the allergic response in people with atopic disorders involves exposure of the immune system to the antigen ( leung 1998 ) , antigen presentation ( fokkens et al 1991 ) , mediator release with amplification signals ( grewal and flavell 1996 ; vercelli et al 1989 ) , and production of antigen specific ige , which binds to mast cells . ( ishizaka and ishizaka 1977 ) . upon re - exposure to the allergen , bridging of the mast cell bound allergen specific ige results in the release of preformed and newly synthesized bioactive and pro - inflammatory mediators ( hirano 1989 ) , which results in the symptoms of allergic rhinitis and chronic idiopathic urticaria , and contributes to the symptoms of atopic dermatitis and allergic asthma . the us food and drug administration ( fda ) approved an oral suspension of fexofenadine on october 16 , 2006 . the approval is for twice - daily dosing , for the treatment of symptoms associated with seasonal allergic rhinitis , in patients 2 to 11 years of age , and for the treatment of symptoms of chronic idiopathic urticaria , in patients 6 months to 11 years of age . the studies cited in this text provide information based upon other oral formulations of fexofenadine . information based upon efficacy studies financially supported only by the manufacturer is not included , unless stated in the text . morrison and sahasranaman ( 2007 ) administered fexofenadine 30 mg by tablet or by oral suspension to 53 normal adult subjects . their subjects reached maximum blood fexofenadine concentrations at 1 hour for the oral suspension and 1.5 hour for the tablet . they found equivalent areas under the curves for the oral suspension and the tablet formulation , suggesting bioequivalence of fexofenadine oral suspension and fexofenadine capsules . in a study focusing on the oral formulations , grubbe et al ( 2007 ) evaluated the pharmacokinetics of fexofenadine oral suspension in 50 children , aged 2 to 5 years , which demonstrated the mean maximum plasma concentration of 224 ng / ml , and the mean area under the plasma concentration curve of 898 ng - h / ml . in capsule formulations in a double - blind , two - way crossover study in children with allergic rhinitis ( with a mean age of 9.8 years , a mean height of 134 cm and a mean weight of 32.1 kg ) , simons et al ( 1996 ) administered 30 or 60 mg of fexofenadine as a capsule and demonstrated the mean maximum plasma concentrations after the 30 mg dose of 78 ng / ml , and the mean maximum concentrations after the 60 mg dose of 286 ng / ml . they found no dose - dependent kinetics in the doses studied and no difference in the clearance rates or the mean terminal elimination half - life values after both doses . in another capsule and tablet formulation study designed as open - label , randomized crossover studies in healthy male non - smokers 18 to 43 years of age , within 10% of ideal body weight , stoltz et al ( 1997 ) found that the relative bioavailability of fexofenadine capsules is 89% to 93% compared to the tablet formulation . food decreased the area under the curves by 17% for the capsule and by 25% for the tablet compared to administration of the fexofenadine under a fasting state . in an industry - based1 study , robbins et al ( 1998 ) studied the pharmacokinetics of fexofenadine in 24 healthy male adult volunteers . the drug was undetectable at 48 hours after a single dose , and percent drug recovered in the urine ranged from 7.6% to 11.8% . in another industry - based study , russell et al ( 1998 ) found similar pharmacokinetics , in healthy male adults , for both the single dose and twice - daily dose of fexofenadine , administered as an oral solution , with 80% of the administered drug passing through the intestinal tract ( russell et al 1998 ) . these two studies suggest that the majority of the drug is excreted through the intestinal tract , with a small component via the kidneys , mostly unchanged . although high doses of fexofenadine do not appear to provide much toxicity , interaction with other drugs that use the p450 cyp3a4 degradation pathway , p - glycoprotein and the organic anion transporter peptides , prominent transporter proteins , may increase the risks of adverse events ( shukla et al 2008 ) . concomitant exposure to prescription and non - prescription drugs , as well as food , may significantly alter the blood and tissue levels of medications , as well as alter the risks to those medications . factors that may affect the