Disease relevance of chlorpheniramine

• Chlorpheniramine-dependent thrombocytopenia [1].
• Chlorpheniramine and agranulocytosis [2].
• By contrast, intrarenal infusion of 10(-5) mol/min chlorpheniramine, an H1 receptor antagonist, reversibly attenuated reactive hyperemia and the ability of the kidney to autoregulate renal blood flow [3].
• To determine if one drug regimen was superior to the other, eight patients with systemic mastocytosis were admitted to a double-blind, double-crossover study in which the therapeutic efficacy of cromolyn sodium was compared with that of a combination of chlorpheniramine and cimetidine [4].
• The efficacy of terfenadine, a nonsedating H1 antihistamine, in the management of chronic idiopathic urticaria was compared with chlorpheniramine and placebo in a parallel multicenter trial [5].

Psychiatry related information on chlorpheniramine

• Three histamine H1-receptor antagonists, chlorpheniramine, diphenhydramine and tripelennamine, were tested alone or in combination with morphine, amphetamine and scopolamine on locomotor activity in mice [6].
• Animals treated with chlorpheniramine in the caudal and in the rostral nucleus accumbens displayed higher rates of ipsihemispheric self-stimulation behavior [7].
• The present study was designed to compare the effects of astemizole and chlorpheniramine, alone and in combination with alcohol, on an objective measure of psychomotor performance relating to car-driving ability [8].
• 3 The subjects as a group reported improved alertness (P less than 0.05) and improved wakefulness (P less than 0.05) 0.5 h and 3.5 h respectively after ingestion of terfenadine, and were less energetic (P less than 0.05) 7.0 h after ingestion of chlorpheniramine [9].
• RESULTS: Compared with placebo, chlorpheniramine increased the latencies to sleep onset and rapid eye movement (REM) sleep (p < or = 0.05 for both), and reduced the duration of REM sleep (p <or= 0.01), but this was not observed with fexofenadine [10].

High impact information on chlorpheniramine

• Letter: Chlorpheniramine-induced bone-marrow suppression [11].
• Because chlorpheniramine but not cimetidine inhibited the response, EDRF was released by the H1-histaminergic receptor (n = 5-8) [12].
• The effects of chlorpheniramine on autoregulation of glomerular filtration rate also were evaluated [3].
• Histamine augmentation of IFN-gamma-induced phagocytosis was blocked by the H1 antagonists pyrilamine and chlorpheniramine, but not by the H2 antagonist cimetidine [13].
• The 5-HT effects were blocked by the 5-HT antagonists spiperone, ketanserin, LY53857, mCPP, and PAPP, but not by the histamine antagonists pyrilamine, chlorpheniramine, or cimetidine [13].

Chemical compound and disease context of chlorpheniramine

• Comparison of the therapeutic efficacy of cromolyn sodium with that of combined chlorpheniramine and cimetidine in systemic mastocytosis. Results of a double-blind clinical trial [4].
• Suppression of symptoms and signs of allergic rhinitis and suppression of the histamine-induced wheal and flare responses occurred when mean serum chlorpheniramine concentration ranged from 2.3 to 12.1 and 4.1 to 10.0 ng/ml, respectively [14].
• The groups that received 2 sprays of azelastine per nostril once and twice daily and the chlorpheniramine group had statistically significantly more improvement in total rhinitis symptoms than the placebo group without serious adverse events [15].
• Flurbiprofen proved nearly as effective as chlorpheniramine in reducing severity of induced rhinitis [16].
• In patients with alcohol-related liver disease, the elimination half-life of diphenhydramine was increased from 9 to 15 hours, while in patients with chronic renal disease that of chlorpheniramine was very greatly prolonged [17].

Biological context of chlorpheniramine

• Pharmacokinetics and efficacy of chlorpheniramine in children [14].
• METHODS: We performed a study of the action of chlorpheniramine, terfenadine, brompheniramine, cetirizine, cyproheptadine, clemastine, and astemizole compared with placebo on histamine-induced skin wheals and bronchoconstriction in a single group of patients with asthma [18].
• Only chlorpheniramine, when given for seven doses, improved the baseline FEV1 and forced expiratory flow during middle half of forced vital capacity (FEF25%-75%) [19].
• However, it is only weakly antagonized at bronchial H1-receptors by conventional antihistamines such as chlorpheniramine and clemastine, achieving dose ratios of 2 to 4 at maximally tolerated doses [20].
• The results indicate that a single dose of chlorpheniramine produces a significant increase in the threshold of histamine-induced bronchoconstriction as measured by the provocative histamine dose producing 20% decrease in 1-sec forced expiratory volume (PD20-FEV1), and this effect was significantly enhanced after seven doses [19].

