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COPAXONE(GLATIRAMER ACETATE)injection

2014-06-15 02:55:07  作者:新特药房  来源:互联网  浏览次数:518  文字大小:【】【】【
简介: 可舒松注射剂Glatiramer(Copaxone) -核准用於治疗多发性硬化症Copaxone由全球知名的以色列药厂TEVA所研发制造,於1996年获美国FDA核准用於治疗多发性硬化症,目前已於43个主要国家上市.在具有较多多发性硬 ...

可舒松注射剂Glatiramer(Copaxone) -核准用於治疗多发性硬化症
Copaxone由全球知名的以色列药厂TEVA所研发制造,於1996年获美国FDA核准用於治疗多发性硬化症,目前已於43个主要国家上市.在具有较多多发性硬化症患者的西方国家中,Copaxone的疗效与耐受性皆获得十足的肯定.除了许多研究与临床经验证实其能大幅度地减低患者的复发率,改善失能的病况,减少脑部损伤之外,Copaxone的副作用发生率少,有助於提升患者的耐受性.另外,相关研究亦显示Copaxone较之干扰素更能显著地降低复发率,防止神经进一步的损伤与恶化,而且也具有更好的耐受性.在其它长期使用的疗效研究里(6年至最长12年不等),Copaxone亦证实能持续地延缓患者其神经学上病程的恶化或者让患者维持稳定的病况,减少脑内损伤并防止神经元大量遭受破坏终至丧失功能的恶化情形。
性质
Copaxone是一种合成的胜肽类化合物,由以下4种胺基酸组成: L-glutamic acid, L-alanine, L-lysine与L-tyrosine,平均分子量为4,700-11,000 daltons.药品为白色至灰白色的灭菌,冻晶粉末,包装另附注射用水以调制成注射溶液之用.主要作为单次皮下注射以治疗多发性硬化症.
作用机转
Copaxone主要藉由调控多发性硬化症患者体内的免疫进程以达到治疗的目的.进入体内后,Copaxone与免疫系统内的调控因子结合并进入中枢神经,透过一连串的免疫作用扭转多发性硬化症患者其自体免疫进程;亦即刺激「有害」或前发炎性的T细胞转换为「有益的」或抗发炎的T细胞.Copaxone可直接作用於神经细胞损伤部位并直接减少发炎情形.这些效益都有助於减少多发性硬化症患者其复发率,以及有效降低其进一步的损伤.
临床疗效
临床已有许多研究证实Copaxone可有效降低复发型多发性硬化症患者其复发频率.这些研究包括密切地监控患者投药后的复发情形,相伴症状改善的评估,以及MRI(核磁共振造影)所显示的损伤部位改善情形.另外亦有研究针对Copaxone对於维护患者生理功能的影响作评估,结果显示Copaxone可减少活动性损伤发展为永久的神经性损害,恢复轴突功能以及神经元的完整性,亦即Copaxone防止患者中枢神经内进一步的损害与病况的恶化.
副作用
最常见的副作用为注射部位的刺激反应,包括:红斑,疼痛,肿胀,搔痒,水肿,发炎与过敏反应.其它有能於注射后立即发生的症状包括:血管扩张,胸痛,呼吸困难和心悸.这些反应可於注射后几分钟内即发生,持续数分钟后即逐渐消失;通常这些副作用多属轻微,极少因此需要接受治疗.
药品交互作用
目前尚未有Copaxone与其它药品产生交互作用的相关研究.现存的临床研究里并未发现Copaxone与现有其它治疗多发性硬化症的药品之间有任何显著的药品交互作用,包括同时给药的corticosteroids
(皮质类固醇)投予长达28天.目前尚无Copaxone并用干扰素的影响研究.
禁忌
已知对Copaxone成份glatiramer acetate或对mannitol过敏者.
怀孕
哺乳期间(目前未知Copaxone是否会分泌至乳汁中而影响餵乳婴儿)
警语
Copaxone的唯一建议投予途径为皮下注射,不该作静脉注射.
剂量与用法
Copaxone的建议投予剂量为每天20 mg皮下(皮肤下脂肪层)注射.


