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Published in Caroline Ashley, Aileen Dunleavy, John Cunningham, The Renal Drug Handbook, 2018
Caroline Ashley, Aileen Dunleavy, John Cunningham
Fexofenadine undergoes negligible metabolism (hepatic or non-hepatic); about 5% of the total dose is metabolised, mostly by the intestinal mucosa, with 0.5–1.5% of the dose undergoing hepatic biotransformation by the cytochrome P450 system. The major route of elimination is believed to be via biliary excretion while up to 10% of ingested dose is excreted unchanged through the urine.
Information on level of drugs into breastmilk
Published in Wendy Jones, Breastfeeding and Medication, 2018
Fexofenadine is a non-sedating anti-histamine. No adverse reports have been made on its use in lactation. Milk levels of fexofenadine have not been measured but data have been collected on the parent compound terfenadine (Lucas et al. 1995). In a telephone follow-up study of 25 infants exposed to terfendine, three mothers reported irritability in their infants but no medical attention was sought (Ito et al. 1993). Terfenadine itself was withdrawn from use following association with ventricular arrhythmias including torsade de pointes in some patients at high doses or in patients with liver disease. This effect has not been noted with the metabolite. It is licenced for use in children over 6 years.
General pharmacology
Published in Fazal-I-Akbar Danish, Ahmed Ehsan Rabbani, Pharmacology in 7 Days for Medical Students, 2018
Fazal-I-Akbar Danish, Ahmed Ehsan Rabbani
Drug metabolites: Parent molecules of some drugs are inactive. They must therefore first undergo metabolism to yield therapeutically active metabolites. For example, azathioprine, an immunosuppressant drug is inactive per se. It first undergoes metabolism to produce mercaptopurine – a therapeutically active metabolite. Such drugs are called pro-drugs.Both the parent drug and the metabolite of some drugs are active, though partly dissimilar in their therapeutic effects. For example, aspirin (the parent drug) has both platelet-aggregation inhibition and anti-inflammatory effects. Its metabolite salicylic acid, on the other hand, produces only anti-inflammatory effect.Some drugs, per se, are safe, but their metabolites are toxic and are responsible for the adverse effects of that drug. For example, haemorrhagic cystitis, a very well known side effect of cyclophosphamide is caused by its toxic metabolite (acrolein) and not the parent molecule. Some drugs, per se, are toxic, but their metabolites are safer. For example, terfenadine – a non-sedating antihistamine occasionally causes cardiac arrhythmias, but its active metabolite fexofenadine lacks this side effect. Fexofenadine (the metabolite) has thus replaced terfenadine (the parent drug) in clinical practice.
The clinical relationship between histamine-1 receptor antagonists and risk of cancer: a systematic review and meta-analysis
Published in Expert Review of Anticancer Therapy, 2023
Elham Bakhtiari, Nasrin Moazzen, Amir Amirabadi, Hamid Ahanchian
Another possible explanation might be Enhancer of Zester Homolog 2 (EZH2) which is dysregulated in most cancer cell lines [23]. Some recent evidence showed promising cancer-suppressive properties with inhibition of component. There is enhanced proliferation of cancer cell lines when this protein is overexpressed, while there is increased apoptosis of cancer cells with inhibition of it [24]. This oncogenic methyl transferase especially over expressed on aggressive and difficult to treat prostate and breast cancer [25,26]. So it can be considered as a new promising target for treatment of cancer [26]. In a recent animal study, ebastine, which is a second-generation anti-histamine with low or absent potential of transferring to the brain, was investigated for inhibition of EZH2 and compared with chlorpheniramine, fexofenadine, and some other antihistamines. The result has shown that ebastine like astemizole was effective in attenuating EZH2 levels. While fexofenadine or chlorpheniramine was not effective even in higher doses [23]. Targeting this component with antihistamine may be helpful in some cancer treatments; however, some drugs like astemizole and ebastine may cause unwanted events like cardiac arrhythmias [27,28]. So recommending this treatment in the absence of allergic diseases or other clinical indication may not be appropriate.
When topical therapy of atopic dermatitis fails: a guide for the clinician
Published in Expert Review of Clinical Immunology, 2021
Giuseppe Ingrasci, Zoe M. Lipman, Gil Yosipovitch
Oral antihistamines have been a commonly used treatment option for atopic itch due to their FDA approval for use in AD, relative safety, widespread availability, and affordability, both over the counter and through prescription [76]. However, research published in the last two decades has found that the mechanism of itch in AD is predominantly non-histaminergic, implying that antihistaminergic medicines may not be the best therapy option [77]. Furthermore, because no large, randomized, placebo-controlled trials have been reported to date, the body of evidence supporting their use in AD is relatively thin. There is no evidence that second-generation antihistamines, such as fexofenadine, cetirizine, or loratadine, are useful in treating atopic itch, according to a systematic study [78]. Daily fexofenadine reduced pruritus more than placebo in a study of 400 adult AD patients, but the difference was minor and unlikely to be clinically significant [79]. In addition, a phase II clinical trial of the H4R Antagonist, ZPL-389, for adults with moderate-to-severe AD failed to reach the primary endpoint of a significant difference in peak pruritus scores from baseline compared to placebo [80]. Thus, oral antihistamines are not suggested for AD patients who do not have an urticaria component. However, AD patients whose sleep is disrupted due to nocturnal itch aggravations may benefit from the more sedating antihistamines [57].
Pharmacokinetics, toxicological and clinical aspects of ulipristal acetate: insights into the mechanisms implicated in the hepatic toxicity
Published in Drug Metabolism Reviews, 2021
In vitro data demonstrated that UPA appears to be a potent P-gp inhibitor in Caco-2 cells (PGL09-007) with an IC50 value of 0.73 µM at clinically relevant concentrations such as 340 mg/mL. The inhibitory effect was in a similar range as for ketoconazole and cyclosporine at high concentrations. To assess the clinical relevance of this finding, the sensitive P-gp substrate fexofenadine (60 mg) was administered to 18 healthy women alone or in combination with UPA at a single table of 10 mg (Pohl et al. 2015). As the Tmax of UPA was 0.75 h and the t1/2 36 h, it was demonstrated that the administration of UPA 1.5 h prior to the fexofenadine administration produced a high UPA concentration in the intestinal tract during the major absorption process of fexofenadine (Pohl et al. 2015). But data did not evidence clinically relevant effects in the pharmacokinetics of fexofenadine.