Oral Liquid
Relief of symptoms associated with urticaria from 6 months of age. Relief of symptoms
associated with seasonal allergic rhinitis from 2 years of age.
6 – 11 Years Tablets*
Relief of symptoms associated with seasonal allergic rhinitis, allergic rhinitis or urticaria in
children aged 6 to 11 years.
60 mg Tablets
Relief of symptoms associated with allergic rhinitis in adults and children aged 12 years or
older.
120 mg Tablets
Relief of symptoms associated with seasonal allergic rhinitis in adults and children aged 12
years or older.
180 mg Tablets
Relief of symptoms associated with seasonal allergic rhinitis or urticaria in adults and
children aged 12 years or older.

Paediatrics
Allergic Rhinitis and Seasonal Allergic Rhinitis:
Children aged 2 to 11 years: 30 mg twice daily, when required.
Urticaria:
Children aged 6 to 23 months: 15 mg twice daily, when required.
Children aged 2 to 11 years: 30 mg twice daily, when required.
Adults and Children aged 12 years or older
Allergic Rhinitis:
60 mg twice daily, when required.
Seasonal Allergic Rhinitis:
120 mg or 180 mg once daily, when required.
Urticaria:
180 mg once daily, when required.
Dosage adjustment is not required in the elderly or in patients with hepatic or renal
impairment.

Use in renal impairment
Dosage adjustment is not required in patients with renal impairment.
Use in hepatic impairment
Dosage adjustment is not required in patients with hepatic impairment.
Use in the elderly
Dosage adjustment is not required in the elderly.
Paediatric use
Safety and effectiveness of Telfast has not been established in children under 2 years of age
for allergic rhinitis and under 6 months of age for chronic idiopathic urticaria.
Telfast 6 – 11 Years tablets* is intended for paediatric patients 6 to 11 years of age and
Telfast Oral Liquid for children from 6 months.
Effects on laboratory tests
No data available

As fexofenadine undergoes negligible hepatic biotransformation, it is unlikely to interact with
other drugs through hepatic metabolism.
The pharmacokinetics of fexofenadine HCl and pseudoephedrine are not altered when both
drugs are co-administered.
Fexofenadine is a P-glycoprotein (P-gp) and organic-anion-transporting polypeptide (OATP)
substrate. Concomitant use of fexofenadine with P-gp inhibitors or inducers can affect the
exposure to fexofenadine.
Coadministration of fexofenadine with P-gp inhibitors erythromycin or ketoconazole has
been found to result in a 2 - 3 times increase in the level of fexofenadine in plasma. The
changes were not accompanied by any effects on the QT interval and were not associated
with any increase in adverse events compared to the drugs given singly. Fexofenadine had no
effect on the pharmacokinetics of erythromycin or ketoconazole.
A clinical drug-drug interaction study showed that co-administration of apalutamide (a weak
inducer of P-gp) and a single oral dose of 30 mg fexofenadine resulted in a 30 % decrease in
AUC of fexofenadine.

No interaction between fexofenadine and omeprazole has been observed. However, the
administration of an antacid containing aluminium and magnesium hydroxide gel 15 minutes
prior to fexofenadine HCl causes a reduction in bioavailability, most likely due to binding in
the gastrointestinal tract. It is advisable to leave 2 hours between administration of
fexofenadine HCl and aluminium and magnesium hydroxide containing antacids.

