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Intranasal Mometasone Furoate for Treatment
of Allergic Rhinitis
Marco Berlucchi and Barbara Pedruzzi
Department of Pediatric Otorhinolaryngology, Spedali Civili, Brescia, Italy.
Corresponding author email: marco.berlucchi@tin.it

Abstract: Allergic rhinitis (AR) is a chronic nasal disease that affects the upper respiratory tract. This disorder is characterized by
inflammation of the mucous membranes and it manifests with several nasal symptoms accompanied sometimes by non-nasal symptoms.
Best therapy aims to prevent and improve the AR-clinical picture. Steroids have an important role in the treatment of AR. The development
of steroids administrated directly on nasal mucosa has much reduced the systemic adverse affects associated with oral steroids therapy.
Mometasone furoate aqueous nasal spray is a synthetic steroid assessed for intranasal use in the therapy of adults and children affected
by AR. Such topical nasal steroid is an effective molecule improving clinical picture of AR and it is also approved as prophylactic therapy. In this article, apart from a careful description of its successful clinical use the authors review pharmacokinetic/pharmacodynamic
profile, mechanism of action, safety, and efficacy of such steroid molecule.
Keywords: allergic rhinitis, steroids, intranasal steroids, mometasone, steroid therapy

Clinical Medicine Insights: Therapeutics 2010:2 761–769
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Clinical Medicine Insights: Therapeutics 2010:2

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Berlucchi and Pedruzzi

Introduction

Allergic rhinitis (AR) is a common chronic nasal
inflammatory disorder characterized by nasal obstruction,
aqueous rhinorrhea, sneezing, nasal itching, and
postnasal drip.1 Ocular signs and symptoms including
itching, burning, tearing, and redness of the sclera and
ocular mucosa and, moreover, itching of the ear, palate,
and pharynx may be present.2 The symptomatology
begins after exposure and continues until the allergen is
no longer present.3
It has been observed that the prevalence of AR is
increasing.4,5 In adults, it ranges from 5% to 40% and
is related to age and geographical site, whereas in
children it is about 45%.6,7 The increasing prevalence
is possibly due to higher levels of air pollution,
increased numbers of dust mites in houses with
central heating and reduced ventilation, and changes
in the pattern of childhood infection.5,8 Asthma, otitis,
rhinosinusitis, conjunctivitis, and nasal polyposis are
also associated with AR.4,9–11
While AR is not a life-threatening disease, it
nonetheless has a significant impact on the quality
of life. Chronic AR may cause negative effects,
such as sleeplessness, fatigue, irritability, and poor
concentration, as well as decreased performance and
productivity, with negative effects on psychological
and social wellness and high costs for society.5,11–14
AR has been traditionally classified into seasonal
AR (SAR) and perennial AR (PAR) in relation to
the time of exposure.3 SAR is caused usually by
allergies found outdoors, such as pollen and molds,
whereas PAR is most commonly due to allergens
found indoors, such as house dust mites, molds, animal dander, and cockroaches. In 2001, the AR and
its Impact on Asthma (ARIA) group together with
the WHO introduced a new classification system.3 In
Europe, about 50% of the patients have PAR according to traditional SAR/PAR classifications, while
approximately one-third have persistent allergic rhinitis in relation to ARIA classification.15
The first treatment for AR is allergen avoidance. If
this is inadequate, several pharmacological agents are
available [ie, decongestants, sedating and non-sedating
anti-histamines, mast cell stabilizers (chromones),
leukotriene receptor antagonists, intranasal or systemic corticosteroids] that may be administered alone
or in various combinations. Immunotherapy is another
therapeutic option.
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Anti-histamines and intranasal corticosteroids are
the cornerstones of therapy and effectively treat the
symptoms of AR. Several meta-analysis and reviews
have shown that intranasal corticosteroids are superior to anti-histamines for relief of clinical symptoms
of AR, such as nasal congestion, which is considered
the most important AR-related symptom.14 Various
studies have shown that intranasal corticosteroids
begin to control symptoms within the first day of
therapy.16–18 At present, topical nasal corticosteroids
represent the recommended first-line therapy for
moderate to severe cases of AR.14,19,20 Intranasal corticosteroids act on nasal mucosa, where the drug is
needed, minimizing systemic and adverse effects.21
To date, six intranasal corticosteroids are available in
the USA for treatment of AR: beclomethasone dipropionate (BDP), budesonide (BUD), flunisolide, fluticasone propionate (FP), mometasone furoate (MF),
and triamcinolone acetonide (TAA).14  All these
agents are safe and well tolerated. Except for beclomethasone dipropionate, all intranasal corticosteroids
are metabolized quickly to less effective metabolites,
have minimal systemic absorption, and minimal systemic effects.14 The goals of treatment with intranasal
corticosteroids are to maximize effectiveness and
minimize potential systemic adverse effects, while
favoring good patient compliance.
MF is a potent synthetic 17-heterocyclic corticosteroid glucocorticoid, topically active and effective,
initially introduced for treatment of dermatological diseases.22 Subsequently, an aqueous nasal spray
form was found to be effective in AR, non-AR, nasal
polyposis, adenoid hypertrophy, and uncomplicated
rhinosinusitis.22–28 MF has a high affinity for the glucocorticoid receptor and a highly lipophilic nature.
These characteristics contribute to its minimal systemic absorption and prolonged nasal contact time.29

