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GABAPENTIN MORNINGSIDE 600 MG FILM-COATED TABLETS

Active substance(s): GABAPENTIN / GABAPENTIN / GABAPENTIN

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SUMMARY OF PRODUCT CHARACTERISTICS

1

NAME OF THE MEDICINAL PRODUCT
Gabapentin Morningside 600 mg film-coated tablets.

2

QUALITATIVE AND QUANTITATIVE COMPOSITION

Each 600 mg film-coated tablet contains 600 mg of gabapentin.
For the full list of excipients, see section 6.1.

3

PHARMACEUTICAL FORM
Film-coated tablet.
White, convex and elliptic film-coated tablet.

4

CLINICAL PARTICULARS

4.1

Therapeutic indications
Epilepsy
Gabapentin is indicated as adjunctive therapy in the treatment of partial seizures with
and without secondary generalization in adults and children aged 6 years and above
(see section 5.1).
Gabapentin is indicated as monotherapy in the treatment of partial seizures with and
without secondary generalization in adults and adolescents aged 12 years and above.
Treatment of peripheral neuropathic pain
Gabapentin is indicated for the treatment of peripheral neuropathic pain such as
painful diabetic neuropathy and post-herpetic neuralgia in adults.

4.2

Posology and method of administration
Posology
For oral use.
Gabapentin can be given with or without food and should be swallowed whole with
sufficient fluid-intake (e.g. glass of water).
For all indications a titration scheme for the initiation of therapy is described in Table
1, which is recommended for adults and adolescents aged 12 years and above. Dosing
instructions for children under 12 years of age are provided under a separate subheading later in this section.

Table 1
Dosing chart – initial titration
Day 1

Day 2

Day 3

300 mg once a day

300 mg twice a day

300 mg three times a day

Epilepsy
Epilepsy typically requires long-term therapy. Dosage is determined by the treating
physician according to individual tolerance and efficacy. When in the judgment of the
clinician there is a need for dose reduction, discontinuation, or substitution with an
alternative medication, this should be done gradually over a minimum of one week.
Adults and adolescents:
In clinical trials, the effective dosing range was 900 to 3600 mg/day. Therapy may be
initiated by titrating the dose as described in Table 1 or by administering 300 mg
three times a day (TID) on Day 1. Thereafter, based on individual patient response
and tolerability, the dose can be further increased in 300 mg/day increments every 2-3
days up to a maximum dose of 3600 mg/day. Slower titration of gabapentin dosage
may be appropriate for individual patients. The minimum time to reach a dose of
1800 mg/day is one week, to reach 2400 mg/day is a total of 2 weeks, and to reach
3600 mg/day is a total of 3 weeks. Dosages up to 4800 mg/day have been well
tolerated in long-term open-label clinical studies. The total daily dose should be
divided in three single doses, the maximum time interval between the doses should
not exceed 12 hours to prevent breakthrough convulsions.

Children aged 6 years and above:
The starting dose should range from 10 to 15 mg/kg/day and the effective dose is
reached by upward titration over a period of approximately three days. The effective
dose of gabapentin in children aged 6 years and older is 25 to 35 mg/kg/day. Dosages
up to 50 mg/kg/day have been well tolerated in a long-term clinical study. The total
daily dose should be divided in three single doses, the maximum time interval
between doses should not exceed 12 hours.
It is not necessary to monitor gabapentin plasma concentrations to optimize
gabapentin therapy. Further, gabapentin may be used in combination with other
antiepileptic medicinal products without concern for alteration of the plasma
concentrations of gabapentin or serum concentrations of other antiepileptic medicinal
products.
Peripheral neuropathic pain
Adults
The therapy may be initiated by titrating the dose as described in Table 1.
Alternatively, the starting dose is 900 mg/day given as three equally divided doses.
Thereafter, based on individual patient response and tolerability, the dose can be
further increased in 300 mg/day increments every 2-3 days up to a maximum dose of
3600 mg/day. Slower titration of gabapentin dosage may be appropriate for individual
patients. The minimum time to reach a dose of 1800 mg/day is one week, to reach
2400 mg/day is a total of 2 weeks, and to reach 3600 mg/day is a total of 3 weeks.
In the treatment of peripheral neuropathic pain such as painful diabetic neuropathy
and post-herpetic neuralgia, efficacy and safety have not been examined in clinical
studies for treatment periods longer than 5 months. If a patient requires dosing longer
than 5 months for the treatment of peripheral neuropathic pain, the treating physician
should assess the patient’s clinical status and determine the need for additional
therapy.