Effects on fertility
In rat fertility studies, dose-related reductions in implants and increases in postimplantation
losses were observed at oral doses equal to or greater than 150 mg/kg of terfenadine
respectively; these doses produced plasma AUC values of fexofenadine that were equal to or
greater than three times the human therapeutic value respectively (based on a 60 mg twice
daily fexofenadine HCl dose).
Use in pregnancy
Category B2. Reproductive toxicity of fexofenadine in animals was assessed through
terfenadine exposure. No evidence of teratogenicity was observed in animal reproduction
studies (rat and rabbit) when terfenadine was given at oral doses of up to 300 mg/kg/day
throughout organogenesis, which corresponds to levels of systemic fexofenadine exposure 4-
and 32-fold higher, respectively, than those anticipated in clinical use. Decreased pup weight
and survival occurred in rats when terfenadine was given at oral doses of 150 mg/kg/day and
above throughout pregnancy and lactation.
There are no studies in pregnant women exposed to fexofenadine alone or through the
administration of terfenadine.
Use in lactation
Telfast is not recommended for nursing women unless, in the physician’s judgment, the
potential benefit to the patient outweighs the potential risk to the infant. There are no data on
the content of human milk after administering fexofenadine. However, when terfenadine was
administered to nursing mothers, fexofenadine was found to cross into human breast milk.
Exposure of rats to fexofenadine and terfenadine through the administration of terfenadine at
dietary doses of 150 and 300 mg/kg/day throughout pregnancy and lactation (corresponding
to systemic exposure at levels (AUC) approximately 3- and 6-fold higher than those
anticipated in clinical use) caused decreased pup weight gain and survival. The relative risks
of these effects from terfenadine or fexofenadine are unknown. Effects on pups exposed to
fexofenadine only during lactation are unknown.

The effects of this medicine on a person’s ability to drive and use machines were not assessed
as part of its registration.

Telfast is generally well tolerated. In placebo-controlled trials involving seasonal allergic
rhinitis and chronic idiopathic urticaria patients, adverse events were comparable in

fexofenadine- and placebo-treated patients. The most common adverse events reported in
controlled clinical trials were headache, fatigue, dizziness or drowsiness and nausea. No
apparent dose trends were revealed in adverse events.
Events that have been reported during controlled trials involving seasonal allergic rhinitis and
chronic idiopathic urticaria patients with incidences less than 1% and similar to placebo, and
have been reported rarely during postmarketing surveillance include: fatigue, insomnia,
nervousness, and sleep disorders or paroniria. In rare cases, rash, urticaria, pruritus and
hypersensitivity reactions with manifestations such as angioedema, chest tightness, dyspnoea,
flushing and systemic anaphylaxis have been reported.
Adverse events reported in placebo-controlled chronic idiopathic urticaria studies were
similar to those reported in placebo-controlled seasonal allergic rhinitis studies. In placebocontrolled
trials involving paediatric seasonal allergic rhinitis patients (6-11 years of age),
adverse events were similar to those observed in trials involving seasonal allergic rhinitis
patients 12 years and older.
In controlled clinical trials involving paediatric patients 6 months to 5 years of age, there
were no unexpected adverse events in patients treated with fexofenadine hydrochloride.
As with adults, the incidence of adverse events with fexofenadine in paediatric patients was
similar to placebo.

Eye disorders:
Vision blurred (unknown)

To reports any side effect(s):
Saudi Arabia:
• The National Pharmacovigilance Centre (NPC):

- Fax: +966-11-205-7662
- SFDA Call Center: 19999
- E-mail: npc.drug@sfda.gov.sa
- Website: https://ade.sfda.gov.sa/

• Sanofi- Pharmacovigilance: KSA_Pharmacovigilance@sanofi.com

Other GCC States:
- Please contact the relevant competent authority.

There is no clinical experience with a fexofenadine overdose. The maximum single dose
tested in clinical trials is 800 mg in six healthy subjects. In a multiple-dose study, doses of
690 mg every 12 hours for 28.5 days were given to three healthy subjects and, in another
study with forty subjects, a dose of 400 mg every 12 hours was given for 6.5 days. No
clinically significant adverse events were reported in these studies.
In the case of an overdose, standard measures to remove any unabsorbed drug should be
employed. Symptomatic and supportive treatment is recommended. Haemodialysis is not an
effective means of removing fexofenadine from plasma.
For general advice on management of overdose, contact the Poisons Information Centre,
telephone number 13 11 26 (Australia) or the National Poisons Centre, 0800 POISON or
0800 764 766 (New Zealand).

