Last update 21 Nov 2024

Chlorpheniramine Maleate/Pseudoephedrine Hydrochloride

Last update 21 Nov 2024

Overview

R&D Status

Clinical Result

Translational Medicine

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Pseudoephedrine Hydrochloride/Chlorphenamine Maleate, 盐酸伪麻黄碱/马来酸氯苯那敏, CODIMAL-L.A. 12

Target

H1 receptor x α-adrenergic receptor

Mechanism

H1 receptor antagonists(Histamine H1 receptor antagonists), α-adrenergic receptor agonists(Alpha adrenergic receptor agonists)

Therapeutic Areas

Infectious DiseasesRespiratory Diseases

Active Indication-

Inactive Indication

Common Cold

Originator Organization

Schwarz Pharma, Inc.

Active Organization-

Inactive Organization

Schwarz Pharma, Inc.

Drug Highest PhaseWithdrawn

First Approval Date

US (18 Mar 1985),

Common Cold

Regulation-

Structure

Molecular FormulaC20H23ClN2O4

InChIKeyDBAKFASWICGISY-BTJKTKAUSA-N

CAS Registry113-92-8

View All Structures (2)

100 Clinical Results associated with Chlorpheniramine Maleate/Pseudoephedrine Hydrochloride

100 Translational Medicine associated with Chlorpheniramine Maleate/Pseudoephedrine Hydrochloride

100 Patents (Medical) associated with Chlorpheniramine Maleate/Pseudoephedrine Hydrochloride

Literatures (Medical) associated with Chlorpheniramine Maleate/Pseudoephedrine Hydrochloride

01 Dec 2021·Journal of Medical Case Reports

Possible immunoglobulin-E-dependent sugammadex-induced anaphylaxis caused by an epitope other than γ-cyclodextrin: a case report

Article

Author: Horiuchi, Tatsuo ; Sakamoto, Shinya ; Takazawa, Tomonori ; Saito, Shigeru ; Uchiyama, Mutsumi ; Yokohama, Akihiko ; Orihara, Masaki

AbstractBackgroundSugammadex is a synthetic γ-cyclodextrin derivative designed to selectively bind to steroidal neuromuscular blocking agents and reverse their effects. Although many cases of sugammadex-induced anaphylaxis have been reported, few studies have investigated the underlying mechanism.Case presentationA 55-year-old Japanese man underwent a laryngectomy under general anesthesia. One month before laryngectomy, he had undergone laryngoscopy under general anesthesia and received sugammadex administration without causing hypersensitivity. He had no history of allergies. The operation was finished without complications. Shortly after sugammadex administration, his blood pressure dropped to approximately 70 mmHg, and his heart rate increased to 110 beats/minute with systemic erythema. Suspecting anaphylaxis, he was treated with the intravenous injection of phenylephrine, d-chlorpheniramine, and hydrocortisone. After these treatments, his cardiovascular condition stabilized. Eight months after the event, skin prick tests and intradermal tests with all agents used during general anesthesia were performed. Intradermal tests showed positive results only for sugammadex. Subsequently, basophil activation tests with CD203c were performed using sugammadex, γ-cyclodextrin, and positive controls (anti-immunoglobulin-E and formyl-methionyl-leucyl-phenylalanine). In addition to both controls, sugammadex, but not γ-cyclodextrin, induced significant upregulation of CD203c expression. We performed additional basophil activation tests with wortmannin, an inhibitor of phosphoinositide 3-kinase, to investigate the mechanism underlying sugammadex-induced basophil activation. The inhibitory effect of wortmannin on basophil activation due to sugammadex was similar to that of anti-immunoglobulin-E, suggesting an immunoglobulin-E-dependent mechanism. Although the patient showed no hypersensitivity after the first exposure of sugammadex, anaphylaxis appeared after the second administration. Because most cases of sugammadex-induced anaphylaxis reportedly appeared after first administration, this seems to be a rare case.ConclusionsIn the present case, sugammadex-induced anaphylaxis might have occurred through an immunoglobulin-E-dependent mechanism and not involve γ-cyclodextrin as an epitope. Physicians should pay attention to the occurrence of sugammadex-induced anaphylaxis even when the patient has a history of safe administration of sugammadex.