Copaxone 20mg/ml, Solution For Injection, Pre-Filled Syringe
1. Name of the medicinal product
 Copaxone ® 20 mg/ml Solution for Injection, Pre-filled Syringe
2. Qualitative and quantitative composition
1ml solution for injection contains 20 mg glatiramer acetate *, equivalent to 18 mg of glatiramer base per pre-filled syringe
* Glatiramer acetate is the acetate salt of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine and L-lysine, in molar fraction ranges of 0.129-0.153, 0.392-0.462, 0.086-0.100 and 0.300-0.374, respectively. The average molecular weight of glatiramer acetate is in the range of 5,000-9,000 daltons.
For a full list of excipients, see section 6.1.
3. Pharmaceutical form
Solution for Injection, Pre-filled Syringe
Clear solution free of visible particles
4. Clinical particulars
4.1 Therapeutic indications
Copaxone is indicated for the treatment of patients who have experienced a well-defined first clinical episode and are determined to be at high risk of developing clinically definite multiple sclerosis (CDMS) (see Section 5.1).
Copaxone is indicated for the reduction in frequency of relapses in ambulatory patients, (i.e. who can walk unaided) with relapsing, remitting multiple sclerosis (MS) characterised by at least two attacks of neurological dysfunction over the preceding two-year period.
Copaxone is not indicated in primary or secondary progressive MS.
4.2 Posology and method of administration
The recommended dosage in adults is 20 mg of glatiramer acetate (one pre-filled syringe), administered as a subcutaneous injection once daily.
At the present time, it is not known for how long the patient should be treated.
A decision concerning long term treatment should be made on an individual basis by the treating physician.
Paediatric Use: Children and adolescents: No prospective, randomized, controlled clinical trials or pharmacokinetic studies have been conducted in children or adolescents. However, limited published data suggest that the safety profile in adolescents from 12 to 18 years of age receiving Copaxone 20 mg subcutaneously every day is similar to that seen in adults. There is not enough information available on the use of Copaxone in children below 12 years of age to make any recommendation for its use. Therefore, Copaxone should not be used in this population.
Use in the Elderly: Copaxone has not been specifically studied in the elderly.
Use in Patients with Impaired Renal Function: Copaxone has not been specifically studied in patients with renal impairment (see Section 4.4).
Patients should be instructed in self-injection techniques and should be supervised by a health-care professional the first time they self-inject and for 30 minutes after.
A different site for injection should be chosen every day, so this will reduce the chances of any irritation or pain at the site of the injection. Sites for self-injection include the abdomen, arms, hips and thighs.
4.3 Contraindications
Copaxone is contraindicated under the following conditions:
• Hypersensitivity to glatiramer acetate or mannitol.
• Pregnant women
4.4 Special warnings and precautions for use
Copaxone should only be administered subcutaneously. Copaxone should not be administered by intravenous or intramuscular routes.
The initiation of Copaxone treatment should be supervised by a neurologist or a physician experienced in the treatment of MS.
The treating physician should explain to the patient that a reaction associated with at least one of the following: vasodilatation (flushing), chest pain, dyspnoea, palpitations or tachycardia, may occur within minutes of a Copaxone injection. The majority of these symptoms is short-lived and resolves spontaneously without any sequelae. Should a severe adverse event occur, the patient must immediately stop Copaxone treatment and contact his/her physician or any emergency doctor. Symptomatic treatment may be instituted at the discretion of the physician.
There is no evidence to suggest that any particular patient groups are at special risk from these reactions. Nevertheless, caution should be exercised when administering Copaxone to patients with pre-existing cardiac disorders. These patients should be followed up regularly during treatment.
Convulsions and/or anaphylactoid or allergic reactions have been reported rarely.
