Brussels (OTE) – Brussels (ots/PRNewswire)
– 26 scientific abstracts, including two oral presentations,
demonstrate UCB’s ongoing commitment to advancing research for people
living with epilepsies
– Data include an open-label extension study describing the long-term
safety of FINTEPLA®▼ (fenfluramine)[1] and global functioning in
children and adults with Dravet syndrome or Lennox-Gastaut syndrome[2
]
– Data provide insights on developmental and epileptic
encephalopathies (DEEs), including a qualitative study addressing
diagnostic challenges and benefits in adult care settings, and a
caregiver survey exploring the daily impacts of unpredictable
seizures and disruptive behaviors[3],[4]
– Additional focus on defining prolonged seizures and their real-
world impact on patients and caregivers[5],[6],[7]
UCB, a global biopharmaceutical company, today announced it will
present 26 abstracts from its epilepsy portfolio at the International
Epilepsy Congress (IEC) Congress, Lisbon, Portugal, August 30 –
September 3, 2025. Data will focus on developmental and epileptic
encephalopathies (DEEs), such as Dravet syndrome (DS) and Lennox-
Gastaut syndrome (LGS), as well as prolonged seizures, seizure
emergencies and early pipeline research.
Dimitrios Bourikas, Global Medical Head of DEE and Epilepsy ,
UCB, commented: „At UCB, we are committed to driving improvements in
all aspects of care for people living with epilepsies and severe
epileptic conditions. The breadth of data we are presenting at the
International Epilepsy Congress reflects our dedication to advancing
innovative solutions that address real-world patient needs. By
deepening insights into disease mechanisms, treatment outcomes, and
the experiences of both patients and caregivers, we strive to shape a
better future for those affected by epileptic conditions.“
Highlights of data to be presented at IEC :
Fenfluramine:
A combined open-label extension (OLE) study enrolled 412 patients
with DS or LGS who had participated in three previous fenfluramine
studies, reporting no new or unexpected safety signals and long-term
sustained benefit.[2]
Barriers and benefits of identifying patients with DEEs in adult
care settings:
Although the diagnosis of DEEs in children has become routine,
significant diagnostic gaps remain for adults. This qualitative
study, based on interviews with caregivers and healthcare
professionals in the UK, Germany, France, and Spain, found that a
confirmed diagnosis fosters holistic care, which may improve quality
of life (QoL), enhance communication and reduce risk of
hospitalization for patients.[4]
Unpredictable seizures and disruptive behavior in DEEs: Interim
results of a caregiver survey:
An internet-based anonymous 63-question survey was distributed to
caregivers of patients with DEEs by multiple DEE-specific patient
groups. Nearly half of caregivers reported that high rates of
disruptive seizures/behavior led to temporary loss in abilities,
previously associated with reduced quality of life.[3]
Prolonged seizures:
– Research characterizing patient and caregiver experiences of
prolonged seizures describes unmet needs and the significant short-
term and long-term negative impact on quality of life.[7]
– Real-world data from Adelphi’s Prolonged Seizure Disease Specific
Programme™ characterizes the definition, prevalence, and patient
population of prolonged seizures finding that people living with
epilepsy experiencing prolonged seizures encounter significant
seizure worry due to their seizure. In addition, these seizures
regularly progress to status epilepticus and/or seizure clusters,
leading to emergency care and hospital admissions, despite best
practice.[5]
– A post hoc analysis of video-EEG recordings from 725 patients
explores seizure duration and time-point cutoffs for statistically
defining possible and probable prolonged seizures by seizure type,
supporting the 2-minute cutoff for tonic-clonic seizures (
focal/generalized onset) and suggesting a 1 to 3 minutes cutoff for
other seizures, confirming that most seizure are abnormally prolonged
at 2 minutes or less[6]
– Seizure pathways: A qualitative study aimed to understand the end-
to-end care process for acute seizure emergencies finding that a
stronger focus on outpatient guidelines could empower patients and
caregivers to manage prolonged seizures in the outpatient setting,
potentially avoiding unnecessary seizure escalation, injury,
hospitalization and death.[8]
– Acute medication landscape: A global analysis assessed the
availability and reimbursement coverage of seizure acute medications
for use in the outpatient setting.[9]
Lennox-Gastaut syndrome:
Diagnosing LGS is challenging due to the heterogeneity of its
clinical presentation and symptom evolution over time. A group of ten
epilepsy experts from seven countries convened to develop a simple-to
-use checklist for non-specialists to support LGS diagnosis, using
the International League Against Epilepsy criteria as a framework.[10
]
UCB-sponsored symposium: Time matters in developmental and
epileptic encephalopathies
– Date: Monday, September 1st, 13:55 – 15:05
– Overview: The upcoming symposium aims to enhance knowledge and
awareness of the broader impact of DEEs in adulthood – beyond seizure
control. The session will focus on improving diagnosis, understanding
treatment journeys and addressing barriers to care in order to drive
better individual outcomes.
UCB presentations during the International Epilepsy Congress (IEC
) Congress Annual Meeting
Lead Author Abstract Title
DEEs
Wilkinson AL, et al[3] Oral presentation:
Unpredictable Seizures and Disruptive
Behavior in Developmental and
Epileptic Encephalopathies:
Interim Results of a Caregiver
Survey
Specchio N, et al[10] A checklist to support the
diagnosis of Lennox-Gastaut
syndrome
Rodriguez Solis B, et al[4] Barriers and benefits of
identifying patients with DEE in
adult care settings
Soto Insuga V, et al[11] Improving Lives in Dravet
Syndrome: Overcoming Challenges in
the Family Journey
Lothe A, et al[12] A Retrospective Claims Study
Evaluating Mortality in
Patients With Lennox-Gastaut
or
Dravet Syndromes in the United
States
Montero V, et al[13] Lennox-Gastaut Syndrome.
Situation analysis and Family
Journey.
Seizures
Trinka E, et al[5] Describing the Population of
Patients with Prolonged
Seizures: Results from a
Global Real-World
Point In-Time Study
Sile B, et al[6] Seizure Duration and Time-
point Cutoffs for Statistically
Defining a Prolonged Seizure:
A Post-Hoc
Analysis of the SCORE Video-
EEG Database
Kaye D, et al[7] Characterising Patient and
Caregiver Experiences Resulting
from Prolonged Seizures
Sain N, et al[8] Understanding and Optimising
the Seizure Emergency Pathway
Shafer P, et al[9] Global Seizure Rescue
Medication Landscape: Availability &
Reimbursement
Fenfluramine
Nabbout R, et al[14] Impact of Fenfluramine on
Convulsive Seizure Frequency in
Dose-Capped Patients With
Dravet Syndrome
Lagae L, at al[15] A Stratified Analysis of
Efficacy and Safety of Fenfluramine
in Patients With Dravet
Syndrome
Wirrell E, et al[16] Oral presentation: Real-World
Use of Fenfluramine for Dravet
Syndrome: a Retrospective
Cohort
Study Using a National
Pharmacy Database
Gjerulfsen CE, et al[17] Non-seizure benefits of long-
term fenfluramine treatment in
pediatric patients with Dravet
syndrome
Rosendahl A, et al[18] Prospective evaluation of non-
seizure benefits related to
treatment with fenfluramine in
pediatric and
adult patients with Dravet
syndrome
Schoonjans A, et al[2] Tolerability and Safety of
Fenfluramine and Global
Functioning of Patients in a
Combined Open-label
Extension Study of Children
and Adults With Dravet and
Lennox-Gastaut Syndromes
Lothe A, et al[19] A European Study of the
Effectiveness of Risk Minimisation
Measures for Fenfluramine Oral
Solution in Dravet Syndrome
and Lennox-Gastaut Syndrome
Dransfeld CR, et al[20] Use of Fenfluramine and
Cannabidiol in Daily Practice: A
Retrospective Analysis of
German
Prescription Claims
Mittur A, et al[21] Exposure-Response
Relationships of Fenfluramine in Patients
With Dravet Syndrome and
Lennox-Gastaut Syndrome
Zuberi S, et al[22] Post-hoc Analysis of
Fenfluramine for Lennox-Gastaut
Syndrome by Baseline Frequency
Quartiles
of Seizures Associated With a
Fall
Early pipeline:
Rodriguez N, et al[23] AAV gene therapy at neonatal
age in a mouse model of STXBP1
haploinsufficiency
Gomes AR, et al[24] Rescue of neuronal activity in
iPSC-derived STXBP1 in vitro
disease models using viral
vectors
Niespodziany I, et al[25] In vitro electrophysiological
study of hippocampal network
activity in a mouse model of
STXBP1 haploinsufficiency
Herrewegen YVD, et al[26] Expression and quantification
of STXBP1 splice variants in
rodent and primate brain
tissues
Brivaracetam [27]
Zafeiriou D, et al.[28] Brivaracetam Adjunctive
Therapy in Paediatric and Adult
Patients With Focal-Onset
Seizures in
Mid-European Countries: 12-
Month, Real-World Outcomes from
the BRIVA-REG Study
About UCB
UCB, Brussels, Belgium ( www.ucb.com ) is a global
biopharmaceutical company focused on the discovery and development of
innovative medicines and solutions to transform the lives of people
living with severe diseases of the immune system or of the central
nervous system. With approximately 9,000 people in approximately 40
countries, the company generated revenue of Ꞓ5.3 billion in 2023. UCB
is listed on Euronext Brussels (symbol: UCB). Follow us on Twitter: @
UCB_news .
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Important Safety Information about FINTEPLA▼ (fenfluramine) in
the EU [1]
Indications: Treatment of seizures associated with Dravet
syndrome and Lennox-Gastaut syndrome as an add-on therapy to other
anti-epileptic medicines for patients 2 years of age and older.
Dosage and Administration: Please refer to SmPC for full
information. Should be initiated and supervised by physicians with
experience in the treatment of epilepsy. Fintepla is prescribed and
dispensed according to the Fintepla controlled access programme.
Dravet syndrome: Patients who are not taking stiripentol: Starting
dose is 0.1 mg/kg twice daily (0.2 mg/kg/day). After 7 days, if
tolerated, can increase dose to 0.2 mg/kg twice daily (0.4 mg/kg/day)
. After an additional 7 days, if tolerated and further seizure
reduction required, can increase dose to a maximum of 0.35 mg/kg
twice daily (0.7 mg/kg/day), which is the recommended maintenance
dose. Patients requiring more rapid titration may increase the dose
every 4 days. Do not exceed maximum daily dose of 26 mg (13 mg twice
daily). Patients who are taking stiripentol: Starting dose is 0.1
mg/kg twice daily (0.2 mg/kg/day). After 7 days, if tolerated, can
increase dose to 0.2 mg/kg twice daily (0.4 mg/kg/day), which is the
recommended maintenance dose. Patients requiring more rapid titration
may increase the dose every 4 days. Do not exceed a total dose of 17
mg (8.6 mg twice daily). Lennox-Gastaut syndrome: Starting dose is
0.1 mg/kg twice daily (0.2 mg/kg/day). After 7 days, the dose should
be increased to 0.2 mg/kg twice daily (0.4 mg/kg/day), if tolerated.
After an additional 7 days, if tolerated, dose should be increased to
0.35 mg/kg twice daily (0.7 mg/kg/day), which is the recommended
maintenance dose. Do not exceed maximum daily dose of 26 mg (13 mg
twice daily). Discontinuation: When discontinuing treatment, decrease
the dose gradually. As with all anti-epileptic medicines, avoid
abrupt discontinuation when possible to minimize the risk of
increased seizure frequency and status epilepticus. A final
echocardiogram should be conducted 3-6 months after the last dose of
treatment with fenfluramine. Renal impairment: Generally, no dose
adjustment is recommended when administered to patients with mild to
severe renal impairment, however, a slower titration may be
considered. If adverse reactions are reported, a dose reduction may
be needed. Has not been studied in patients with end-stage renal
disease. Not known if fenfluramine or its active metabolite,
norfenfluramine, is dialyzable. Hepatic impairment: Hepatic
impairment: Generally, no dose adjustment is recommended when
Fintepla is administered without concomitant stiripentol to patients
with mild and moderate hepatic impairment (Child-Pugh Class A and B).
In patients with severe hepatic impairment (Child-Pugh C) not
receiving concomitant stiripentol, the maximum dosage is 0.2mg/kg
twice daily, and the maximal total daily dose is 17 mg. There are
limited clinical data on the use of Fintepla with stiripentol in
patients with mild impaired hepatic function. A slower titration may
be considered in patients with hepatic impairment and a dose
reduction may be needed if adverse reactions are reported. No
clinical data is available on the use of Fintepla with stiripentol in
moderate and severe hepatic impairment, therefore not recommended for
use. Elderly: No data available. Paediatric population: Safety and
efficacy in children below 2 years of age not yet established. No
data available.
Contraindications: Hypersensitivity to active substance or any
excipients. Aortic or mitral valvular heart disease and pulmonary
arterial hypertension. Within 14 days of the administration of
monoamine oxidase inhibitors due to an increased risk of serotonin
syndrome.
Warnings and Precautions: Aortic or mitral valvular heart disease
and pulmonary arterial hypertension: Prior to starting treatment,
patients must undergo an echocardiogram to establish a baseline and
exclude any pre-existing valvular heart disease or pulmonary
hypertension. Conduct echocardiogram monitoring every 6 months for
the first 2 years and annually thereafter. If an echocardiogram
indicates pathological valvular changes, consider follow-up earlier
to evaluate whether the abnormality is persistent. If pathological
abnormalities seen on echocardiogram, evaluate the benefit versus
risk of continuing fenfluramine treatment with the prescriber,
caregiver and cardiologist. Once treatment is discontinued for any
reasons, a final echocardiogram should be conducted 3-6 months after
the last dose of treatment with fenfluramine. If echocardiogram
findings suggestive of pulmonary arterial hypertension, perform a
repeat echocardiogram as soon as possible and within 3 months to
confirm these findings. If echocardiogram finding is confirmed
suggestive of an increased probability of pulmonary arterial
hypertension defined as intermediate probability, conduct a benefit-
risk evaluation of continuation of Fintepla by the prescriber, carer
and cardiologist. If echocardiogram suggests a high probability, it
is recommended fenfluramine treatment should be stopped. Decreased
appetite and weight loss: Fenfluramine can cause decreased appetite
and weight loss – an additive effect can occur in combination with
other anti-epileptic medicines such as stiripentol. Monitor the
patient’s weight. Undertake risk-benefit evaluation before starting
treatment if history of anorexia nervosa or bulimia nervosa. Fintepla
controlled access programme: A controlled access programme has been
created to 1) prevent off-label use in weight management in obese
patients and 2) confirm that prescribing physicians have been
informed of the need for periodic cardiac monitoring in patients
taking Fintepla. Somnolence: Fenfluramine can cause somnolence which
could be potentiated by other central nervous system depressants.
Suicidal behaviour and ideation: Suicidal behaviour and ideation have
been reported in patients treated with anti-epileptic medicines in
several indications. Advise patients and caregivers to seek medical
advice should any signs of suicidal behaviour and ideation emerge.
Serotonin syndrome: Serotonin syndrome, a potentially life-
threatening condition, may occur with fenfluramine treatment,
particularly with concomitant use of other serotonergic agents; with
agents that impair metabolism of serotonin such as MAOIs; or with
antipsychotics that may affect the serotonergic neurotransmitter
systems. Carefully observe the patient, particularly during treatment
initiation and dose increases. Increased seizure frequency: A
clinically relevant increase in seizure frequency may occur during
treatment, which may require adjustment in the dose of fenfluramine
and/or concomitant anti-epileptic medicines, or discontinuation of
fenfluramine, should the benefit-risk be negative. Cyproheptadine:
Cyproheptadine is a potent serotonin receptor antagonist and may
therefore decrease the efficacy of fenfluramine. If cyproheptadine is
added to treatment with fenfluramine, monitor patient for worsening
of seizures. If fenfluramine treatment is initiated in a patient
taking cyproheptadine, fenfluramine’s efficacy may be reduced.
Glaucoma: Fenfluramine can cause mydriasis and can precipitate angle
closure glaucoma. Discontinue therapy in patients with acute
decreases in visual acuity. Consider discontinuation if ocular pain
of unknown origin. Effect of CYP1A2 or CYP2B6 inducers: Co-
administration with strong CYP1A2 inducers or CYP2B6 inducers will
decrease fenfluramine plasma concentrations, which may lower the
efficacy of fenfluramine. If co-administration is considered
necessary, the patient should be monitored for reduced efficacy and a
dose increase of fenfluramine could be considered provided that it
does not exceed twice the maximum daily dose (52 mg/day). If a strong
CYP1A2 or CYP2B6 inducer is discontinued during maintenance treatment
with fenfluramine, consider gradual reduction of the fenfluramine
dosage to the dose administered prior to initiating the inducer.
Effect of CYP1A2 or CYP2D6 inhibitors: Initiation of concomitant
treatment with a strong CYP1A2 or CYP2D6 inhibitor may result in
higher exposure and, therefore, adverse events should be monitored,
and a dose reduction may be needed in some patients. Excipients:
Contains sodium ethyl para-hydroxybenzoate (E 215) and sodium methyl
para-hydroxybenzoate (E 219) – may cause allergic reactions (possibly
delayed). It also contains sulfur dioxide (E 220) which may rarely
cause severe hypersensitivity reactions and bronchospasm. Patients
with rare glucose-galactose malabsorption should not take this
medicine. The product contains less than 1 mmol sodium (23 mg) per
the maximum daily dose of 12 mL; essentially ’sodium-free‘. Contains
glucose – may be harmful to teeth. Interactions: Pharmacodynamic
interactions with other CNS depressants increase the risk of
aggravated central nervous system depression. An increase in dose may
be necessary when coadministered with rifampicin or a strong CYP1A2
or CYP2B6 inducer. In in vitro studies coadministration with a strong
CYP1A2 or CYP2D6 inhibitor may result in higher exposure (see section
4.4 of the SmPC). Coadministration with CYP2D6 substrates or MATE1
substrates may increase their plasma concentrations. Co-
administration with CYP2B6 or CYP3A4 substrates may decrease their
plasma concentrations. Pregnancy and lactation: Limited data in
pregnant women. As a precaution, avoid use of Fintepla in pregnancy.
It is unknown whether fenfluramine/metabolites are excreted in human
milk. Animal data have shown excretion of fenfluramine/metabolites in
milk. A decision must be made whether to discontinue breast-feeding
or to discontinue/abstain from Fintepla taking into account the
benefit of breast-feeding for the child and the benefit of therapy
for the woman. Drive and use machines.: Fintepla has moderate
influence on the ability to drive/ use machines as it may cause
somnolence and fatigue. Advise patients not to drive or operate
machinery until they have sufficient experience to gauge whether it
adversely affects their abilities.
Adverse effects: Dravet syndrome: Very common (≥1/10): Upper
respiratory tract infection, decreased appetite, somnolence,
diarrhoea, pyrexia, fatigue, blood glucose decreased, echocardiogram
abnormal (Consisted of trace and mild mitral regurgitation, and trace
aortic regurgitation, which are considered physiologic). Common (
≥1/100 to <1/10): Bronchitis, abnormal behaviour, aggression,
agitation, insomnia, mood swings, ataxia, hypotonia, lethargy,
seizure, status epilepticus, tremor, constipation, salivary
hypersecretion, weight decreased and blood prolactin increased.
Lennox-Gastaut syndrome: Very common (≥1/10): Upper respiratory tract
infection, decreased appetite, somnolence, diarrhoea, vomiting,
fatigue. Common (≥1/100 to <1/10): Bronchitis, influenza, pneumonia,
seizure, status epilepticus, lethargy, tremor, constipation, salivary
hypersecretion, blood prolactin increased, weight decreased, fall.
Refer to SmPC for other adverse reactions.
▼ This medicinal product is subject to additional monitoring.
This will allow quick identification of new safety information.
Healthcare professionals are asked to report any suspected adverse
reactions.
Refer to the European Summary of Product Characteristics for
other adverse reactions and full Prescribing Information:
https://www.ema.europa.eu/en/documents/product-information/fintepla-
epar-product-information_en.pdf .
FINTEPLA® is a registered trademark of the UCB Group of
Companies.
Important Safety Information about BRIVIACT® (brivaracetam) in
the EU [28]
Therapeutic indications: BRIVIACT is indicated as adjunctive
therapy in the treatment of partial-onset seizures with or without
secondary generalisation in adults, adolescents and children from 2
years of age with epilepsy.
Posology and method of administration: The physician should
prescribe the most appropriate formulation and strength according to
weight and dose. It is recommended to parent and care giver to
administer BRIVIACT oral solution with the measuring device (10 ml or
5 ml oral dosing syringe) provided in the carton box. BRIVIACT
solution for injection/infusion is an alternative route of
administration for patients when oral administration is temporarily
not feasible. There is no experience with twice daily intravenous
administration of brivaracetam for a period longer than 4 days.
Adults: The recommended starting dose is 50 or 100 mg/day based on
physician’s assessment of required for seizure reduction versus
potential side effects. Brivaracetam can be taken with or without
food. Based on individual patient response and tolerability, the dose
may be adjusted in the effective dose range of 50 mg/day to 200
mg/day. Children and adolescents weighing 50 kg or more: The
recommended starting dose is 50 mg/day. Brivaracetam may also be
initiated at 100 mg/day based on physician’s assessment of need for
seizure control. The recommended maintenance dose is 100 mg/day.
Based on individual patient response, the dose may be adjusted in the
effective dose range of 50 mg/day to 200 mg/day. Children and
adolescents weighing from 20 kg to less than 50 kg: The recommended
starting dose is 1 mg/kg/day. Brivaracetam may also be initiated at
doses up to 2 mg/kg/day based on physician’s assessment of need for
seizure control. The recommended maintenance dose is 2 mg/kg/day.
Based on individual patient response, the dose may be adjusted in the
effective dose range of 1 mg/kg/day to 4 mg/kg/day. Children weighing
from 10 kg to less than 20 kg: The recommended starting dose is 1
mg/kg/day. Brivaracetam may also be initiated at doses up to 2.5
mg/kg/day based on physician’s assessment of need for seizure
control. The recommended maintenance dose is 2.5 mg/kg/day. Based on
individual patient response, the dose may be adjusted in the
effective dose range of 1 mg/kg/day to 5 mg/kg/day. For adults,
adolescents and children from 2 years of age, the dose should be
administered in two equally divided doses, approximately 12 hours
apart.
If patients miss one dose or more, it is recommended that they
take a single dose as soon as they remember and take the following
dose at the usual morning or evening time. Brivaracetam oral solution
can be diluted in water or juice shortly before swallowing; a
nasogastric tube or a gastrostomy tube may also be used. Brivaracetam
may be initiated with either intravenous or oral administration. When
converting from oral to intravenous administration or vice versa, the
total daily dose and frequency of administration should be
maintained. Brivaracetam may be administered as an intravenous bolus
without dilution or diluted in a compatible diluent and administered
as a 15-minute intravenous infusion. This medicinal product must not
be mixed with other medicinal products. Brivaracetam bolus injection
or intravenous infusion has not been studied in acute conditions,
e.g. status epilepticus, and is therefore not recommended for such
conditions. For patients from 16 years of age, if brivaracetam has to
be discontinued, it is recommended that the dose is reduced gradually
by 50 mg/day on a weekly basis. For patients below the age of 16
years, if brivaracetam has to be discontinued, it is recommended that
the dose is reduced by a maximum of half the dose every week until a
dose of 1 mg/kg/day (for patients with a body weight less than 50 kg)
or 50 mg/day (for patients with body weight of 50 kg or more) is
reached. After 1 week of treatment at 50 mg/day, a final week of
treatment at 20 mg/day is recommended. No dose adjustment is needed
for elderly patients (≥65 years of age) or for those with renal
impairment. Based on data in adults, no dose adjustment is necessary
in paediatric patients with impaired renal function. No clinical data
are available on paediatric patients with renal impairment.
Brivaracetam is not recommended for patients with end-stage renal
disease undergoing dialysis due to lack of data. Exposure to
brivaracetam was increased in patients with chronic liver disease. In
patients with hepatic impairment, the following adjusted doses,
administered in 2 divided doses, approximately 12 hours apart, are
recommended for all stages of hepatic impairment: In adults,
adolescents and children weighing ≥50 kg, a 50 mg/day starting dose
is recommended, with a maximum daily dose of 150 mg/day. For
adolescents and children weighing from 20 kg to <50 kg, a 1 mg/kg/day
is recommended, with a maximum daily dose of 3 mg/kg/day. For
children weighing from 10 kg to <20 kg, a 1 mg/kg/day is recommended,
with a maximum daily dose of 4 mg/kg/day. No clinical data are
available in paediatric patients with hepatic impairment. The
efficacy of brivaracetam in paediatric patients aged less than 2
years has not yet been established.
Contraindications: Hypersensitivity to the active substance,
other pyrrolidone derivatives or any of the excipients. Special
warnings and precautions for use: Suicidal ideation and behaviour
have been reported in patients treated with anti-epileptic drugs (
AEDs) in several indications, including brivaracetam. Patients should
be monitored for signs of suicidal ideation and behaviours and
appropriate treatment should be considered. Patients (and caregivers)
should be advised to seek medical advice should any signs of suicidal
ideation or behaviour emerge. Clinical data on the use of
brivaracetam in patients with pre-existing hepatic impairment are
limited. Dose adjustments are recommended for patients with hepatic
impairment. Brivaracetam film-coated tablets contain lactose.
Patients with rare hereditary problems of galactose intolerance,
total lactase deficiency or glucose-galactose malabsorption should
not take brivaracetam. Brivaracetam film-coated tablets, solution for
injection/infusion and oral solution contain less than 1 mmol sodium
(23mg) per tablet/vial/ml respectively, that is to say essentially
’sodium free‘. Brivaracetam oral solution contains 168 mg sorbitol (
E420) in each ml. Patients with hereditary fructose intolerance (HFI)
should not take this medicinal product. The oral solution contains
methyl parahydroxybenzoate (E218), which may cause allergic reactions
(possibly delayed). Brivaracetam oral solution contains propylene
glycol (E1520).
Interaction with other medicinal products and other forms of
interaction: In clinical studies, although patient numbers were
limited, brivaracetam had no observed benefit over placebo among
patients taking concomitant levetiracetam. No additional safety or
tolerability concern was observed. In an interaction study between
brivaracetam 200 mg single dose and ethanol 0.6 g/L continuous
infusion in healthy volunteers, there was no pharmacokinetic
interaction, but the effect of alcohol on psychomotor function,
attention and memory was approximately doubled with the intake of
brivaracetam. Intake of brivaracetam with alcohol is not recommended.
In vitro data suggest that brivaracetam has a low interaction
potential. The main disposition pathway of brivaracetam® is by
CYPindependent hydrolysis; a second pathway involves hydroxylation
mediated by CYP2C19. Brivaracetam plasma concentrations may increase
when co-administered with CYP2C19 strong inhibitors (e.g.
fluconazole, fluvoxamine), but the risk of a clinically relevant
CYP2C19 mediated interaction is considered to be low. Limited
clinical data are available implying that coadministration of
cannabidiol may increase the plasma exposure of brivaracetam,
possibly through CYP2C19 inhibition, but the clinical relevance is
uncertain. In healthy subjects, co-administration with the strong
enzyme inducer rifampicin (600 mg/day for 5 days), decreased
brivaracetam area under the plasma concentration curve (AUC) by 45%.
Prescribers should consider adjusting the dose of brivaracetam in
patients starting or ending treatment with rifampicin. Brivaracetam
plasma concentrations are decreased when co-administered with strong
enzyme-inducing AEDs (carbamazepine, phenobarbital, phenytoin) but no
dose adjustment is required. Other strong enzyme inducers such as St
John’s wort (Hypericum perforatum) may decrease the systemic exposure
of brivaracetam. Starting or ending treatment with St John’s wort
should be done with caution. Brivaracetam at 50 or 150 mg/day did not
affect the AUC of midazolam (metabolised by CYP3A4). The risk of
clinically relevant CYP3A4 interactions is considered low. In vitro
studies have shown that brivaracetam exhibits little or no inhibition
of CYP450 isoforms except for CYP2C19 and may therefore increase
plasma concentrations of medicinal products metabolised by CYP2C19 (
e.g. lansoprazole, omeprazole, diazepam). Brivaracetam did not induce
CYP1A1/2 but induced CYP3A4 and CYP2B6 in vitro. No CYP3A4 induction
was found in vivo. CYP2B6 induction has not been investigated in vivo
and brivaracetam may decrease plasma concentrations of medicinal
products metabolised by CYP2B6 (e.g. efavirenz). In vitro interaction
studies to determine the potential inhibitory effects on transporters
concluded that there were no clinically relevant effects, except for
OAT3. In vitro, brivaracetam inhibits OAT3 with a half maximal
inhibitory concentration 42-fold higher than the Cmax at the highest
clinical dose. Brivaracetam 200 mg/day may increase plasma
concentrations of medicinal products transported by OAT3.
Brivaracetam is a moderate reversible inhibitor of epoxide hydrolase,
resulting in an increased concentration of carbamazepine epoxide, an
active metabolite of carbamazepine. In controlled clinical studies,
carbamazepine epoxide plasma concentration increased by a mean of 37%
, 62% and 98% with little variability at Brivaracetam doses of 50
mg/day, 100 mg/day and 200 mg/day, respectively. No safety risks were
observed. There was no additive effect of brivaracetam and valproate
on the AUC of carbamazepine epoxide. No dose adjustment is needed
when brivaracetam is co-administered with carbamazepine,
phenobarbital or phenytoin. Brivaracetam had no clinically relevant
effect on the plasma concentrations of clobazam, clonazepam,
lacosamide, lamotrigine, levetiracetam, oxcarbazepine, phenobarbital,
phenytoin, pregabalin, topiramate, valproic acid or zonisamide. There
are no data available on the effects of clobazam, clonazepam,
lacosamide, pregabalin or zonisamide on brivaracetam plasma
concentrations. Co-administration of brivaracetam (100 mg/day) with
an oral contraceptive containing ethinylestradiol (0.03 mg) and
levonorgestrel (0.15 mg) did not influence the pharmacokinetics of
either substance. However, when brivaracetam was coadministered at a
dose of 400 mg/day (twice the recommended maximum daily dose), a
reduction in estrogen and progestin AUCs of 27% and 23%,
respectively, was observed without impact on suppression of
ovulation. Pregnancy: Data on the use of brivaracetam in pregnant
women are limited. There are no data on placental transfer in humans,
but brivaracetam was shown to readily cross the placenta in rats. The
potential risk for humans is unknown. Animal studies did not detect
any teratogenic potential of brivaracetam. In clinical studies,
adjunctive brivaracetam used concomitantly with carbamazepine induced
a dose-related increase in the concentration of the active
metabolite, carbamazepine-epoxide. There are insufficient data to
determine the clinical significance of this effect in pregnancy.
Brivaracetam should not be used during pregnancy unless clinically
necessary. Breast-feeding: Brivaracetam is excreted in human breast
milk. The decision to discontinue either breastfeeding or
brivaracetam should be made based on the benefit of the medicinal
product to the mother. In case of co-administration of brivaracetam
and carbamazepine, the amount of carbamazepine-epoxide excreted in
breast milk could increase. The clinical significance remains
unknown. Fertility: No human data on the effect of brivaracetam on
fertility are available. There was no effect on fertility in rats.
Effects on ability to drive and use machines : Brivaracetam has minor
or moderate influence on the ability to drive and use machines.
Patients should be advised not to drive a car or to operate other
potentially hazardous machines until they are familiar with the
effects of brivaracetam on their ability to perform such activities.
Undesirable effects: The most frequently reported adverse reactions
with brivaracetam were somnolence (14.3%) and dizziness (11.0%); they
were usually mild-to-moderate in intensity. Somnolence and fatigue
were reported at a higher incidence with increasing dose. Very common
adverse reactions (≥1%-<10%) were influenza, decreased appetite,
depression, anxiety, insomnia, irritability, convulsion, vertigo,
upper respiratory tract infections, cough, nausea, vomiting,
constipation and fatigue. Neutropenia was reported in 6/1099 (0.5%)
of brivaracetam and none (0/459) of the placebo-treated patients.
Four of these subjects had decreased neutrophil counts at baseline.
None of the neutropenia cases were severe, required any specific
treatment or led to discontinuation of brivaracetam and none had
associated infections. Suicidal ideation was reported in 0.3% (3/1099
) of brivaracetam and 0.7% (3/459) of placebo-treated patients. In
short-term clinical studies of brivaracetam in patients with
epilepsy, there were no cases of completed suicide and suicide
attempt; however, both were reported in open-label extension studies.
The safety profile of brivaracetam observed in children from 1 month
of age was consistent with the safety profile observed in adults. In
the open label, uncontrolled, long-term studies suicidal ideation was
reported in 4.7 % of paediatric patients (assessed from 6 years
onwards, more common in adolescents) compared with 2.4 % of adults
and behavioural disorders were reported in 24.8 % of paediatric
patients compared with 15.1 % of adults. The majority of events were
mild or moderate in intensity, were non-serious, and did not lead to
discontinuation of study drug. An additional adverse reaction
reported in children was psychomotor hyperactivity (4.7 %). No
specific pattern of adverse event (AE) was identified in children
from 1 month to < 4 years of age when compared to older paediatric
age groups. No significant safety information was identified
indicating the increasing incidence of a particular AE in this age
group. As data available in children younger than 2 years of age are
limited, brivaracetam is not indicated in this age range. Limited
clinical data are available in neonates. Reactions suggestive of
immediate (Type I) hypersensitivity have been reported in a small
number of brivaracetam patients (9/3022) during clinical development.
Overdose: There is limited clinical experience with brivaracetam
overdose in humans. Somnolence and dizziness have been reported in a
healthy subject taking a single dose of 1,400 mg of brivaracetam. The
following adverse reactions were reported with brivaracetam overdose:
nausea, vertigo, balance disorder, anxiety, fatigue, irritability,
aggression, insomnia, depression, and suicidal ideation in the
postmarketing experience. In general, the adverse reactions
associated with brivaracetam overdose were consistent with the known
adverse reactions. There is no specific antidote for overdose with
brivaracetam. Treatment of an overdose should include general
supportive measures. Since <10% of brivaracetam is excreted in urine,
haemodialysis is not expected to significantly enhance brivaracetam
clearance.
Refer to the European Summary of Product Characteristics for
other adverse reactions and full Prescribing Information:
https://www.ema.europa.eu/en/documents/product-information/briviact-
epar-product-information_en.pdf
BRIVIACT® is a registered trademark of the UCB Group of
Companies.
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