficiency ten times lower than dexamphetamine.[4] Unlike typical amphetamine-like compounds, in vitro research shows that Fencafamin does not inhibit the activity of MAO enzymes, and exhibits greatly reduced adrenergic activity.[5] Additional in vivo research hint that FCF may exert some efffects not only via indirect activation of dopamine receptors but also possible mild downstream activity at opioid and NMDA receptors, given that some related structures show mild affinities at those receptor sites, low doses of FCF can cause paradoxical relaxation, and some reinforcing effects of FCF are blocked by naloxone.[6]


Further Scientific research:

The available data for DiEt-FCF is scarce – almost entirely comprising two German patents from the 1960s, describing a variety of compounds synthesized and tested to optimize the efficacy of the related Amino-Norcamphane series of compounds.  The patents cover only the synthesis of the series and some preliminary pharmacodynamic investigations in the mouse. 

The following pharmacological information was disclosed for DiEt-FCF, the N,N-diethyl compound of the series:

  • The lowest effective dosage for the CNS-stimulant screening test in mice: 1 – 3 mg/kg per os
  • LD50 in mice: ~100 mg/kg per os (therapeutic index between 33 and 100)
  • Effectiveness compared to the prior art N,N-dimethyl compound: 3 to 4 fold more potent as a CNS stimulant.
    In comparison, Fencamfamin (mono N-ethyl compound) was 2 to 3 fold more potent than the N,N-dimethyl analog.[1],[7],[8]


Human studies: 

No clinical trials or studies with human participants have been undertaken for DiEt-FCF.  However, a number of clinical studies have been carried out with the related compound Fencamfamin (FCF):

In a small study for the treatment of narcolepsy, the following findings were reported: 60 mg of FCF improved subjective rating scales for alertness (drowsy-alert, dreamy-attentive), motor coordination (clumsy-well coordinated), energy (lethargic-energetic), and mood (sad-happy) to an equal or greater extent than 30mg of dexamphetamine.  Compared to dexamphetamine, Fencamfamin was noted as having a longer (12 hour) elimination half life, but showed equal efficacy, similar duration of stimulating effects, and fewer dose limiting side effects such as anxiety, headache, palpitations or "on edge" feelings that were more frequently induced by dexamphetamine.  The study also stated that: "Tolerance may lead to the use of very high doses of amphetamines - for example, over 100 mg daily - but this may not be so great a problem with either fencamfamin or mazindol. Also, misuse of these compounds may be less than with amphetamine, although any effective central stimulant drug that causes euphoria presents a potential hazard. There are only a few reports of tolerance or addiction to mazindol and/or fencamfamin. Amphetamine, fencamfamin, and mazindol all raise mood." [4]

In a few small early studies of FCF, the following findings were reported: "Several European investigators have reported beneficial effects of fencanfamin ... in a broad range of disorders involving depressed mood." [9]

In a small study of the urinary excretion of FCF, the following findings were reported: After oral consumption of 0.4mg of Fencamfamine HCl per kg of bodyweight, the biological half life of FCF in man was found to average approximately 16 hours.  The primary metabolite was found to be the desethylated analog, 2-amino-3-phenylnorbornane (one may speculate that if the in vivo routes of DiEt-FCF metabolism were studied, they might also be found to include N-desethylation). The physiochemical properties of FCF indicated that only 95% of FCF was ionized at pH 7.4, and the 5% proportion of non-ionized FCF has high lipid solubility enabling membrane permeation; correspondingly the urinary excretion profile in the study showed a high renal excretion rate during the first hours, indicating that FCF was rapidly absorbed from the gastrointestinal tract (a finding that remained uninfluenced by variation of the pharmaceutical formulation in which the substance was administered).[10]. 

In another earlier small study of the urinary excretion of FCF, the following findings were reported: After oral consumption of 20mg of Fencamfamine HCl, the biological half life of FCF in man was found to average approximately 12 hours.[11]

In a small study of the effects of various stimulants on sleep, 20mg of Fencamfamine HCl, (like methylphenidate), was found not to change sleep onset latency or stage 3 sleep latency, and not to reduce SWS (slow wave sleep), but was found to delay the first REM period and reduce the duration and percentage of REM sleep.[12]


Clinical Reviews:

No clinical reviews exist for this compound.


