Clinical data | |
---|---|
Trade names | Clarinex, Aerius, Allex, others [1] [2] |
AHFS/ Drugs.com | Monograph |
MedlinePlus | a602002 |
License data |
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Pregnancy category |
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Routes of administration | By mouth (tablets, solution) |
ATC code | |
Legal status | |
Legal status |
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Pharmacokinetic data | |
Bioavailability | Rapidly absorbed |
Protein binding | 83 to 87% |
Metabolism | UGT2B10, CYP2C8 |
Metabolites | 3-Hydroxydesloratadine |
Onset of action | within 1 hour [3] |
Elimination half-life | 27 hours [3] |
Duration of action | up to 24 hours [3] |
Excretion | 40% as conjugated metabolites into urine Similar amount into the feces |
Identifiers | |
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CAS Number | |
PubChem CID | |
IUPHAR/BPS | |
DrugBank | |
ChemSpider | |
UNII | |
KEGG | |
ChEBI | |
ChEMBL | |
CompTox Dashboard ( EPA) | |
ECHA InfoCard | 100.166.554 |
Chemical and physical data | |
Formula | C19H19ClN2 |
Molar mass | 310.83 g·mol−1 |
3D model ( JSmol) | |
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(verify) |
Desloratadine (trade names Clarinex and Aerius) is a tricyclic H1 inverse agonist that is used to treat allergies. It is an active metabolite of loratadine. [3]
It was patented in 1984 and came into medical use in 2001. [4]
Desloratadine is used to treat allergic rhinitis, nasal congestion and chronic idiopathic urticaria ( hives). [5] It is the major metabolite of loratadine and the two drugs are similar in safety and effectiveness. [5] Desloratadine is available in many dosage forms and under many trade names worldwide. [6]
An emerging indication for desloratadine is in the treatment of acne, as an inexpensive adjuvant to isotretinoin and possibly as maintenance therapy or monotherapy. [7] [8]
The most common side-effects are fatigue (1.2% [9]), dry mouth (3% [9]), and headache (0.6% [9]). [5]
Co-administration with erythromycin, ketoconazole, azithromycin, fluoxetine or cimetidine resulted in elevated blood plasma concentrations of desloratadine and its metabolite 3-hydroxydesloratadine in studies. However, no clinically relevant changes were observed. [10] [11]
Desloratadine is a selective H1- antihistamine which functions as an inverse agonist at the histamine H1 receptor. [12]
At very high doses, is also an antagonist at various subtypes of the muscarinic acetylcholine receptors. This effect is not relevant for the drug's action at therapeutic doses. [13]
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 proteins. [11]
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. [14] Both desloratadine and 3-hydroxydesloratadine are eliminated via urine and feces with a half-life of 27 hours in normal metabolizers. [11] [15]
It exhibits only peripheral activity since it does not readily cross the blood–brain barrier; hence, it does not normally cause drowsiness because it does not readily enter the central nervous system. [16]
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. [14]
2% of Caucasian people and 18% of people from African descent are desloratadine poor metabolizers. In these people, the drug reaches threefold highest plasma concentrations six to seven hours after intake, and has a half-life of about 89 hours. However, the safety profile for these subjects is not worse than for extensive (normal) metabolizers. [11] [15]
Desloratadine is a metabolite of loratadine. The onset of action is within 1 hour. Peak serum concentrations of desloratadine appear 3 hours after dosing. The mean elimination half-life of desloratadine is 27 hours and that of its metabolite is 36 hours. The consumption of food does not interfere with the absorption of desloratadine. Wheal inhibition is detected 1 hour after administration and may last 24 hours.
Clinical data | |
---|---|
Trade names | Clarinex, Aerius, Allex, others [1] [2] |
AHFS/ Drugs.com | Monograph |
MedlinePlus | a602002 |
License data |
|
Pregnancy category |
|
Routes of administration | By mouth (tablets, solution) |
ATC code | |
Legal status | |
Legal status |
|
Pharmacokinetic data | |
Bioavailability | Rapidly absorbed |
Protein binding | 83 to 87% |
Metabolism | UGT2B10, CYP2C8 |
Metabolites | 3-Hydroxydesloratadine |
Onset of action | within 1 hour [3] |
Elimination half-life | 27 hours [3] |
Duration of action | up to 24 hours [3] |
Excretion | 40% as conjugated metabolites into urine Similar amount into the feces |
Identifiers | |
| |
CAS Number | |
PubChem CID | |
IUPHAR/BPS | |
DrugBank | |
ChemSpider | |
UNII | |
KEGG | |
ChEBI | |
ChEMBL | |
CompTox Dashboard ( EPA) | |
ECHA InfoCard | 100.166.554 |
Chemical and physical data | |
Formula | C19H19ClN2 |
Molar mass | 310.83 g·mol−1 |
3D model ( JSmol) | |
| |
| |
(verify) |
Desloratadine (trade names Clarinex and Aerius) is a tricyclic H1 inverse agonist that is used to treat allergies. It is an active metabolite of loratadine. [3]
It was patented in 1984 and came into medical use in 2001. [4]
Desloratadine is used to treat allergic rhinitis, nasal congestion and chronic idiopathic urticaria ( hives). [5] It is the major metabolite of loratadine and the two drugs are similar in safety and effectiveness. [5] Desloratadine is available in many dosage forms and under many trade names worldwide. [6]
An emerging indication for desloratadine is in the treatment of acne, as an inexpensive adjuvant to isotretinoin and possibly as maintenance therapy or monotherapy. [7] [8]
The most common side-effects are fatigue (1.2% [9]), dry mouth (3% [9]), and headache (0.6% [9]). [5]
Co-administration with erythromycin, ketoconazole, azithromycin, fluoxetine or cimetidine resulted in elevated blood plasma concentrations of desloratadine and its metabolite 3-hydroxydesloratadine in studies. However, no clinically relevant changes were observed. [10] [11]
Desloratadine is a selective H1- antihistamine which functions as an inverse agonist at the histamine H1 receptor. [12]
At very high doses, is also an antagonist at various subtypes of the muscarinic acetylcholine receptors. This effect is not relevant for the drug's action at therapeutic doses. [13]
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 proteins. [11]
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. [14] Both desloratadine and 3-hydroxydesloratadine are eliminated via urine and feces with a half-life of 27 hours in normal metabolizers. [11] [15]
It exhibits only peripheral activity since it does not readily cross the blood–brain barrier; hence, it does not normally cause drowsiness because it does not readily enter the central nervous system. [16]
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. [14]
2% of Caucasian people and 18% of people from African descent are desloratadine poor metabolizers. In these people, the drug reaches threefold highest plasma concentrations six to seven hours after intake, and has a half-life of about 89 hours. However, the safety profile for these subjects is not worse than for extensive (normal) metabolizers. [11] [15]
Desloratadine is a metabolite of loratadine. The onset of action is within 1 hour. Peak serum concentrations of desloratadine appear 3 hours after dosing. The mean elimination half-life of desloratadine is 27 hours and that of its metabolite is 36 hours. The consumption of food does not interfere with the absorption of desloratadine. Wheal inhibition is detected 1 hour after administration and may last 24 hours.