Fexofenadine 180mg/5ml oral solution
Requires a prescription from a doctor or prescriber
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Yellow Card
Report side effects (MHRA)
Drug safety updates
MHRA alerts for Fexofenadine
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Fexofenadine
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Fexofenadine
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
WHO defined daily dose (DDD)
120 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 16 · Randomised trials: 6 · 1999–2026
Showing the 50 most relevant studies, sorted by most relevant.
Coumau C, Csajka C
2025
- Terfenadine
- Digoxin
- Dabigatran
P-glycoprotein is a critical efflux transporter that may significantly affect the pharmacokinetics of various drugs by influencing their absorption, distribution and elimination. While European and American regulatory guidelines provide lists of P-glycoprotein modulators, they lack specificity concerning in vivo studies and clear guidance on inducers, creating uncertainty in their clinical relevance. A systematic search on in vivo clinical studies involving healthy volunteers using fexofenadine, dabigatran and digoxin as P-glycoprotein substrates has been performed in accordance with the PRISMA guidelines. A total of 151 studies assessing the impact of P-glycoprotein modulators on the concentration-time profile of P-glycoprotein substrates were retrieved. Additionally, data on the P-glycoprotein modulators' effect on cytochrome P450 3A4 induction or inhibition were also collected. P-gp modulators were classified as potent, moderate, weak or non-interactors for P-glycoprotein, with or without cytochrome P450 3A4 impact, on the basis of the area under the concentration-time curve ratio. This classification was adapted from the Food and Drug Administration criteria for cytochrome interactions. This systematic review identified 49 area under the plasma concentration-time curve ratio values corresponding to P-glycoprotein inhibitors, 23 to P-glycoprotein inducers and 131 to non-interactors. Of these, only 32.5% and 41.1% were classified as weak to potent, respectively. Only 0.7% of inhibitors and no inducers were classified as potent. This suggests that most P-glycoprotein modulators have a limited impact on drug exposure. The potential for interaction increases when P-glycoprotein modulators also affect cytochrome P450 3A4, which is the case for 59.9% of P-glycoprotein modulators. However, some moderate P-glycoprotein modulators may have clinically significant effects depending on the therapeutic margin of the substrate and the clinical context.
Abstract licence: CC BY-NC
Kim JS, Stybayeva G, Hwang SH
2026
ObjectivesAllergic rhinitis (AR) can substantially compromise daily functioning and well-being, and many patients require more than a single agent to obtain satisfactory symptom control. This study examined whether adding montelukast to antihistamine could manage AR symptoms and quality-of-life outcomes effectively.MethodsA review was performed in PubMed, Embase, Medline, Scopus, the Cochrane Library, and Google Scholar to identify eligible studies reported through April 2025. Eligible studies compared combination therapy with montelukast plus antihistamine against antihistamine monotherapy and reported nasal symptoms or rhinoconjunctivitis quality of life questionnaire (RQLQ) scores. Treatment effects were further examined by antihistamine class.ResultsFifteen studies including 2,882 subjects were analyzed. Combination therapy significantly improved daytime nasal symptoms (standardized mean difference [SMD] [95% CI], 0.44 [0.21-0.67]), nighttime nasal symptoms (0.12 [0.01-0.23]), and RQLQ scores (0.14 [0.00-0.27]) versus monotherapy. Individual nasal or ocular symptoms, sneezing, nasal obstruction, and rhinorrhea improved significantly, while nasal itching and ocular symptoms did not. Combinations with desloratadine and levocetirizine showed greater benefits than those with loratadine or fexofenadine.ConclusionMontelukast-antihistamine combination therapy reduced overall symptoms and improved quality of life versus antihistamine monotherapy. The magnitude of benefit appears to vary depending on the specific antihistamine used, highlighting the possible value of individualized treatment strategies in the treatments of AR.
Abstract licence: CC BY-NC
Ansotegui IJ, Bousquet J, Canonica GW, et al.
