Disease relevance of triprolidine

• Wheal-and-flare areas and pruritus decreased after the triprolidine dose [1].
• Since histamine has been shown to act as a growth factor in malignant melanoma cells, we decided to evaluate the in vitro effect of diphenhydramine and other H1 histamine receptor antagonists, such as terfenadine, astemizol and triprolidine on four malignant human melanoma cell lines [2].
• No mutagenic activity was observed for triprolidine and hydroxymethyl triprolidine by reversion of Salmonella typhimurium strains TA97, TA98, TA100, and TA104 at concentrations up to 1000 and 200 micrograms/plate, respectively [3].
• The abilities of triprolidine 2.5 mg and pseudoephedrine 60 mg, alone and in combination, to protect against an increase in nasal airway resistance (NAR) after histamine challenge were determined in eighteen individuals with grass pollen allergy [4].
• In addition, results quite similar to those with cyproheptadine were obtained with the other two antihistamines, triprolidine almost devoid of antiserotonin activity and oxatomide, in testing with BDF1 mice sensitized using Bordetella pertussis organisms [5].

Psychiatry related information on triprolidine

• Hallucinations in a child after drinking triprolidine/pseudoephedrine linctus [6].
• Measurements of the amplitude and latency of the P3b component of the event-related potential (ERP), simple reaction time (SRT) and four psychomotor tests (VAS, DSST, DSp and CFF) were made on 12 male subjects (aged 19-24 years) 1.0-1.5 and 4.0-4.5 h after single oral doses of triprolidine (7.5 mg), terfenadine (60 mg) and placebo [7].
• It may be concluded that mizolastine (5 mg and 15 mg) is free from disruptive effects on cognitive function and psychomotor performance, in contrast to terfenadine 60 mg, triprolidine 10 mg and mizolastine 45 mg [8].

High impact information on triprolidine

• An investigation of the H1-receptor antagonist triprolidine: pharmacokinetics and antihistaminic effects [1].
• Both doses of triprolidine caused subjective central nervous system effects after 1.5 hours, and triprolidine, 5 mg, still had some detectable effects on subjective rating scales after 3 hours [9].
• The new H1-antagonist acrivastine (BW825C) in doses of 4, 8, and 16 mg was compared with triprolidine HCl (2.5 and 5 mg) in a double-blind crossover study in 12 subjects [9].
• 6. The histamine responses were abolished by triprolidine (1 microM), but unaffected by ranitidine (1 microM), indicating that an Hi receptor subtype is activated by histamine [10].
• Histamine responses were sensitive to the H1 receptor antagonist triprolidine (10 microM) and the nonselective potassium channel blocker barium (1 mM) but were unaffected by the H2 receptor antagonist tiotidine (10 microM) and the H3 receptor antagonist, clobenpropit (5 microM) [11].

Biological context of triprolidine

• TLC analysis demonstrated that the absolute oral bioavailability of triprolidine (1-mg/kg dose) in the dog was low (4%) [12].
• The triprolidine-elicited increase in food intake was suppressed by rauwolscine at a dose of 40 microg [13].
• Data on the effect of an antihistamine (triprolidine 10 mg) on visuo-motor coordination and dynamic visual acuity were used to establish interactions between these skills [14].
• In contrast, the brain-to-plasma AUC ratio between KO and WT was comparable for hydroxyzine, diphenhydramine, and triprolidine [15].
• Triprolidine had no effects on pupil size and respiration, but reduced salivation slightly [16].

Anatomical context of triprolidine

• Histamine increased contractions of both circular and longitudinal smooth muscles in oviduct segments, an effect that was antagonized by triprolidine or thioperamide but not by ranitidine [17].
• The carboxylic acid analog of triprolidine (219C69) was found to be the major metabolite in urine and feces, accounting for an average of 57.6% of the administered dose [18].
• Pseudoephedrine and triprolidine in plasma and breast milk of nursing mothers [19].
• Blood samples were collected via the femoral artery for 36 h and the plasma concentrations of triprolidine were determined by HPLC [20].
• Affinity constants for triprolidine (E and Z) in guinea-pig ileum showed a potency ratio of approximately 600 whereas at cerebellar sites this ratio was only approximately 100, suggesting that the H1 receptor in these two tissues may not be identical [21].

