Adults:
KROMAFINA tablets are indicated for the management of nausea and vomiting
induced by cytotoxic chemotherapy and radiotherapy.
KROMAFINA tablets are indicated for the prevention of post-operative nausea and
vomiting (PONV). For treatment of established PONV, administration by injection is
recommended.
 

Paediatric Population:
KROMAFINA is indicated for the management of chemotherapy-induced nausea and
vomiting (CINV) in children aged ≥6 months.
No studies have been conducted on the use of orally administered ondansetron in
the prevention and treatment of PONV in children aged ≥1 month, administration by
IV injection is recommended for this purpose.
 

Chemotherapy and radiotherapy induced nausea and vomiting.
Adults:
The emetogenic potential of cancer treatment varies according to the doses and
combinations of chemotherapy and radiotherapy regimens used. The selection of
dose regimen should be determined by the severity of the emetogenic challenge.
Emetogenic Chemotherapy and Radiotherapy: KROMAFINA can be given either by
rectal, oral (tablets or syrup), intravenous or intramuscular administration.
For oral administration: 8mg taken 1 to 2 hours before chemotherapy or radiation
treatment, followed by 8 mg every 12 hours for a maximum of 5 days to protect
against delayed or prolonged emesis.
For highly emetogenic chemotherapy: a single dose of up to 24 mg KROMAFINA
taken with 12 mg oral dexamethasone sodium phosphate, 1 to 2 hours before
chemotherapy, may be used.
To protect against delayed or prolonged emesis after the first 24 hours, oral or rectal
treatment with KROMAFINA may be continued for up to 5 days after a course of
treatment.
The recommended dose for oral administration is 8 mg to be taken twice daily.

Paediatric Population:
CINV in children aged ≥ 6 months and adolescents
The dose for CINV can be calculated based on body surface area (BSA) or weight –
see below. In paediatric clinical studies, ondansetron was given by IV infusion diluted
in 25 to 50 mL of saline or other compatible infusion fluid and infused over not less
than 15 minutes.
Weight-based dosing results in higher total daily doses compared to BSA-based
dosing (see section 4.4).
There are no data from controlled clinical trials on the use of KROMAFINA in the
prevention of delayed or prolonged CINV. There are no data from controlled clinical
trials on the use of KROMAFINA for radiotherapy-induced nausea and vomiting in
children.
Dosing by BSA:
KROMAFINA should be administered immediately before chemotherapy as a single
intravenous dose of 5 mg/m2. The single intravenous dose must not exceed 8 mg.

Oral dosing can commence 12 hours later and may be continued for up to 5 days
(Table 1).
The total dose over 24 hours (given as divided doses) must not exceed adult dose of
32 mg.

Table 1: BSA-based dosing for Chemotherapy - Children aged ≥ 6 months and
adolescents

a The intravenous dose must not exceed 8 mg.
b The total dose over 24 hours (given as divided doses) must not exceed adult dose
of 32 mg

Dosing by bodyweight:
Weight-based dosing results in higher total daily doses compared to BSA-based
dosing (see sections 4.4. and 5.1).
KROMAFINA should be administered immediately before chemotherapy as a single
intravenous dose of 0.15 mg/kg. The single intravenous dose must not exceed 8 mg.
Two further intravenous doses may be given in 4-hourly intervals.
Oral dosing can commence 12 hours later and may be continued for up to 5 days
(Table 2).
The total dose over 24 hours (given as divided doses) must not exceed adult dose of
32 mg.

Table 2: Weight-based dosing for Chemotherapy - Children aged ≥6 months and
adolescents

a The intravenous dose must not exceed 8 mg.
b The total dose over 24 hours (given as divided doses) must not exceed adult dose
of 32 mg.

Elderly:
No alteration of oral dose or frequency of administration is required.
Patients with Renal Impairment:
No alteration of daily dosage or frequency of dosing, or route of administration are
required.
 

Patients with Hepatic Impairment:
Clearance of KROMAFINA is significantly reduced and serum half-life significantly
prolonged in subjects with moderate or severe impairment of hepatic function. In
such patients a total daily dose of 8 mg should not be exceeded.
Patients with Poor Sparteine/Debrisoquine Metabolism:
The elimination half-life of ondansetron is not altered in subjects classified as poor
metabolisers of sparteine and debrisoquine. Consequently in such patients repeat
dosing will give drug exposure levels no different from those of the general
population. No alteration of daily dosage or frequency of dosing is required.
Post operative nausea and vomiting (PONV):
 

Adults:
For the prevention of PONV: KROMAFINA can be administered orally or by
intravenous or intramuscular injection.
For oral administration: 16 mg taken one hour prior to anaesthesia.
For the treatment of established PONV: Intravenous or intramuscular administration
is recommended.
 

