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Desloratadine
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== Pharmacology == === Pharmacodynamics === Desloratadine is a selective H<sub>1</sub>-[[antihistamine]] which functions as an [[inverse agonist]] at the [[HRH1|histamine H<sub>1</sub> receptor]].<ref name="Desloratedine">{{cite journal | vauthors = Canonica GW, Blaiss M | title = Antihistaminic, anti-inflammatory, and antiallergic properties of the nonsedating second-generation antihistamine desloratadine: a review of the evidence | journal = The World Allergy Organization Journal | volume = 4 | issue = 2 | pages = 47β53 | date = February 2011 | pmid = 23268457 | pmc = 3500039 | doi = 10.1097/WOX.0b013e3182093e19 }}</ref> At very high doses, is also an [[receptor antagonist|antagonist]] at various subtypes of the [[muscarinic acetylcholine receptor]]s. This effect is not relevant for the drug's action at therapeutic doses.<ref>{{cite web|url=http://www.ema.europa.eu/docs/en_GB/document_library/EPAR_-_Scientific_Discussion/human/000313/WC500022748.pdf|title=Aerius: EPAR β Scientific Discussion|publisher=[[European Medicines Agency]]|date=3 April 2006|access-date=13 October 2017|archive-date=16 March 2018|archive-url=https://web.archive.org/web/20180316170856/http://www.ema.europa.eu/docs/en_GB/document_library/EPAR_-_Scientific_Discussion/human/000313/WC500022748.pdf|url-status=dead}}</ref> === Pharmacokinetics === Desloratadine is well absorbed from the gut and reaches highest [[blood plasma]] concentrations after about three hours. In the bloodstream, 83 to 87% of the substance are bound to [[plasma protein]]s.<ref name="EPAR" /> Desloratadine is metabolized to 3-hydroxydesloratadine in a three-step sequence in normal metabolizers. First, N-glucuronidation of desloratadine by [[UGT2B10]]; then, 3-hydroxylation of desloratadine N-glucuronide by [[CYP2C8]]; and finally, a non-enzymatic deconjugation of 3-hydroxydesloratadine N-glucuronide.<ref name="kazmi-april-2015">{{cite journal | vauthors = Kazmi F, Barbara JE, Yerino P, Parkinson A | title = A long-standing mystery solved: the formation of 3-hydroxydesloratadine is catalyzed by CYP2C8 but prior glucuronidation of desloratadine by UDP-glucuronosyltransferase 2B10 is an obligatory requirement | journal = Drug Metabolism and Disposition | volume = 43 | issue = 4 | pages = 523β533 | date = April 2015 | pmid = 25595597 | doi = 10.1124/dmd.114.062620 }}</ref><ref name="further characterization">{{cite journal | vauthors = Kazmi F, Yerino P, Barbara JE, Parkinson A | title = Further Characterization of the Metabolism of Desloratadine and Its Cytochrome P450 and UDP-glucuronosyltransferase Inhibition Potential: Identification of Desloratadine as a Relatively Selective UGT2B10 Inhibitor | journal = Drug Metabolism and Disposition | volume = 43 | issue = 9 | pages = 1294β1302 | date = September 2015 | pmid = 26135009 | doi = 10.1124/dmd.115.065011 | doi-access = free }}</ref> Both desloratadine and 3-hydroxydesloratadine are eliminated via urine and feces with a [[biological half-life|half-life]] of 27 hours in normal metabolizers.<ref name="EPAR" /><ref name="Drugs.com">{{cite web | title=Desloratadine Monograph for Professionals | website=Drugs.com | date=22 October 2024 | url=https://www.drugs.com/monograph/desloratadine.html | access-date=24 March 2025}}</ref> [[File:3-Hydroxydesloratadine skeletal.svg|class=skin-invert-image|thumb|left|3-Hydroxydesloratadine is the main [[metabolite]].]] It exhibits only peripheral activity since it does not readily cross the [[bloodβbrain barrier]]; hence, it does not normally cause [[drowsiness]] because it does not readily enter the [[central nervous system]].<ref>{{cite journal | vauthors = Mann RD, Pearce GL, Dunn N, Shakir S | title = Sedation with "non-sedating" antihistamines: four prescription-event monitoring studies in general practice | journal = BMJ | volume = 320 | issue = 7243 | pages = 1184β1186 | date = April 2000 | pmid = 10784544 | pmc = 27362 | doi = 10.1136/bmj.320.7243.1184 }}</ref> Desloratadine does not have a strong effect on a number of tested enzymes in the [[cytochrome P450]] system. It was found to weakly inhibit [[CYP2B6]], [[CYP2D6]], and [[CYP3A4]]/[[CYP3A5]], and not to inhibit [[CYP1A2]], [[CYP2C8]], [[CYP2C9]], or [[CYP2C19]]. Desloratadine was found to be a potent and relatively selective inhibitor of [[UGT2B10]], a weak to moderate inhibitor of [[UGT2B17]], [[UGT1A10]], and [[UGT2B4]], and not to inhibit [[UGT1A1]], [[UGT1A3]], [[UGT1A4]], [[UGT1A6]], [[UGT1A9]], [[UGT2B7]], [[UGT2B15]], [[UGT1A7]], and [[UGT1A8]].<ref name="further characterization" /> {{clear left}} === Pharmacogenomics === 2% of [[Caucasian race|Caucasian]]s and 18% of people from African descent are desloratadine [[poor metabolizer]]s. In these people, the drug reaches threefold higher plasma concentrations at seven hours after intake, and it has a half-life of 89 hours (compared to a 27-hour half-life in normal metabolizers). Adverse effects were reported at similar rates in poor metabolizers, suggesting that it is not clinically relevant.<ref name="EPAR" /><ref name="Drugs.com" />
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