Associations of triprolidine with other chemical compounds

• Neither triprolidine nor terfenadine changed P3b amplitude or latency although VAS, CFF and DSST scores were significantly altered by triprolidine at 1.0-1.5 h after dosage [7].
• Two other H1 antagonists, chemically unrelated to mepyramine, diphenhydramine (9 mg kg-1, i.p.) and triprolidine (0.5 mg kg-1, i.p.), inhibited IL-8-induced migration to a similar extent (approximately 50-60%), whereas the H2 antagonist, ranitidine (5 mg kg-1, i.p.) was without effect.(ABSTRACT TRUNCATED AT 250 WORDS)[22]
• Perfusion of the NBM with either H1 (mepyramine or triprolidine) or H2 (cimetidine) receptor antagonists failed to alter ACh spontaneous release from the cortex, however, H1 but not H2 receptor antagonists antagonized the releases of cortical ACh elicited by histamine and methylhistaprodifen [23].
• 4. The inhibitory effect of 100 microM histamine was completely prevented by the highly selective histamine H3 receptor antagonist, clobenpropit but was resistant to antagonism by triprolidine and cimetidine, antagonists at histamine H1 and H2 but not H3 receptors [24].
• First-generation histamine H1-receptor antagonists, such as diphenhydramine, triprolidine, hydroxyzine or chlorpheniramine (chlorphenamine), frequently cause somnolence or other CNS adverse effects [25].

Gene context of triprolidine

• The inhibitory effect of histamine could be reversed by the H2 histamine receptor (HR2) antagonists cimetidine and ranitidine both in PMBC and in CD19-depleted cells, but not with triprolidine, an H1 receptor antagonist, suggesting that the inhibition of IFNgamma production is mediated through H2 receptors in these cell populations [26].
• During in vitro differentiation parallel culture incubations were performed by adding H1 receptor antagonist triprolidine, H2 receptor antagonist tiotidine, the tamoxifene derivate DPPE which blocks the intracellular binding of histamine, and an irreversible blocker of histidine decarboxylase, alpha-fluoromethyl histamine (alpha-FMH) [27].
• Subjective reports of sedation (LARS) were significantly greater at 2 h and 4 h following triprolidine administration on day 1 and ebastine (30 mg) was rated as sedative 4 h following administration on day 5 [28].
• Comparison of pseudoephedrine and triprolidine, alone and in combination in preventing nasal congestion in subjects with allergic rhinitis using nasal histamine challenge [4].
• Freely-fed rats were i.c.v. injected with an histamine H1-receptor antagonist, triprolidine (82 microg), and/or an alpha 2-adrenoceptor antagonist, rauwolscine (0, 20 and 40 microg), and food intake (n=8 each) over 2 h was measured [13].

Analytical, diagnostic and therapeutic context of triprolidine

• Serum and urine triprolidine concentrations were measured by high-performance liquid chromatography [1].
• 1 The effects of triprolidine and cyclizine on the histamine skin response, performance tests and subjective effects were examined in a controlled, double-blind study in eight healthy volunteers [29].
• Thus, after oral administration of triprolidine, a mean of 49.1% of the dose was excreted as 219C69, 12.0% as metabolite 2, 3.4% as metabolite 3, and 0.6% as triprolidine, while after intravenous administration, a mean of 50.8% of the dose was excreted as 219C69, 11.1% as metabolite 2, 4.2% as metabolite 3, and 0.8% as triprolidine [30].
• These antisera were used to develop a radioimmunoassay (RIA) for triprolidine in human plasma with a sensitivity limit of 0.1 ng/mL (0.01 ng of actual mass) [12].
• The noradrenaline content in perfusates collected by a microdialysis probe aimed at the PVN was significantly (p<0.05) increased by the presence of triprolidine in the perfusates [13].

References