Instruction for all areas of indication
In patients with poor general health, i.e., low body weight, after organ transplantation
etc., the dose should be titrated more slowly, either by using smaller dosage strengths
or longer intervals between dosage increases.
Use in elderly patients (over 65 years of age)
Elderly patients may require dosage adjustment because of declining renal function
with age (see Table 2). Somnolence, peripheral oedema and asthenia may be more
frequent in elderly patients.

Use in patients with renal impairment
Dosage adjustment is recommended in patients with compromised renal function as
described in Table 2 and/or those undergoing haemodialysis. Gabapentin 100 mg
capsules can be used to follow dosing recommendations for patients with renal
insufficiency.

Table 2
DOSAGE OF GABAPENTIN IN ADULTS BASED ON RENAL FUNCTION
Creatinine Clearance (ml/min)

Total Daily Dose (mg/day)

≥80

900-3600

50-79

600-1800

30-49

300-900

15-29

150b-600

<15c

150b-300

a Total daily dose should be administered as three divided doses. Reduced dosages
are for patients with renal impairment (creatinine clearance < 79 ml/min).
b To be administered as 300 mg every other day.
c For patients with creatinine clearance <15 ml/min, the daily dose should be reduced
in proportion to creatinine clearance (e.g., patients with a creatinine clearance of 7.5
ml/min should receive one-half the daily dose that patients with a creatinine clearance
of 15 ml/min receive).
Use in patients undergoing haemodialysis
For anuric patients undergoing haemodialysis who have never received gabapentin, a
loading dose of 300 to 400 mg, then 200 to 300 mg of gabapentin following each 4
hours of haemodialysis, is recommended. On dialysis-free days, there should be no
treatment with gabapentin.
For renally impaired patients undergoing haemodialysis, the maintenance dose of
gabapentin should be based on the dosing recommendations found in Table 2. In
addition to the maintenance dose, an additional 200 to 300 mg dose following each 4hour haemodialysis treatment is recommended.

4.3

Contraindications

Hypersensitivity to the active substance or to any of the excipients listed in section
6.1.

4.4

Special warnings and precautions for use
Suicidal ideation and behavior have been reported in patients treated with antiepileptic agents in several indications. A meta-analysis of randomised placebo
controlled trials of anti-epileptic drugs has also shown a small increased risk of
suicidal ideation and behavior. The mechanism of this risk is not known and the
available data do not exclude the possibility of an increased risk for gabapentin.
Therefore patients should be monitored for signs of suicidal ideation and behaviours
and appropriate treatment should be considered. Patients (and caregivers of patients)
should be advised to seek medical advice should signs of suicidal ideation or behavior
emerge.
If a patient develops acute pancreatitis under treatment with gabapentin,
discontinuation of gabapentin should be considered (see section 4.8).
Although there is no evidence of rebound seizures with gabapentin, abrupt
withdrawal of anticonvulsants in epileptic patients may precipitate status epilepticus
(see section 4.2).
As with other antiepileptic medicinal products, some patients may experience an
increase in seizure frequency or the onset of new types of seizures with gabapentin.
As with other anti-epileptics, attempts to withdraw concomitant anti-epileptics in
treatment refractive patients on more than one anti-epileptic, in order to reach
gabapentin monotherapy have a low success rate.
Gabapentin is not considered effective against primary generalized seizures such as
absences and may aggravate these seizures in some patients. Therefore, gabapentin
should be used with caution in patients with mixed seizures including absences.