2025
Buendía JA, Patino DG
2025
IntroductionAllergic rhinitis (AR) is highly prevalent worldwide, often leading to substantial healthcare costs and diminished patient quality of life. Although guidelines frequently recommend intranasal corticosteroids, oral second-generation antihistamines remain commonly used in many low- and middle-income countries. We performed a cost-utility analysis of newer-generation oral H1 antihistamines for adults with intermittent AR in Colombia.Materials and methodsA 28-day decision-tree model compared multiple antihistamines' costs and quality-adjusted life years (QALYs). Inputs included clinical effectiveness and adverse-event probabilities from systematic reviews and network meta-analyses. All costs, expressed in 2024 US dollars (1 USD = 4,400 COP), were adjusted for inflation. Net monetary benefits (NMB) were calculated using willingness-to-pay thresholds for Colombia (US$ 5130). Probabilistic sensitivity analyses were conducted to assess uncertainty in key parameters.ResultsCetirizine 10 mg and fexofenadine 180 mg were the only undominated strategies, exhibiting higher NMB values than other antihistamines. Deterministic analysis showed that cetirizine had a lower total cost (22.15 USD) and an ICER of 349.62 USD per QALY gained. In contrast, fexofenadine provided a slight gain in effectiveness at a modest incremental cost. Probabilistic analysis confirmed fexofenadine as cost-effective option across a wide range of thresholds, with cetirizine remaining a strong contender at lower thresholds.ConclusionIn this cost-utility analysis of oral H1 antihistamines for adults with intermittent allergic rhinitis in Colombia, cetirizine 10 mg and fexofenadine 180 mg emerged as the cost-effective options, offering high net monetary benefits and remaining undominated in deterministic and probabilistic analyses.
Abstract licence: CC BY-NC-ND
Kim JS, Stybayeva G, Hwang SH
2025
Allergic rhinitis (AR) significantly impairs quality of life and often necessitates combination therapies for optimal symptom control. This study aimed to evaluate the efficacy of montelukast-antihistamine combination therapy in patients with AR by using a network meta-analysis. A comprehensive search was conducted using PubMed, Embase, MEDLINE, Scopus, the Cochrane Library, and Google Scholar up to April 2025. The treatment strategies included montelukast alone, antihistamine monotherapies (loratadine, desloratadine, levocetirizine, and fexofenadine), their respective combinations with montelukast, including bilastine. Outcomes included daytime and nighttime symptom scores, Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ), and individual symptoms. Both pairwise and network meta-analyses were conducted. Thirty studies (4,486 patients) were included. Montelukast combinations with desloratadine (standardized mean difference [SMD] = -0.51), levocetirizine (SMD = -0.44), and loratadine (SMD = -0.31) significantly improved daytime nasal symptoms compared to montelukast alone. Only montelukast-levocetirizine improved nighttime symptoms (SMD = -0.21) and RQLQ (SMD = -0.48). The combinations with desloratadine or levocetirizine were superior for nasal obstruction, sneezing, and itching, while nasal discharge improved only with montelukast-levocetirizine. No treatment significantly improved eye symptoms. Surface under the cumulative ranking curve rankings generally favored combination therapies, though trends varied by outcome. Desloratadine monotherapy ranked highest for nasal itching. Although some comparisons require cautious interpretation, montelukast-based combination therapy demonstrated greater efficacy than monotherapy for multiple AR symptoms. These results highlight the importance of selecting therapeutic strategies based on the predominant symptom profile of individual patients.
Abstract licence: CC BY-NC
R. M. Gómez, P. Moreno, E. Compalati, et al.
The World Allergy Organization Journal, 2023
Cheng-zhi Huang, Zhi-hui Jiang, Jian Wang, et al.
BMC Pharmacology & Toxicology, 2019
Basma Mahrous El-fatatry, S. El-Haggar, Osama M Ibrahim, et al.
International Urology and Nephrology, 2023
Yeh HF, Chu YS, Hwang SJ, et al.
