Leaflet ESMYA 5mg tablets

Product code: W61258001 Quantity: 28

Indicated for: contraception

Route of administration: oral

Substance: ulipristal acetate (hormonal contraceptive)

ATC: G03XB02 (Genito urinary system and sex hormones | Other sex hormones and modulators of the genital system | Progesterone receptor modulators)

Precautions:
Breastfeeding warning
Breastfeeding warning

Use during breastfeeding only on medical advice.

Pregnancy warning
Pregnancy warning

Use during pregnancy only on medical advice.

Ulipristal acetate is a medication primarily used for the treatment of uterine fibroids and as an emergency contraceptive. It is a selective progesterone receptor modulator (SPRM) that works by inhibiting the activity of progesterone, a hormone essential for fibroid growth and ovulation.

In the treatment of uterine fibroids, ulipristal is administered orally, usually in courses lasting several months, to reduce the size of fibroids and associated symptoms such as heavy bleeding and pelvic pain. As an emergency contraceptive, it is used to prevent pregnancy after unprotected sexual intercourse if taken within 120 hours.

Common side effects include headache, nausea, abdominal discomfort, and changes in the menstrual cycle. In rare cases, allergic reactions or liver function impairment may occur.

Ulipristal acetate is an effective and versatile medication used both in the management of uterine fibroids and as a method of emergency contraception.

General data about ESMYA 5mg

  • Substance: ulipristal acetate
  • Date of latest medicines list: 01-03-2025
  • Product code: W61258001
  • Concentration: 5mg
  • Pharmaceutical form: tablets
  • Quantity: 28
  • Product type: Original
  • Prescription status: P-RF - Medicines dispensed with a medical prescription that is retained by the pharmacy and cannot be renewed.

Marketing authorisation

  • Manufacturer: CENEXI - FRANTA
  • Holder: GEDEON RICHTERPLC - UNGARIA
  • Number: 750/2012/01
  • Shelf life: 2 years

Pharmaceutical forms available for ulipristal acetate

Concentrations available for ulipristal acetate

  • 30mg
  • 5mg

Contents of the package leaflet for the medicine ESMYA 5mg tablets

1. NAME OF THE MEDICINAL PRODUCT

Esmya 5 mg tablets

2. QUALITATIVE AND QUANTITATIVE COMPOSITION

Each tablet contains 5 mg of ulipristal acetate.

For the full list of excipients, see section 6.1.

3. PHARMACEUTICAL FORM

Tablet.

White to off-white, round biconvex tablet of 7 mm engraved with “ES5” on one face.

4. CLINICAL PARTICULARS

4.1 Therapeutic indications

Ulipristal acetate is indicated for intermittent treatment of moderate to severe symptoms of uterinefibroids in adult women who have not reached menopause when uterine fibroid embolisation and/orsurgical treatment options are not suitable or have failed.

4.2 Posology and method of administration

Esmya treatment is to be initiated and supervised by physicians experienced in the diagnosis andtreatment of uterine fibroids.

Posology

The treatment consists of one tablet of 5 mg to be taken once daily for treatment courses of up to3 months each. Tablets may be taken with or without food.

Treatments should only be initiated when menstruation has occurred:

- The first treatment course should start during the first week of menstruation.

- Re-treatment courses should start at the earliest during the first week of the second menstruationfollowing the previous treatment course completion.

The treating physician should explain to the patient the requirement for treatment free intervals.

Repeated intermittent treatment has been studied up to 4 intermittent courses.

If a patient misses a dose, the patient should take ulipristal acetate as soon as possible. If the dose wasmissed by more than 12 hours, the patient should not take the missed dose and simply resume theusual dosing schedule.

Special population

Renal impairment

No dose adjustment is recommended in patients with mild or moderate renal impairment. In theabsence of specific studies, ulipristal acetate is not recommended in patients with severe renalimpairment unless the patient is closely monitored (see sections 4.4 and 5.2).

Paediatric population

There is no relevant use of ulipristal acetate in the paediatric population. The safety and efficacy ofulipristal acetate was only established in women of 18 years and older.

Method of administration

Medicinal product no longer authorised

Oral use. Tablets should be swallowed with water.

4.3 Contraindications

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

Pregnancy and breastfeeding.

Genital bleeding of unknown aetiology or for reasons other than uterine fibroids.