drug  drug and drug  food interactions include biodegradative pathways and transport mechanisms , particularly via the multi - drug transporters p - glycoprotein and organic anion transporter ( table 1 ) ( adenot et al 2004 ; akiyama et al 1988 ; baltes et al 2007 ; charuk et al 1994 ; chiou et al 2000 ; choi et al 1998 ; crowe et al 2006a , b ; didiodato and sharom 1997 ; doran et al 2005 ; ejsing et al 2007 ; elsinga et al 2004 ; faassen et al 2003 ; feng et al 2008 ; fromm 2000 ; garrigues et al 2002 ; gouaze et al 2005 ; hanko et al 2003 ; hayeshi et al 2006 ; ibrahim et al 2000 ; ito et al 1997 ; jette et al 1995 ; johnson 2002 ; ketabi - kiyanvash et al 2003 ; kim and kim 2002 ; king et al 2001 ; lee and lee 2002 ; leung and bendayan 1999 ; ling 1992 ; litman et al 2003 ; loo et al 2003 ; makowski and pikula 1997 ; mollgard et al 2001 ; neuhoff et al 2000 ; orlowski and garrigos 1999 ; pascaud et al 1998 ; rebbeor and senior 1998 ; safa and safa 2004 ; savolainen et al 2002 ; schinkel et al 1996 ; sharom 1997 ; shirasaka et al 2006 ; shukla et al 2008 ; smit et al 1998 ; storch et al 2007 ; terao et al 1996 ; wang et al 2006 ; weiss et al 2003 ) . although sterioisomers are commonly found to have some preferential biological and pharmacological effects ( bielory et al ) , miura et al ( 2007 ) did not find any difference in the pharmacokinetics of fexofenadine enantiomers in healthy subjects . in addition , alfentanil , a selective inhibitor of the p450 cyp3a4 degradative pathway , did not significantly compete with fexofenadine ( kharasch et al 2005 ) . therefore , it appears that fexofenadine does not significantly interact with the p450 cyp3a degradative pathway . however , in a study using mdr1a/1b knockout mice , tahara et al ( 2005 ) showed that p - glycoprotein does have a role in moving fexofenadine from the brain to the plasma , and from the plasma to the liver , but had no effect on fexofenadine biliary excretion . cvetkovic et al ( 1999 ) found that the human organic anion transporting polypeptide mediates c - labeled fexofenadine cellular uptake . the bile acid transporter , human sodium taurocholate co - transporting polypeptide , did not exhibit such activity . the authors identified p - glycoprotein as a fexofenadine efflux transporter , using the llc - pk1 cell , a polarized epithelial cell line that lacks p - glycoprotein , and a derivative cell line ( l - mdr1 ) , which overexpresses p - glycoprotein . oral and intravenous administration of c - labeled fexofenadine to mice lacking mdr1-encoded p - glycoprotein resulted in 5- and 9-fold increases in the drug s plasma and brain levels , respectively , compared with wild - type mice . a number of drug inhibitors of p - glycoprotein effectively inhibited organic anion transporting polypeptide . because organic anion transporting polypeptide transporters and p - glycoprotein co - localize in organs of importance to drug disposition , such as the liver , their activity may provide an explanation for the mechanism(s ) responsible for fexofenadine disposition , and suggests potentially similar roles in the disposition of other xenobiotics ( cvetkovic et al 1999 ) . inhibitors of p - glycoprotein ( ketoconazole , itraconazole , verapamil , and erythromycin ) inhibited the intestinal absorption of fexofenadine . however , inhibitors of multidrug resistant associated protein ( indomethacin , probenecid ) and organic anion transporting polypeptide ( rifamycin ) had no effect upon fexofenadine transport . rifampin increases fexofenadine clearance , presumably by the induction of p - glycoprotein ( hamman et al 2001 ) . fexofenadine does not appear to affect the pharmacokinetics of omeprazole , a substrate of p - glycoprotein , suggesting that these two drugs have different transport mechanisms , or fexofenadine does not saturate p - glycoprotein . drescher et al ( 2002 ) described a number of distinct p - glycoprotein mutations that may affect the transport of fexofenadine . the mdr1 g2577t / c3435 t haplotype of p - glycoprotein , in the presence of itraconazole , altered the disposition of fexofenadine , with no change in the elimination half - life and the renal clearance of fexofenadine . itraconazole resulted in a 3-fold increase in the peak concentration of fexofenadine and the area under the curve . this suggests that the interaction between itraconazole and fexofenadine may occur at the gut wall before reaching the portal vein circulation . however , subjects with the 2677aa/3435cc haplotype had lower plasma fexofenadine concentrations than those with the g2677t / a and c3435 t haplotypes ( yi et al 2004 ) . these findings suggest that p - glycoprotein is responsible for the intestinal absorption of fexofenadine . van heeswijk et al ( 2006 ) studied the time - dependent interaction between lopinavir / ritonavir and fexofenadine . ritonavir and lopinavir / ritonavir increased the area under the plasma concentration - time curve for fexofenadine . they did not observe a change in the fexofenadine elimination half - life . they postulated that the increased area under the curve related to increased bioavailability due to p - glycoprotein inhibition . st john s wort , in a single dose of 900 mg , inhibits the intestinal transport of fexofenadine , increasing the maximum plasma concentration of fexofenadine by 45% . st john s wort decreases the oral clearance of fexofenadine by 20% , without changing the half - life and renal clearance ( milne et al 2000 ; petri et al 2004 ; shon et al 2005 ; takahata et al 2004 ; tannergren et al 2003 ; uno et al 2006 ; wang et al 2002 ) . these data suggest that fexofenadine may affect the blood levels of other drugs through its interaction with p - glycoprotein . probenecid has been shown to inhibit the interaction of fexofenadine with the organic anion transporter 3 ( oat3 ) in the kidney ( tahara et al 2006 ) . however , as the renal excretion of fexofenadine is small ( < 10% ) , the effect upon systemic fexofenadine levels is limited ( robbins et al 1998 ) . organic anion transporter protein 1b3 preferentially accepts fexofenadine over organic anion transporter proteins 1b1 and 2b1 in human embryonic kidney cells , suggesting that organic anion transporter protein 1b3 is a transporter involved in hepatic uptake of fexofenadine ( shimizu et al 2005 ) . although fexofenadine does not undergo significant metabolism by the p450 cyp 3a4 , it does interact with a numbers of drugs at p - glycoprotein and the organic anion transporter polypeptides . these interactions may increase the blood levels of a number of drugs , and increase the risk of adverse effects with concomitant administration of those drugs . administration of fexofenadine with grapefruit juice reduces the bioavailability of fexofenadine ( banfield et al 2002 ) . this reduction in bioavailability , which also occurs with apple juice , appears to result from preferential inhibition of organic anion transporter polypeptide mediated transport ( dresser et al 2002 , 2005 ; kamath et al 2005 ) . these data have led to the recommendation that patients should not ingest apple or grapefruit juice while taking fexofenadine . at 1 to 2 hours following the ingestion of fexofenadine , both the 30 mg and 60 mg doses suppressed the epicutaneous wheal response to histamine through 24 hours post dosing and suppressed the epicutaneous flare response to histamine through 8 hours post dosing ( simons et al 2003 ) . in another study , fexofenadine inhibited the histamine - induced wheal and flare with a maximum effect reached between 1 and 2 hours and lasting through the 12-hour dosing schedule for 60 mg , while the fexofenadine 120 mg dose inhibited the histamine - induced wheal and flare for 23 hours . the authors did not note tolerance to the anti - histamine effect over a period of 28 days ( russell et al 1998 ) . allocco et al ( 2002 ) , with grants from the nih and industry , studied the effect of fexofenadine upon the early response to nasal allergen challenge and demonstrated that fexofenadine reduced symptoms and vascular permeability . their data suggest that while fexofenadine antagonizes mediators of the acute allergic response , it does not prevent mast cell degranulation . older anti - histamines have anti - cholinergic properties that may induce increased intraocular pressure , leading to glaucoma and prostatism associated with urinary retention . however , in a cholinergic linked capsaicin - induced cough model , pretreatment with fexofenadine had no adverse effect ( dicpinigaitis et al 2003 ) . in an industry - sponsored study , juergens et al ( 2006a ) evaluated the effect of fexofenadine on arachidonic acid metabolism in cultured human monocytes . lipopolysaccharide stimulated human monocytes from healthy volunteers co - cultured with and without fexofenadine , followed by stimulation with zymosan , led to inhibition of ltc4 , ltd4 , and lte4 production . fexofenadine also inhibited lipopolysaccharide - stimulated production of pge2 and pgf2 , which the authors suggest may explain the beneficial effects of fexofenadine upon nasal congestion . in addition , fexofenadine selectively inhibited cyclo - oxygenase 2 , which may also contribute to its apparent anti - inflammatory properties ( juergens et al 2006b ) . sakairi et al ( 2005 ) , in an industry - based study , demonstrated that fexofenadine inhibited the increase in nasal airway resistance in a guinea pig antigen - induced model of rhinitis . the authors suggest that fexofenadine may inhibit the release of chemical mediators , including thromboxane , to reduce antigen - induced nasal airway resistance , in part by its inhibitory effect on cyclo - oxygenase 2 . asano et al ( 2007 ) , in an industry - sponsored study , evaluated the effect of nitric oxide production by fexofenadine from nasal fibroblasts , which demonstrated inhibition of inos mrna , with the suppression of tnf-induced no production from nasal fibroblasts . mice treated for 2 and 3 weeks with fexofenadine had diminished lps - induced no production with inhibition of inos mrna expression in lung tissues , suggesting a role for fexofenadine in asthma . however , brannan et al ( 2001 ) and fardon et al ( 2005 ) did not show a direct benefit of fexofenadine in patients with asthma . fexofenadine treatment appeared to decrease endothelial leukocyte adhesion molecule-1 ( elam-1 ) , vascular cell adhesion molecule-1 ( vcam-1 ) , and tryptase in subjects with chronic idiopathic urticaria , suggesting that fexofenadine may express other anti - inflammatory properties by the modulation of these cytokines ( cassano et al 2002 ) . abdelaziz et al ( 1998 ) studied the effects of fexofenadine on eosinophil - induced changes in electrical resistance and adherence to human nasal endothelial cells , as well as the effects of fexofenadine on eosinophil adherence and chemotaxis , in the presence and absence of opsonized latex beads . fexofenadine significantly attenuated the decrease in electrical resistance of the human nasal epithelial cells with exposure to both eosinophils and opsonized latex beads . human nasal epithelial cells , on exposure to eosinophils with opsonized latex beads , released rantes , il-8 , gm - csf , and sicam-1 . fexofenadine diminished the release of these chemokines with human nasal epithelial cell exposure to eosinophils and opsonized latex beads . in the presence of ifn and tnf , fexofenadine decreased the expression of icam-1 , increased the percentage of apoptotic cells , but did not change the expression of lfa-1 . fexofenadine did not change the expression of keratinocyte expression of il-8 and mig , but fexofenadine did down - modulate keratinocyte rantes , i - tac , mdc , and tarc , suggesting that fexofenadine had a selective effect on th2 cytokines , a mechanism by which fexofenadine provided an anti - inflammatory effect . however , fexofenadine significantly inhibited the ability of peripheral blood leukocytes to produce il-4 , but not ifn- with cry j 1 stimulation ( asano et al 2004b ) . fexofenadine pretreatment reduced the intranasal levels of il-6 and tnf in subjects given an intranasal challenge of parietaria officinalis ( ciprandi et al 2004 ) . watanabe et al ( 2004 ) studied the effect of fexofenadine upon eosinophilia and systemic anaphylaxis in mice infected with trichinella spiralis . fexofenadine provided a dose - dependent suppression of eosinophilia in c57bl/6 mice but not in mast cell - deficient w / w mice . fexofenadine suppressed rectal temperature , a marker for systemic anaphylaxis , in c57bl/6 mice . in an ige - anti - ige model of anaphylaxis in cbf1 mice , fexofenadine suppressed this same marker of anaphylaxis , without an effect on peripheral il-5 or eotaxin levels . fexofenadine diminished mrna expression of rantes , as well as limited the elaboration of eotaxin from nasal polyp fibroblasts , in response to lps ( asano et al 2004a ) . fexofenadine inhibited the production of matrix metal - loproteinases ( mmp ) mmp-2 and mmp-9 from nasal polyp and mucosal fibroblasts in response to tnf- , and inhibited mmp mrna expression and nf-b , but not tissue inhibitor of metalloproteinase ( timp-1 and timp-2 ) ( asano et al 2004c ) . fexofenadine improved performance on the digit symbol substitution test , but it did not have a blocking effect upon the dopamine transporter ( theunissen et al 2006a , b ) fexofenadine is primarily