Breast Engorgement, Erectile Dysfunction, Pelvic Prolapse, Priapism, Prostatic Disorder, Smear Cervix Abnormal, Testicular Disorder, Vaginal Haemorrhage, Vulvovaginal Disorder
 
General Disorders And Administration Site Conditions
 Asthenia, Chest Pain*, Injection Site Reactions*§, Pain*
 Chills*, Face Oedema*, Injection Site Atrophy♣, Local Reaction*, Oedema Peripheral, Oedema, Pyrexia
 Cyst, Hangover, Hypothermia, Inflammation, Injection Site Necrosis, Mucous Membrane Disorder
 
Injury, Poisoning And Procedural Complications
 
  Post Vaccination Syndrome

* More than 2% (>2/100) higher incidence in the Copaxone treatment group than in the placebo group. Adverse reaction without the * symbol represents a difference of less than or equal to 2%.

§ The term 'Injection site reactions' (various kinds) comprises all adverse events occurring at the injection site excluding injection site atrophy and injection site necrosis, which are presented separately within the table.

♣Includes terms which relate to localized lipoatrophy at the injection sites.

Rare (>1/10000, <1/1000) reports of anaphylactoid reactions were collected from MS patients treated with Copaxone in uncontrolled clinical trials and from post-marketing experience with Copaxone.

4.9 Overdose

 A few cases of overdose with Copaxone (up to 80 mg glatiramer acetate) have been reported. These cases were not associated with any adverse reactions other than those mentioned in Section 4.8.

There is no clinical experience with doses higher than 80 mg glatiramer acetate.

In clinical trials, daily doses of up to 30 mg glatiramer acetate for up to 24 months were not associated with adverse reactions other than those mentioned in Section 4.8.

In case of overdose, patients should be monitored and the appropriate symptomatic and supportive therapy instituted.

5. PHARMACOLOGICAL PROPERTIES

5.1 Pharmacodynamic properties

 Pharmacotherapeutic group: Other cytokines and immunomodulators

ATC code: L03AX13

The mechanism(s) by which glatiramer acetate exerts its effects in patients with MS is (are) not fully elucidated. However, it is thought to act by modifying immune processes that are currently believed to be responsible for the pathogenesis of MS. This hypothesis is supported by findings of studies that have been carried out to explore the pathogenesis of experimental allergic encephalomyelitis (EAE), a condition induced in several animal species through immunisation against central nervous system derived material containing myelin and often used as an experimental animal model of MS. Studies in animals and in MS patients suggest that upon its administration, glatiramer acetate-specific suppressor T cells are induced and activated in the periphery.

RRMS :

A total of 269 patients have been treated with Copaxone in three controlled trials. The first was a two-year study involving 50 patients (Copaxone n=25, placebo n=25) who were diagnosed with relapsing-remitting MS by the then-applicable standard criteria, and who had at least two attacks of neurological dysfunction (exacerbations) during the preceding two years. The second study ap