Uterine, cervical, ovarian or breast cancer.

Underlying hepatic disorder.

4.4 Special warnings and precautions for use

Ulipristal acetate should only be prescribed after careful diagnosis. Pregnancy should be precludedprior to treatment. If pregnancy is suspected prior to initiation of a new treatment course, a pregnancytest should be performed.

Contraception

Concomitant use of progestagen-only pills, a progestagen-releasing intrauterine device or combinedoral contraceptive pills is not recommended (see section 4.5). Although a majority of women taking atherapeutic dose of ulipristal acetate have anovulation, a non hormonal contraceptive method isrecommended during treatment.

Endometrial changes

Ulipristal acetate has a specific pharmacodynamic action on the endometrium:

Changes in the histology of the endometrium may be observed in patients treated with ulipristalacetate. These changes are reversible after treatment cessation.

These histological changes are denoted as “Progesterone Receptor Modulator Associated Endometrial

Changes” (PAEC) and should not be mistaken for endometrial hyperplasia (see sections 4.8 and 5.1).

In addition, reversible increase of the endometrium thickness may occur under treatment.

In case of repeated intermittent treatment, periodic monitoring of the endometrium is recommended.

This includes annual ultrasound to be performed after resumption of menstruation during off-treatmentperiod.

If endometrial thickening is noted, which persists after return of menstruations during off-treatmentperiods or beyond 3 months following the end of treatment courses, and/or an altered bleeding patternis noted (see section 'Bleeding pattern' below), investigation including endometrial biopsy should beperformed in order to exclude other underlying conditions, including endometrial malignancy.

In case of hyperplasia (without atypia), monitoring as per usual clinical practice (e.g. a follow-upcontrol 3 months later) would be recommended. In case of atypical hyperplasia, investigation andmanagement as per usual clinical practice should be performed.

The treatment courses should each not exceed 3 months as the risk of adverse impact on theendometrium is unknown if treatment is continued without interruption.

Bleeding pattern

Patients should be informed that treatment with ulipristal acetate usually leads to a significantreduction in menstrual blood loss or amenorrhea within the first 10 days of treatment. Should theexcessive bleeding persist, patients should notify their physician. Menstrual periods generally returnwithin 4 weeks after the end of each treatment course.

If, during repeated intermittent treatment, after the initial reduction in bleeding or amenorrhea, analtered persistent or unexpected bleeding pattern occurs, such as inter-menstrual bleeding,investigation of the endometrium including endometrial biopsy should be performed in order toexclude other underlying conditions, including endometrial malignancy.

Medicinal product no longer authorised

Repeated intermittent treatment has been studied up to 4 intermittent treatment courses.

Renal impairment

Renal impairment is not expected to significantly alter the elimination of ulipristal acetate. In theabsence of specific studies, ulipristal acetate is not recommended for patients with severe renalimpairment unless the patient is closely monitored (see section 4.2).

Hepatic injury

During the post-marketing experience, cases of liver injury and hepatic failure, some requiring livertransplantation have been reported (see section 4.3).

Liver function tests must be performed before starting treatment. Treatment must not be initiated iftransaminases (alanine transaminase (ALT) or aspartate aminotransferase (AST)) exceed 2 x ULN(isolated or in combination with bilirubin >2 x ULN).

During treatment, liver function tests must be performed monthly during the first 2 treatment courses.

For further treatment courses, liver function must be tested once before each new treatment course andwhen clinically indicated.

If a patient during treatment shows signs or symptoms compatible with liver injury (fatigue, asthenia,nausea, vomiting, right hypochondrial pain, anorexia, jaundice), treatment should be stopped and thepatient should be investigated immediately, and liver function tests performed.

Patients who develop transaminase levels (ALT or AST) > 3 times the upper limit of normal duringtreatment should stop treatment and be closely monitored.

In addition liver testing should be performed 2- 4 weeks after treatment has stopped.

Concomitant treatments

Co-administration of moderate (e.g. erythromycin, grapefruit juice, verapamil) or potent (e.g.ketoconazole, ritonavir, nefazodone, itraconazole, telithromycin, clarithromycin) CYP3A4 inhibitorsand ulipristal acetate is not recommended (see section 4.5).

Concomitant use of ulipristal acetate and potent CYP3A4 inducers (e.g. rifampicin, rifabutin,carbamazepine, oxcarbazepine, phenytoin, fosphenytoin, phenobarbital, primidone, St John´s wort,efavirenz, nevirapine, long term use of ritonavir) is not recommended (see section 4.5).

Asthma patients

Use in women with severe asthma insufficiently controlled by oral glucocorticoids is notrecommended.

4.5 Interaction with other medicinal products and other forms of interaction

Potential for other medicinal products to affect ulipristal acetate:

Hormonal contraceptives

Ulipristal acetate has a steroid structure and acts as a selective progesterone receptor modulator withpredominantly inhibitory effects on the progesterone receptor. Thus hormonal contraceptives andprogestagens are likely to reduce ulipristal acetate efficacy by competitive action on the progesteronereceptor. Therefore concomitant administration of medicinal products containing progestagen is notrecommended (see section 4.4 and 4.6).

CYP3A4 inhibitors

Following administration of the moderate CYP3A4 inhibitor erythromycin propionate (500 mg twicedaily for 9 days) to healthy female volunteers, Cmax and AUC of ulipristal acetate increased 1.2 and2.9 fold, respectively; the AUC of the active metabolite of ulipristal acetate increased 1.5 fold whilethe Cmax of the active metabolite decreased (0.52 fold change).

Following administration of the potent CYP3A4 inhibitor ketoconazole (400 mg once daily for 7 days)to healthy female volunteers, Cmax and AUC of ulipristal acetate increased 2 and 5.9 fold, respectively;

Medicinal prodct no longer authorisedthe AUC of the active metabolite of ulipristal acetate increased 2.4 fold while the Cmax of the activemetabolite decreased (0.53 fold change).

No dose adjustment is considered necessary for administration of ulipristal acetate to patientsreceiving concomitant mild CYP3A4 inhibitors. Co-administration of moderate or potent CYP3A4inhibitors and ulipristal acetate is not recommended (see section 4.4).

CYP3A4 inducers

Administration of the potent CYP3A4 inducer rifampicin (300 mg twice daily for 9 days) to healthyfemale volunteers markedly decreased Cmax and AUC of ulipristal acetate and its active metabolite by90% or more and decreased ulipristal acetate half-life by 2.2-fold corresponding to an approximately10-fold decrease of ulipristal acetate exposure. Concomitant use of ulipristal acetate and potent

CYP3A4 inducers (e.g. rifampicin, rifabutin, carbamazepine, oxcarbazepine, phenytoin, fosphenytoin,phenobarbital, primidone, St John´s wort, efavirenz, nevirapine, long term use of ritonavir) is notrecommended (see section 4.4).

Medicinal products affecting gastric pH

Administration of ulipristal acetate (10 mg tablet) together with the proton pump inhibitoresomeprazole (20 mg daily for 6 days) resulted in approximately 65% lower mean Cmax, a delayed tmax(from a median of 0.75 hours to 1.0 hours) and 13% higher mean AUC. This effect of medicinalproducts that increase gastric pH is not expected to be of clinical relevance for daily administration ofulipristal acetate tablets.

Potential for ulipristal acetate to affect other medicinal products:

Hormonal contraceptives

Ulipristal acetate may interfere with the action of hormonal contraceptive medicinal products(progestagen only, progestagen releasing devices or combined oral contraceptive pills) andprogestagen administered for other reasons. Therefore concomitant administration of medicinalproducts containing progestagen is not recommended (see sections 4.4 and 4.6). Medicinal productscontaining progestagen should not be taken within 12 days after cessation of ulipristal acetatetreatment.

P-gp substrates

In vitro data indicate that ulipristal acetate may be an inhibitor of P-gp at clinically relevantconcentrations in the gastrointestinal wall during absorption.

Simultaneous administration of ulipristal acetate and a P-gp substrate has not been studied and aninteraction cannot be excluded. In vivo results show that ulipristal acetate (administered as a single10 mg tablet) 1.5 hour before administration of the P-gP substrate fexofenadine (60 mg) has noclinically relevant effects on the pharmacokinetic of fexofenadine. It is therefore recommended thatco-administration of ulipristal acetate and P-gp substrates (e.g. dabigatran etexilate, digoxin,fexofenadine) should be separated in time by at least 1.5 hours.

4.6 Fertility, pregnancy and lactation

Contraception in females

Ulipristal acetate is likely to adversely interact with progestagen-only pills, progestagen-releasingdevices or combined oral contraceptive pills, therefore, concomitant use is not recommended.

Although a majority of women taking a therapeutic dose of ulipristal acetate have anovulation, a nonhormonal contraceptive method is recommended during treatment (see sections 4.4 and 4.5).

Pregnancy

Ulipristal acetate is contraindicated during pregnancy (see section 4.3).

There are no or limited amount of data from the use of ulipristal acetate in pregnant women.

Although no teratogenic potential was observed, animal data are insufficient with regard toreproduction toxicity (see section 5.3).

Medicinal productlonger authorised

Breastfeeding

Available toxicological data in animals have shown excretion of ulipristal acetate in milk (for detailssee section 5.3). Ulipristal acetate is excreted in human milk. The effect on newborn/infants has notbeen studied. A risk to the newborns/infants cannot be excluded. Ulipristal acetate is contraindicatedduring breastfeeding (see sections 4.3 and 5.2).

Fertility

A majority of women taking a therapeutic dose of ulipristal acetate have anovulation, however, thelevel of fertility while taking multiple doses of ulipristal acetate has not been studied.

4.7 Effects on ability to drive and use machines

Ulipristal acetate may have minor influence on the ability to drive or use machines as mild dizzinesshas been observed after ulipristal acetate intake.

4.8 Undesirable effects

Summary of the safety profile

The safety of ulipristal acetate has been evaluated in 1,053 women with uterine fibroids treated with5 mg or 10 mg ulipristal acetate during Phase III studies. The most common finding in clinical trialswas amenorrhea (79.2%), which is considered as a desirable outcome for the patients (see section 4.4).

The most frequent adverse reaction was hot flush. The vast majority of adverse reactions were mildand moderate (95.0%), did not lead to discontinuation of the medicinal product (98.0%) and resolvedspontaneously.

Among these 1,053 women, the safety of repeated intermittent treatment courses (each limited to3 months) has been evaluated in 551 women with uterine fibroids treated with 5 or 10 mg ulipristalacetate in two phase III studies (including 446 women exposed to four intermittent treatment coursesof whom 53 were exposed to eight intermittent treatment courses) and demonstrated a similar safetyprofile to that observed for one treatment course.

Tabulated list of adverse reactions

Based on pooled data from four phase III studies in patients with uterine fibroids treated for 3 months,the following adverse reactions have been reported. Adverse reactions listed below are classifiedaccording to frequency and system organ class. Within each frequency grouping, adverse reactions arepresented in order of decreasing seriousness. Frequencies are defined as 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) and not known (cannot be estimated from available data).

Medicinal pr duct no longer authorised

Adverse reactions during treatment course 1

System Organ Very common Common Uncommon Rare Frequency

Class Not known

Immune system Drugdisorders hypersensitivity*

Psychiatric Anxietydisorders Emotional disorder

Nervous system Headache* Dizzinessdisorders

Ear and labyrinth Vertigodisorders

Respiratory, Epistaxisthoracic andmediastinaldisorders

Gastrointestinal Abdominal pain Dry mouth Dyspepsiadisorders Nausea Constipation Flatulence

Hepatobiliary Hepaticdisorders failure*

Skin and Acne Alopecia** Angioedemasubcutaneous Dry skintissue disorders Hyperhidrosis

Musculoskeletal Musculoskeletal Back painand connective paintissue disorders

Renal and urinary Urinarydisorders incontinence

Reproductive Amenorrhea Hot flush* Uterine Ovarian cystsystem and breast Endometrial Pelvic pain haemorrhage* ruptured*disorders thickening* Ovarian cyst* Metrorrhagia Breast swelling

Breast Genital dischargetenderness/pain Breast discomfort

General disorders Fatigue Oedemaand administration Astheniasite conditions

Investigations Weight increased Blood cholesterolincreased

Blood triglyceridesincreased

* see section 'Description of selected adverse reactions'

** The verbatim term “mild hair loss” was coded to the term “alopecia”

When comparing repeated treatment courses, overall adverse reactions rate was less frequent insubsequent treatment courses than during the first one and each adverse reaction was less frequent orremained in the same frequency category (except for dyspepsia which was classified as uncommon intreatment course 3 based on one patient occurence).

Description of selected adverse reactions

Hepatic failure

During the post-marketing experience, cases of hepatic failure have been reported. In a small numberof these cases, liver transplantation was required. The frequency of occurrence of hepatic failure andpatient risk factors are unknown.

Medicinal product o longer authorised

Endometrial thickening

In 10-15% of patients, thickening of the endometrium (> 16 mm by ultrasound or MRI at end oftreatment) was observed with ulipristal acetate by the end of the first 3-month treatment course. Insubsequent treatment courses, endometrial thickening was less frequently observed (4.9% and 3.5% ofpatients by the end of second and fourth treatment course, respectively). The endometrial thickeningreverses when treatment is stopped and menstrual periods resume.

In addition, reversible changes to the endometrium are denoted PAEC and are different fromendometrial hyperplasia. If hysterectomy or endometrial biopsy specimens are sent for histology, thenthe pathologist should be informed that the patient has taken ulipristal acetate (see sections 4.4and 5.1).

Hot flush

Hot flushes were reported by 8.1% of patients but the rates varied across trials. In the activecomparator controlled study the rates were 24% (10.5% moderate or severe) for ulipristal acetate and60.4% (39.6% moderate or severe) for leuprorelin-treated patients. In the placebo-controlled study, therate of hot flushes was 1.0% for ulipristal acetate and 0% for placebo. In the first 3-month treamentcourse of the two long term Phase III trials, the frequency was 5.3% and 5.8% for ulipristal acetate,respectively.

Drug hypersensitivity

Drug hypersensitivity symptoms such as generalised oedema, pruritus, rash, swelling face or urticariawere reported by 0.4% of patients in Phase III trials.

Headache

Mild or moderate severity headache was reported in 5.8% of patients.

Ovarian cyst

Functional ovarian cysts were observed during and after treatment in 1.0% of patients and in most ofthe cases spontaneously disappeared within a few weeks.

Uterine haemorrhage

Patients with heavy menstrual bleeding due to uterine fibroids are at risk of excessive bleeding, whichmay require surgical intervention. A few cases have been reported during ulipristal acetate treatmentor within 2-3 months after ulipristal acetate treatment was stopped.

Reporting of suspected adverse reactions

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.

4.9 Overdose

Experience with ulipristal acetate overdose is limited.

Single doses up to 200 mg and daily doses of 50 mg for 10 consecutive days were administered to alimited number of subjects, and no severe or serious adverse reactions were reported.

5. PHARMACOLOGICAL PROPERTIES

5.1 Pharmacodynamic properties

Pharmacotherapeutic group: Sex hormones and modulators of the genital system, progesteronereceptor modulators. ATC code: G03XB02.

Medicinal roduct no longer authorised

Ulipristal acetate is an orally-active synthetic selective progesterone receptor modulator characterisedby a tissue-specific partial progesterone antagonist effect.

Mechanism of action

Ulipristal acetate exerts a direct effect on the endometrium.

Ulipristal acetate exerts a direct action on fibroids reducing their size through inhibition of cellproliferation and induction of apoptosis.

Pharmacodynamic effects

Endometrium

When daily administration of a 5 mg dose is commenced during a menstrual cycle most subjects(including patients with myoma) will complete their first menstruation but will not menstruate againuntil after treatment is stopped. When ulipristal acetate treatment is stopped, menstrual cyclesgenerally resume within 4 weeks.

The direct action on the endometrium results in class-specific changes in histology termed PAEC.

Typically, the histological appearance is an inactive and weakly proliferating epithelium associatedwith asymmetry of stromal and epithelial growth resulting in prominent cystically dilated glands withadmixed oestrogen (mitotic) and progestin (secretory) epithelial effects. Such a pattern has beenobserved in approximately 60% of patients treated with ulipristal acetate for 3 months. These changesare reversible after treatment cessation. These changes should not be confused with endometrialhyperplasia.

About 5% of patients of reproductive age experiencing heavy menstrual bleeding have an endometrialthickness of greater than 16 mm. In about 10-15% of patients treated with ulipristal acetate theendometrium may thicken (> 16 mm) during the first 3-month treatment course. In case of repeatedtreatment courses, endometrial thickening was less frequently observed (4.9% of patients after secondtreatment course and 3.5% after fourth treatment course). This thickening disappears after treatment iswithdrawn and menstruation occurs. If endometrial thickness persists after return of menstruationsduring off-treatment periods or beyond 3 months following the end of treatment courses, it may needto be investigated as per usual clinical practice to exclude other underlying conditions.

Pituitary

A daily dose of ulipristal acetate 5 mg inhibits ovulation in the majority of patients as indicated byprogesterone levels maintained at around 0.3 ng/ml.

A daily dose of ulipristal acetate 5 mg partially suppresses FSH levels but serum oestradiol levels aremaintained in the mid-follicular range in the majority of patients and are similar to levels in patientswho received placebo.

Ulipristal acetate does not affect serum levels of TSH, ACTH or prolactin.

Clinical efficacy and safety

Pre-operative use:

The efficacy of fixed doses of ulipristal acetate 5 mg and 10 mg once daily was evaluated in two

Phase 3 randomised, double-blind, 13 week studies recruiting patients with very heavy menstrualbleeding associated with uterine fibroids. Study 1 was double-blind placebo controlled. Patients in thisstudy were required to be anaemic at Study entry (Hb < 10.2 g/dl) and all patients were to receive oraliron 80 mg Fe++ in addition to study medicinal product. Study 2 contained the active comparator,leuprorelin 3.75 mg given once per month by intramuscular injection. In Study 2, a double-dummymethod was used to maintain the blind. In both studies menstrual blood loss was assessed using the

Pictorial Bleeding Assessment Chart (PBAC). A PBAC >100 within the first 8 days of menses isconsidered to represent excessive menstrual blood loss.

Medicinal product no longer authorised

In study 1, a statistically significant difference was observed in reduction in menstrual blood loss infavour of the patients treated with ulipristal acetate compared to placebo (see Table 1 below), resultingin faster and more efficient correction of anaemia than iron alone. Likewise, patients treated withulipristal acetate had a greater reduction in myoma size, as assessed by MRI.

In study 2, the reduction in menstrual blood loss was comparable for the patients treated with ulipristalacetate and the gonadotrophin releasing hormone-agonist (leuprorelin). Most patients treated withulipristal acetate stopped bleeding within the first week of treatment (amenorrhea).

The size of the three largest myomas was assessed by ultrasound at the end of treatment (Week 13)and for another 25 weeks without treatment in patients who did not have hysterectomy ormyomectomy performed. Myoma size reduction was generally maintained during this follow-upperiod in patients originally treated with ulipristal acetate but some re-growth occurred in patientstreated with leuprorelin.

Table 1: Results of primary and selected secondary efficacy assessments in Phase III studies

Study 1 Study 2

Parameter Placebo Ulipristal Ulipristal Leuprorelin Ulipristal Ulipristalacetate acetate 3.75 mg/ acetate acetate5 mg/day 10 mg/day month 5 mg/day 10 mg/day

N=48 N=95 N=94 N=93 N=93 N=95

Menstrualbleeding

Median PBAC at 376 386 330 297 286 271baseline

Median change at -59 -329 -326 -274 -268 -268week 13

Patients inamenorrhea at 3 69 76 741 2 70 (75.3%) 85 (89.5%)week 13 (6.3%) (73.4%) (81.7%) (80.4%)

Patients whosemenstrualbleeding became 9 86 86 82normal (PBAC < (18.8%) (91.5%) (92.5%)1 (89.1%) 84 (90.3%) 93 (97.9%)75) at week 13

Median change inmyoma volume 3from baseline to +3.0% -21.2% -12.3%4 -53.5% -35.6% -42.1%week 13aa In Study 1, change from baseline in total myoma volume was measured by MRI. In Study 2, change in the volume of thethree largest myomas was measured by ultrasound. Bold values in shaded squares indicate that there was a significantdifference in the comparisons between ulipristal acetate and the control. These were always in favour of ulipristal acetate.

P values: 1 = <0.001, 2 = 0.037, 3= <0.002, 4 = <0.006.

Repeated intermittent use:

The efficacy of repeated treatment courses fixed doses of ulipristal acetate 5 mg or 10 mg once dailywas evaluated in two Phase 3 studies assessing up to 4 intermittent 3-month treatment courses inpatients with heavy menstrual bleeding associated with uterine fibroids. Study 3 was on open-labelstudy assessing ulipristal acetate 10 mg, where each of the 3-month treatment was followed by 10 daysof double-blind treatment with progestin or placebo. Study 4 was a randomized, double-blind clinicalstudy assessing ulipristal acetate 5 or 10 mg.

Studies 3 and 4 showed efficacy in controlling uterine fibroid symptoms (e.g. uterine bleeding) andreducing fibroid size after 2 and 4 courses.

Medicinal product no longer authorised

In study 3, treatment efficacy has been shown over > 18 months of repeated intermittent treatment(4 courses of 10 mg once daily), 89.7% of patients were in amenorrhea at the end of the treatmentcourse 4.

In study 4, 61.9% and 72.7% of patients were in amenorrhea at the end of both treatmentcourse 1 and 2 combined (5 mg dose and 10 mg dose, respectively, p=0.032); 48.7 % and 60.5 % werein amenorrhea at the end of all four treatment courses combined (5 mg dose and 10 mg dose,respectively, p=0.027). At the end of treatment course 4, 158 (69.6%) subjects and 164 (74.5%)subjects were assessed as being in amenorrhea, in the 5 mg dose and 10 mg dose respectively(p=0.290).

Table 2: Results of primary and selected secondary efficacy assessments in long term Phase III studies

Parameter After treatment course 2 After treatment course 4(two times 3 months of treatment) (four times 3 months of treatment)

Study 3a Study 4 Study 3 Study 4

Patients starting 10 mg/day 5 mg/day 10 mg/day 10 mg/day 5 mg/day 10 mg/daytreatment N=132 N=213 N=207 N=107 N=178 N=176course 2 or 4

Patients in N=131 N=205 N=197 N=107 N=227 N=220amenorrheab,c 116 152 162 96 158 164(88.5%) (74.1%) (82.2%) (89.7%) (69.6%) (74.5%)

Patients with NA N=199 N=191 NA N=202 N=192controlled 175 168 148 144bleedingb,c, d (87.9%) (88.0%) (73.3%) (75.0%)

Median change -63.2% -54.1% -58.0% -72.1% -71.8% -72.7%in myomavolume frombaselinea Treatment course 2 assessment corresponds to Treatment course 2 plus one menstrual bleeding.b Patients with missing values were exluded from the analysis.c N and % include withdrawn patientsd Controlled bleeding was defined as no episodes of heavy bleeding and a maximum of 8 days of bleeding (not includingdays of spotting) during the last 2 months of a treatment course.

In all Phase III studies including repeated intermittent treatment studies, a total of 7 cases ofhyperplasia were observed out of 789 patients with adequate biopsies (0.89%). The vast majorityspontaneously reversed to normal endometrium after resumption of menstruation during theoff-treatment period. The incidence of hyperplasia did not increase with repeated treatment courses,including data on 340 women who received up to 4 courses of ulipristal acetate 5 or 10 mg and limiteddata of 43 women who received up to 8 courses of ulipristal acetate 10 mg. The observed frequency isin line with control groups and prevalence reported in literature for symptomatic pre-menopausalwomen of this age group (mean of 40 years).

Paediatric population

The European Medicines Agency has waived the obligation to submit the results of studies with

Esmya in all subsets of the paediatric population in leiomyoma of uterus (see section 4.2 forinformation on paediatric use).

5.2 Pharmacokinetic properties

Absorption

Following oral administration of a single dose of 5 or 10 mg, ulipristal acetate is rapidly absorbed,with a Cmax of 23.5 ± 14.2 ng/ml and 50.0 ± 34.4 ng/ml occurring approximately 1 h after ingestion,and with an AUC0-∞ of 61.3 ± 31.7 ng.h/ml and 134.0 ± 83.8 ng.h/ml, respectively. Ulipristal acetate israpidly transformed into a pharmacologically active metabolite with a Cmax of 9.0 ± 4.4 ng/ml and

Medicinal product no longer autho ised20.6 ± 10.9 ng/ml also occurring approximately 1 h after ingestion, and with an AUC0-∞ of26.0 ± 12.0 ng.h/ml and 63.6 ± 30.1 ng.h/ml respectively.

Administration of ulipristal acetate (30 mg tablet) together with a high-fat breakfast resulted inapproximately 45% lower mean Cmax, a delayed tmax (from a median of 0.75 hours to 3 hours) and 25%higher mean AUC0-∞ compared with administration in the fasted state. Similar results were obtainedfor the active mono-N-demethylated metabolite. This kinetic effect of food is not expected to be ofclinical relevance for daily administration of ulipristal acetate tablets.

Distribution

Ulipristal acetate is highly bound (>98%) to plasma proteins, including albumin, alpha-l-acidglycoprotein, high density lipoprotein and low density lipoprotein.

Ulipristal acetate and its active mono-N-demethylated metabolite are excreted in breast milk with amean AUCt milk/plasma ratio of 0.74 ± 0.32 for ulipristal acetate.

Biotransformation/Elimination

Ulipristal acetate is readily converted to its mono-N-demethylated and subsequently to itsdi-N-demethylated metabolites. In vitro data indicate that this is predominantly mediated by thecytochrome P450 3A4 isoform (CYP3A4). The main route of elimination is through faeces and lessthan 10% is excreted in the urine. The terminal half-life of ulipristal acetate in plasma following asingle dose of 5 or 10 mg is estimated to be about 38 hours, with a mean oral clearance (CL/F) ofabout 100 l/h.

In vitro data indicate that ulipristal acetate and its active metabolite do not inhibit CYP1A2, 2A6, 2C9,2C19, 2D6, 2E1, and 3A4, or induce CYP1A2 at clinically relevant concentrations. Thusadministration of ulipristal acetate is unlikely to alter the clearance of medicinal products that aremetabolised by these enzymes.

In vitro data indicate that ulipristal acetate and its active metabolite are not P-gp (ABCB1) substrates.

Special populations

No pharmacokinetic studies with ulipristal acetate have been performed in women with impaired renalor hepatic function. Due to the CYP-mediated metabolism, hepatic impairment is expected to alter theelimination of ulipristal acetate, resulting in increased exposure. Esmya is contraindicated in patientswith hepatic disorder (see section 4.3 and 4.4).

5.3 Preclinical safety data

Non-clinical data reveal no special hazard for humans based on conventional studies of safetypharmacology, repeated dose toxicity, and genotoxicity.

Most findings in general toxicity studies were related to its action on progesterone receptors (and athigher concentrations on glucocorticoid receptors), with antiprogesterone activity observed atexposures similar to therapeutic levels. In a 39-week study in cynomolgus monkeys, histologicalchanges resembling PAEC were noted at low doses.

Due to its mechanism of action, ulipristal acetate has an embryolethal effect in rats, rabbits (atrepeated doses above 1 mg/kg), guinea pigs and in monkeys. The safety for a human embryo isunknown. At doses which were low enough to maintain gestation in the animal species, no teratogenicpotential was observed.

Reproduction studies performed in rats at doses giving exposure in the same range as the human dosehave revealed no evidence of impaired fertility due to ulipristal acetate in treated animals or theoffspring of treated females.

Carcinogenicity studies (in rats and mice) showed that ulipristal acetate is not carcinogenic.

Mdicinal product no longer athorised

6. PHARMACEUTICAL PARTICULARS

6.1 List of excipients

Microcrystalline cellulose

Mannitol

Croscarmellose sodium

Talc

Magnesium stearate

6.2 Incompatibilities

Not applicable.

6.3 Shelf life

3 years.

6.4 Special precautions for storage

Keep the blisters in the outer carton in order to protect from light.

6.5 Nature and contents of container

Alu/PVC/PE/PVDC or Alu/PVC/PVDC blister.

Pack of 28, 30 and 84 tablets.

Not all pack sizes may be marketed.

6.6 Special precautions for disposal and other handling

No special requirements.

7. MARKETING AUTHORISATION HOLDER

Gedeon Richter Plc.

Gyömrői út 19-21.1103 Budapest

Hungary

8. MARKETING AUTHORISATION NUMBER(S)

EU/1/12/750/001

EU/1/12/750/002

EU/1/12/750/003

EU/1/12/750/004

EU/1/12/750/005

9. DATE OF FIRST AUTHORISATION/RENEWAL OF THE AUTHORISATION

Date of first authorisation: 23 February 2012

Date of latest renewal: 14 November 2016

Medicinal product no longer authorised

10. DATE OF REVISION OF THE TEXT

DD/MM/YYYY

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

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

Medicinal product no longer authorised