Mechanism of Action, Metabolism,
and Pharmacokinetic Profile

MF has a chemical structure similar to cortisol. The
presence of a double bond in the 1, 2 position on ring A
and of an esterified furoate moiety in the 17α position
leads to high glucocorticoid activity and major affinity
to the glucocorticoid receptor, respectively. Occupying
a lipophilic pocket in the glucocorticoid receptor,
the furoate moiety increases receptor binding and
activation.20 The binding between glucocorticoids and
Clinical Medicine Insights: Therapeutics 2010:2

Intranasal mometasone furoate for allergic rhinitis

the glucocorticoid receptor produces a complex that
enters the cell nucleus and regulates the expression of
pro- and anti-inflammatory genes. The binding affinity with synthetic glucocorticoids, which is higher
than with endogenous cortisol, correlates with several
parameters of pharmacologic activity such as topical
anti-inflammatory activity, glucocorticoid-induced
dermal blanching activity, inhibition of T-cell cytokine
production, inhibition of histamine and vascular cell
adhesion molecule-1 levels.
When compared with FP, BUD and TAA, MF
has the highest relative receptor affinity (RAA).
This important characteristic indicates that a drug
with higher affinity will occupy the same number of
receptors at a lower drug concentration than a drug
with a lower affinity.20
The glucocorticoids act through 2 pathways:
1) transactivation, when the receptor complex binds
to glucocorticoid-response elements in the promoter
region of glucocorticoid-responsive genes and
activates the transcription of anti-inflammatory genes,
and 2) transrepression, when the receptor complex
represses transcription of pro-inflammatory genes.
Differences in the transactivation-action among intranasal corticosteroids have been found in vitro experiments; MF was more potent than FP, TAA and BUD.
Transrepression is a complicated process that involves
the glucocorticoid receptor complex, inhibitory transcription factors and cofactors, and DNA. MF and FP
are effective in inhibiting pro-inflammatory activity.
Intranasal corticosteroid administration allows
slow uptake through nasal mucosa with a high
time of contact between steroidal molecule and
nasal mucosa.30  A prolonged nasal residency time
depends on the presence of slowly dissolving drug
particles.31 An increase in lipophilicity usually results
in drug particles that dissolve more slowly in nasal
mucosa, so that the intranasal residency time is longer. Lipophilic suspension-based formulations have
a higher nasal residency time than hydrophilic or
solution-based formulations.30 Slow-dissolving, lipophilic, suspension-based formulations represent a
way to increase the nasal residence time of intranasal corticosteroids. A second mechanism to increase
nasal residence time is through the formation of lipophilic esters in target cells. A glucocorticoid molecule with a free C-21-hydroxy group enters the cell
where it is transformed into lipophilic esters that are
Clinical Medicine Insights: Therapeutics 2010:2