Serious hypersensitivity reactions (e.g. bronchospasm, anaphylaxis or urticaria) may rarely occur. If reactions are severe, appropriate treatment should be instituted and Copaxone should be discontinued.
Glatiramer acetate-reactive antibodies were detected in patients' sera during daily chronic treatment with Copaxone. Maximal levels were attained after an average treatment duration of 3-4 months and, thereafter, declined and stabilised at a level slightly higher than baseline.
There is no evidence to suggest that these glatiramer acetate-reactive antibodies are neutralising or that their formation is likely to affect the clinical efficacy of Copaxone.
In patients with renal impairment, renal function should be monitored while they are treated with Copaxone. Whilst there is no evidence of glomerular deposition of immune complexes in patients, the possibility cannot be excluded.
4.5 Interaction with other medicinal products and other forms of interaction
Interaction between Copaxone and other medicinal products have not been formally evaluated.
There are no data on interaction with interferon beta.
An increased incidence of injection site reactions has been seen in Copaxone patients receiving concurrent administration of corticosteroids.
In vitro work suggests that glatiramer acetate in blood is highly bound to plasma proteins but that it is not displaced by, and does not itself displace, phenytoin or carbamazepine. Nevertheless, as Copaxone has, theoretically, the potential to affect the distribution of protein bound substances, concomitant use of such medicinal products should be monitored carefully.
4.6 Fertility, pregnancy and lactation
Pregnancy: There are no adequate data from the use of glatiramer acetate in pregnant women. Animal studies are insufficient with respect to effects on pregnancy; embryonal/foetal development, parturition and postnatal development (see Section 5.3). The potential risk for humans is unknown. Copaxone is contraindicated during pregnancy.
A contraceptive cover should be considered whilst using this medicinal product.
Breast-feeding: Data regarding excretion of glatiramer acetate, its metabolites or antibodies in human milk are unavailable. Caution should be exercised when Copaxone is administered to a nursing mother. The relative risk and benefit to the mother and child should be taken into consideration.
4.7 Effects on ability to drive and use machines
No studies on the effects on the ability to drive and use machines have been performed.
4.8 Undesirable effects
In all clinical trials, injection-site reactions were seen to be the most frequent adverse reactions and were reported by the majority of patients receiving Copaxone. In controlled studies, the proportion of patients reporting these reactions, at least once, was higher following treatment with Copaxone (70%) than placebo injections (37%). The most commonly reported injection-site reactions, which were more frequently reported in Copaxone vs. placebo-treated patients, were erythema, pain, mass, pruritus, oedema, inflammation and hypersensitivity.
A reaction associated with at least one or more of the following symptoms: vasodilatation, chest pain, dyspnoea, palpitation or tachycardia has been described as the Immediate Post-Injection Reaction. This reaction may occur within minutes of a Copaxone injection. At least one component of this Immediate Post-Injection Reaction was reported at least once by 31% of patients receiving Copaxone compared to 13% of patients receiving placebo.
All adverse reactions, which were more frequently reported in Copaxone vs. placebo-treated patients, are presented in the table below. This data was derived from four pivotal, double-blind, placebo-controlled clinical trials with a total of 512 patients treated with Copaxone and 509 patients treated with placebo for up to 36 months. Three trials in relapsing-remitting MS (RRMS) included a total of 269 patients treated with Copaxone and 271 patients treated with placebo for up to 35 months. The fourth trial in patients who have experienced a first clinical episode and were determined to be at high risk of developing clinically definite MS included 243 patients treated with Copaxone and 238 patients treated with placebo for up to 36 months.

System Organ Class (SOC)

Very Common (>1/10)

Common (>1/100,<=1/10)

Uncommon (>1/1000,<=1/100)

Infections And Infestations

Infection, Influenza

Bronchitis, Gastroenteritis, Herpes Simplex, Otitis Media, Rhinitis, Tooth Abscess, Vaginal Candidiasis*

Abscess, Cellulitis, Furuncle, Herpes Zoster, Pyelonephritis

Neoplasms Benign, Malignant And Unspecified (Incl Cysts And Polyps)

 

Benign Neoplasm Of Skin, Neoplasm

Skin Cancer

Blood And Lymphatic System Disorders

 

Lymphadenopathy*

Leukocytosis, Leukopenia, Splenomegaly Thrombocytopenia, Lymphocyte Morphology Abnormal

Immune System Disorders

 

Hypersensitivity

 

Endocrine Disorders

   

Goitre, Hyperthyroidism

Metabolism And Nutrition Disorders

 

Anorexia, Weight Increased*

Alcohol Intolerance, Gout, Hyperlipidaemia, Blood Sodium Increased, Serum Ferritin Decreased

Psychiatric Disorders

Anxiety*, Depression

Nervousness

Abnormal Dreams, Confusional State, Euphoric Mood, Hallucination, Hostility, Mania, Personality Disorder, Suicide Attempt

Nervous System Disorders

Headache,

Dysgeusia, Hypertonia, Migraine, Speech Disorder, Syncope, Tremor*

Carpal Tunnel Syndrome, Cognitive Disorder, Convulsion, Dysgraphia, Dyslexia, Dystonia, Motor Dysfunction, Myoclonus, Neuritis, Neuromuscular Blockade, Nystagmus, Paralysis, Peroneal Nerve Palsy, Stupor, Visual Field Defect

Eye Disorders

 

Diplopia, Eye Disorder*

Cataract, Corneal Lesion, Dry Eye, Eye Haemorrhage, Eyelid Ptosis, Mydriasis, Optic Atrophy

Ear And Labyrinth Disorders

 

Ear Disorder

 

Cardiac Disorders

 

Palpitations*, Tachycardia*

Extrasystoles, Sinus Bradycardia, Tachycardia Paroxysmal

Vascular Disorders

Vasodilatation*

 

Varicose Vein

Respiratory, Thoracic And Mediastinal Disorders

Dyspnoea*

Cough, Rhinitis Seasonal

Apnoea, Epistaxis, Hyperventilation, Laryngospasm, Lung Disorder, Choking sensation

Gastrointestinal Disorders

Nausea*

Anorectal Disorder, Constipation, Dental Caries, Dyspepsia, Dysphagia, Faecal Incontinence, Vomiting*

Colitis, Colonic Polyp, Enterocolitis, Eructation, Oesophageal Ulcer, Periodontitis Rectal Haemorrhage, Salivary Gland Enlargement

Hepatobiliary Disorders

 

Liver Function Test Abnormal

Cholelithiasis, Hepatomegaly

Skin And Subcutaneous Tissue Disorders

Rash*

Ecchymosis, Hyperhidrosis, Pruritus, Skin Disorder*, Urticaria

Angioedema, Dermatitis Contact, Erythema Nodosum, Skin Nodule

Musculoskeletal And Connective Tissue Disorders

Arthralgia, Back Pain*

Neck Pain

Arthritis, Bursitis, Flank Pain, Muscle Atrophy, Osteoarthritis

Renal And Urinary Disorders

 

Micturition Urgency, Pollakiuria, Urinary Retention

Haematuria, Nephrolithiasis, Urinary Tract Disorder, Urine Abnormality

Pregnancy, Puerperium And Perinatal Conditions

   

Abortion

Reproductive System And Breast Disorders

   