prescribed for its h1 antagonist activity . however , it appears to have effects upon other mast cell mediators , as well as mediators produced by other cell types . fexofenadine , in addition to antagonizing h1 receptors , decreases the production of ltc4 , ltd4 , and lte4 , pge2 , and pgf2 , inhibits cyclo - oxygenase 2 , inhibits the generation of thromboxane ( perhaps through cyclo - oxygenase 2 ) , and limits the inos generation of no , as well as the generation of icam-1 , elam-1 , vcam-1 , rantes , i - tac , mdc , tarc , mmp-2 , mmp-9 , and tryptase . these effects may decrease the inflammatory responses initiated by an acute allergic reaction and provide a basis for future development of h1 antagonists with stronger anti - inflammatory effects . fexofenadine reduced airway sensitivity to mannitol compared to placebo . however , fexofenadine did not alter the final percent reduction in fev1 ( brannan et al 2001 ) . in transfer experiments , fexofenadine prevented the development of airway hyper - responsiveness as well as primary sensitization and challenge , with a decrease in bronchoalveolar lavage and tissue eosinophilia , lymphocyte numbers , and th2 cytokine production ( gelfand et al 2002 ) . however , fexofenadine did not have an additive effect to inhaled corticosteroid therapy or on inflammatory markers in subjects with atopic asthma ( fardon et al 2005 ) . in children aged 2 to 5 years with allergic rhinitis , fexofenadine had a frequency of adverse effects no different from placebo . the most frequently involved adverse events were upper respiratory tract infection , fever , infection , and vomiting . of the adverse events , 8.2% were attributable to the placebo , and 9.5% to fexofenadine . there were no clinically relevant differences for laboratory measures , vital signs , and physical examinations ( milgrom et al 2007 ) . grubbe et al ( 2007 ) evaluated effects of fexofenadine oral suspension in 50 children , aged 2 to 5 years . ngamphaiboon et al ( 2005 ) studied the efficacy and safety of fexofenadine 30 mg in pediatric patients with allergic rhinitis . , they did not appreciate  meaningful change in any electrocardiogram  . in a double blind , two - way crossover study , simons et al ( 1996 ) administered 30 or 60 mg of fexofenadine as a capsule to 14 children with allergic rhinitis ( mean age of 9.8 years , with a mean height of 134 cm and a mean weight of 32.1 kg ) . somnolence occurred in one child 10 hours after the ingestion of a 30 mg dose . they found that fexofenadine administered before or after the onset of cedar pollinosis prevented or controlled nasal obstruction , sneeze , and rhinorrhea . in a multi - center placebo controlled safety and efficacy study of 861 subjects with moderate to severe autumn allergic rhinitis , fexofenadine at doses of 120 mg and 180 mg fexofenadine , given once daily , significantly reduced total symptom score ( for nasal congestion ) , through the 24-hour trough . there were no differences between the two doses of fexofenadine and placebo groups in adverse events , as both subjects and controls reported headache as the most common adverse event ( casale et al 1999 ) . fexofenadine had no effect on the quality of life and work productivity in adult subjects with seasonal allergic rhinitis during the peak season for cedar pollinosis ( okubo et al 2005 ) . bronsky et al ( 1998 ) studied 550 subjects who had previously responded to other anti - histamines for seasonal allergic rhinitis , for 17 days . subjects sustained significant improvements in total symptom score 1 to 3 hours after the first dose at doses of 40 mg , 60 mg , and 120 mg , all twice daily . these authors did not find increases in the qtc intervals in their subjects treated with fexofenadine . in an industry - sponsored study , meltzer et al ( 2004 ) studied the safety and efficacy of fexofenadine in children with seasonal allergic rhinitis . they polled data from 3 double - blind , randomized , placebo - controlled , parallel group , 2-week trials in children ages 6 to 11 years with seasonal allergic rhinitis . the studies used 30 mg twice daily while 2 other studies also used 15 or 60 mg twice daily . fexofenadine at 30 mg twice daily significantly reduced the total symptom score , sneeze , rhinorrhea , itchy nose / mouth / throat / ears , itchy watery red eyes , and nasal congestion . kawashima et al ( 2002 ) found that doses as low as 20 mg twice daily were effective in the treatment of