released in the target tissue.20 For MF, suspensionbased glucocorticoid formulations are removed from
nasal mucosa by the mucociliary transport system to
the nasopharynx and are then swallowed. The mucociliary clearance rates vary in different sites of the
nose, and so an optimal residency time depends on
the anatomic region of drug delivery.
Systemic adverse effects of corticosteroids
occur when plasma concentrations exceed
normal physiological ranges or modify diurnal
hormonal regulation.32 The hypothalamic-pituitaryadrenal axis (HPAA) controls the cortisol level
reducing cortisol secretion when additional exogenous steroid is added. Long-term use of systemic
corticosteroid therapy may produce adverse effects
such as HPAA suppression,33 impairment of linear
bone growth,34 and inhibition of growth hormone
(GH) release.34 Moreover, glucocorticoids can inhibit
osteoblast function, collagen synthesis, chondrocyte
mitosis, and decrease absorption and increase excretion of calcium. Some authors have reported a
decrease in total bone mass, bone mineral density,
serum osteocalcin and alkaline phosphatase in adults,
whereas adverse effects on bone metabolism have not
been observed in children.20
Systemic activity of intranasal corticosteroids is
in relation to systemic bioavailability, plasma protein
binding, systemic clearance, and pharmacologic
activity.30 The systemic bioavailability of MF is
0.46%, while it ranges from 0.42% to 0.51% for FP;
it is 31%, 44%, and 46% for BUD, BDP, and TAA,
respectively.20,35
Moreover, systemic bioavailability depends on
systemic absorption through the nasal and gastrointestinal tracts.36 Thirty percent of an intranasal
corticosteroid dose remains in the nose, whereas 70%
is swallowed.37 This latter steroid fraction may be
likely absorbed by the gastrointestinal tract. Drugs
administrated as a suspension (lipophilic drugs) such
as MF dissolve slowly after prolonged contact with
nasal mucosa, and mucociliary clearance removes
solid drug particles from nasal mucosa. Thus, only a
small fraction of the delivered dose enters the nasal
tissues and bloodstream. Removal of solid drug
particles from the nose by mucociliary clearance leads
to a very small amount of systemic spill-over, while
the amount of MF remaining in the nasal cavities is
sufficient to obtain a therapeutic effect.21
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Berlucchi and Pedruzzi

MF is relatively stable in human plasma, with a
half-life ranging from 18.4 to 24 hours.38,39 Its degradation results in 9, 11-epoxide MF and 2 additional
minor degradation products.20 The binding affinity
of 9, 11-epoxide MF for glucocorticoids receptor
is 2 to 4 times higher than dexamethasone (DEX),
and it has been suggested that the 9, 11-epoxide MF
metabolite may contribute to systemic glucocorticoid
exposure.20
The liver metabolizes intranasal corticosteroids
efficiently since they are high-extraction drugs with
clearance values close to liver blood flow.30 In human
hepatocytes, 2 primary metabolites (ie, 6beta-OH
MF and MET1) and 2 minor metabolites have been
identified. It is interesting to note that 6beta-OH MF
has an affinity for the glucocorticoid receptor that is
7 times greater than DEX.39
Once-daily morning administration of intranasal
corticosteroids is predicted to have a minimal effect
on diurnal HPAA rhythm.32 Endogenous cortisol
levels are at their physiological nadir in the morning and the GH secretion has its peak in the late
evening, so the administration of intranasal corticosteroids in the morning should not change daytime cortisol levels and the normal circadian rhythm
of HPPA.32
In a review of literature performed in 2008,
Hochhaus et  al20 concluded that MF-treatment did
not produce demonstrable effects on HPPA even
when the drug was administered at up to 20 times
the recommended daily dose.40 Furthermore, plasma
cortisol, urinary free cortisol, and 8 am plasma
cortisol were similar in patients who received a
single dose of oral MF, intranasal MF, or placebo.41
Moreover, pediatric patients showed no significant
changes in mean cortisol concentrations or 24-hours
urinary-free cortisol concentrations. Finally, the
available data suggests that in children and adults MF
has a favourable tolerability profile.20

Safety

In 2007, Herman14  reviewed double-blind, placebocontrolled studies of once-daily administration of intranasal corticosteroids and concluded that the overall
occurrence of adverse events was similar between the
different intranasal steroids investigated. There was no
significant suppression of serum cortisol values before
or after adrenocorticotropin hormone stimulation for
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any of the treatment groups that used FP, TAA, or
BDP.42 There was no statistically significant modification on markers for adrenocortical activity, bone formation, or white cell count for BUD, TAA, or MF.43
Healthy volunteers treated with FP showed lower
overnight urinary cortisol levels compared with
­placebo treatment, but no significant effects on HPAA
function (24-hours plasma cortisol levels and 24-hours
and fractioned urinary cortisol levels), markers of
bone formation (osteocalcin levels), and white blood
cells count were seen with BUD, MF, or TAA.42
In 1999, Berkowitz et  al44 assessed treatmentemergent adverse events in patients treated with MF.
Adverse events considered by the investigators to be
possibly or probably treatment-related were headache
and pharyngitis, with severe coughing and pruritus
occurring only rarely. No serious adverse effects were
reported. After 5 years, Suissa et al45 published a population-based cohort study with nested case-control
analysis of elderly patients who were administered
respiratory medications (monitored for 4 years), and
found no effects on the rate of hip or upper extremity
fractures with intranasal corticosteroids.
Safety studies, conducted before and after
12  months of treatment with MF, have evaluated
potential glaucoma and/or cataract formation,46 shortterm lower-leg growth,47 and assessed the effects of
MF on growth and statural growth.48  No significant
changes from baseline in intraocular pressures or
posterior subcapsular cataracts were observed at the
end of the study, and no clinically-relevant changes
in vital signs, electrocardiograms, clinical laboratory
values or nasal examinations were reported for MF.46
Even if in pediatric patients a decrease in growth
velocity, adrenal suppression and growth failure have
been reported receiving intranasal ­corticosteroids
such as BDP,49 no effects on growth velocity and/or the
function HPPA have been observed using MF nasal
spray at therapeutic doses.41,48
The use of intranasal corticosteroids could
potentially increase the risk of nasal irritation,
dryness, bleeding, epistaxis, septal perforations,
sneezing, and coughing. However, biopsies of nasal
mucosa before and after 1 year of treatment with MF
in adults showed improvement of the appearance of
the epithelium and reduction of the inflammatory cell
infiltrate (such as eosinophils and mast cells) and no
signs of mucosa atrophy.50
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Intranasal mometasone furoate for allergic rhinitis

Finally, the incidence of adverse events in children
treated with MF was comparable to that in patients
treated with placebo or active control, and the most
frequent adverse event was epistaxis. Pharyngitis,
sneezing, and headache were mild and of short
duration.

Immunopathological Mechanisms
of Action

AR is an immunological disease mediated by
immunoglobulin E (IgE) that involves inflammation of
the nasal membrane after exposure to an allergen.51 AR
involves an initial sensitization during which
allergen-specific IgE binds to receptors on mast cells
and basophils, followed by an allergic/inflammatory
response at subsequent re-exposure to the allergen.52
In nasal mucosa, this process leads to cross-linking of
IgE on the surface of mucosal cells, mast cells, and
basophils, along with ­degranulation of ­inflammatory
cells, causing the release of ­preformed ­mediators
such as histamine within 5  minutes after allergen
contact (early-phase response). Next (usually within
15 ­minutes), there is synthesis of mediators (ie, leukotrienes, prostaglandins, ­platelet-activating ­factor,
and several cytokines) that produce ­vasodilatation,
increase glandular secretions and sensory nerve
stimulation leading to the immediate symptoms of
AR such as sneezing, rhinorrhea, itching, and nasal
congestion.52
The late-phase response, which occurs approximately 4–24 hours after allergen exposure is
­characterized by recruitment of inflammatory cells
from blood (ie, basophils, eosinophils, lymphocytes,
and monocytes) that release additional ­inflammatory
mediators promoting inflammation and tissue
­damage.20 This results in an increase of symptoms,
particularly nasal congestion.52
MF acts at multiple points in the allergic inflammation pathway. Traditionally, corticosteroids showed
a large effect on the late-phase response, although
Frieri et al53 reported that MF also has a small effect
on the early-phase response. The anti-inflammatory
effects of intranasal corticosteroids are mediated
through inhibition of pro-inflammatory cytokines (ie,
IL-1, IL-3, IL-4 and IL-5) and decrease the number of
inflammatory cells.20 It has been documented that at
least in vitro, MF is the most steroid potent inhibitor
of IL-4 and IL-5 release from CD4+ cells.
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IL-4 and IL-5 are T-helper cell type 2 (Th2)-secreted
pro-inflammatory cytokines that regulate mast cell
activation and degranulation, eosinophil differentiation, and IgE production. INF-gamma is a T-helper
cell type 1 (Th1)-secreted cytokine that ­downregulates
the effects of the Th2 cytokines. MF acts by ­reversing
the exaggerated Th2 response that contributes to the
pathophysiology of allergic ­disease.54 In a review
of randomized trials evaluating eosinophil levels
in nasal mucosa of patients with AR and undergoing ­intranasal MF-treatment or placebo for 2 weeks,
Hochhaus20 observed that MF-subjects showed a
reduction in eosinophils and basophils from baseline
after 6 hours (late phase), whereas subjects treated
with placebo had no significant difference in nasal
eosinophil l­evels from baseline.
MF also inhibits expression of ­chemoattractant
cytokines such as IL-3, IL-4 and IL-5 and is 3 to
4 times more potent than DEX or BDP in ­inhibiting
the migration of rat eosinophils.55 Moreover, MF
enhances eosinophil apoptosis.56  Lastly, activation
of the adhesion-molecule system is crucial to the
pathogenesis of inflammatory cell infiltration in nasal
mucosa, and thus the inhibition by MF may protect
against cell injury due to inflammation.57

Efficacy

The efficacy of MF in the treatment of allergic
­rhinitis has been demonstrated in several clinical
studies and by means of its clinical utilization. This
­important ­feature is highlighted particularly in a
review ­performed by Italian researchers, who ­carried
out a meta-analysis of randomized, double-blind, placebo-controlled clinical trials after a ­comprehensive
search of the MEDLINE, LILACS, SCOPUS, and
the Cochrane Library databases.7 By this analysis,
1534 subjects and 1464 one represented MF- and
placebo-group, respectively. A significant reduction
in total nasal symptom scores such as congestion,
rhinorrhea, snezzing, and nasal itching was observed
in the MF participants. ­Furthermore, the study group
showed a significant reduction of total non-nasal
symptom scores (ie, cough, ocular, otic, palate, ant
throat complaints). This evaluation provided a level
Ia evidence for the efficacy of MF in the therapy of
AR vs. placebo. Finally, such topical nasal steroid is
also effective in preventing the onset of symptoms in
patients with AR.58
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Berlucchi and Pedruzzi

Patient Preference

Good management of AR is also dependent on patient
compliance and acceptance of planned ­treatment.
Factors that may influence patient compliance to
treatment include efficacy, safety, dosing regimen,
patient preference, and cost-effectiveness. MF has a
once-daily dosing regimen and good clinical efficacy
in treatment of AR. Its rapid onset of action (within
7 hours after a single intranasal dose), as well as its
once-daily dosing schedule, offer an attractive option
for patients with AR.44
The sensory attributes of intranasal ­corticosteroids
can influence adherence to therapy,59 and patients have
expressed preferences considering various attributes of
different nasal sprays.60 In 1999, Gerson et al61 ­studied
the characteristics of TAA, FP and BDP in a doubleblind, crossover study of adult patients with AR and
found that TAA had a lower odor strength and a more
preferred odor than either BDP or FP. There were no
differences in taste intensities, but patients preferred
the taste of TAA over FP or BDP. TAA had also
higher moistness in the nose and throat than BDP.
Patient-rated overall likeability was higher for TAA
than for FP. Three years later, ­Bachert and ­El-Akkad62
compared assessments of sensory attributes from
patients with AR after a single dose administration
of FP, MF, and TAA in a multicenter, randomized,
­double-blind, crossover study. Immediately after
drug administration, TAA provided significantly
­better comfort ­during administration, less irritation,
less odor strength, preferred odor, more moistness
of nose and throat, milder taste, and preferred taste
compared with MF. TAA had less odor strength, preferred odor, more moistness of the nose and throat,
and a milder taste than FP. Two minutes after drug
administration, TAA had less aftertaste than FP or MF
and produced less irritation. In the same year, Gross
et al63 comparing sensory attributes of TAA and FP,
found that TAA has a greater incidence of running
out of the nose and sneezing than FP, but TAA has
less offensive smell and treatment-related stinging
and burning than FP. In 2003, Berger et  al64 studying the differences between FP and TAA, also found
that patients treated with the latter reported less odor
than those ­administered FP, although no significant
differences were found in any other attributes. Shah
et  al65 ­studied the perceptions of patients and their
like/dislike of sensory attributes for BUD or FP in two
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randomized, patient-blind, crossover studies in adult
patients with AR. BUD was rated as more pleasing
than FP at the recommended starting dose, as well as
more pleasing than FP at one-half the recommended
starting dose. Patients preferred BUD and indicated a
greater overall satisfaction with the sensory features
of BUD than FP. BUD had less scent or taste or aftertaste after using than FP. Patients preferred the spray
force and moisture content of BUD than FP. In 2004,
Stokes et al66 had the same overall results of Bachert
and El-Akkad.62 TAA had less odor, less taste, less
dryness of nose and throat, and less aftertaste than FP
and MF. Patients had also a greater preference for the
odor of TAA and greater overall likeability for TAA
than FP or MF, and preferred a prescription for TAA
over FP or MF. Finally, Mahadevia et  al59  studied
six sensory attributes of intranasal corticosteroids:
taste, smell, aftertaste, throat rundown, nose runout,
and feel of spray in nose and throat. They found that
preference for sensory attributes and willingness to
adhere to therapy decreased with increasing intensity,
and that the most important attribute was aftertaste.
The results of patient preference studies show that
the recommended once-daily starting doses of BUD
and TAA were preferred by adults over FP and MF.14
BUD appeared to have less aftertaste than FP, and
TAA appeared to have less aftertaste than either FP or
MF.14 BUD and TAA had very similar inert ingredients:
they lack phenylethyl ­alcohol, which is present in MF
and FP and may cause ­unpleasant sensations (such
as burning or stinging in the nose).14,65,67 Phenylethyl
alcohol has a floral scent, and BUD and TAA were
rated as having less scent or odor, and a more preferred
odor than MF or FP. Recently, a new ­scent-free
­formulation of MF has been marketed.
The number of sprays per nostril for both BUD
and FP in adolescent and pediatric patients is 1 puff
per nostril to obtain the recommended starting dose.
For TAA and MF, the number of puffs is 2 per nostril
for adolescent patients and 1 per nostril in pediatric
patients (less than 12 years).14 BUD has the lowest
spray volume and the least number of sprays per nostril of all the once-daily intranasal corticosteroids.14,68

