79794-75-5CCOC(=O)N1CCC(=C2c3ccc(Cl)cc3CCc3cccnc32)CC1JCCNYMKQOSZNPW-UHFFFAOYSA-NLoratadine is a benzocycloheptapyridine that is 6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridine substituted by a chloro group at position 8 and a 1-(ethoxycarbonyl)piperidin-4-ylidene group at position 11. It is a H1-receptor antagonist commonly employed in the treatment of allergic disorders. It has a role as a geroprotector, a H1-receptor antagonist, a cholinergic antagonist and an anti-allergic agent. It is a tertiary carboxamide, an ethyl ester, an organochlorine compound, a N-acylpiperidine and a benzocycloheptapyridine. It is functionally related to a desloratadine.
79794-75-5Pharmaceutical
Pharmaceuticals
Pharmaceuticals -> Listed in ZINC15
Log P= 5.20 at pH 7.4
5.20
4.4
Breast Feeding; Lactation; Milk, Human; Antihistamines; Antipruritics; Nonsedating Antihistamines
FDA approved drugs -> Active ingredient
FDA approved drugs -> Active ingredient
Pharmaceuticals
Antiallergics and medicines used in anaphylaxis
134-136 °C
134-136 °C
134 - 136 °C
187.4 Ų [M+H]+ [CCS Type: DT; Buffer gas: N2; Ionization: ESI+; Dataset: TOXCAST; Source Identifier: DTXSID2023224]
185.8 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]
안전 정보는 참고용이며, 공급업체의 물질안전보건자료(SDS), 관련 법규 및 전문가 평가를 대체하지 않습니다.
This chemical does not meet GHS hazard criteria for 0.9% (1 of 111) of reports.
Warning
H315 (48.6%): Causes skin irritation [Warning Skin corrosion/irritation]
P203, P261, P264, P264+P265, P271, P272, P273, P280, P302+P352, P304+P340, P305+P351+P338, P318, P319, P321, P332+P317, P333+P317, P337+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)
Aggregated GHS information provided per 111 reports by companies from 8 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
This chemical does not meet GHS hazard criteria for 2.3% (2 of 86) of reports.
Status: Active Update: 27-04-2018 https://echa.europa.eu/registration-dossier/-/registered-dossier/21649
1-Piperidinecarboxylic acid, 4-(8-chloro-5,6-dihydro-11H-benzo5,6cyclohepta1,2-bpyridin-11-ylidene)-, ethyl ester: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.
Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).
Rosa F; Reprod Toxicol 9 (6): 583 (1995). New medical entities widely used in fertile women: post marketing surveillance priorities.
Bergman HD; South Pharm J 86: 17-21 (1994). Major new drugs: review of 1993. The pharmacology, pharmacokinetics, uses, efficacy and adverse effects of /new drug products are reviewed/.
Haria M, et al; Drugs 48: 617-37 (1994). Loratadine: reapprasial of its pharmacological properties and therapeutic use in allergic disorders.
R06AX13
R - Respiratory system
QR - Respiratory system
R06AX13
Like other 2nd generation antihistamines, loratadine is selective for peripheral H1 receptors. Loratadine does not penetrate effectively into the central nervous system and has poor affinity for CNS H1-receptors. These qualities result in a lack of CNS depressant effects such as drowsiness, sedation, and impaired psychomotor function.
Histamine release is a key mediator in allergic rhinitis and urticaria. As a result, loratadine exerts it's effect by targeting H1 histamine receptors. Loratadine binds to H1 histamine receptors found on the surface of epithelial cells, endothelial cells, eosinophils, neutrophils, airway cells, and vascular smooth muscle cells among others. H1 histamine receptors fall under the wider umbrella of G-protein coupled receptors, and exist in a state of equilibrium between the active and inactive forms. Histamine binding to the H1-receptor facilitates cross linking between transmembrane domains III and V, stabilizing the active form of the receptor. On the other hand, antihistamines bind to a different site on the H1 receptor favouring the inactive form. Hence, loratadine can more accurately be classified as an "inverse agonist" as opposed to a "histamine antagonist", and can prevent or reduce the severity of histamine mediated symptoms.