Paediatric population:
PONV in children aged ≥ 1 month and adolescents
Oral formulation:
No studies have been conducted on the use of orally administered ondansetron in
the prevention or treatment of post-operative nausea and vomiting; slow IV injection
(not less than 30 seconds) is recommended for this purpose.
Injection:
For prevention of PONV in paediatric patients having surgery performed under
general anaesthesia, a single dose of ondansetron may be administered by slow
intravenous injection (not less than 30 seconds) at a dose of 0.1 mg/kg up to a
maximum of 4 mg either prior to, at or after induction of anaesthesia.

For the treatment of PONV after surgery in paediatric patients having surgery
performed under general anaesthesia, a single dose of KROMAFINA may be
administered by slow intravenous injection (not less than 30 seconds) at a dose of
0.1 mg/kg up to a maximum of 4 mg.
There are no data on the use of KROMAFINA in the treatment of PONV in children
below 2 years of age.
 

Elderly:
There is limited experience in the use of KROMAFINA in the prevention and
treatment of post-operative nausea and vomiting in the elderly, however
KROMAFINA is well tolerated in patients over 65 years receiving chemotherapy.
Patients with Renal impairment:
No alteration of daily dosage or frequency of dosing, or route of administration are
required.
 

Patients with Hepatic impairment:
Clearance of KROMAFINA is significantly reduced and serum half life significantly
prolonged in subjects with moderate or severe impairment of hepatic function. In
such patients a total daily dose of 8 mg should not be exceeded.
 

Patients with poor Sparteine/Debrisoquine Metabolism:
The elimination half-life of ondansetron is not altered in subjects classified as poor
metabolisers of sparteine and debrisoquine. Consequently in such patients repeat
dosing will give drug exposure levels no different from those of the general
population. No alteration of daily dosage or frequency of dosing is required.

Hypersensitivity reactions have been reported in patients who have exhibited
hypersensitivity to other selective 5HT3 receptor antagonists. Respiratory events
should be treated symptomatically and clinicians should pay particular attention to
them as precursors of hypersensitivity reactions.
Ondansetron prolongs the QT interval in a dose-dependent manner (see section
5.1). In addition, post- marketing cases of Torsade de Pointes have been reported in

patients using ondansetron. Avoid ondansetron in patients with congenital long QT
syndrome. Ondansetron should be administered with caution to patients who have or
may develop prolongation of QTc, including patients with electrolyte abnormalities,
congestive heart failure, bradyarrhythmias or patients taking other medicinal
products that lead to QT prolongation or electrolyte abnormalities.
Hypokalaemia and hypomagnesaemia should be corrected prior to ondansetron
administration.
There have been post-marketing reports describing patients with serotonin syndrome
(including altered mental status, autonomic instability and neuromuscular
abnormalities) following the concomitant use of ondansetron and other serotonergic
drugs (including selective serotonin reuptake inhibitors (SSRI) and serotonin
noradrenaline reuptake inhibitors (SNRIs)). If concomitant treatment with
ondansetron and other serotonergic drugs is clinically warranted, appropriate
observation of the patient is advised.
As ondansetron is known to increase large bowel transit time, patients with signs of
subacute intestinal obstruction should be monitored following administration.
In patients with adenotonsillar surgery prevention of nausea and vomiting with
ondansetron may mask occult bleeding. Therefore, such patients should be followed
carefully after ondansetron.
Patients with rare hereditary problems of galactose intolerance, Lapp lactasedeficiency
or glucose- galactose malabsorption should not take this medicine.
 

Paediatric Population:
Paediatric patients receiving ondansetron with hepatotoxic chemotherapeutic agents
should be monitored closely for impaired hepatic function.
 

CINV: When calculating the dose on an mg/kg basis and administering three doses
at 4-hour intervals, the total daily dose will be higher than if one single dose of 5
mg/m2 followed by an oral dose is given. The comparative efficacy of these two
different dosing regimens has not been investigated in clinical trials. Cross-trial
comparison indicates similar efficacy for both regimens (see section 5.1).