Drug Rash with Eosinophilia and Systemic Symptoms (DRESS)
Severe, life-threatening, systemic hypersensitivity reactions such as Drug rash with
eosinophilia and systemic symptoms (DRESS) have been reported in patients taking
antiepileptic drugs including gabapentin (see section 4.8).
It is important to note that early manifestations of hypersensitivity, such as fever or
lymphadenopathy, may be present even though rash is not evident. If such signs or
symptoms are present, the patient should be evaluated immediately. Gabapentin
should be discontinued if an alternative etiology for the signs or symptoms cannot be
established.

No systematic studies in patients 65 years or older have been conducted with
gabapentin. In one double blind study in patients with neuropathic pain, somnolence,
peripheral oedema and asthenia occurred in a somewhat higher percentage in patients
aged 65 years or above, than in younger patients. Apart from these findings, clinical
investigations in this age group do not indicate an adverse event profile different from
that observed in younger patients.
The effects of long-term (greater than 36 weeks) gabapentin therapy on learning,
intelligence, and development in children and adolescents have not been adequately
studied. The benefits of prolonged therapy must therefore be weighed against the
potential risks of such therapy.

Laboratory tests
False positive readings may be obtained in the semi-quantitative determination of
total urine protein by dipstick tests. It is therefore recommended to verify such a
positive dipstick test result by methods based on a different analytical principle such
as the Biuret method, turbidimetric or dye-binding methods, or to use these
alternative methods from the beginning.

4.5

Interaction with other medicinal products and other forms of interaction
In a study involving healthy volunteers (N=12), when a 60 mg controlled-release
morphine capsule was administered 2 hours prior to a 600 mg gabapentin capsule,
mean gabapentin AUC increased by 44% compared to gabapentin administered
without morphine. Therefore, patients should be carefully observed for signs of CNS
depression, such as somnolence, and the dose of gabapentin or morphine should be
reduced appropriately.
No interaction between gabapentin and phenobarbital, phenytoin, valproic acid, or
carbamazepine has been observed.
Gabapentin steady-state pharmacokinetics are similar for healthy subjects and
patients with epilepsy receiving these antiepileptic agents.
Coadministration of gabapentin with oral contraceptives containing norethindrone
and/or ethinyl estradiol, does not influence the steady-state pharmacokinetics of either
component.
Coadministration of gabapentin with antacids containing aluminium and magnesium,
reduces gabapentin bioavailability up to 24%. It is recommended that gabapentin be
taken at the earliest two hours following antacid administration.
Renal excretion of gabapentin is unaltered by probenecid.

A slight decrease in renal excretion of gabapentin that is observed when it is
coadministered with cimetidina is not expected to be of clinical importance.

4.6

Fertility, pregnancy and lactation
Risk related to epilepsy and antiepileptic medicinal products in general
The risk of birth defects is increased by a factor of 2 – 3 in the offspring of mothers
treated with an antiepileptic medicinal product. Most frequently reported are cleft lip,
cardiovascular malformations and neural tube defects. Multiple antiepileptic drug
therapy may be associated with a higher risk of congenital malformations than
monotherapy, therefore it is important that monotherapy is practiced whenever
possible. Specialist advice should be given to women who are likely to become
pregnant or who are of childbearing potential and the need for antiepileptic treatment
should be reviewed when a woman is planning to become pregnant. No sudden
discontinuation of antiepileptic therapy should be undertaken as this may lead to
breakthrough seizures, which could have serious consequences for both mother and
child. Developmental delay in children of mothers with epilepsy has been observed
rarely.
It is not possible to differentiate if the developmental delay is caused by genetic,
social factors, maternal epilepsy or the antiepileptic therapy.
Risk related to gabapentin
There are no adequate data from the use of gabapentin in pregnant women.
Studies in animals have shown reproductive toxicity (see section 5.3). The potential
risk for humans is unknown. Gabapentin should not be used during pregnancy unless
the potential benefit to the mother clearly outweighs the potential risk to the foetus.
No definite conclusion can be made as to whether gabapentin is associated with an
increased risk of congenital malformations when taken during pregnancy, because of
epilepsy itself and the presence of concomitant antiepileptic medicinal products
during each reported pregnancy.
Gabapentin is excreted in human milk. Because the effect on the breast-fed infant is
unknown, caution should be exercised when gabapentin is administered to a breast-

feeding mother. Gabapentin should be used in breast-feeding mothers only if the
benefits clearly outweigh the risks.