All of the available H1 receptor antagonists are reversible, competitive inhibitors of the interaction of histamine with H1 receptors. /H1 Receptor Antagonists/
H1 antagonists inhibit most responses of smooth muscle to histamine. /H1 Antagonists Receptors/
Within the vascular tree, the H1 antagonists inhibit both the vasoconstrictor effects of histamine and, to a degree, the more rapid vasodilator effects that are mediated by H1 receptors on endothelial cells. /H1 Receptor Antagonists/
H1 antagonists strongly block the action of histamine that results in increased capillary permeability and formation of edema and wheal. /H1 Receptor Antagonists/
For more Mechanism of Action (Complete) data for LORATADINE (6 total), please visit the HSDB record page.
불러오는 중…
DTXSID2023224CHEMBL998CHEBI:6538187.4 Ų [M+H]+ [CCS Type: TW; Method: Major Mix IMS/Tof Calibration Kit (Waters)]
185.71 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]
White Crystalline Solid
Corey JP; Otolaryngol Head Neck Surg 109 (3 pt 2): 584-92 (1993). Advances in the pharmacotherapy of allergic rhinitis: second generation H1 receptor antagonists.
For more Special Reports (Complete) data for LORATADINE (7 total), please visit the HSDB record page.
Skin Irrit. 2 (66.3%)
Skin Irrit. 2 (48.6%)
SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.
Treatment of overdosage would reasonably consist of emesis (ipecac syrup), except in patients with impaired consciousness, followed by the administration of activated charcoal to absorb any remaining drug. If vomiting is unsuccessful, or contraindicated, gastric lavage should be performed with normal saline. Saline cathartics may also be of value for rapid dilution of bowel contents. Loratadine is not eliminated by hemodialysis. It is not known if loratadine is eliminated by peritoneal dialysis. (L1712)
Concurrent use may potentiate the CNS depressant effects of either these medications /alcohol or other CNS depression-producing medications/ or antihistamines; also, concurrent use of maprotiline or tricyclic antidepressants may potentiate the anticholinergic effects of either antihistamines or these medications. /Antihistamines/
Anticholinergic effects may be potentiated when these medications /anticholinergics or other medications with anticholinergic activity/ are used concurrently with antihistamines; patients should be advised to report occurrence of gastrointestinal problems promptly since paralytic ileus may occur with concurrent therapy. /Antihistamines/
Concurrent use of monoamine oxidase (MAO) inhibitors with antihistamines may prolong the intensify the anticholinergic and CNS depressant effects of antihistamines; concurrent use is not recommended. /Antihistamines/
Concurrent use /of ototoxic medications/ with antihistamines may mask the symptoms of ototoxicity such as tinnitus, dizziness, or vertigo. /Antihistamines/
For more Interactions (Complete) data for LORATADINE (6 total), please visit the HSDB record page.
Although loratadine is a relatively safe and effective medication for treating allergic rhinitis, its primary adverse effects include headaches, dizziness, and gastrointestinal distress (diarrhea, abdominal pain, nausea, and vomiting). Loratadine may also cause sedation (a rare adverse effect), mydriasis, and xerostomia. These effects are primarily due to the drug's anticholinergic properties; anticholinergic adverse effects are minimal at therapeutic dosage. In a patient undergoing long-term loratadine treatment, a rare case of bilateral cystoid macular edema has been described, which resolved after discontinuation of loratadine. The potential pathophysiology remains unclear. It may involve dysfunction of H1-receptor–expressing retinal neurons and associated signal transduction, toxicity affecting Müller cells or retinal pigment epithelium cells, and intracellular fluid accumulation.
Signs and Symptoms of Overdose
Loratadine competes with free histamine and exhibits specific, selective peripheral H<sub>1</sub> antagonistic activity. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms (eg. nasal congestion, watery eyes) brought on by histamine. Loratadine has low affinity for cholinergic receptors and does not exhibit any appreciable alpha-adrenergic blocking activity in-vitro. Loratadine also appears to suppress the release of histamine and leukotrienes from animal mast cells, and the release of leukotrienes from human lung fragments, although the clinical importance of this is unknown.