2025
- Drugs, Chinese Herbal
- Acetylcysteine
- Medicine, Chinese Traditional
BackgroundGlobus, a non-painful sensation of a lump in the throat, affects nearly half of the population. Its etiology remains uncertain, and standardized treatment is lacking. Ban-Xia-Hou-Pu-Tang (BXHPT, ), a classical formula for "Plum Pit Qi" ( ), closely resembles globus in traditional Chinese medicine. This study investigated the traditional Chinese medicine constitution of patients with globus and evaluated the efficacy and safety of BXHPT combined with western therapy.MethodsA single-blinded, randomized, placebo-controlled trial was conducted in patients with globus pharyngeus. Participants received either fexofenadine, famotidine, and acetylcysteine plus BXHPT (group A) or plus placebo (group B) for 4 weeks. The Constitution in Chinese Medicine Questionnaire, Reflux Symptom Index (RSI), Glasgow Edinburgh Throat Scale (GETS), Beck Anxiety Inventory (BAI), Beck Depression Inventory-II (BDI-II), and Reflux Finding Score (RFS) were assessed. Hepatic and renal safety were monitored.ResultsNinety-two patients completed the trial. Both groups showed significant improvements in RFS, RSI, GETS, BAI, and BDI-II. Group A had greater RFS reduction at week 2 (8.03 ± 1.57 vs 10.12 ± 1.75; p ConclusionBXHPT combined with western therapy provided additional improvement in laryngoscopic findings without safety concerns, supporting its potential as an effective adjunctive treatment for globus sensation.
Abstract licence: CC BY-NC-ND
Khafagy ES, Ashmawy AM, Abu Lila AS, et al.
2026
This study evaluates the repurposed application of an expired non-sedating antihistamine drug (ENSAD), fexofenadine hydrochloride, as a high-performance "green" corrosion inhibitor for copper in 1.0 M HCl. Gravimetric results demonstrate a concentration-dependent inhibition efficiency reaching 96.4% at 120 ppm, with remarkable long-term stability (> 92.5% efficiency after 72 h). Adsorption behavior followed the Langmuir isotherm model, indicating the formation of a stable monolayer. The calculated Gibbs free energy (∆Goads =-33.8 kJ mol- 1) confirms a comprehensive physicochemical adsorption mechanism involving both electrostatic attraction and chemical coordination. Thermodynamic investigations revealed that the addition of ENSAD increased the activation energy from 30.36 to 53.89 kJ mol⁻¹, creating a substantial energy barrier against metallic dissolution. Electrochemical studies (PDP and EIS) confirmed ENSAD as a mixed-type inhibitor that significantly enhances charge transfer resistance (Rct). Quantum chemical parameters, including a low energy gap (ΔEg = 2.361 eV) and high softness (S = 0.424 eV- 1), corroborate the high reactivity and electron-donating capability of the molecule's heteroatoms (N, O) and π-systems. Surface characterization (SEM/EDX) visually and chemically confirmed the presence of a robust organic film. These findings position ENSAD as a technically viable, thermally stable, and sustainable alternative for corrosion protection in industrial acid cleaning and low-temperature desalination stages.
Abstract licence: CC BY-NC-ND
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
11-15 hours
Mechanism
The H1 histamine receptor is responsible for mediating hypersensitivity and allergic reactions.
Food interactions
2 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
33%
[L10779]
…
Half-life
11-15 hours
[L10779][A1495]
Protein binding
60-70%
Volume of distribution
5.4-5.8 L/kg
[A1495]
Metabolism
5%
[L4269][A1495]
…
Elimination
80%
[A1495]
…
Clearance
50.6 L/h
[L10779]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L4269]
In Canada, fexofenadine carries the same indications but is approved only for patients ≥12 years old.
[L10779]
Fexofenadine is also available in combination with [pseudoephedrine] for the symptomatic treatment of season allergic rhinitis in patients ≥12 years old.
[L10800]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 436 interactions
[L4269]
If overdosage occurs, employ symptomatic and supportive treatment.
Hemodialysis does not effectively remove fexofenadine from the blood and is therefore of no benefit.
[L4269]
Fexofenadine is considered an “inverse agonist” of the H1 receptor because it binds to and stabilizes the inactive form of the receptor, preventing its activation and subsequent downstream effects.[A1495] It has a potent and selective affinity for H1 receptors, and there is no evidence that it carries antidopaminergic, antiserotonergic, anticholinergic, sedative, or adrenergic blocking activity.[L10779] Fexofenadine does not cross the blood-brain barrier and thus is unlikely to cause significant CNS effects.[L10779]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L10779]
The Tmax following oral administration is approximately 1-3 hours.
[L10779][A1495]
The steady-state AUCss(0-12h) and Cmax following twice daily dosing of 60mg are 1367 ng/mL.h and 299 ng/mL, respectively.