4.7

Effects on ability to drive and use machines
Gabapentin may have minor or moderate influence on the ability to drive and use
machines. Gabapentin acts on the central nervous system and may cause drowsiness,
dizziness or other related symptoms. Even, if they were only of mild or moderate
degree, these undesirable effects could be potentially dangerous in patients driving or
operating machinery. This is especially true at the beginning of the treatment and
after increase in dose.

4.8

Undesirable effects

The adverse reactions observed during clinical studies conducted in epilepsy
(adjunctive and monotherapy) and neuropathic pain have been provided in a single list
below by class and frequency (very common (≥ 1/10); common (≥1/100 to <1/10);
uncommon (≥1/1000 to <1/100); rare (≥1/10,000 to <1/1,000); very rare (< 1/10000).
Where an adverse reaction was seen at different frequencies in clinical studies, it was
assigned to the highest frequency reported.
Additional reactions reported from post-marketing experience are included as
frequency Not known (cannot be estimated from the available data) in italics in the
list below.
Within each frequency grouping, undesirable effects are presented in order of
decreasing seriousness.
Body System
Infections and infestations
Very Common
Common
Blood and the lymphatic system
disorders
Common

Adverse drug reactions
Viral infection
Pneumonia, respiratory infection, urinary
tract infection, infection, otitis media

leucopenia

Not known
Immune system disorders
Uncommon
Not known

Metabolism and Nutrition Disorders
Common
Psychiatric disorders
Common

Not known
Nervous system disorders
Very Common
Common

Uncommon
Not known
Eye disorders
Common

thrombocytopenia
allergic reactions (e.g. urticaria)
hypersensitivity syndrome, a systemic
reaction with a variable presentation that
can include fever, rash, hepatitis,
lymphadenopathy, eosinophilia, and
sometimes other signs and symptoms
anorexia, increased appetite
hostility, confusion and emotional
lability, depression, anxiety, nervousness,
thinking abnormal
hallucinations
somnolence, dizziness, ataxia
convulsions, hyperkinesias, dysarthria,
amnesia, tremor, insomnia, headache,
sensations such as paresthesia,
hypaesthesia, coordination abnormal,
nystagmus, increased, decreased, or
absent reflexes
hypokinesia
other movement disorders (e.g.
choreoathetosis, dyskinesia, dystonia)
visual disturbances such as amblyopia,
diplopia

Ear and Labyrinth disorders
Common
vertigo
Not known
tinnitus
Cardiac disorders
Uncommon
palpitations
Vascular disorders
Common
hypertension, vasodilatation
Respiratory, thoracic and mediastinal disorders
Common
dyspnoea, bronchitis, pharyngitis, cough,
rhinitis
Gastrointestinal disorders
Common
vomiting, nausea, dental abnormalities,
gingivitis, diarrhea, abdominal pain,
dyspepsia, constipation, dry mouth or
throat, flatulence
Not known
pancreatitis
Hepatobiliary disorders
Not known
hepatitis, jaundice
Skin and subcutaneous tissue disorders
Common
facial oedema, purpura most often

described as bruises resulting from
physical trauma, rash, pruritus, acne
Not known
Stevens-Johnson syndrome, angioedema,
erythema multiforme, alopecia, drug rash
with eosinophilia and systemic symptoms
(see section 4.4)
Musculoskeletal, connective tissue and bone disorders
Common
arthralgia, myalgia, back pain, twitching
Not known
myoclonus
Renal and urinary disorders
Not known
acute renal failure, incontinence
Reproductive system and breast
disorders
Common
impotence
Not known
breast hypertrophy, gynaecomastia
General disorders and administration site conditions
Very Common
fatigue, fever
Common
peripheral oedema, abnormal gait,
asthenia, pain, malaise, flu syndrome
Uncommon
generalized oedema
Not known
withdrawal reactions (mostly anxiety,
insomnia, nausea, pains, sweating), chest
pain. Sudden unexplained deaths have
been reported where a causal
relationship to treatment with gabapentin
has not been established
Investigations
Common
WBC (white blood cell count) decreased,
weight gain
Uncommon
elevated liver function tests SGOT
(AST), SGPT (ALT) and bilirubin
Not known
blood glucose fluctuations in patients
with diabetes
Injury and poisoning
Common
accidental injury, fracture, abrasion
Under treatment with gabapentin cases of acute pancreatitis were reported. Causality
with gabapentin is unclear (see section 4.4).
In patients on haemodialysis due to end-stage renal failure, myopathy with elevated
creatine kinase levels has been reported.
Respiratory tract infections, otitis media, convulsions and bronchitis were reported
only in clinical studies in children. Additionally, in clinical studies in children,
aggressive behaviour and hyperkinesias were reported commonly.