The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical. [http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=79794-75-5]
Somnolence, tachycardia, and headache have been reported with overdoses greater than 10 mg (40 to 180 mg).
The second generation H1 antagonists (eg, terfenadine, astemizole, loratadine) have no effect on muscarinic receptors.
Drug Induced Liver Injury Rank (DILIrank 2.0)
Loratadine
vNo-DILI-concern
0
No match
DOI:10.1016/j.drudis.2016.02.015
In mutagenicity studies, there was no evidence of mutagenic potential in reverse (Ames) or forward point mutation (CHO-HGPRT) assays, or in the assay for DNA damage (rat Primary Hepatocyte Unscheduled DNA Assay) or in two assays for chromosomal aberrations (Human Peripheral Blood Lymphocyte Clastogenesis Assay and the Mouse Bone Marrow Erythrocyte Micronucleus Assay). In the Mouse Lymphoma Assay, a positive finding occurred in the nonactivated but not the activated phase of the study.
In an 18 month oncogenicity study in mice and a 2 year study in rats, loratadine was administered in the diet at doses up to 40 mg/kg (mice) and 25 mg/kg (rats). In the carcinogenicity studies, pharmacokinetic assessments were carried out to determine animal exposure to the drug. AUC data demonstrated that the exposure of mice given 40 mg/kg of loratadine was 3.6 (loratadine) and 18 (active metabolite) times higher than a human given 10 mg/kg. Exposure of rats given 25 mg/kg of loratadine was 28 (loratadine) and 67 (active metabolite) times higher than a human given 10 mg/day. Male mice given 40 mg/kg had a significantly higher incidence of hepatocellular tumors (combined adenomas and carcinomas) than concurrent controls. In rats, a significantly higher incidence of hepatocellular tumors (combined adenomas and carcinomas) was observed in males given 10 mg/kg and males and females given 25 mg/kg. The clinical significant of these findings during long-term use of Claritin tablets is not known. /Claritin/
Loratadine administration produced hepatic microsomal enzyme induction in the mouse at 40 mg/kg and rat at 25 mg/kg, but not at lower doses.
There was no evidence of animal teratogenicity in studies performed in rats and rabbits at oral doses up to 96 mg/kg (75 times and 150 times, respectively, the recommended daily human dose on a mg/sq m basis).
Decreased fertility in male rats, shown by lower female conception rates, occurred at approximately 64 mg/kg and was reversible with cessation of dosing. Loratadine had no effect on male or female fertility or reproduction in the rat at doses of approximately 24 mg/kg.
Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).
The elimination half life is approximately 10 hours for loratadine and 20 hours for descarboethoxyloratadine.
The mean elimination half-lives found in studies in normal adult subjects (n= 54) were 8.4 hours (range= 3 to 20 hours) for loratadine and 28 hours (range= 8.8 to 92 hours) for the major active metabolites (descarboethoxyloratadine).
Loratadine undergoes extensive first pass metabolism in the liver and is primarily metabolized by CYP3A4, CYP2D6, CYP1A1 and CYP2C19. Less involved CYP enzymes include CYP1A2, CYP2B6, CYP2C8, CYP2C9 and CYP3A5. CYP3A4 and CYP2D6 are mainly responsible for metabolizing loratadine to descarboethoxyloratadine. This primary metabolite is 4 times more pharmacologically active than loratadine. In addition, a study demonstrates that descarboethoxyloratadine is first glucuronidated by UGT2B10, then hydroxylated by CYP2C8 to form 3-hydroxydesloratadine. Further glucuronidation of 3-hydroxydesloratadine facilitates excretion.
The second generation H1 antagonists astemizole, loratadine,and terfenadine are rapidly absorbed from the gastrointestinal tract and metabolized in the liver to active metabolites by the hepatic microsomal p450 system.