Pharmacotherapeutic group: Antihistamine for systemic use, ATC code: R06A X26
Mechanism of action
The antihistaminic effects of fexofenadine have been demonstrated in animal systems in vitro
and in vivo. Oral administration of fexofenadine to guinea pigs, indicated that fexofenadine
antagonised histamine-induced skin wheals in a dose-dependent manner. Fexofenadine and
terfenadine antagonised the contractile effects of histamine in the guinea pig ileum in vitro.
In this model fexofenadine was found to be a more selective histamine antagonist than
terfenadine.
Fexofenadine inhibited antigen-induced bronchospasm in sensitised guinea pigs and, at high
doses (>100-fold higher than those required for antihistaminic activity), inhibited histamine
release from peritoneal mast cells of the rat. In laboratory animals, no anticholinergic or
alpha-1-adrenergic receptor blocking effects were observed. Radiolabelled tissue
distribution studies in rat indicated that fexofenadine does not cross the blood-brain barrier.
Fexofenadine is not associated with significant ECG abnormalities. Studies have shown that
fexofenadine does not affect the action potential or ion channel currents (IK, ICa, INa) in
either guinea pig or neonatal rat myocytes. Fexofenadine was 583 times less potent than
terfenadine in blocking a delayed rectifier potassium channel cloned from human heart.
Additionally, doses of fexofenadine ten times greater than the dose of terfenadine that
produces prolongation of QTC intervals do not prolong QTC intervals in anaesthetised
rabbits and conscious dogs.

Clinical trials
An escalating acute dose study demonstrated antihistaminic activity via skin wheal and flare
inhibition at doses ranging from 40 mg to 800 mg, with maximum inhibition reaching a
plateau at a dose of 130 mg. An escalating repeat dose study demonstrated increasing skin
flare inhibition at twice daily doses ranging from 20 mg to 690 mg. During both acute dose
and repeat dose studies, an antihistaminic effect was observed within one hour, achieving
maximum effect within 2 - 4 hours and lasting a minimum of 12 hours. There was no
evidence of tolerance to these effects after 28 days of dosing.
In dose ranging studies, fexofenadine HCl was shown to relieve the symptoms of seasonal
allergic rhinitis, significantly reducing total symptom scores (including scores for sneezing,
rhinorrhoea, itchy nose, palate and/or throat, and itchy, watery, red eyes) over a dosage range
of 40 mg to 240 mg twice daily. In a double-blind, placebo-controlled trial of 208 patients
with chronic idiopathic urticaria, fexofenadine HCl 180 mg and 240 mg once daily for 6
weeks were found to significantly reduce total symptom scores (number of wheals (hives)
and pruritus).
In a double-blind, placebo-controlled clinical efficacy study involving 821 patients with
seasonal allergic rhinitis, fexofenadine HCl 120 mg and 180 mg once daily were found to be
significantly superior to placebo in relieving symptoms of seasonal allergic rhinitis, including
sneezing, rhinorrhoea, itchy nose, palate and/or throat, itchy, red or watery eyes and nasal
congestion, after 24 hours. There was no statistically significant difference in efficacy