4.9

Overdose
Acute, life-threatening toxicity has not been observed with gabapentin overdoses of
up to 49 g. Symptoms of the overdoses included dizziness, double vision, slurred
speech, drowsiness, lethargy and mild diarrhoea. All patients recovered fully with
supportive care. Reduced absorption of gabapentin at higher doses may limit drug
absorption at the time of overdosing and, hence, minimize toxicity from overdoses.
Although gabapentin can be removed by haemodialysis, based on prior experience it
is usually not required.However, in patients with severe renal impairment,
haemodialysis may be indicated.
An oral lethal dose of gabapentin was not identified in mice and rats given doses as
high as 8000 mg/kg.
Signs of acute toxicity in animals included ataxia, laboured breathing, ptosis,
hypoactivity, or excitation.

5

PHARMACOLOGICAL PROPERTIES

5.1

Pharmacodynamic properties
Pharmacotherapeutic groups: Other antiepileptics. ATC code: N03AX12
The precise mechanism of action of gabapentin is not known.
Gabapentin is structurally related to the neurotransmitter GABA (gammaaminobutyric acid) but its mechanism of action is different from that of several other
active substances that interact with GABA synapses including valproate, barbiturates,
benzodiazepines, GABA transaminase inhibitors, GABA uptake inhibitors, GABA
agonists, and GABA prodrugs. In vitro studies with radiolabeled gabapentin have
characterized a novel peptide binding site in rat brain tissues including neocortex and
hippocampus that may
relate to anticonvulsant and analgesic activity of gabapentin and its structural
derivatives. The binding site for gabapentin has been identified as the alpha2-delta
subunit of voltage-gated calcium channels.
Gabapentin at relevant clinical concentrations does not bind to other common drug or
neurotransmitter receptors of the brain including GABAA, GABAB, benzodiazepine,
glutamate, glycine or N-methyl-daspartate receptors.

Gabapentin does not interact with sodium channels in vitro and so differs from
phenytoin and
carbamazepine. Gabapentin partially reduces responses to the glutamate agonist Nmethyl-D-aspartate (NMDA) in some test systems in vitro, but only at concentrations
greater than 100 μM, which are not achieved in vivo. Gabapentin slightly reduces the
release of monoamine neurotransmitters in vitro.
Gabapentin administration to rats increases GABA turnover in several brain regions
in a manner similar to valproate sodium, although in different regions of brain. The
relevance of these various actions of gabapentin to the anticonvulsant effects remains
to be established. In animals, gabapentin readily enters the brain and prevents seizures
from maximal electroshock, from chemical convulsants including inhibitors of
GABA synthesis, and in genetic models of seizures.
A clinical trial of adjunctive treatment of partial seizures in paediatric subjects,
ranging in age from 3 to 12 years, showed a numerical but not statistically significant
difference in the 50% responder rate in favour of the gabapentin group compared to
placebo. Additional post-hoc analyses of the responder rates by age did not reveal a
statistically significant effect of age, either as a continuous or dichotomous variable
(age groups 3-5 and 6-12 years). The data from this additional post-hoc analysis are
summarised in the table below:
Response (≥50% Improved) by Treatment and Age MITT*
Population
Age
Category

Placebo

Gabapentin

PValue

< 6 Years
Old

4/21
(19.0%)

4/17
(23.5%)

0.7362

6 to 12 Years
Old

17/99
(17.2%)

20/96
(20.8%)

0.5144

*The modified intent to treat population was defined as all patients randomised to
study medication who also had evaluable seizure diaries available for 28 days during
both the baseline and double-blind phases.

