Dibenzosuberone is used for the organic synthesis. Dibenzosuberone derivatives are potent inhibitors of p38 mitogen-activated protein kinase. They may foster a new generation of anti-inflammatory drugs. Dibenzosuberone derivatives are potential tricyclic antidepressants and anti-tumor agents.

Amitriptylinoxide (amitriptyline N-oxide, Amioxid, Ambivalon) is a tricyclic antidepressant, which was introduced in Europe in the 1970s for the treatment of depression. Amitriptylinoxide (AMINO) produces similar effects to the drug Amitriptyline (AMI), which makes sense because it is a metabolite of Amitriptyline. AMINO and AMI potentiate the depletion of 5-hydroxytryptamine (5-HT) induced by p-chloroamphetamine in the rat brain and it may be considered as evidence that both drugs do not inhibit 5-HT uptake in vivo. Neither AMINO nor AMI affects the rat brain level of 5-HT but at higher doses they elevate the 5-hydroxy-indoleacetic acid concentrations. AMINO antagonizes the head twitch reaction induced by 5-hydroxytryptophan in mice and tryptamine convulsions in rats. The hyperthermia induced by fenfluramine (in rats at a high ambient temperature) as well as the stimulation of the hind limb flexor reflex in spinal rats, induced by fenfluramine or LSD, are also inhibited. AMINO antagonizes the 5-HT-induced increase in blood pressure in pithed rats. All the above effects are similar to those induced by AMI, only the active doses of AMINO are higher. The results presented indicate that AMINO, like AMI, inhibits NA uptake and is a 5-HT antagonist. Amitriptylinoxide is considered to work more quickly with fewer side effects than Amitriptyline and is regarded as being equal in terms of efficacy. The way the drug works is nearly identical to Amitriptyline, except it affects the Alpha-1 receptors to a significantly lesser extent (60x less) and has among the weakest effects on acetylcholine receptors. Half maximal inhibition of acetylcholine receptor binding occurred for amitriptylinoxide at 18 mumol/l (amitriptyline: 0.32 mumol/l). Comparing all studied antidepressants for muscarinic acetylcholine receptor binding, amitriptylinoxide had the weakest affinity of all tested tricyclic compounds. Also the affinity of amitriptylinoxide for alpha-receptor binding was about 60 fold less than that of amitriptyline. For all antidepressants investigated, the lowest affinities were found for benzodiazepine, opiate and beta-receptor binding. The weak affinities of amitriptylinoxide for various receptors may be responsible for its reduced side-effects, while it still retains potent antidepressant properties by stabilising the amitriptyline-level in the brain.