01 Mar 2008·Human Psychopharmacology: Clinical and ExperimentalQ4 · MEDICINE

Effects of a sedative antihistamine, D‐chlorpheniramine, on regional cerebral perfusion and performance during simulated car driving

Q4 · MEDICINE

Article

Author: Arai, Hiroyuki ; Watanuki, Shoichi ; Okamura, Nobuyuki ; Mochizuki, Hideki ; Tashiro, Manabu ; Itoh, Masatoshi ; Sakurada, Yumiko ; Yanai, Kazuhiko ; Maruyama, Masahiro ; Horikawa, Etsuo

AbstractObjectivesThe sedative side effects of antihistamines have been recognized to be potentially dangerous in car driving, but the mechanism underlying these effects has not yet been elucidated to date. The aim of the present study is to examine regional cerebral blood flow (rCBF) responses during a simulated car‐driving task following oral administration of D‐chlorpheniramine using positron emission tomography (PET) and [15O]H2O, based on a single‐blind cross‐over study‐design.MethodsRight‐handed, healthy male volunteers (n = 14) drove a car in a simulated environment following oral administration of D‐chlorpheniramine repetab 6 mg or placebo. Their rCBF was measured using PET with [15O]H2O in the following three conditions: (1) resting, (2) active driving, and (3) passive driving. All ‘in‐car’ views during the simulated driving were videotaped and used for rating driving performance.ResultsPerformance evaluation revealed that the number of lane deviations significantly increased in the D‐chlorpheniramine condition compared with the placebo condition (p < 0.01). Subjective sleepiness was not significantly different between the two drug conditions. The regions of diminished brain responses following D‐chlorpheniramine treatment were detected in the parietal, temporal and visual cortices, and in the cerebellum. The regions of augmented rCBF responses were found in the orbitofrontal cortex and cerebellar vermis.ConclusionThese results suggest that D‐chlorpheniramine tends to suppress visuo‐spatial cognition and visuo‐motor coordinating functions rather than attention and motor functions during car driving. Copyright © 2008 John Wiley & Sons, Ltd.

01 May 2002·British Journal of Clinical PharmacologyQ2 · MEDICINE

The roles of CYP2D6 and stereoselectivity in the clinical pharmacokinetics of chlorpheniramine

Q2 · MEDICINE

Article

Author: Karen M. Fried ; Raymond L. Woosley ; Andrea E. Young ; Sally Usdin Yasuda ; Peter Zannikos ; Irving W. Wainer

Aims To examine the stereoselective disposition of chlorpheniramine and to evaluate the role of CYP2D6 in chlorpheniramine pharmacokinetics in humans.Methods Eight healthy volunteers (six extensive metabolizers with respect to CYP2D6 and two poor metabolizers) received a single 8 mg oral dose of rac‐chlorpheniramine either given alone or following administration of quinidine 50 mg every 6 h for 2 days prior to the study day and every 6 h thereafter until the end of the study. Plasma concentrations of (S)‐(+)‐ and (R)‐(−)‐enantiomers of chlorpheniramine were determined using liquid chromatography/mass spectrometry.Results In extensive metabolizers, mean Cmax was greater (12.55±1.51 ng ml−1vs 5.38±0.44 ng ml−1) and CLoral was lower (0.49±0.08 l h−1 kg−1vs 1.07±0.15 l h−1 kg−1) for (S)‐(+)‐ than for (R)‐(−)‐chlorpheniramine (P<0.005). For (S)‐(+)‐chlorpheniramine, administration of quinidine, an inhibitor of CYP2D6, resulted in an increase in Cmax to 13.94±1.51 (P<0.01), a reduction in CLoral to 0.22±0.03 l h−1 kg−1 (P<0.01), and a prolongation of elimination half‐life from 18.0±2.0 h to 29.3±2.0 h (P<0.001). Administration of quinidine decreased CLoral for (R)‐(−)‐chlorpheniramine to 0.60±0.10 l h−1 kg−1 (P<0.005). In CYP2D6 poor metabolizers, systemic exposure was greater after chlorpheniramine alone than in extensive metabolizers, and administration of quinidine resulted in a slight increase in CLoral.Conclusions Stereoselective elimination of chlorpheniramine occurs in humans, with the most pharmacologically active (S)‐(+)‐enantiomer cleared more slowly than the (R)‐(−)‐enantiomer. CYP2D6 plays a role in the metabolism of chlorpheniramine in humans.

100 Deals associated with Chlorpheniramine Maleate/Pseudoephedrine Hydrochloride

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Chlorpheniramine Maleate/Pseudoephedrine Hydrochloride

Overview

Basic Info

Structure

Related

R&D Status

Clinical Result

Translational Medicine

Deal

Core Patent

Clinical Trial

Approval

Regulation