5.2

Pharmacokinetic properties

Absorption
Following oral administration, peak plasma gabapentin concentrations are observed
within 2 to 3 hours. Gabapentin bioavailability (fraction of dose absorbed) tends to
decrease with increasing dose. Absolute bioavailability of a 300 mg capsule is

approximately 60%. Food, including a high-fat diet, has no clinically significant effect
on gabapentin pharmacokinetics.
Gabapentin pharmacokinetics are not affected by repeated administration. Although
plasma gabapentin concentrations were generally between 2 μg/ml and 20 μg/ml in
clinical studies, such concentrations were not predictive of safety or efficacy.
Pharmacokinetic parameters are given in Table 3.
Table 3
Summary of gabapentin mean (%CV) steady-state pharmacokinetic parameters
following every eight hours administration
Pharmacokinetic
parameter

400 mg
(N = 14)

300 mg
(N = 7)

800 mg
(N=14)

Mean %

CV

Mean %

CV

Mean

%CV

Cmax (μg/ml)

4.02

(24)

5.74

(38)

8.71

(29)

tmax (hr)

2.7

(18)

2.1

(54)

1.6

(76)

T1/2 (hr)

5.2

(12)

10.8

(89)

10.6

(41)

AUC (0-8)

24.8

(24)

34.5

(34)

51.4

(27)

NA

NA

47.2

(25)

34.4

(37)

μg•hr/ml)
Ae% (%)

Cmax = Maximum steady state plasma concentration
tmax = Time for Cmax
T1/2 = Elimination half-life
AUC(0-8) = Steady state area under plasma concentration-time curve from time 0 to 8
hours postdose
Ae% = Percent of dose excreted unchanged into the urine from time 0 to 8
hourspostdose
NA = Not available
Distribution
Gabapentin is not bound to plasma proteins and has a volume of distribution equal to
57.7 litres. In patients with epilepsy, gabapentin concentrations in cerebrospinal fluid
(CSF) are approximately 20% of corresponding steady-state trough plasma
concentrations. Gabapentin is present in the breast milk of breast-feeding women.
Metabolism
There is no evidence of gabapentin metabolism in humans. Gabapentin does not
induce hepatic mixed function oxidase enzymes responsible for drug metabolism.
Elimination

Gabapentin is eliminated unchanged solely by renal excretion. The elimination halflife of gabapentin is independent of dose and averages 5 to 7 hours.
In elderly patients, and in patients with impaired renal function, gabapentin plasma
clearance is reduced.
Gabapentin elimination-rate constant, plasma clearance, and renal clearance are
directly proportional to creatinine clearance.
Gabapentin is removed from plasma by haemodialysis. Dosage adjustment in patients
with
compromised renal function or undergoing haemodialysis is recommended (see
section 4.2).
Gabapentin pharmacokinetics in children were determined in 50 healthy subjects
between the ages of 1 month and 12 years. In general, plasma gabapentin
concentrations in children > 5 years of age are similar to those in adults when dosed
on a mg/kg basis.
Linearity/Non-linearity
Gabapentin bioavailability (fraction of dose absorbed) decreases with increasing dose
which imparts non-linearity to pharmacokinetic parameters which include the
bioavailability parameter (F) e.g. Ae%, CL/F, Vd/F. Elimination pharmacokinetics
(pharmacokinetic parameters which do not include F such as CLr and T1/2), are best
described by linear pharmacokinetics. Steady state plasma gabapentin concentrations
are predictable from single-dose data.
5.3

Preclinical safety data
Carcinogenesis
Gabapentin was given in the diet to mice at 200, 600, and 2000 mg/kg/day and to rats
at 250, 1000, and 2000 mg/kg/day for two years. A statistically significant increase in
the incidence of pancreatic acinar cell tumors was found only in male rats at the
highest dose. Peak plasma drug concentrations in rats at 2000 mg/kg/day are 10 times
higher than plasma concentrations in humans given 3600 mg/day. The pancreatic
acinar cell tumors in male rats are low-grade malignancies, did not affect survival, did
not metastasize or invade surrounding tissue, and were similar to those seen in
concurrent controls. The relevance of these pancreatic acinar cell tumors in male rats
to carcinogenic risk in humans is unclear.
Mutagenesis
Gabapentin demonstrated no genotoxic potential. It was not mutagenic in vitro in
standard assays using bacterial or mammalian cells. Gabapentin did not induce
structural chromosome aberrations in mammalian cells in vitro or in vivo, and did not
induce micronucleus formation in the bone marrow of hamsters.