There is no evidence that ondansetron either induces or inhibits the metabolism of
other drugs commonly coadministered with it. Specific studies have shown that there
are no interactions when ondansetron is administered with alcohol, temazepam,
furosemide, alfentanil, tramadol, morphine, lidocaine, thiopental, or propofol.
Ondansetron is metabolised by multiple hepatic cytochrome P-450 enzymes:
CYP3A4, CYP2D6 and CYP1A2. Due to the multiplicity of metabolic enzymes

capable of metabolising ondansetron, enzyme inhibition or reduced activity of one
enzyme (e.g. CYP2D6 genetic deficiency) is normally compensated by other
enzymes and should result in little or no significant change in overall ondansetron
clearance or dose requirement.
Caution should be exercised when ondansetron is coadministered with drugs that
prolong the QT interval and/or cause electrolyte abnormalities (see section 4.4).
Use of ondansetron with QT prolonging drugs may result in additional QT
prolongation. Concomitant use of ondansetron with cardiotoxic drugs (e.g.
anthracyclines (such as doxorubicin, daunorubicin) or trastuzumab), antibiotics (such
as erythromycin), antifungals (such as ketoconazole), antiarrhythmics (such as
amiodarone) and beta blockers (such as atenolol or timolol) may increase the risk of
arrhythmias. (See section 4.4).
Serotonergic Drugs (e.g. SSRIs and SNRIs): There have been post-marketing
reports describing patients with serotonin syndrome (including altered mental status,
autonomic instability and neuromuscular abnormalities) following the concomitant
use of ondansetron and other serotonergic drugs (including SSRIs and SNRIs) (see
section 4.4).
Apomorphine: Based on reports of profound hypotension and loss of consciousness
when ondansetron was administered with apomorphine hydrochloride, concomitant
use with apomorphine is contraindicated.
Phenytoin, Carbamazepine and Rifampicin: In patients treated with potent inducers
of CYP3A4 (i.e. phenytoin, carbamazepine, and rifampicin), the oral clearance of
ondansetron was increased and ondansetron blood concentrations were decreased.
Tramadol: Data from small studies indicate that ondansetron may reduce the
analgesic effect of tramadol.

Women of childbearing potential
Women of childbearing potential should consider the use of contraception.
 

Pregnancy
Based on human experience from epidemiological studies, ondansetron is suspected
to cause orofacial malformations when administered during the first trimester of
pregnancy.
In one cohort study including 1.8 million pregnancies, first trimester ondansetron use
was associated with an increased risk of oral clefts (3 additional cases per 10 000
women treated; adjusted relative risk, 1.24, (95% CI 1.03-1.48)).

The available epidemiological studies on cardiac malformations show conflicting
results.
Animal studies does not indicate direct or indirect harmful effects with respect to
reproductive toxicity.
Ondansetron should not be used during the first trimester of pregnancy.
 

Breast-feeding
Tests have shown that ondansetron passes into the milk of lactating animals. It is
therefore recommended that mothers receiving KROMAFINA should not breast-feed
their babies.
 

Fertility
There is no information on the effects of ondansetron on human fertility.

In psychomotor testing ondansetron does not impair performance nor cause
sedation. No detrimental effects on such activities are predicted from the
pharmacology of ondansetron.

Adverse events are listed below by system organ class and frequency. Frequencies
are defined as: very common (≥1/10), common (≥1/100 to <1/10), uncommon
(≥1/1000 to <1/100), rare (≥1/10,000 to <1/1000) and very rare (<1/10,000). Very
common, common and uncommon events were generally determined from clinical
trial data. The incidence in placebo was taken into account. Rare and very rare
events were generally determined from post-marketing spontaneous data.
The following frequencies are estimated at the standard recommended doses of
ondansetron. The adverse event profiles in children and adolescents were
comparable to that seen in adults.

Immune system disorders
Rare: Immediate hypersensitivity reactions sometimes severe, including anaphylaxis.

Nervous system disorders
Very common: Headache.
Uncommon: Seizures, movement disorders (including extrapyramidal reactions such as dystonic
reactions, oculogyric crisis and dyskinesia) (1).
Rare: Dizziness predominantly during rapid IV administration.

Eye disorders
Rare: Transient visual disturbances (eg. blurred vision) predominantly during IV
administration.
Very rare: Transient blindness predominantly during IV administration (2).

Cardiac disorders
Uncommon: Arrhythmias, chest pain with or without ST segment depression, bradycardia.
Rare: QTc prolongation (including Torsade de Pointes).
 

Vascular disorders
Common: Sensation of warmth or flushing.
Uncommon: Hypotension.
 

Respiratory, thoracic and mediastinal disorders
Uncommon: Hiccups.
 