Toxicological studies:

No studies have been carried out to assess the potential toxicological properties of this compound in human subjects.


Animal studies: 

No animal studies have been published for this compound aside from those referenced in initial patents.



[1] Patent DE1219478 (B). (1966) Merck AG. Verfahren zur Herstellung analeptisch wirksamer N-substituierter Aminonorcamphanderivate bzw. von deren Saeureadditionssalzen und quartaeren Ammoniumverbindungen. Application number DE1960M047503 Available from:  

[2] NIH. National Library of Medicine. (2020). Fencamfamin. Pubchem [online] Available at:

[3] Drugbank [2020] Fencamfamin. [online] available at:

[4] J ShindlerM SchachterS Brincat, and J D Parkes (April 1985). "Amphetamine, mazindol, and fencamfamin in narcolepsy". . 290 (6476): 1167-1170. doi: 10.1136/bmj.290.6476.1167. PMCID: PMC1418853. PMID: 2859077

[5] Seyfried CA (August 1983). "Dopamine uptake inhibiting versus dopamine releasing properties of fencamfamine: an in vitro study". Biochemical Pharmacology. 32 (15): 2329–31. doi: 10.1002/bdd.2510020103. PMID 7236868.

[6] Planeta C, Aizenstein ML, DeLucia R (January 1995). "Reinforcing properties of fencamfamine: involvement of dopamine and opioid receptors". Pharmacology, Biochemistry, and Behavior. 50 (1): 35–40. doi:10.1016/0091-3057(94)00236-CPMID 7700952.

[7] Patent 913,866 DE110159 (B) (1961). Merck AG. Improvements in or relating to amino-norcamphane compounds. Application number DE1959M042332. Available from:

[8] Patent US3148118A (1962).Inventors Thesing Jan, Seitz Georg, Hotovy Rudolf, Sommer Siegmund. Improvements in or relating to amino-norcamphane compounds. Application number US200069A. Available from:

[9] Gonzalez, R. G., Bishop, M. P., & Gallant, D. M. (1964). Fencamfamin Versus Placebo in Depressed Patients. The Journal of New Drugs, 4(5), 284–287. doi:10.1002/j.1552-4604.1964.tb00373.x 
Cermak, I., et al (1961). Psychotonic characteristics of 2-ethylaniino-3 -phenylnorcamphiane (Reactivan) and its possibilities in psychotherapy. Munch. med. Wochenschr. 103:1343 . 
Groll, E. (1961). The therapy of the decrease of performance. Landarzt 37:391
Grund, G., and Steinbach, R. W. (1961). Faulty performance at place of work, and its therapy with Reactivan. Munch. med. Wochenschr. 103:1837
Holliday, A. R., and Devery, W. J. (1962). Clin. Pharmacol. Ther. 3, 5-10
Gurtler, J. (June 1962). The use of Reactivan as a supplemental therapy in the treatment of tuberculosis. Praxis 51:600.

[10] F T DelbekeM Debackere (Mar 1981). "Detection and metabolism of fencamfamine and the influence of acetazolamide on its urinary excretion". Biopharm Drug Dispos. 2 (1): 17–30. doi:10.1002/bdd.2510020103PMID 7236868

[11] T B VreeJ M van Rossum (Aug 1969). "Suppression of renal excretion of fencamfamine in man". Eur J Pharmacol. 7 (2): 227–230. doi:10.1016/0014-2999(69)90016-8. PMID 4390567

[12] A N NicholsonB M Stone (Feb 1980). "Heterocyclic amphetamine derivatives and caffeine on sleep in man". Br J Clin Pharmacol. 9 (2): 195–203. doi:10.1111/j.1365-2125.1980.tb05833.x PMCID: PMC1429858. PMID 6101960

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.