Impairment of Fertility

No adverse effects on fertility or reproduction were observed in rats at doses up to
2000 mg/kg (approximately five times the maximum daily human dose on a mg/m2
of body surface area basis).

Teratogenesis
Gabapentin did not increase the incidence of malformations, compared to controls, in
the offspring of mice, rats, or rabbits at doses up to 50, 30 and 25 times respectively,
the daily human dose of 3600 mg, (four, five or eight times, respectively, the human
daily dose on a mg/m2 basis).
Gabapentin induced delayed ossification in the skull, vertebrae, forelimbs, and
hindlimbs in rodents, indicative of fetal growth retardation. These effects occurred
when pregnant mice received oral doses of 1000 or 3000 mg/kg/day during
organogenesis and in rats given 500, 1000, or 2000 mg/kg prior to and during mating
and throughout gestation. These doses are approximately 1 to 5 times the human dose
of 3600 mg on a mg/m2 basis.
No effects were observed in pregnant mice given 500 mg/kg/day (approximately 1/2
of the daily human dose on a mg/m2 basis).
An increased incidence of hydroureter and/or hydronephrosis was observed in rats
given 2000 mg/kg/day in a fertility and general reproduction study, 1500 mg/kg/day
in a teratology study, and 500, 1000, and 2000 mg/kg/day in a perinatal and postnatal
study. The significance of these findings is unknown, but they have been associated
with delayed development. These doses are also approximately 1 to 5 times the
human dose of 3600 mg on a mg/m2 basis.
In a teratology study in rabbits, an increased incidence of post-implantation fetal loss,
occurred in doses given 60, 300, and 1500 mg/kg/day during organogenesis. These
doses are approximately 1/4 to 8 times the daily human dose of 3600 mg on a mg/m2
basis.

6

PHARMACEUTICAL PARTICULARS

6.1

List of excipients
Tablet core:
Povidone K-90

Crospovidone,
Poloxamer 407
Magnesium stearate
Film coat:
Opadry 20A28569 (hydroxypropylcellulose, talc)

6.2

Incompatibilities
Not applicable.

6.3

Shelf life
2 years

6.4

Special precautions for storage
Do not store above 25ºC. In order to protect from light and moisture, store in the
original package.

6.5

Nature and contents of container

Film-coated tablets are packed in PVC+PVDC/Alu blister or OPA/Alu blister.
Each carton contains 10, 50 60, 90 or 100 film-coated tablets.
Not all pack sizes may be marketed.

6.6

Special precautions for disposal
No special requirements.
Any unused medicinal product or waste material should be disposed of in accordance
with local requirements.

7

MARKETING AUTHORISATION HOLDER
Morning side Healthcare Limited
115 Narborough Road
Leicester
LE3 0PA
UK

8

MARKETING AUTHORISATION NUMBER(S)
PL 20117/0055

9

DATE OF FIRST AUTHORISATION/RENEWAL OF THE
AUTHORISATION
27/04/2012

10

DATE OF REVISION OF THE TEXT
11/07/2014

Expand Transcript

Source: Medicines and Healthcare Products Regulatory Agency

Disclaimer: Every effort has been made to ensure that the information provided here is accurate, up-to-date and complete, but no guarantee is made to that effect. Drug information contained herein may be time sensitive. This information has been compiled for use by healthcare practitioners and consumers in the United States. The absence of a warning for a given drug or combination thereof in no way should be construed to indicate that the drug or combination is safe, effective or appropriate for any given patient. If you have questions about the substances you are taking, check with your doctor, nurse or pharmacist.

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