Pharmacokinetic studies following single and multiple oral doses of loratadine in 115 volunteers showed that loratadine is rapidly absorbed and extensively metabolized to an active metabolite (descarboethoxyloratadine).
In vitro studies with human liver microsomes indicate that loratadine is metabolized to descarboethoxyloratadine predominately by p450 CYP3A4 and, to a lesser extent, by p450 CYP2D6.
H1 receptor antagonists are among the many drugs that induce hepatic microsomal enzymes, and they may facilitate their own metabolism. /H1 Receptor Antagonists/
The non-sedating anti-histamine, loratadine ... was admin orally in the diet to mature male rats at dosages of 4, 10 and 25 mg/kg/day for 2 wk. The effects of these treatments on liver microsomal cytochrome P450 were evaluated by immunochemical and biochemical techniques, and were compared with the effects of treating rats with three different inducers of cytochrome P450, namely phenobarbital, 3-methylcholanthrene and dexamethasone. Treatment of rats with loratadine caused a dose dependent incr in the levels of P450 2Bl and 2B2, the major phenobarbital inducible P450 enzymes, as determined by Western immunoblotting. At the highest dosage tested, loratadine was less effective than phenobarbital as an inducer of 2Bl and 2B2, although the induction of these proteins could be detected immunochemically even at the lowest dosage of loratadine tested. Consistent with these observations, treatment of rats with loratadine caused a dose dependent incr in the rate of two reactions that are catalyzed predominantly by 2Bl/2, namely testosterone 16 beta-hydroxylation and 7-pentoxyresorufin O-dealkylation. At the highest dosage tested, loratadine caused a 7.3- and 8.5-fold incr in the rate of testosterone 16 beta-hydroxylation and 7-pentoxyresorufin O-dealkylation, respectively, compared with a and 45-fold incr caused by phenobarbital treatment. Treatment of rats with loratadine caused a 1.4 to 2.0-fold incr in the 2 beta-, 6 beta- and 15 beta-hydroxylation of testosterone, which was associated with a similar incr in the levels of immunoreactive P450 3Al and/or 3A2. As an inducer of P450 3Al/2, loratadine was slightly less effective than phenobarbital, and was considerably less effective than dexamethasone, which caused a 10- to 33-fold increase in testosterone 2 beta-, 6 beta- and 15 beta-hydroxylase activity. At the dosages tested, loratadine did not increase the levels of P450 lAl, the major 3-methylcholanthrene inducible P450 enzyme, as determined by Western immunoblotting. The rate of 7-ethoxyresorufin O-dealkylation, which is catalyzed predominantly by P450 lAl, incr 1.9-fold after loratidine treatment, but this incr was less than that caused by phenobarbital treatment (2.2-fold), and was considerably less than that caused by 3-methylcholanthrene treatment (33-fold). The effects of treating mature male mice with loratadine on liver microsomal cytochrome P450 resembled the effects observed in rats. These results indicate that loratadine is a phenobarbital type inducer of liver microsomal cytochrome P450 in rats and mice.
CHILDRENS ALLERGY RELIEF
Histamine H1 Receptor Antagonists [MoA]; Histamine-1 Receptor Antagonist [EPC]
Agents, usually topical, that relieve itching (pruritus).
Agents that are used to treat allergic reactions. Most of these drugs act by preventing the release of inflammatory mediators or inhibiting the actions of released mediators on their target cells. (From AMA Drug Evaluations Annual, 1994, p475)
A class of non-sedating drugs that bind to but do not activate histamine receptors (DRUG INVERSE AGONISM), thereby blocking the actions of histamine or histamine agonists. These antihistamines represent a heterogenous group of compounds with differing chemical structures, adverse effects, distribution, and metabolism. Compared to the early (first generation) antihistamines, these non-sedating antihistamines have greater receptor specificity, lower penetration of BLOOD-BRAIN BARRIER, and are less likely to cause drowsiness or psychomotor impairment.