between the two doses of fexofenadine, however the 180mg dose did show a trend toward
greater reduction in the mean total symptom score.
In a double blind placebo controlled study, 861 patients aged 12 – 65 years were randomised
to receive either 120 mg fexofenadine or 180 mg fexofenadine or placebo, once daily for a 2
week period. The primary efficacy measure was change from baseline of average total
symptom score. Both doses provided significant (p 0.05) improvement in symptoms of
seasonal allergic rhinitis, compared to placebo. While there was no statistically significant
difference in efficacy between the two doses, the 180 mg dose showed a trend toward greater
reduction in the average total symptom score.
In a double blind placebo controlled study investigating quality-of-life, 845 patients aged 12
65 years were randomised to receive 120 mg fexofenadine or 180 mg fexofenadine or
placebo once daily for a 2 week period. The primary efficacy measures were change from
baseline in a quality-of-life score and in a work / activity impairment score. Patients
receiving either 120 mg or 180 mg dose reported a significant (p 0.006) improvement in
overall quality-of-life score and a significant (p0.004) reduction in work / activity
impairment score, compared to placebo. No statistical comparison was made between the
effects of the two doses of fexofenadine.
The incidence of drowsiness in controlled clinical seasonal allergic rhinitis trials was similar
when comparing patients treated with fexofenadine and placebo. There was no dose-related
increase in drowsiness.
The effects of fexofenadine on the QTc interval have been investigated in a variety of studies
at doses up to 800 mg/day. There were no statistically significant differences in QTc interval
between fexofenadine and placebo treated patients. Similarly, there were no statistically
significant differences from placebo or dose-related changes in other ECG parameters as a
result of fexofenadine treatment.
Also, no statistically significant change in QTc intervals was observed in long term studies in
healthy subjects given fexofenadine HCl 60 mg twice daily for 6 months and 240 mg once
daily for 12 months, when compared to placebo.
Interaction studies in healthy volunteers between fexofenadine and erythromycin or
ketoconazole demonstrated that although the plasma AUC for fexofenadine increased
approximately 2 - 3 fold, there were no significant effects on mean or maximal QTc, nor were
there any effects on the incidence of adverse events. Although these plasma levels were
above those seen with the recommended dose, they were within the range of plasma levels
achieved in controlled dose ranging clinical trials. Fexofenadine had no effect on the
pharmacokinetics of erythromycin or ketoconazole (see 4.5 INTERACTIONS WITH
OTHER MEDICINES AND OTHER FORMS OF INTERACTIONS for further
information).
Across the clinical trials, patients between the ages of 12 to 16 years have received doses
ranging from 20 mg to 240 mg twice daily. Adverse events were similar in this group
compared to patients above the age of 16 years.

Fexofenadine HCl is rapidly absorbed into the body following oral administration, with tmax
occurring approximately 1 - 3 hours post-dose. Following administration of a single 60 mg
oral dose to healthy volunteers, fexofenadine HCl was rapidly absorbed, with a mean Cmax of
209 ng/mL. Following the administration of single oral doses of 120 mg and 180 mg
fexofenadine HCl, the mean Cmax values were approximately 427 ng/mL and 494 ng/mL,
respectively.
The absolute bioavailability following fexofenadine HCl administration was estimated to be
33%. Coadministration with food has no clinically significant effect on the absorption of
fexofenadine HCl.
The single and multiple dose pharmacokinetics of fexofenadine are linear for oral doses up to
120 mg bd. A dose of 240 mg bd produced a slightly greater than proportional increase
(8.8%) in steady state area under the curve, indicating that fexofenadine pharmacokinetics are
practically linear at daily doses between 40 mg and 240 mg. Fexofenadine is 60% to 70%
bound to plasma proteins.
Fexofenadine undergoes negligible metabolism. Following a single radiolabelled 60 mg oral
dose, approximately 80% and 11% of the total [14C]-fexofenadine dose was excreted in
faeces and urine respectively.
The plasma concentration vs. time profiles of fexofenadine follow a bi-exponential decline
with a mean terminal elimination half-life ranging from 14 to 15 hours following multiple
dosing.
The pharmacokinetics of fexofenadine in seasonal allergic rhinitis patients are similar to
those in healthy subjects.
Studies indicated that females may be exposed to higher plasma levels than males, however,
there was no indication of any difference in efficacy or in the frequency of adverse events
reported. Elderly patients, patients with hepatic impairment and patients with cardiac disease
exposed to fexofenadine by administration of terfenadine showed no statistically significant
differences in pharmacokinetic parameters for fexofenadine compared to healthy individuals.
Although peak plasma level and half-life were increased 68% and 15% respectively in elderly
patients and 54% and 19% respectively in patients with renal disease, regardless of disease
severity, these levels are within the range of plasma levels shown to be tolerated in short term
dose ranging trials.
The pharmacokinetics of fexofenadine in children and adults are similar, including tmax,
clearance (corrected for body surface area), t1/2 and volume of distribution, because
fexofenadine undergoes negligible metabolism, with 80% of the dose being eliminated
unchanged in the faeces. In contrast, other H1-receptor antagonists, which are extensively
metabolised in the hepatic cytochrome P450 system, usually have shorter half-life values in
children than adults.
In children, studies indicate that 30 or 60 mg fexofenadine suppresses the histamine induced
wheal and flare within 1 to 2 hours, with both doses producing similar mean maximal
suppression.