Gastrointestinal disorders
Common: Constipation.
 

Hepatobiliary disorders
Uncommon: Asymptomatic increases in liver function tests (3).
1. Observed without definitive evidence of persistent clinical sequelae.
2. The majority of the blindness cases reported resolved within 20 minutes. Most
patients had received chemotherapeutic agents, which included cisplatin. Some
cases of transient blindness were reported as cortical in origin.
3. These events were observed commonly in patients receiving chemotherapy with
cisplatin.

Symptoms and Signs
There is limited experience of ondansetron overdose. In the majority of cases,
symptoms were similar to those already reported in patients receiving recommended
doses (see section 4.8). Manifestations that have been reported include visual
disturbances, severe constipation, hypotension and a vasovagal episode with
transient second-degree AV block
Ondansetron prolongs the QT interval in a dose-dependent fashion. ECG monitoring
is recommended in cases of overdose.
 

Paediatric population
Paediatric cases consistent with serotonin syndrome have been reported after
inadvertent oral overdoses of ondansetron (exceeded estimated ingestion of 4
mg/kg) in infants and children aged 12 months to 2 years.
 

Treatment
There is no specific antidote for ondansetron, therefore in all cases of suspected
overdose, symptomatic and supportive therapy should be given as appropriate.
Further management should be as clinically indicated or as recommended by the
national poisons centre, where available.
The use of ipecacuanha to treat overdose with ondansetron is not recommended, as
patients are unlikely to respond due to the anti-emetic action of ondansetron itself.

Mechanism of Action
Ondansetron is a potent, highly selective 5HT3 receptor-antagonist. Its precise mode
of action in the control of nausea and vomiting is not known. Chemotherapeutic
agents and radiotherapy may cause release of 5HT in the small intestine initiating a
vomiting reflex by activating vagal afferents via 5HT3 receptors. Ondansetron blocks

the initiation of this reflex. Activation of vagal afferents may also cause a release of
5HT in the area postrema, located on the floor of the fourth ventricle, and this may
also promote emesis through a central mechanism. Thus, the effect of ondansetron
in the management of the nausea and vomiting induced by cytotoxic chemotherapy
and radiotherapy is probably due to antagonism of 5HT3 receptors on neurons
located both in the peripheral and central nervous system.
The mechanisms of action in post-operative nausea and vomiting are not known but
there may be common pathways with cytotoxic induced nausea and vomiting.
Ondansetron does not alter plasma prolactin concentrations.
The role of ondansetron in opiate-induced emesis is not yet established.

QT Prolongation
The effect of ondansetron on the QTc interval was evaluated in a double blind,
randomized, placebo and positive (moxifloxacin) controlled, crossover study in 58
healthy adult men and women.
Ondansetron doses included 8 mg and 32 mg infused intravenously over 15 minutes.
At the highest tested dose of 32 mg, the maximum mean (upper limit of 90% CI)
difference in QTcF from placebo after baseline-correction was 19.6 (21.5) msec. At
the lower tested dose of 8 mg, the maximum mean (upper limit of 90% CI) difference
in QTcF from placebo after baseline-correction was 5.8 (7.8) msec. In this study,
there were no QTcF measurements greater than 480 msec and no QTcF
prolongation was greater than 60 msec.

Paediatric population:
CINV
The efficacy of ondansetron in the control of emesis and nausea induced by cancer
chemotherapy was assessed in a double-blind randomised trial in 415 patients aged
1 to 18 years (S3AB3006). On the days of chemotherapy, patients received either
ondansetron 5 mg/m2 intravenous and ondansetron 4 mg orally after 8 to 12 hours or
ondansetron 0.45 mg/kg intravenous and placebo orally after 8 to 12 hours. Postchemotherapy
both groups received 4 mg ondansetron syrup twice daily for 3 days.
Complete control of emesis on worst day of chemotherapy was 49% (5
mg/m2 intravenous and ondansetron 4 mg orally) and 41% (0.45 mg/kg intravenous
and placebo orally). Post-chemotherapy both groups received 4 mg ondansetron
syrup twice daily for 3 days. There was no difference in the overall incidence or
nature of adverse events between the two treatment groups.
A double-blind randomised placebo-controlled trial (S3AB4003) in 438 patients aged
1 to 17 years demonstrated complete control of emesis on worst day of
chemotherapy in:

• 73% of patients when ondansetron was administered intravenously at a dose of 5
mg/m2 intravenous together with 2 to 4 mg dexamethasone orally
• 71% of patients when ondansetron was administered as syrup at a dose of 8 mg
together with 2 to 4 mg dexamethasone orally on the days of chemotherapy.
Post-chemotherapy both groups received 4 mg ondansetron syrup twice daily for 2
days. There was no difference in the overall incidence or nature of adverse events
between the two treatment groups.
The efficacy of ondansetron in 75 children aged 6 to 48 months was investigated in
an open-label, non-comparative, single-arm study (S3A40320). All children received
three 0.15 mg/kg doses of intravenous ondansetron, administered 30 minutes before
the start of chemotherapy and then at 4 and 8 hours after the first dose. Complete
control of emesis was achieved in 56% of patients.
Another open-label, non-comparative, single-arm study (S3A239) investigated the
efficacy of one intravenous dose of 0.15 mg/kg ondansetron followed by two oral
ondansetron doses of 4 mg for children aged < 12 years and 8 mg for children aged
≥ 12 years (total no. of children n = 28). Complete control of emesis was achieved in
42% of patients.
 

PONV
The efficacy of a single dose of ondansetron in the prevention of post-operative
nausea and vomiting was investigated in a randomised, double-blind, placebocontrolled
study in 670 children aged 1 to 24 months (post-conceptual age ≥ 44
weeks, weight ≥ 3 kg). Included subjects were scheduled to undergo elective surgery
under general anaesthesia and had an ASA status ≤ III. A single dose of
ondansetron 0.1 mg/kg was administered within five minutes following induction of
anaesthesia. The proportion of subjects who experienced at least one emetic
episode during the 24-hour assessment period (ITT) was greater for patients on
placebo than those receiving ondansetron (28% vs. 11%, p <0.0001).
Four double-blind, placebo-controlled studies have been performed in 1469 male
and female patients (2 to 12 years of age) undergoing general anaesthesia. Patients
were randomised to either single intravenous doses of ondansetron (0.1 mg/kg for
paediatric patients weighing 40 kg or less, 4 mg for paediatric patients weighing
more than 40 kg; number of patients = 735) or placebo (number of patients = 734).
Study drug was administered over at least 30 seconds, immediately prior to or
following anaesthesia induction. Ondansetron was significantly more effective than
placebo in preventing nausea and vomiting. The results of these studies are
summarised in Table 3.

Following oral administration, ondansetron is passively and completely absorbed
from the gastrointestinal tract and undergoes first pass metabolism. Peak plasma
concentrations of about 30 ng/mL are attained approximately 1.5 hours after an 8 mg
dose. For doses above 8 mg the increase in ondansetron systemic exposure with
dose is greater than proportional; this may reflect some reduction in first pass
metabolism at higher oral doses. Mean bioavailability in healthy male subjects,
following the oral administration of a single 8 mg tablet, is approximately 55 to 60%.
Bioavailability, following oral administration, is slightly enhanced by the presence of
food but unaffected by antacids.
The disposition of ondansetron following oral, intramuscular (IM) and intravenous
(IV) dosing is similar with a terminal half life of about 3 hours and steady state
volume of distribution of about 140 L. Equivalent systemic exposure is achieved after
IM and IV administration of ondansetron.
A 4mg intravenous infusion of ondansetron given over 5 minutes results in peak
plasma concentrations of about 65 ng/mL. Following intramuscular administration of
ondansetron, peak plasma concentrations of about 25 ng/mL are attained within 10
minutes of injection.
Following administration of ondansetron suppository, plasma ondansetron
concentrations become detectable between 15 and 60 minutes after dosing.
Concentrations rise in an essentially linear fashion, until peak concentrations of 20-
30 ng/mL are attained, typically 6 hours after dosing. Plasma concentrations then
fall, but at a slower rate than observed following oral dosing due to continued
absorption of ondansetron. The absolute bioavailability of ondansetron from the
suppository is approximately 60% and is not affected by gender. The half life of the
elimination phase following suppository administration is determined by the rate of
ondansetron absorption, not systemic clearance and is approximately 6 hours.
Females show a small, clinically insignificant, increase in half-life in comparison with
males.

Ondansetron is not highly protein bound (70-76%). Ondansetron is cleared from the
systemic circulation predominantly by hepatic metabolism through multiple
enzymatic pathways. Less than 5% of the absorbed dose is excreted unchanged in
the urine. The absence of the enzyme CYP2D6 (the debrisoquine polymorphism)
has no effect on ondansetron's pharmacokinetics. The pharmacokinetic properties of
ondansetron are unchanged on repeat dosing.