[L10779]
Fexofenadine AUC is decreased by >20% when coadministered with fruit juices (e.g. apple, orange, grapefruit) due to their inhibition of OATP transporters - for this reason, prescribing information recommends administering fexofenadine only with water.
[A188754]
Similarly, coadministration of fexofenadine with a high-fat meal appears to decrease AUC and Cmax by >20%.
[L4269]
[L10779][A1495]
[L10779]
[A1495]
[L4269][A1495]
The only identified metabolites are a methyl ester of fexofenadine (3.6% of the total dose) and MDL 4829 (1.5% of the total dose).
[L10779]
The enzymes responsible for this metabolism have not been elucidated.
[A1495]
The principal pathways of fexofenadine elimination are biliary and renal.
[L10779]
[L10779]
Proteins and enzymes this drug interacts with in the body
PMID:33828102 PMID:8280179
Through the H1 receptor, histamine mediates the contraction of smooth muscles and increases capillary permeability due to contraction of terminal venules. Also mediates neurotransmission in the central nervous system and thereby regulates circadian rhythms, emotional and locomotor activities as well as cognitive functions (By similarity)
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:10358072 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (dehydroepiandrosterone 3-sulfate, 17-beta-glucuronosyl estradiol, and estrone 3-sulfate), as well as eicosanoids (prostaglandin E2, thromboxane B2, leukotriene C4, and leukotriene E4), and thyroid hormones (T4/L-thyroxine, and T3/3,3',5'-triiodo-L-thyronine) .
PMID:10358072 PMID:10601278 PMID:10873595 PMID:11159893 PMID:12196548 PMID:12568656 PMID:15159445 PMID:15970799 PMID:16627748 PMID:17412826 PMID:19129463 PMID:26979622
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Involved in the clearance of endogenous and exogenous substrates from the liver .
PMID:10358072 PMID:10601278
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins), such as pravastatin and pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:10601278 PMID:15159445 PMID:15970799
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drug methotrexate .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver .
PMID:16624871 PMID:16627748
Shows a pH-sensitive substrate specificity towards prostaglandin E2 and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions PMID:19129463
PMID:10779507 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (17-beta-glucuronosyl estradiol, dehydroepiandrosterone sulfate (DHEAS), and estrone 3-sulfate), as well as eicosanoid leukotriene C4, prostaglandin E2 and L-thyroxine (T4) .
PMID:10779507 PMID:11159893 PMID:12568656 PMID:15159445 PMID:17412826 PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions .
PMID:19129463
Shows a pH-sensitive substrate specificity towards sulfated steroids, taurocholate and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Involved in the clearance of bile acids and organic anions from the liver .
PMID:22232210
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins) such as pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:15159445
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drugs methotrexate and paclitaxel .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver PMID:16624871 PMID:16627748
PMID:10873595 PMID:11159893 PMID:11932330 PMID:12724351 PMID:14610227 PMID:16908597 PMID:18501590 PMID:20507927 PMID:22201122 PMID:23531488 PMID:25132355 PMID:26383540 PMID:27576593 PMID:28408210 PMID:29871943 PMID:34628357
Responsible for the transport of estrone 3-sulfate (E1S) through the basal membrane of syncytiotrophoblast, highlighting a potential role in the placental absorption of fetal-derived sulfated steroids including the steroid hormone precursor dehydroepiandrosterone sulfate (DHEA-S) .
PMID:11932330 PMID:12409283
Also facilitates the uptake of sulfated steroids at the basal/sinusoidal membrane of hepatocytes, therefore accounting for the major part of organic anions clearance of liver .
PMID:11159893
Mediates the intestinal uptake of sulfated steroids .
PMID:12724351 PMID:28408210
Mediates the uptake of the neurosteroids DHEA-S and pregnenolone sulfate (PregS) into the endothelial cells of the blood-brain barrier as the first step to enter the brain .
PMID:16908597 PMID:25132355
Also plays a role in the reuptake of neuropeptides such as substance P/TAC1 and vasoactive intestinal peptide/VIP released from retinal neurons .
PMID:25132355
May act as a heme transporter that promotes cellular iron availability via heme oxygenase/HMOX2 and independently of TFRC .