A dose of 5mL of Telfast Oral Liquid containing 30 mg of fexofenadine HCl is bioequivalent
to a 30 mg dose of Telfast tablets. Following oral administration of a 30 mg dose of Telfast
Oral Liquid to healthy adult subjects, the mean Cmax was 118.0 ng/mL and occurred at
approximately 1.0 hour.

Genotoxicity
Fexofenadine showed no genotoxic activity in a series of assays for gene mutations and
chromosomal damage.
Carcinogenicity
The carcinogenic potential and reproductive toxicity of fexofenadine HCl were assessed
using terfenadine studies. No evidence of carcinogenicity was observed when mice and rats
were given daily oral doses of 50 and 150 mg/kg of terfenadine for 18 and 24 months,
respectively; these doses resulted in plasma AUC values of fexofenadine that were two to
four times the human therapeutic value (based on a 60 mg twice daily fexofenadine HCl
dose).

Telfast tablets contain the following excipients: croscarmellose sodium, pregelatinised maize
starch, microcrystalline cellulose, magnesium stearate, hypromellose, povidone, titanium
dioxide, colloidal anhydrous silica, macrogol 400, Pigment Blend Pink PB1254 (ARTG PI
No.3225) and Pigment Blend Yellow PB1255 (ARTG PI No.3226).
Telfast Oral Liquid contains 6 mg/mL of fexofenadine HCl. Telfast Oral Liquid also contains
the following excipients: polypropylene glycol, edetate disodium, propyl hydroxybenzoate,
butyl hydroxybenzoate, xanthan gum, poloxamer 407, titanium dioxide, sodium phosphate
monobasic monohydrate, sodium phosphate dibasic heptahydrate, artificial raspberry cream
flavour (ARTG PI No. 12546), sucrose, xylitol and purified water.

Incompatibilities were either not assessed or not identified as part of the registration of this
medicine.

Telfast 120 mg Tablets
Store below 30C.
Telfast 180 mg Tablets
Store below 30C.

Telfast 120 mg Tablets
Available in blister packs of 10 and 30 tablets.
Telfast 180 mg Tablets
Available in blister packs of 10, 30, 50 and 70 tablets.

In Australia, any unused medicine or waste material should be disposed of by taking to your
local pharmacy.

Fexofenadine occurs as a fine white to off-white powder. It is freely soluble in methanol,
soluble in ethanol, slightly soluble in water (3.6 mg/mL) and only very slightly soluble in
chloroform and hexane.
Fexofenadine is the carboxylic acid metabolite of terfenadine. It is an orally-active non
sedating histamine H1-receptor antagonist that is administered as the hydrochloride salt in
Telfast. The chemical name is benzeneacetic acid, 4-[1-hydroxy-4-[4-
(hydroxydiphenylmethyl)-1-piperidinyl]butyl]- ,-dimethyl-, hydrochloride.
Chemical structure
Fexofenadine HCl is an equimolar mixture of two enantiomers. It has the following structure: