ZILBRYSQ 32.4mg injection solution in pre-filled syringe medication leaflet

Zilbrysq 16.6 mg solution for injection in pre-filled syringe

Zilbrysq 23 mg solution for injection in pre-filled syringe

Zilbrysq 32.4 mg solution for injection in pre-filled syringe

Zilbrysq 16.6 mg solution for injection in pre-filled syringe

Each pre-filled syringe contains zilucoplan sodium equivalent to 16.6 mg zilucoplan in 0.416 mL(40 mg/mL).

Zilbrysq 23 mg solution for injection in pre-filled syringe

Each pre-filled syringe contains zilucoplan sodium equivalent to 23 mg zilucoplan in 0.574 mL(40 mg/mL).

Zilbrysq 32.4 mg solution for injection in pre-filled syringe

Each pre-filled syringe contains zilucoplan sodium equivalent to 32.4 mg zilucoplan in 0.810 mL(40 mg/mL).

For the full list of excipients, see section 6.1.

Solution for injection (injection)

The solution is clear to slightly opalescent and colourless, free of visible particles. The pH andosmolality of the solution are approximately 7.0 and 300 mOsm/kg respectively.

Zilbrysq is indicated as an add-on to standard therapy for the treatment of generalised myastheniagravis (gMG) in adult patients who are anti-acetylcholine receptor (AChR) antibody positive.

Zilbrysq is intended for use under the guidance and supervision of healthcare professionalsexperienced in the management of patients with neuromuscular disorders.

Before starting therapy, patients must be vaccinated against Neisseria meningitidis. If treatment needsto start less than 2 weeks after vaccination, the patient must receive appropriate prophylactic antibiotictreatment until 2 weeks after the first vaccination dose (see sections 4.3 and 4.4).

The recommended dose should be given as a subcutaneous injection once daily and administeredabout the same time every day.

Table 1: Total daily dose by body weight range

Body weight Dose* Number of pre-filledsyringes by colour< 56 kg 16.6 mg 1 (Rubine red)≥ 56 to < 77 kg 23 mg 1 (Orange)≥ 77 kg 32.4 mg 1 (Dark blue)

*The recommended dose corresponds to approximately 0.3 mg/kg.

Zilucoplan has not been studied in gMG patients with a Myasthenia Gravis Foundation of America(MGFA) Class V.

If a dose is missed, it should be administered the same day; then, normal dosing should be continuedthe following day. No more than one dose should be administered per day.

No dose adjustment is required in elderly patients (see section 5.2). Experience with zilucoplan inelderly patients in clinical studies is limited.

No dose adjustment is required for patients with renal impairment (creatinine clearance ≥15 mL/min).

There are no data on patients requiring dialysis.

No dose adjustment is required for patients with mild and moderate hepatic impairment (Child-Pughscore of 9 or lower).

The safety and efficacy of Zilbrysq in patients with severe hepatic impairment have not beenestablished. No dose recommendation can be made (see section 5.2).

The safety and efficacy of Zilbrysq in children below the age of 18 years have not been established.

No data are available.

This medicinal product is administered by subcutaneous injection.

Suitable injection sites include front of the thighs, abdomen and the back of the upper arms.

Injection sites should be rotated and injections should not be given in areas where the skin is tender,erythematous, bruised, indurated or where the skin has scars or stretch marks.

Zilbrysq is intended to be self-administered by the patient and/or another person who has beenproperly trained to administer subcutaneous injections and following the detailed instructions given inthe instructions for use at the end of the package leaflet.

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

Patients who are not currently vaccinated against Neisseria meningitidis (see section 4.4).

Patients with unresolved Neisseria meningitidis infection.

Neisseria infections

Meningococcal infection

Due to its mechanism of action, the use of zilucoplan may increase the patient’s susceptibility toinfections with Neisseria meningitidis. As a precautionary measure, all patients must be vaccinatedagainst meningococcal infections, at least 2 weeks prior to the start of treatment.

If treatment needs to start less than 2 weeks after vaccination against meningococcal infections, thepatient must receive appropriate prophylactic antibiotic treatment until 2 weeks after the firstvaccination dose. Meningococcal vaccines reduce but do not completely eliminate the risk ofmeningococcal infections.

Vaccines against serogroups A, C, Y, W, and where available, serogroup B, are recommended forpreventing the commonly pathogenic meningococcal serogroups. Vaccination and prophylacticantibiotic treatment should occur according to most current relevant guidelines.

During treatment, patients should be monitored for signs and symptoms of meningococcal infectionand evaluated immediately if infection is suspected. In case of a suspected meningococcal infection,appropriate measures such as treatment with antibiotics and discontinuation of treatment, should betaken until the meningococcal infection can be ruled out. Patients should be instructed to seekimmediate medical advice if signs or symptoms of meningococcal infections occur.

Prescribers should be familiar with the educational materials for the management of meningococcalinfections and provide a patient alert card and patient/carer guide to patients treated with zilucoplan.

Other Neisseria infections

In addition to Neisseria meningitidis, patients treated with zilucoplan may also be susceptible toinfections with other Neisseria species, such as gonococcal infections. Patients should be informed onthe importance of gonorrhea prevention and treatment.

Prior to initiating zilucoplan therapy, it is recommended that patients initiate immunizations accordingto current immunization guidelines.

This medicinal product contains less than 1 mmol sodium (23 mg) per pre-filled syringe, that is to sayessentially ‘sodium-free’.

No interaction studies have been performed. Based on results from in vitro testing, zilucoplan will notinhibit or induce drug metabolising enzymes (CYPs and UGTs) and common transporters in aclinically relevant manner.

Based on the potential inhibitory effect of zilucoplan on complement-dependent cytotoxicity ofrituximab, zilucoplan may reduce the expected pharmacodynamic effects of rituximab.

There are no data from the use of zilucoplan in pregnant women.

Animal studies do not indicate direct or indirect harmful effects with respect to reproductive toxicity(see section 5.3).

Treatment of pregnant women with Zilbrysq should only be considered if the clinical benefitoutweighs the risks.

It is unknown whether zilucoplan is excreted in human milk or absorbed systemically after oralingestion by the newborns/infants. A risk to the newborns/infants cannot be excluded.

A decision must be made whether to discontinue breast-feeding or to discontinue zilucoplan therapytaking into account the benefit of breastfeeding for the child and the benefit of therapy for the woman.

The effect of zilucoplan on human fertility has not been evaluated. In some non-human primatefertility and repeat-dose toxicity studies, findings of uncertain clinical relevance were observed inmale and female reproductive organs (see section 5.3).

Zilbrysq has no or negligible influence on the ability to drive and use machines.

The most frequently reported adverse reactions were injection site reactions (injection site bruising(13.9%) and injection site pain (7.0%)) and upper respiratory tract infections (nasopharyngitis (5.2%),upper respiratory tract infection (3.5%) and sinusitis (3.5%)).

Table 2 presents the adverse reactions from the pooled placebo-controlled (n=115) and open-labelextension (n=213) studies in gMG together with a classification of the frequency in the zilucoplantreated patients, using the following convention: very common (≥ 1/10), common (≥ 1/100 to < 1/10),uncommon (≥ 1/1 000 to < 1/100), rare (≥ 1/10 000 to < 1/1 000), very rare (< 1/10 000), not known(cannot be estimated from the available data). Within each frequency grouping, adverse reactions arepresented in the order of decreasing seriousness.

Table 2: Adverse reactions

System organ class Frequency Adverse reaction

Infections and infestations Very common Upper respiratory tractinfections*

Gastrointestinal disorders Common Diarrhoea

Skin and subcutaneous tissue Common Morphoea*adisorders

General disorders and Very common Injection site reactions*administration site conditions

Investigations Common Lipase increased*

Common Amylase increased*

Uncommon Blood eosinophils increased*

*See paragraph Description of selected adverse reactions.aMorphoea was reported only in long-term open-label clinical studies. The maximum duration ofexposure to ZLP during the long-term clinical studies was more than 4 years.

The most common reactions were injection site bruising, pain, nodule, pruritus and haematoma. Allcases were mild or moderate in severity, and less than 3% of reactions led to treatmentdiscontinuation.

Upper respiratory tract infections

The most common infections were nasopharyngitis, upper respiratory tract infection and sinusitis.

More than 95% of the cases were mild or moderate in severity and did not lead to treatmentdiscontinuation. In pooled placebo-controlled studies, upper respiratory tract infections were reportedin 13.0% of patients treated with zilucoplan and in 7.8% of patients treated with placebo.

Pancreatic enzymes increased

Cases of lipase increase (5.2%) and/or amylase increase (6.1%) were observed. These elevations weretransient and rarely led to treatment discontinuation. The majority occurred within 2 months of startingzilucoplan and normalized within 2 months.

Blood eosinophils increased

Elevations of blood eosinophils were observed. These were transient and not leading to treatmentdiscontinuation. The majority occurred within 2 months of starting zilucoplan and normalized within1 month.

Morphoea

Cases of morphoea were observed after long-term treatment during the open-label extension study.

The majority of the cases had a time to onset longer than one year after start of treatment, were mild ormoderate in severity and did not lead to treatment discontinuation.

Reporting suspected adverse reactions after authorisation of the medicinal product is important. Itallows continued monitoring of the benefit/risk balance of the medicinal product. Healthcareprofessionals are asked to report any suspected adverse reactions via the national reporting systemlisted in Appendix V.

In a healthy volunteer study where 32 participants were exposed to doses twice the recommended dose(corresponding to approximately 0.6 mg/kg; Table 1), administered subcutaneously for up to 7 days,safety data were consistent with the safety profile of the recommended dose.

In cases of overdose, it is recommended that patients are monitored closely for any adverse reactions,and appropriate supportive measures should be instituted immediately.

Pharmacotherapeutic group: Immunosuppressants, complement inhibitors, ATC code: L04AJ06

Zilucoplan is a 15 amino acid, synthetic macrocyclic peptide that inhibits the effects of thecomplement protein C5 through a dual mechanism of action. It specifically binds to C5, therebyinhibiting its cleavage by the C5 convertase to C5a and C5b, which results in a downregulation of theassembly and cytolytic activity of the membrane attack complex (MAC). Additionally, by binding tothe C5b moiety of C5, zilucoplan sterically hinders binding of C5b to C6, which prevents thesubsequent assembly and activity of the MAC, should any C5b be formed.

The pharmacodynamic effect of zilucoplan was analysed through the ability of inhibiting ex vivo,complement-induced sheep red blood cell (sRBC) lysis.

Data from the phase 2 and phase 3 studies demonstrate rapid, complete (> 95%) and sustainedcomplement inhibition with zilucoplan when dosed according to Table 1.

The safety and efficacy of zilucoplan were evaluated in a 12-week multicentre, randomised,double-blind placebo-controlled study MG0010 (RAISE) and the open-label extension study MG0011(RAISE-XT).

Study MG0010 (RAISE)

A total of 174 patients were enrolled, who were at least 18 years of age, had acetylcholine-receptorantibody positive generalised myasthenia gravis, a Myasthenia Gravis- Activities of Daily Living(MG­ADL) Score of ≥ 6 and a Quantitative Myasthenia Gravis (QMG Score) of ≥ 12 (see Table 3).

Patients were treated once daily with either zilucoplan (dosed according to Table 1) or placebo with 86and 88 patients randomised to each treatment group, respectively. Stable standard of care (SOC)therapy was allowed. The majority of patients received treatment for gMG at baseline which includedparasympathomimetics (84.5%), systemic corticosteroids (63.2%) and nonsteroidalimmunosuppressants (51.1%).

The primary endpoint was the change from baseline to week 12 in MG-ADL total score.

Key secondary endpoints were the change from baseline to week 12 in QMG total score, in

Myasthenia Gravis Composite (MGC) total score and in MG Quality of Life (MG-QoL15r) total score(Table 4).

MG-ADL clinical responders were defined as having at least a 3-point decrease and QMG responderswere defined as having at least a 5-point decrease without rescue therapy.

Table 3: Baseline demographic and disease characteristics of patients enrolled in study MG0010

Zilucoplan (n=86) Placebo (n=88)

Age, years, mean (SD) 52.6 (14.6) 53.3 (15.7)

Age at onset, years, mean (SD) 43.5 (17.4) 44.0 (18.7)

Age ≥ 65 22 (25.6) 26 (29.5)

Gender, male, n (%) 34 (39.5) 41 (46.6)

Baseline MG-ADL score mean (SD) 10.3 (2.5) 10.9 (3.4)

Baseline QMG score mean (SD) 18.7 (3.6) 19.4 (4.5)

Baseline MGC score, mean (SD) 20.1 (6.0) 21.6 (7.2)

Baseline MG-QoL 15r score, mean (SD) 18.6 (6.6) 18.9 (6.8)

Duration of disease, years, mean (SD) 9.3 (9.5) 9.0 (10.4)

MGFA class at screening, n (%) Class II 22 (25.6) 27 (30.7)

MGFA class at screening, n (%) Class III 60 (69.8) 57 (64.8)

MGFA class at screening, n (%) Class IV 4 (4.7) 4 (4.5)

Table 4 presents the change from baseline at week 12 in the total scores for MG-ADL, QMG, MGCand MGQoL15r. Mean baseline scores were 10.9 and 10.3 for MG-ADL, 19.4 and 18.7 for QMG,21.6 and 20.1 for MGC and 18.9 and 18.6 for MG-QoL15r for placebo and zilucoplan groups,respectively.

Table 4: Change from baseline at week 12 in total scores for MG-ADL, QMG, MGC and MG-QoL15r

Endpoints: Zilucoplan (n=86) Placebo (n=88) Zilucoplan change p-value*

Change from LS meanbaseline in total difference vs.score at week 12: placebo (95% CI)

LS Mean (95%

CI)

MG-ADL -4.39 (-5.28, -3.50) -2.30 (-3.17, -1.43) -2.09 (-3.24, -0.95) < 0.001

QMG -6.19 (-7.29, -5.08) -3.25 (-4.32, -2.17) -2.94 (-4.39, -1.49) < 0.001

MGC -8.62 (-10.22, -7.01) -5.42 (-6.98, -3.86) -3.20 (-5.24, -1.16) 0.0023

MG-QoL15r -5.65 (-7.17, -4.12) -3.16 (-4.65, -1.67) -2.49 (-4.45, -0.54) 0.0128

*Analysis based on a MMRM ANCOVA model

The treatment effect in the zilucoplan group for all 4 endpoints started rapidly at week 1, furtherincreased to week 4 and was sustained through week 12.

At week 12, a clinically meaningful and highly statistically significant improvement in MG-ADL totalscore (Figure 1) and in QMG total score was observed for zilucoplan versus placebo.

Figure 1: Change from baseline in MG ADL total score

Analysis based on MMRM ANCOVA model

Clinically meaningful change = 2-point change in MG-ADL score

At week 12, 73.1% of the patients in the zilucoplan group were MG-ADL clinical responders withoutrescue therapy, vs. 46.1% in the placebo group (p<0.001). Fifty-eight percent (58.0%) of the patientsin the zilucoplan group were QMG clinical responders without rescue therapy, vs. 33.0% in theplacebo group (p=0.0012).

At week 12, the cumulative portion of patients that needed rescue therapy was 5% in the zilucoplangroup and 11% in the placebo group. Rescue therapy was defined as intravenous immunoglobulin G(IVIG) or plasma exchange (PLEX).

Study MG0011 (RAISE-XT)

Two hundred patients who completed a placebo-controlled phase 2 study (MG0009) or the phase 3study (MG0010) continued in the open-label extension study MG0011 in which all patients receivedzilucoplan (dosed according to Table 1) daily. Primary objective was long-term safety. Secondaryefficacy endpoints were change from double-blind study baseline in MG-ADL, QMG, MGC and

MG-QoL15r score at week 24. For former MG0010 participants, results are shown below (Table 5).

Table 5: Mean change from double-blind study baseline (MG0010) to week 24 (week 12 in MG0011)and week 60 (week 48 in MG0011) in total scores for MG-ADL, QMG, MGC and MG-QoL15r

Endpoints: Change from Zilucoplan (n=82) Placebo/zilucoplan (n=84)baseline in total score atweek 24 and week 60: LS

Mean (SE)

MG-ADL

Week 24 -5.46 (0.59) -5.20 (0.52)

Week 60 -5.16 (0.61) -4.37 (0.54)

QMG

Week 24 -7.10 (0.80) -7.19 (0.69)

Week 60 -6.44 (0.83) -6.15 (0.71)

MGC

Week 24 -10.37 (1.15) -11.12 (1.00)

Week 60 -8.89 (1.20) -9.01 (1.04)

MG-QoL15r

Week 24 -8.09 (0.96) -7.96 (0.89)

Week 60 -7.22 (0.99) -6.09 (0.91)

Analysis based on a MMRM ANCOVA model where rescue therapy and discontinuation are imputed astreatment failure; Death are imputed the worst possible score (e.g. score 24 for MG-ADL).

SE = Standard error

Figure 2: Mean change from double-blind study baseline to week 60 for total MG ADL score

In MG0010 and MG0011 (RAISE-XT), the patients were tested for anti-drug antibody (ADA)positivity and anti-polyethylene glycol (PEG) antibody positivity.

In both studies, antibody titres were low and there was no evidence of an impact on pharmacokineticsor pharmacodynamics and no clinically meaningful impact on efficacy or safety.

In MG0010 and MG0011, 2 patients (2.4%) each in the zilucoplan/zilucoplan and placebo/zilucoplangroup were positive for treatment emergent ADA and anti-PEG antibodies. Thirteen subjects (16%)per arm were treatment emergent anti-PEG antibody positive while ADA negative. Two patients(2.4%) per arm were anti-PEG negative while treatment emergent ADA positive.

The European Medicines Agency has deferred the obligation to submit the results of studies withzilucoplan in one or more subsets of the paediatric population in the treatment of myasthenia gravis.

See section 4.2 for information on paediatric use.

Following single and multiple daily subcutaneous administration of the zilucoplan recommended dose(Table 1) in healthy subjects, zilucoplan reached peak plasma concentration generally between 3 to6 hours post-dose.

In study MG0010 in patients with gMG, after daily repeated subcutaneous administration of thezilucoplan recommended dose (Table 1), plasma concentrations of zilucoplan were consistent, withsteady state trough concentrations being reached by week 4 and maintained through week 12.

Exposures after subcutaneous administration of single zilucoplan doses in the abdomen, thigh, orupper arm were comparable.

Zilucoplan and the active (RA103488) and major inactive (RA102758) circulating metabolites arehighly bound to plasma proteins (> 99%). The mean volume of distribution for zilucoplan (Vc/F)using a population pharmacokinetic analysis is 3.51 L. Zilucoplan is not a substrate for common drugtransporters.

Zilucoplan is not a substrate of major CYP enzymes. In plasma, 2 metabolites, the active (RA103488)and major inactive metabolite (RA102758) were detected. The formation of RA103488 is mainly dueto cytochrome CYP450 4F2. RA103488 has pharmacological activity similar to zilucoplan but ispresent at a much lower concentration compared to zilucoplan. The contribution of RA103488 topharmacological activity is low. Further, as a peptide, zilucoplan is expected to be degraded intosmaller peptides and amino acids via catabolic pathways.

Zilucoplan inhibits MRP3 in vitro at therapeutic concentrations; the clinical relevance of thisinhibition is unknown.

As a peptide, zilucoplan is expected to be degraded into smaller peptides and amino acids via catabolicpathways. The mean plasma terminal elimination half-life was approximately 172 hours (7-8 days).

The half-life was 220 hours and 96 hours respectively for the active (RA103488) and major inactivemetabolite (RA102758). The excretion of zilucoplan and its metabolites (RA103488 and RA102758)measured in both urine and faeces was negligible. The pegylated part of zilucoplan is anticipated to beexcreted mainly via the kidneys and the main degradation of fatty acid part is via β-oxidation toacetyl-CoA.

In the population pharmacokinetic analysis (doses corresponding to 0.05 to 0.6 mg/kg), zilucoplanpharmacokinetics is characterised by target dependent drug disposition with less than doseproportional increase in exposure with increasing doses, and after multiple doses compared to singledose.

Antibodies

The incidences of ADA and anti-PEG antibodies in the phase 3 study in patients with gMG werecomparable between the zilucoplan treatment group and the placebo treatment group (see section 5.1).

The ADA and anti-PEG antibody status of patients treated with zilucoplan did not affect zilucoplanconcentrations.

Weight

Population pharmacokinetic analysis on data collected across studies in gMG showed that body weightsignificantly influences the pharmacokinetics of zilucoplan. Zilucoplan dosing is based on bodyweight categories (see section 4.2), no further dose adjustment is needed.

Based on population pharmacokinetic analysis, age did not influence the pharmacokinetics ofzilucoplan. No dose adjustment is required.

The effect of renal impairment on the pharmacokinetics of zilucoplan and its metabolites was studiedin an open-label phase 1 study, where a single-dose of the zilucoplan recommended dose (Table 1)was administered to healthy subjects and subjects with severe renal impairment (creatinine clearancebetween 15 and <30 mL/min).

Systemic exposure to zilucoplan and the major inactive metabolite RA102758 was not different insubjects with severe renal impairment compared to subjects with normal renal function. The exposureto the active metabolite RA103488 was approximately 1.5-fold higher in subjects with severe renalimpairment compared to subjects with normal renal function.

Based on the pharmacokinetic results, no dose adjustment is required in patients with renalimpairment.

The effects of moderate hepatic impairment (as defined by a Child-Pugh score between 7 and 9) on thepharmacokinetics of zilucoplan and its metabolites were studied in an open-label phase 1 study, wherea single dose of the zilucoplan recommended dose (Table 1) was administered to healthy subjects andsubjects with moderate hepatic impairment.

Systemic exposure to zilucoplan was 24% lower in subjects with moderate impaired liver functioncompared to healthy subjects, which was in line with a higher systemic and peak exposures of bothmetabolites in subjects with hepatic impairment compared to healthy subjects. Zilucoplan peakexposure as well as terminal half-life were comparable between both groups. Furtherpharmacodynamic analysis did not identify meaningful differences in complement levels or inhibitionof complement activity between both groups. Based on these results, no dose adjustment is required inpatients with mild and moderate hepatic impairment.

Racial and ethnic groups

In a phase 1 clinical study in healthy Caucasian and Japanese subjects, the pharmacokinetic profile ofzilucoplan and its two metabolites (RA102758 and RA103488) was compared following a single dose(Table 1) and after multiple dosing for 14 days. Results were generally similar between both groups.

The population pharmacokinetic analysis for zilucoplan showed that there are no differences betweenthe different race categories (Black/African American, Asian/Japanese, and Caucasians). No doseadjustment is required.

In the population pharmacokinetic analysis, no difference in pharmacokinetics between genders wasobserved. No dose adjustment is required.

In repeat-dose toxicity studies performed in non-human primates, there were vesiculardegeneration/hyperplasia of epithelial cells and mononuclear cell infiltrates in various tissues atclinically relevant exposure. In the pancreas, this sometimes manifested as pancreatic acinar celldegeneration, some with fibrosis and ductal degeneration/regeneration and was accompanied withincreased plasma concentrations of amylase and lipase. In female reproductive organs (vagina, cervix,uterus), mononuclear cell infiltrates with epithelial degeneration and cervical squamous metaplasiawere seen. In a monkey male fertility study, minimal to slight germ line degeneration/depletion wasobserved at clinically relevant exposures but severity did not increase with dose. No impact onspermatogenesis was observed.The findings in non-human primates are of uncertain clinical relevanceand some are possibly related to infections secondary to the pharmacological effect of zilucoplan, butother mechanisms cannot be excluded. The findings did not correlate with any effects on embryofetaldevelopment or pregnancy outcomes (pregnancy loss, parturition, pregnancy outcomes, or infant post-natal development) in non-human primates at similar dose levels.

No carcinogenicity studies were conducted with zilucoplan.

Sodium dihydrogen phosphate, monohydrate

Disodium phosphate (anhydrous)

Sodium chloride

Water for injections

Not applicable

3 years

Store in a refrigerator (2 °C-8 °C).

Do not freeze.

Keep the pre-filled syringe in the outer carton in order to protect from light.

Patients may store the pre-filled syringe at room temperature in the original carton up to 30 °C for asingle period of maximum 3 months. Once Zilbrysq has been stored at room temperature, it should notbe placed back into the refrigerator and should be discarded if not used within the 3 months period orby the expiry date, whichever occurs first.

Pre-filled syringe (type I glass) with a 29G ½” thin wall needle closed with a greyfluoropolymer-laminated bromobutyl rubber plunger stopper. The needle is protected with a rigidneedle shield consisting of a thermoplastic elastomer needle shield and a polypropylene rigid shield.

Each pre-filled syringe is pre-assembled with a needle safety device, a finger grip and a colouredplunger:

Zilbrysq 16.6 mg solution for injection in pre-filled syringe0.416 mL solution for injection in pre-filled syringe with rubine red plunger

Zilbrysq 23 mg solution for injection in pre-filled syringe0.574 mL solution for injection in pre-filled syringe with orange plunger

Zilbrysq 32.4 mg solution for injection in pre-filled syringe0.810 mL solution for injection in pre-filled syringe with dark blue plunger

Pack size of 7 pre-filled syringes for 16.6 mg, 23 mg and 32.4 mg solution for injection.

Multipack containing 28 (4 packs of 7) pre-filled syringes.

Not all pack sizes may be marketed.

Any unused medicinal product or waste material should be disposed of in accordance with localrequirements.

UCB Pharma S.A.

Allée de la Recherche 60

B-1070 Bruxelles

Belgium

Zilbrysq 16.6 mg solution for injection in pre-filled syringe

EU/1/23/1764/001

EU/1/23/1764/002

Zilbrysq 23 mg solution for injection in pre-filled syringe

EU/1/23/1764/003

EU/1/23/1764/004

Zilbrysq 32.4 mg solution for injection in pre-filled syringe

EU/1/23/1764/005

EU/1/23/1764/006

Date of first authorisation: 01 December 2023

Detailed information on this medicinal product is available on the website of the European Medicines

Agency http://www.ema.europa.eu.