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, Immediate Post-Injection Reaction, 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.
In the fourth trial noted above, an open-label treatment phase followed the placebo-controlled period (see Section 5.1). No change in the known risk profile of Copaxone was observed during the open-label follow-up period of up to 5 years.
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 included 251 patients treated for up to 35 months (Copaxone n=125, placebo n=126) and the third study was a nine-month study involving 239 patients (Copaxone n=119, placebo n=120) where inclusion criteria were similar to those in the first and second studies with the additional criterion that patients had to have at least one gadolinium-enhancing lesion on the screening MRI.
In clinical trials in MS patients receiving Copaxone, a significant reduction in the number of relapses, compared with placebo, was seen.
In the largest controlled study, the relapse rate was reduced by 32% from 1.98 under placebo to 1.34 under glatiramer acetate.
Exposure data are available for up to twelve years in 103 patients treated with Copaxone.
Copaxone has also demonstrated beneficial effects over placebo on MRI parameters relevant to relapsing-remitting MS.
Copaxone had, however, no beneficial effect on progression of disability in relapsing-remitting MS patients.
There is no evidence that Copaxone treatment has an effect on relapse duration or severity.
There is currently no evidence for the use of Copaxone in patients with primary or secondary progressive disease.
Single Clinical Event Suggestive of MS:
One placebo-controlled study involving 481 patients (Copaxone n=243, placebo n=238) was performed in patients with a well-defined, single, unifocal neurological manifestation and MRI features highly suggestive of MS (at least two cerebral lesions on the T2-weighted MRI above 6 mm diameter). Any disease other than multiple sclerosis that could better explain signs and symptoms of the patient had to be excluded. An open-label treatment phase followed the placebo-controlled period: following conversion to clinically definite multiple sclerosis (CDMS) or after three years of treatment, or upon proof of overwhelming effect, whichever came first, all patients were assigned to active drug treatment in an open-label phase for an additional period of two years, not exceeding a maximal total treatment duration of 5 years. Of the 243 patients initially randomized to Copaxone, 198 continued Copaxone treatment in the open-label phase. Of the 238 patients initially randomized to placebo, 211 switched to Copaxone treatment in the open-label phase.
During the placebo-controlled period of up to three years, Copaxone delayed the progression from the first clinical event to clinically definite multiple sclerosis (CDMS) according to Poser criteria in a statistically significant and clinically meaningful manner, corresponding to a risk reduction of 45% (Hazard Ratio = 0.55; 95% CI [0.40; 0.77], p-value=0.0005). The proportion of patients who converted to CDMS was 43% for the placebo group and 25% in the Copaxone group.
The favourable effect of treatment with Copaxone over placebo was also demonstrated in two secondary MRI endpoints , i.e. number of new T2 lesions and T2 lesion volume.
Post-hoc subgroup analyses were performed in patients with various baseline characteristics to identify a population at high risk to develop the second attack. For subjects with baseline MRI with at least one T1 Gd-enhancing lesion and 9 or more T2 lesions, conversion to CDMS was evident for 50% of the placebo subjects vs. 28% of the Copaxone subjects in 2.4 years. For subjects with 9 or more T2 lesions at baseline, conversion to CDMS was evident for 45% of the placebo subjects vs. 26% on Copaxone in 2.4 years. However, the impact of early treatment with Copaxone on the long term evolution of the disease is unknown even in these high-risk subgroups as the study was mainly designed to assess the time to the second event. In any case, treatment should only be considered for patients classified at high risk.
The effect shown in the placebo-controlled phase was sustained in the long-term follow-up period of up to 5 years. The time progression from the first clinical event to CDMS was prolonged with earlier Copaxone treatment as compared to delayed treatment, reflecting a 41% risk reduction with earlier versus later treatment (Hazard Ratio = 0.59; 95% CI [0.44; 0.80], p-value=0.0005). The proportion of subjects in the Delayed Start group who progressed was higher (49.6%) compared to those in the Early Start group (32.9%).
A consistent effect in favour of early treatment over delayed treatment across time was shown for the analysis of cumulative number of lesions until end of each year in new T1 Gd-enhancing lesions, new T2 lesions and new T1 hypointense lesions. An effect in reductions in favor of early versus delayed treatment was observed for the total number of new T1 Gd-enhancing lesions, T1 Gd-enhancing lesions volume, as well as the total number of new T1 hypointense lesions measured over the entire study period.
No appreciable differences between the Early Start and Delayed Start cohorts were observed for either hypointense T1 lesions volume or brain atrophy over 5 years. However, analysis of brain atrophy at LOV (adjusted to treatment exposure) showed a reduction in favour of early treatment with GA.
5.2 Pharmacokinetic properties
 Pharmacokinetic studies in patients have not been performed. In vitro data and limited data from healthy volunteers indicate that with subcutaneous administration of glatiramer acetate, the active substance is readily absorbed and that a large part of the dose is rapidly degraded to smaller fragments already in subcutaneous tissue.
5.3 Preclinical safety data
 Preclinical data reveal no special hazard for humans based on studies of safety pharmacology, repeated dose toxicity, toxicity to reproduction, genotoxicity or carcinogenicity, beyond the information included in other sections of the SPC. Due to the lack of pharmacokinetic data in humans, margins of exposure between humans and animals can not be established.
Immune complex deposition in the glomeruli of the kidney was reported in a small number of rats and monkeys treated for at least 6 months. In a 2 years rat study, no indication of immune complex deposition in the glomeruli of the kidney was seen.
Anaphylaxis after administration to sensitised animals (guinea pigs or mice) was reported. The relevance of these data for humans is unknown.
Toxicity at the injection site was a common finding after repeated administration in animals.
6. Pharmaceutical particulars
6.1 List of excipients
 Mannitol
Water for Injections
6.2 Incompatibilities
In the absence of compatibility studies, this medicinal product must not be mixed with other medicinal products.
6.3 Shelf life
2 years
6.4 Special precautions for storage
Keep the container in the outer carton, in order to protect from light.
Store in refrigerator (2°C to 8°C).
If the pre-filled syringes cannot be stored in a refrigerator, they can be stored at room temperature (15°C to 25°C), once for up to 1 month.
After this one month period, if the Copaxone 20 mg/ml pre-filled syringes have not been used and are still in their original packaging, they must be returned to storage in a refrigerator (2°C to 8°C).
6.5 Nature and contents of container
A pre-filled syringe containing Copaxone solution for injection consists of a 1 ml long colourless type I glass syringe barrel with staked needle, a plastic plunger rod, a rubber plunger stopper and a needle shield.
Copaxone is available in packs containing 7, 28 or 30 pre-filled syringes of 1 ml solution for injection or a multipack containing 90 (3 packs of 30) pre-filled syringes of 1 ml solution for injection.
Not all pack sizes may be marketed.
6.6 Special precautions for disposal and other handling
 For single use only. Any unused product or waste material must be discarded.
7. Marketing authorisation holder
 Teva Pharmaceuticals Ltd
Ridings Point
Whistler Drive
Castleford
West Yorkshire
WF10 5HX United Kingdom
8. Marketing authorisation number(s)
 PL 10921/0023
9. Date of first authorisation/renewal of the authorisation
Date of first authorization: 7 April 2003
10. Date of revision of the text
26/04/2013
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注:以下产品不同的上市国和不同价格,购买以咨询为准!
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产地国家: 美国
原产地英文商品名:
COPAXONE INJECTION KIT 20MG/PRE-FILLED SYRINGE 30SYRINGES/BOX
原产地英文药品名:
GLATIRAMER ACETATE
中文参考商品译名:
可舒松注射剂套装 20毫克/注射器/套 30套/盒
中文参考药品译名:
醋酸格拉替雷
生产厂家中文参考译名:
美国梯瓦公司
生产厂家英文名:
TEVA
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产地国家: 意大利
原产地英文商品名:
COPAXONE 20mg/ml/syringe 28syringes/box
原产地英文药品名:
GLATIRAMER ACETATE
中文参考商品译名:
可舒松 20毫克/毫升/注射器 28注射器/盒
中文参考药品译名:
醋酸格拉替雷
生产厂家中文参考译名:
梯瓦
生产厂家英文名:
TEVA
---------------------------------------------------------------
产地国家: 瑞士
原产地英文商品名:
COPAXONE 20mg/ml/syringe 28syringes/box
原产地英文药品名:
GLATIRAMER ACETATE
中文参考商品译名:
可舒松 20毫克/毫升/注射器 28注射器/盒
中文参考药品译名:
醋酸格拉替雷
生产厂家中文参考译名:
梯瓦
生产厂家英文名:
TEVA
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产地国家: 以色列
原产地英文商品名:
COPAXONE 20mg/ml/syringe 30syringes/box
原产地英文药品名:
GLATIRAMER ACETATE
中文参考商品译名:
可舒松 20毫克/毫升/注射器 30注射器/盒
中文参考药品译名:
醋酸格拉替雷
生产厂家中文参考译名:
梯瓦
生产厂家英文名:
TEVA
--------------------------------------------------------
产地国家: 加拿大
原产地英文商品名:
COPAXONE INJECTION KIT 20MG/PRE-FILLED SYRINGE 30SYRINGES/BOX
原产地英文药品名:
GLATIRAMER ACETATE
中文参考商品译名:
可舒松注射剂套装 20毫克/注射器/套 30套/盒
中文参考药品译名:
醋酸格拉替雷
生产厂家中文参考译名:
美国梯瓦公司
生产厂家英文名:
TEVA

责任编辑:admin


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