Special Patient Populations:
Gender
Gender differences were shown in the disposition of ondansetron, with females
having a greater rate and extent of absorption following an oral dose and reduced
systemic clearance and volume of distribution (adjusted for weight).
 

Children and Adolescents (aged 1 month to 17 years)
In paediatric patients aged 1 to 4 months (n=19) undergoing surgery, weight
normalised clearance was approximately 30% slower than in patients aged 5 to 24
months (n=22) but comparable to the patients aged 3 to 12 years. The half-life in the
patient population aged 1 to 4 month was reported to average 6.7 hours compared to
2.9 hours for patients in the 5 to 24 month and 3 to 12 year age range. The
differences in pharmacokinetic parameters in the 1 to 4 month patient population can
be explained in part by the higher percentage of total body water in neonates and
infants and a higher volume of distribution for water soluble drugs like ondansetron.
In paediatric patients aged 3 to 12 years undergoing elective surgery with general
anaesthesia, the absolute values for both the clearance and volume of distribution of
ondansetron were reduced in comparison to values with adult patients. Both
parameters increased in a linear fashion with weight and by 12 years of age, the
values were approaching those of young adults. When clearance and volume of
distribution values were normalised by body weight, the values for these parameters
were similar between the different age group populations. Use of weight-based
dosing compensates for age- related changes and is effective in normalising
systemic exposure in paediatric patients.
Population pharmacokinetic analysis was performed on 428 subjects (cancer
patients, surgery patients and healthy volunteers) aged 1 month to 44 years
following intravenous administration of ondansetron. Based on this analysis,
systemic exposure (AUC) of ondansetron following oral or IV dosing in children and
adolescents was comparable to adults, with the exception of infants aged 1 to 4
months. Volume was related to age and was lower in adults than in infants and
children. Clearance was related to weight but not to age with the exception of infants
aged 1 to 4 months. It is difficult to conclude whether there was an additional
reduction in clearance related to age in infants 1 to 4 months or simply inherent
variability due to the low number of subjects studied in this age group. Since patients

less than 6 months of age will only receive a single dose in PONV a decreased
clearance is not likely to be clinically relevant.
 

Elderly
Early Phase I studies in healthy elderly volunteers showed a slight age-related
decrease in clearance, and an increase in half-life of ondansetron. However, wide
inter-subject variability resulted in considerable overlap in pharmacokinetic
parameters between young (< 65 years of age) and elderly subjects (≥ 65 years of
age) and there were no overall differences in safety or efficacy observed between
young and elderly cancer patients enrolled in CINV clinical trials to support a
different dosing recommendation for the elderly.
Based on more recent ondansetron plasma concentrations and exposure-response
modelling, a greater effect on QTcF is predicted in patients ≥75 years of age
compared to young adults. Specific dosing information is provided for patients over
65 years of age and over 75 years of age for intravenous dosing.
 

Renal impairment
In patients with renal impairment (creatinine clearance 15-60 mL/min), both systemic
clearance and volume of distribution are reduced following IV administration of
ondansetron, resulting in a slight, but clinically insignificant, increase in elimination
half-life (5.4 hours). A study in patients with severe renal impairment who required
regular haemodialysis (studied between dialyses) showed ondansetron's
pharmacokinetics to be essentially unchanged following IV administration.
 

Hepatic impairment
Following oral, intravenous or intramuscular dosing in patients with severe hepatic
impairment, ondansetron's systemic clearance is markedly reduced with prolonged
elimination half-lives (15-32 hours) and an oral bioavailability approaching 100% due
to reduced pre-systemic metabolism. The pharmacokinetics of ondansetron following
administration as a suppository have not been evaluated in patients with hepatic
impairment.

No additional data of relevance

ANHYDROUS LACTOSE
MICROCRYSTALLINE CELLULOSE
PARTIALLY PREGELATINIZED MAIZE
STARCH
COLLOIDAL SILLCONE DIOXIDE
MAGNESIUM STEARATE
PURIFIED WATER
OPADRY 03B52375 YELLOW – Coating Material

Not applicable.

Store below 30°C

KROMAFINA Tablets 4mg come in blister packs of 10 tablets comprising
aluminium/PVC blister film and aluminium foil lidding.
KROMAFINA Tablets 8mg come in blister packs of 10 tablets comprising
aluminium/PVC blister film and aluminium foil lidding.

Any unused medicinal product or waste material should be disposed of in
accordance with local requirements, Keep out of the reach & sight of children