Reactivan

Fencamfamin

Clinical data
Pregnancy category	?
Routes of administration	Oral
ATC code	N06BA06 (WHO)
Legal status
Legal status	CA: Schedule IV DE: Anlage II (Authorized trade only, not prescriptible) US: Schedule IV
Pharmacokinetic data
Biological half-life	16 hours
Identifiers
IUPAC name N-Ethyl-3-phenyl-norbornan-2-amine
CAS Number	1209-98-9 N
PubChem CID	14584
DrugBank	DB01463 Y
ChemSpider	13922 Y
UNII	NME1I5IGBK
KEGG	D07343 Y
ChEMBL	CHEMBL7010 Y
Chemical and physical data
Formula	C15H21N
Molar mass	215.34 g·mol−1
3D model (JSmol)	Interactive image
SMILES CCNC1C(C2CCC1C2)C3=CC=CC=C3
InChI InChI=1S/C15H21N/c1-2-16-15-13-9-8-12(10-13)14(15)11-6-4-3-5-7-11/h3-7,12-16H,2,8-10H2,1H3 Y Key:IKFBPFGUINLYQI-UHFFFAOYSA-N Y
NY (what is this?)

Fencamfamin (INN), also known as fencamfamine or by the brand names Glucoenergan and Reactivan, is a stimulant which was developed by Merck in the 1960s.

Fencamfamin is still used, though rarely, for treating depressive day-time fatigue, lack of concentration and lethargy, particularly in individuals who have chronic medical conditions, as its favourable safety profile makes it the most suitable drug in some cases.

Fencamfamin is well tolerated and causes minimal circulatory effects. Extended use may result in a dryness of the mouth.

Not to be used with heart diseases, angina pectoris and decompensated cardiac insufficiency, glaucoma, hyper-excitability and thyrotoxicosis or while treated with monoamine oxidase inhibitors.

Symptoms of overdose are nausea, agitation and restlessness, dryness of the mouth, dizziness and tremor. In gross overdosage also associated with dyspnoea, tachycardia, disorientation and convulsions.

In a study on slices of rat corpus striatum and substantia nigra fencamfamin acted as an indirect dopamine agonist. It released dopamine by a similar mechanism to amphetamines, but was ten times less potent than dexamphetamine at producing this effect. The main mechanism of action was instead inhibition of dopamine reuptake. Also unlike amphetamines, fencamfamin does not inhibit the action of monoamine oxidase enzymes. It was concluded that, at least in the models employed, the in vitro profile of fencamfamin is more similar to that of nomifensine, a reportedly pure uptake inhibitor, than to d-amphetamine.

In animal experiments on place preference fencamfamin produced a significant place preference only at the dose of 3.5 mg/kg. The experiments suggested a relation to dopamine D1 receptors, and also to opioid receptors in the reinforcement produced by fencamfamin, as place preference was blocked by the selective dopamine D1 antagonist SCH 23390 and by the opioid antagonist naloxone. A similar place preference, which was blocked by naloxone and by SCH 23390 and by raclopride, has been seen in a study on rats with drinking water. Animals treated with naloxone before the conditioning sessions showed a place aversion instead of the place preference found in saline-treated animals. Naloxone also reduced drinking. It was proposed that naloxone induced a state of frustrative nonreward. It was suggested that both dopamine and (endogenous) opioids are important for water-induced reinforcement. Possible interactions between these two neurotransmitter systems were discussed.