Place in Therapy

Due to their high efficacy for controlling nasal
symp­toms,14  intranasal corticosteroids are recommended as first-line prescription treatment for
Clinical Medicine Insights: Therapeutics 2010:2

Intranasal mometasone furoate for allergic rhinitis

­ oderate-to-severe cases of SAR and PAR.3,69,70
m
­Several double-blind, placebo-controlled trials
assessing the efficacy of intranasal corticosteroids
such as MF have shown that once-daily administration
is well tolerated and more effective than placebo in the
treatment of SAR, although there are few differences
in efficacy and tolerability among the once-daily
intranasal corticosteroids.14
Furthermore, the safety and efficacy of MF in
the prophylaxis and treatment of SAR and PAR in
adults has been studied.46 A dose of 100 or 200  µg
­once-daily is effective in relieving ­moderate-­to-­severe
symptoms of SAR and PAR in patients older than
12 years.71,72  When administrated about 4 weeks
before the onset of the ragweed season, MF is also
effective and well-­tolerated in the prophylactic
­treatment of SAR.58
A dose of 100 µg once-daily is the optimal ­dosage,
considering efficacy and safety, for children from 3
to 11 years of age with SAR or PAR. This dosage
provides greater symptomatic relief, is well tolerated,
and has a low potential for systemic effects because
plasma concentrations of MF in children were
­virtually undetectable.46

Conclusions

Mometasone furoate nasal spray is an ­intranasal
­corticosteroid that has a number of qualities that
are important in achieving nasal selectivity with
­minimal systemic adverse effects. Data from
­clinical, animal, and in vitro studies indicate that
MF has ­pharmacokinetic and pharmacodynamic
characteristics that make it well suited for intranasal administration. Furthermore, the efficacy and
safety profiles in clinical use are consistent with its
pharmacokinetic and pharmacodynamic properties.
Lipophilic MF in a suspension-based delivery system has a long nasal residence time and rapid hepatic
clearance, with a high plasma protein binding that
contributes to very low systemic bioavailability. No
evidence of growth retardation has been observed at
the recommended dose, and no evidence of HPAA
suppression in adults or children has been seen. MF
is an intranasal ­corticosteroid that is well tolerated,
effective and safe in treatment of SAR and PAR in
adults and children. MF is also good for prophylactic treatment of SAR, starting 2–4 weeks before
allergen season.
Clinical Medicine Insights: Therapeutics 2010:2

Patient adherence and acceptance of treatment
r­ egimen are also important factors as intranasal
­corticosteroids have particular sensory attributes.
Since MF is available in an aqueous formulation
without alcohol, with less nasal mucosa irritation
and aftertaste and no scent/odor, patients may show
greater compliance to treatment.

Disclosure

This manuscript has been read and approved by
all authors. This paper is unique and is not under
­consideration by any other publication and has not
been published elsewhere. The authors and peer
reviewers of this paper report no conflicts of ­interest.
The authors confirm that they have permission to
reproduce any copyrighted material.

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