Loratadine is rapidly absorbed and achieves peak plasma concentration in 1-2 hours, while it's main metabolite achieves peak plasma concentration in 3-4 hours. In the rapid dissolve formulation, the pharmacokinetic parameters of loratadine are as follows: Cmax = 2.56 ng/ml, Tmax = 1.14 hrs, AUC = 6.14 ng x hr/ml. In the rapid dissolve formulation, the pharmacokinetic parameters of descarboethoxyloratadine are as follows: Cmax = 3.72 ng/ml, Tmax = 1.97 hr, AUC = 49.1 ng x hr/ml. In the conventional formulation, the pharmacokinetic parameters of loratadine are as follows: Cmax = 2.11 ng/ml, Tmax = 1.00 hr, AUC = 4.64 ng x hr/ml In the conventional formulation, the pharmacokinetic parameters of descarboethoxyloratadine are as follows: Cmax = 3.66 ng/ml, Tmax = 1.97 hr, AUC = 48.4 ng x hr/ml
Over a 10 day period, 40% of loratadine is excreted in the urine, and 42% is eliminated in the faeces.
The volume of distribution of loratadine is 120 L/Kg.
The clearance of loratadine after single oral doses of 20 mg and 40 mg are 12 L/h/kg and 9 L/h/kg respectively. P-glycoprotein is involved in the clearance of many 2nd generation antihistamines, including loratadine, from the central nervous system. 1st generation antihistamines are not cleared by P-glycoprotein, which may help explain why they have a different central nervous system adverse effect profile compared to their 2nd generation counterparts. It appears that an antihistamine with higher affinity for p-glycoprotein will have a lower incidence of CNS adverse effects.
H1 antagonists are eliminated more rapidly by children than by adults and more slowly in those with severe liver disease. /H1 Receptor Antagonists/
The H1 antagonists are well absorbed from the gastrointestinal tract. Following oral administration, peak plasma concentrations are achieved in 2 to 3 hours ... . /H1 Receptor Antagonists/
Antihistaminic
Use (kg; approx.) in Germany (2009): >750
Used to treat allergies. A self-medication that is used alone or in combination with pseudoephedrine sulfate for the symptomatic relief of seasonal allergic rhinitis. Also used for the symptomatic relief of pruritus, erythema, and urticaria associated with chronic idiopathic urticaria in patients (not for children under 6 unless directed by a clincian).
Claritin 10 mg tablets; Claritin-D 5 mg loratadine in the tablet coating for immediate release and 120 mg pseudoephedrine sulfate, USP equally distributed between the tablet for immediate release and the barrier coated extended release core.
개요Loratadine is a non-sedating antihistamine indicated for use in allergic rhinitis and chronic urticaria. Its major advantage over other non-sedating antihistamines such as astemizole and terfenadine is its very fast onset of action. Loratadine is claimed not to cross the blood-brain barrier.
용도Loratadine, is used as a peripheral histamine H1 receptor agonist. It is also used as an orally active antiallergic agent. It is an important raw material and intermediate used in Organic Synthesis, Pharmaceuticals, Agrochemicals and Dyestuff.
일반 설명Loratadine, 4-(8-chloro-5,6-dihydro-11Hbenzo[5,6]-cyclohepta[1,2-b]pyridin-l 1-ylidene-1-carboxylic acid ethyl ester, is a white to off-white powder insoluble in water but very soluble in acetone, alcohols, and chloroform. Loratadine is structurally related to the antihistamines azatadine and cyproheptadine, and to some tricyclic antidepressants. It differs from azatadine, in that a neutral carbamate group has replaced the basic tertiary amino moiety, and a phenyl ring has been substituted with a chlorine atom. Loratadine is a selective peripheral H1-antihistamine with a receptor-binding profile like that of the other members of this series, except that it has more antiserotonergic activity. Thus, it produces no substantial CNS or autonomic side effects or cardiac toxicity. Loratadine displays potency comparable with that of astemizole and greater than that of terfenadine. Loratadine is indicated for the relief of nasal and nonnasal symptoms of seasonal allergic rhinitis. In the presence of a CYP3A4 inhibitor ketoconazole, loratadine is metabolized to descarboethoxyloratadine predominantly by CYP2D6.