PMID:35714613
Also transports heme by-product coproporphyrin III (CPIII), and may be involved in their hepatic disposition .
PMID:26383540
Mediates the uptake of other substrates such as prostaglandins D2 (PGD2), E1 (PGE1) and E2 (PGE2), taurocholate, L-thyroxine, leukotriene C4 and thromboxane B2 (PubMed:10873595, PubMed:14610227, PubMed:19129463, PubMed:29871943, Ref.25). May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable). Shows a pH-sensitive substrate specificity which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:14610227 PMID:19129463 PMID:22201122
The exact transport mechanism has not been yet deciphered but most likely involves an anion exchange, coupling the cellular uptake of organic substrate with the efflux of an anionic compound .
PMID:19129463 PMID:20507927 PMID:26277985
Hydrogencarbonate/HCO3(-) acts as a probable counteranion that exchanges for organic anions .
PMID:19129463
Cytoplasmic glutamate may also act as counteranion in the placenta .
PMID:26277985
An inwardly directed proton gradient has also been proposed as the driving force of E1S uptake with a (H(+):E1S) stoichiometry of (1:1) PMID:20507927
PMID:19129463 PMID:7557095
Responsible for intestinal absorption of bile acids (By similarity). Transports dehydroepiandrosterone 3-sulfate (DHEAS), a major circulating steroid secreted by the adrenal cortex, as well as estrone 3-sulfate and 17beta-estradiol 17-O-(beta-D-glucuronate) .
PMID:11159893 PMID:12568656 PMID:19129463 PMID:23918469 PMID:25560245 PMID:9539145
Mediates apical uptake of all-trans-retinol (atROL) across human retinal pigment epithelium, which is essential to maintaining the integrity of the visual cycle and thus vision .
PMID:25560245
Involved in the uptake of clinically used drugs .
PMID:17301733 PMID:20686826 PMID:27777271
Capable of thyroid hormone transport (both T3 or 3,3',5'-triiodo-L-thyronine, and T4 or L-tyroxine) .
PMID:19129463 PMID:20358049
Also transports prostaglandin E2 .
PMID:19129463
Plays roles in blood-brain and -cerebrospinal fluid barrier transport of organic anions and signal mediators, and in hormone uptake by neural cells (By similarity). May also play a role in the reuptake of neuropeptides such as substance P/TAC1 and vasoactive intestinal peptide/VIP released from retinal neurons .
PMID:25132355
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drugs methotrexate and paclitaxel .
PMID:23243220
Shows a pH-sensitive substrate specificity which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions .
PMID:19129463
May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
PMID:10220572 PMID:10421658 PMID:11500505 PMID:16332456
Mediates hepatobiliary excretion of mono- and bis-glucuronidated bilirubin molecules and therefore play an important role in bilirubin detoxification .
PMID:10421658
Also mediates hepatobiliary excretion of others glucuronide conjugates such as 17beta-estradiol 17-glucosiduronic acid and leukotriene C4 .
PMID:11500505
Transports sulfated bile salt such as taurolithocholate sulfate .
PMID:16332456
Transports various anticancer drugs, such as anthracycline, vinca alkaloid and methotrexate and HIV-drugs such as protease inhibitors .
PMID:10220572 PMID:11500505 PMID:12441801
Confers resistance to several anti-cancer drugs including cisplatin, doxorubicin, epirubicin, methotrexate, etoposide and vincristine PMID:10220572 PMID:11500505
PMID:10359813 PMID:11581266 PMID:15083066
Transports glucuronide conjugates such as bilirubin diglucuronide, estradiol-17-beta-o-glucuronide and GSH conjugates such as leukotriene C4 (LTC4) .
PMID:11581266 PMID:15083066
Transports also various bile salts (taurocholate, glycocholate, taurochenodeoxycholate-3-sulfate, taurolithocholate- 3-sulfate) (By similarity). Does not contribute substantially to bile salt physiology but provides an alternative route for the export of bile acids and glucuronides from cholestatic hepatocytes (By similarity). May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable).
Can confer resistance to various anticancer drugs, methotrexate, tenoposide and etoposide, by decreasing accumulation of these drugs in cells PMID:10359813 PMID:11581266
PMID:14586168 PMID:15644426 PMID:15846473 PMID:16455804 PMID:31553721
Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) .