chronic idiopathic urticaria , and in another study , kawashima et al ( 2003 ) found that fexofenadine improved the pruritus associated with atopic dermatitis more than placebo . with assistance from industry , nelson et al ( 2000 ) tested the efficacy of fexofenadine in the treatment of chronic idiopathic urticaria . they noted no significant differences in the responses to doses between 60 mg twice daily and 240 mg twice daily . all subjects noted improvement in pruritus severity , number of wheals , and interference with sleep . handa et al ( 2004 ) did not find great benefit of fexofenadine n the treatment of chronic idiopathic urticaria . in an open - label , non - comparative study , kulthanan et al ( 2001 ) studied the efficacy and toxicity of fexofenadine in the treatment of chronic idiopathic urticaria . fexofenadine reduced the number of wheals , the severity of itch , interference with sleep , and interference with daily activities . the adverse events included headache , drowsiness , dizziness , increased appetite with weight gain , and cough . with industry support , russell et al ( 1998 ) studied the fexofenadine dose and subject tolerance to fexofenadine , as well as the drug single dose and steady - state pharmacokinetics in 87 adult subjects . their subjects tolerated doses of fexofenadine ranging from 10 to 800 mg , with no clinically significant trends for cardiac conduction parameters , vital signs , adverse event reporting , or clinical laboratory parameters despite exposure to fexofenadine plasma concentrations as high as 12,250 ng / ml . at doses of 15 and 30 mg twice daily in children aged 6 months to 2 years with allergic rhinitis , treatment - emergent adverse events were similar between the placebo and treatment groups . there were no differences between fexofenadine and placebo for vital signs , electrocardiographic results , or physical examination results ( hampel et al 2007 ) . an industry study of the effect of fexofenadine in a single dose up to 800 mg and multiple doses of 690 mg did not appear to change the qtc interval ( pratt et al 1999 ) . pinto et al ( et al 1999 ) described a patient on fexofenadine with a prolonged qtc interval . while on fexofenadine , the patient experienced an episode of syncope , with injury to a tooth . taken off the fexofenadine , the patient s qtc interval normalized . when replaced on fexofenadine 180 mg daily , qtc interval increased and the patient experienced an episode of polymorphic ventricular tachycardia , which progressed to ventricular fibrillation . the authors did not find an alternative reason for the prolonged qtc interval or the ventricular arrhythmia . craig - mcfeely et al ( 2000 , 2001 ) surveyed general practitioners in britain for adverse events to fexofenadine . they found no reports of drug interactions . cardiac events , including palpitations , chest pain , arrhythmia , and chest tightness , but without reports of qtc interval lengthening , resolved upon cessation of the drug . hindmarch et al with industry support , studied the effect of fexofenadine upon cognitive and psychomotor function ( hindmarch et al 1999 , 2002 ; kamei et al 2003 ; ridout et al 2003a , b ) . the authors tested critical flicker fusion ( cff ) , choice reaction time ( crt ) , and assessment of subjective sedation ( lars ) after up to 180 mg fexofenadine , from 1 to 24 hours . stone et al ( 1999 ) studied the central effects of fexofenadine ( 120 , 180 and 240 mg ) on digit symbol substitution , tracking and vigilance tasks and on objective sleepiness ( multiple sleep latency test ) and subjective sleepiness . potter et al ( 2003 ) were unable to find differences in reaction time , decision - making , and driver behavior with and without fexofenadine 180 mg compared to placebo . nicholson et al ( 2000 ) found that fexofenadine in doses of 120 g , 180 mg , and 240 mg did not affect digit symbol substitution , tracking , vigilance tasks , multiple sleep latencies , and subjective sleepiness . mansfield et al ( 2003 ) found that fexofenadine at a dose of 180 mg did not change self - reported drowsiness , omission errors , and response time . bower et al ( 2003 ) studied the effects of single - dose fexofenadine , diphenhydramine , and placebo on cognitive performance in flight personnel . although diphenhydramine resulted in significant psychomotor decrements , the effect of fexofenadine was not different from placebo . in an industry - supported study , tashiro