Anatomical context of chlorpheniramine

• Although chlorpheniramine effectively blocked tickling and the reflex-mediated symptoms, sneezing and hypersecretion, ranitidine had no effect, which suggests an H1 and not an H2 effect on sensory nerve endings in the airway epithelium [21].
• However, pretreatment of the normal T lymphocytes with cimetidine (an H-2 histamine receptor antagonist) led to a demonstrable loss in their allo-suppressor properties, whereas pretreatment with chlorpheniramine (an H-1 histamine receptor antagonist) had no such effect [22].
• The response to histamine of EOA was inhibited by treatment with indomethacin (10(-6) mol/l) or tranylcypromine (10(-4) mol/l), a PGI2 synthesis inhibitor, only when the endothelium was present, but additional treatment with chlorpheniramine did not further inhibit relaxation [23].
• During the drug-free test for conditioned place preference, when a choice among the four quadrants was provided, those rats injected with 10.0 microg chlorpheniramine in the caudal nucleus accumbens spent more time in the treatment corral, indicative of a positively rewarding drug action [7].
• The in vitro metabolism of 3-(p-chlorophenyl)-3-(2-pyridyl)-N, N-dimethylpropylamine (chlorpheniramine, I) by rabbit liver microsomes was examined [24].

Associations of chlorpheniramine with other chemical compounds

• Single doses of hydroxyzine, 50 mg; chlorpheniramine, 16 mg; and promethazine, 50 mg; induced significant suppression of skin test reactivity at 2 hr, whereas the suppression produced by tripelennamine, 100 mg; diphenhydramine, 50 mg; and cyproheptadine, 16 mg; did not differ significantly from that produced by placebo [25].
• In seven patients, skin test suppression by these two doses of terfenadine each administered for 3 days, was compared to that produced in an earlier study by 3 days of treatment with chlorpheniramine (8 mg three times a day) [26].
• SCH 1000 prevented methacholine-induced bronchoconstriction and chlorpheniramine prevented methacholine-induced bronchoconstriction [27].
• The stimulation by 4-methylhistamine of cyclic AMP formation was markedly inhibited by metiamide, but not by chlorpheniramine, a histamine H1-receptor antagonist [28].
• Two chiral compounds, bovine serum albumin (BSA) and ovomucoid (OVM) from chicken egg white, were encapsulated in tetramethoxysilane-based hydrogel and their chiral selectivity was evaluated for the separation of some selected enantiomers (tryptophan, benzoin, eperisone, chlorpheniramine) [29].

Gene context of chlorpheniramine

• The ED50 was increased 10-fold by 0.1 microM chlorpheniramine (a histamine H1-receptor selective antagonist) [30].
• Promethazine and chlorpheniramine inhibited CYP2D6 at concentrations that are very close to their therapeutic plasma concentrations [31].
• Treatment was compared with placebo and the H1 receptor antagonist chlorpheniramine [32].
• In each subject the challenges were repeated, on separate days, after intravenous injections of either sodium chloride solution (150 nmol/l: saline) placebo, chlorpheniramine (an H1-receptor antagonist), cimetidine (an H2-receptor antagonist) or after both antagonists together [33].
• The effect of compound 48/80 on plasma insulin-like growth factor I was significantly attenuated by oral administration of the histamine H1 receptor antagonist (chlorpheniramine), but not by the histamine H2 receptor antagonists (cimetidine and ranitidine) [34].

Analytical, diagnostic and therapeutic context of chlorpheniramine

• Ten subjects received chlorpheniramine, 24 mg per day, and placebo in a double-blind crossover study [35].
• In six subjects a double-blind study (chlorpheniramine vs. saline solution) confirmed the effectiveness of the doses administered in the open study [36].
• Capillary electrophoresis, nuclear magnetic resonance and mass spectrometry studies of opposite chiral recognition of chlorpheniramine enantiomers with various cyclodextrins [37].
• Single doses of each product were administered orally in a 5-way crossover study, plasma samples were collected at specific time intervals, and chlorpheniramine levels assayed by HPLC [38].
• A method was developed for the rapid quantitative analysis of chlorpheniramine in plasma, saliva and urine using high-performance liquid chromatography [39].

References