PMID:14586168 PMID:15846473 PMID:15864504 PMID:22108572 PMID:23832370
Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain .
PMID:11306713 PMID:14586168 PMID:15846473
E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange .
PMID:26377792
Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule .
PMID:11907186
Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate .
PMID:22108572 PMID:23832370
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside .
PMID:15644426
May participate in the detoxification/ renal excretion of drugs and xenobiotics, such as the histamine H(2)-receptor antagonists fexofenadine and cimetidine, the antibiotic benzylpenicillin (PCG), the anionic herbicide 2,4-dichloro-phenoxyacetate (2,4-D), the diagnostic agent p-aminohippurate (PAH), the antiviral acyclovir (ACV), and the mycotoxin ochratoxin (OTA), by transporting these exogenous organic anions across the cell membrane in exchange for dicarboxylates such as 2-oxoglutarate .
PMID:11669456 PMID:15846473 PMID:16455804
Contributes to the renal uptake of potent uremic toxins (indoxyl sulfate (IS), indole acetate (IA), hippurate/N-benzoylglycine (HA) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)), pravastatin, PCG, E1S and dehydroepiandrosterone sulfate (DHEAS), and is partly involved in the renal uptake of temocaprilat (an angiotensin-converting enzyme (ACE) inhibitor) .
PMID:14675047
May contribute to the release of cortisol in the adrenals .
PMID:15864504
Involved in one of the detoxification systems on the choroid plexus (CP), removes substrates such as E1S or taurocholate (TC), PCG, 2,4-D and PAH, from the cerebrospinal fluid (CSF) to the blood for eventual excretion in urine and bile (By similarity). Also contributes to the uptake of several other organic compounds such as the prostanoids prostaglandin E(2) and prostaglandin F(2-alpha), L-carnitine, and the therapeutic drugs allopurinol, 6-mercaptopurine (6-MP) and 5-fluorouracil (5-FU) (By similarity). Mediates the transport of PAH, PCG, and the statins pravastatin and pitavastatin, from the cerebrum into the blood circulation across the blood-brain barrier (BBB).
In summary, plays a role in the efflux of drugs and xenobiotics, helping reduce their undesired toxicological effects on the body (By similarity)
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
Appears to function in modulating the activity of the immune system during the acute-phase reaction
Involved compounds
ATC R06AX26
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Fexofenadine
Additional database identifiers
Drugs Product Database (DPD)
11456
ChemSpider
3231
BindingDB
22874
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5182
GenAtlas
HRH1
GeneCards
HRH1
GenBank Gene Database
Z34897
GenBank Protein Database
510296
Guide to Pharmacology
262
UniProt Accession
HRH1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8499
GeneCards
ORM2
GenBank Gene Database
BC015964
GenBank Protein Database
16359000
UniProt Accession
A1AG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10959
GenAtlas
SLCO1B1
GeneCards
SLCO1B1
GenBank Gene Database
AF060500
GenBank Protein Database
5051630
Guide to Pharmacology
1220
UniProt Accession
SO1B1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10961
GeneCards
SLCO1B3
GenBank Gene Database
AJ251506
GenBank Protein Database
9187497
Guide to Pharmacology
1221
UniProt Accession
SO1B3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10962
GenAtlas
SLCO2B1
GeneCards
SLCO2B1
GenBank Gene Database
AB026256
GenBank Protein Database
5006263
Guide to Pharmacology
1224
UniProt Accession
SO2B1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10956
GeneCards
SLCO1A2
GenBank Gene Database
U21943
GenBank Protein Database
885978
Guide to Pharmacology
1219
UniProt Accession
SO1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:53
GenAtlas
ABCC2
GeneCards
ABCC2
GenBank Gene Database
U63970
GenBank Protein Database
1764162
Guide to Pharmacology
780
UniProt Accession
MRP2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:54
GenAtlas
ABCC3
GeneCards
ABCC3
GenBank Gene Database
AB010887
GenBank Protein Database
3132270
UniProt Accession
MRP3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10972
GeneCards
SLC22A8
GenBank Gene Database
AF097491
GenBank Protein Database
4378059
Guide to Pharmacology
1027
UniProt Accession
S22A8_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72