et al ( 2005 ) studied the effect of fexofenadine upon brake reaction time , while using a cellular phone . compared to hydroxyzine , fexofenadine did not impair brake reaction time in otherwise healthy subjects . weiler et al ( 2000 ) compared the effects of fexofenadine , diphenhydramine , and alcohol on driving performance . subjects received one of these drugs or placebo , weekly , 1 hour prior to driving . lane keeping ( steering instability and crossing the centerline ) was impaired after alcohol and diphenhydramine use compared with fexofenadine use . self - reported drowsiness did not predict lack of coherence and weakly related to the minimum following distance , steering instability , and left lane excursion . in a review by banerji et al ( 2007 ) , the authors found that fexofenadine was less sedating than diphenhydramine . graft et al ( 2001 ) , in an industry - sponsored study , demonstrated the safety of fexofenadine in 875 children , 6 to 11 years of age , treated for seasonal allergic rhinitis . ten of their subjects ( 5 in the fexofenadine group and 5 in the placebo group ) stopped the medication because of an adverse event , which included upper respiratory congestion , otitis media , and asthma , although the authors could not link any of the adverse events to the drug . saraswat et al ( 2006 ) presented a case of stable psoriasis , who developed a severe pustular flare within 24 hours of taking fexofenadine . following resolution of the pustular psoriasis , they rechallenged the patient with fexofenadine , with recurrence of the rash . these studies support the contention that fexofenadine is effective for the treatment of allergic rhinits and chronic idiopathic urticaria , perhaps without benefit to patients with asthma . with the possible exception of rare adverse cardiac and cutaneous events , fexofenadine appears no more toxic than placebo when administered in the absence of other drugs . the fda approved fexofenadine for treatment of the symptoms of allergic rhinitis and chronic idiopathic urticaria . however , concern remains regarding fexofenadine s interactions with other medications that use the p - glycoprotein and the organic anion transporter peptides , which may result in an increased risk of adverse events to those other medications . this concern comes from the pharmacokinetic data , which suggest that although only a small proportion of fexofenadine is metabolized , fexofenadine moves into and out of the blood and tissues by at least p - glycoprotein and organic anion transporter peptides , which transport a number of other medications . in addition to blocking h1 receptors , fexofenadine appears to diminish the production of ltc4 , ltd4 , and lte4 , pge2 , and pgf2 ; inhibits cyclo - oxygenase 2 ; inhibits the generation of thromboxane ( perhaps through cyclo - oxygenase 2 ) ; and limits inos generation of no , as well as icam-1 , elam-1 , vcam-1 , rantes , i - tac , mdc , tarc , mmp-2 , mmp-9 , and tryptase , which may contribute to its benefit .
fexofenadine is a selective , non - sedating h1 receptor antagonist , marketed in the united states since 2000 . 
 the fda approved an oral suspension in 2006 , for the treatment of seasonal allergic rhinitis and chronic idiopathic urticaria in children . 
 the tablet , capsule , and oral suspension are bioequivalent . 
 although fexofenadine does not use p450 cyp 3a4 it does interact with a number of drugs at p - glycoprotein and organic anion transporter polypeptides 
 . the risk of toxicity from other drugs may increase with the administration of fexofenadine . 
 orange and grapefruit juices reduce the bioavailability of fexofenadine . 
 fexofenadine has been shown to have an impact on inflammatory mediators , other than histamine , such as decreasing the production of ltc4 , ltd4 , lte4 , pge2 , and pgf2 ; inhibiting cyclo - oxygenase 2 , thromboxane ; limiting inos generation of no ; decreasing cytokine levels ( icam-1 , elam-1 , vcam-1 , rantes , i - tac , mdc , tarc , mmp-2 , mmp-9 , tryptase ) ; and diminishing eosinophil adherence , chemotaxis , and opsonization of particles . 
 these effects may provide benefit to some of the inflammatory responses of an acute allergic reaction and provide a basis for future development of h1 antagonists with stronger anti - inflammatory effects . 
 these studies also support the contention that fexofenadine is effective for the treatment of allergic rhinits and chronic idiopathic urticaria .