Disease relevance of Desopimon

• The early changes in experimental myopathy induced by chloroquine and chlorphentermine [1].
• There was no change in the ratio of right ventricular to left ventricular weight in the rats treated with chlorphentermine, supporting the views that this drug does not cause pulmonary hypertension [2].
• Chronic administration of chlorphentermine to rats resulted in a reduction of body weight compared to a normal control group [2].
• Gentamicin or chlorphentermine induction of phospholipidosis in the developing organism: role of tissue and species in manifestation of toxicity [3].
• The role of hyperoxygenation in facilitating the induction of pulmonary histiocytosis by low doses of chlorphentermine [4].

Psychiatry related information on Desopimon

• Augmentation in antioxidant defense mechanisms in rat alveolar macrophages following induction of phospholipidosis with chlorphentermine [5].
• Cross-fostering and starvation experiments revealed that the lethality was not due to aberrant maternal behavior by the chlorphentermine-treated dams or malnutrition of the neonates [6].
• 2. After stable discrimination performances were attained in each group, stimulus generalization studies were conducted with amphetamine, fenfluramine, and chlorphentermine [7].

High impact information on Desopimon

• Metabolic inhibitors (KCN, 2,4-dinitrophenol, and ouabain) and other cationic, amphiphilic drugs (chlorcyclizine, chlorphentermine, and imipramine) were added individually to the cell cultures containing amiodarone or desethylamiodarone [8].
• The order of potency for substituting for AMPH was: mazindol greater than AMPH = phenmetrazine = phentermine greater than chlorphentermine = phendimetrazine = diethylpropion greater than clortermine = mefenorex [9].
• In the present experiments, the influence of the amphiphilic drugs ambroxol, imipramine, chloroquine and chlorphentermine on the hydrolysis of dipalmitoyl-phosphatidylcholine (DPPC) unilamellar liposomes by bee venom phospholipase A2 (PLase A2) was studied [10].
• Role of the alveolar macrophage in the induction of pulmonary phospholipidosis by chlorphentermine. I. Drug and phospholipid levels [11].
• The effects of chlorphentermine on the bioenergetics and activity of monoamine oxidase in mitochondria from the brain of the rat were examined [12].

Chemical compound and disease context of Desopimon

• Ultrastructural and biochemical studies were carried out on three groups of experimental models which were induced by a single subcutaneous daily dose of 10 to 40 mg./kg. body weight of chlorphentermine hydrochloride [13].
• The bradycardias observed after iva chlorphentermine were much less pronounced than those associated with iva clonidine at comparable vasodepressor doses [14].

Biological context of Desopimon

• Effect of desmethylimipramine on the kinetics of chlorphentermine accumulation in isolated perfused rat lung [15].
• These data indicate that chlorphentermine functions as an uncoupler of oxidative phosphorylation [12].
• In three species chronic treatment with the anorectic drug chlorphentermine causes a profound alteration of the phospholipid/lipid metabolism in the organism, resulting in an increase of the fractions of phospholipids and lipids, e.g. in lungs, livers and adrenals [16].
• These latter areas may arise secondary to exocytosis, to fusion of lipid vesicles with the plasma membrane, or to a direct action of chlorphentermine on the membrane [17].
• Effect of desmethylimipramine on tissue distribution and anorectic activity of chlorphentermine in rats [18].

Anatomical context of Desopimon

• Multinucleation in alveolar macrophages from rats treated with chlorphentermine [19].
• Chlorphentermine-induced alterations in the response of human lymphocytes to mitogens [20].
• Chlorphentermine-induced biochemical alterations in mitochondrial membranes [21].
• Chlorphentermine binding in rat lung subcellular fractions and its displacement by desmethylimipramine [22].
• The effects of chlorphentermine (CP) on bioenergetics and monoamine oxidase activity in rat liver mitochondria were examined [21].

Associations of Desopimon with other chemical compounds

• Gentamicin or chlorphentermine (1 mg/egg) failed to induce a phospholipidosis in chick embryo kidney and liver [3].
• The effect of phenobarbital on chlorphentermine-induced alveolar foam cells in rats [23].
• 1 A gas-liquid chromatography procedure for the determination of chlorphentermine (I), N-hydroxychlorphentermine (II) and alpha,alpha-dimethyl-alpha-nitro-beta-(4-chlorophenyl)ethane (IV) in urine has been developed [24].
• Whereas 20 mg/kg chlorphentermine for 7 days failed to markedly alter the incorporation of thymidine into kidney and liver DNA, significant enhancement was noted in neonates receiving 40 or 60 mg/kg drug and quantitatively greater incorporation occurred when the agent was given for 21 days [25].
• The metabolic fate of several amphetamine drugs, namely amphetamine, norephedrine, chlorphentermine and phenmetrazine, in the rhesus monkey and the tamarin and two non-primate species has been investigated and compared to that found for man [26].

Gene context of Desopimon

• Chlorphentermine (CP) is a cationic, amphiphilic drug (CAD) that has been studied widely for its ability to induce phospholipidosis, a disorder characterized by excessive accumulation of cellular phospholipid and ultrastructural development of lysosomal lamellar bodies (LLBs) in the cell [27].

Analytical, diagnostic and therapeutic context of Desopimon

• Histological examination of the lung after treatment with chlorphentermine showed evidence of this drug-induced lipidosis [2].
• N-[11C-methyl]chlorphentermine ([11C]NMCP) and N,N-[11C-dimethyl]chlorphentermine ([11C]NDMCP) were prepared from chlorphentermine and 11CH3I in DMF and evaluated in rats as brain blood-flow agents for positron emission tomography (PET) [28].
• Chlorphentermine (2.5 x 10-7-2.5 x 10-5 M) was rapidly taken up over the 10-min perfusion period, and the rate of uptake was well described by a biexponential equation [15].
• Early changes in chlorphentermine myopathy of rat studied by freeze fracturing [17].
• Daily oral administration of either 20, 40 or 60 mg/kg chlorphentermine for 7 days significantly increased liver and kidney DNA levels, which were not elevated further even after a 3 week treatment period [25].

References