Clapitax, 75 mg 28 pcs

Name: Clapitax, 75 mg 28 pcs
SKU: 336687
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EAN: 8906072523121 SKU: 336687 Categories: Blood Circulation, Cardiovascular, Medicine

Description

Pharmacological group:

anti-aggregant

ATX code: B01AC04

Pharmacological action

Pharmacodynamics

Clopidogrel is a prodrug, one of whose active metabolites is a platelet aggregation inhibitor. Active metabolite of clopidogrel selectively inhibits binding of ADP (adenosine diphosphate) to P2Y12 receptor of platelets and subsequent ADP-mediated activation of GPIIb/IIIa complex, resulting in suppression of platelet aggregation. Through irreversible binding, platelets remain immune to ADP stimulation for the remainder of their lives (approximately 7-10 days), and recovery of normal platelet function occurs at a rate consistent with the rate of platelet renewal.

The aggregation of platelets caused by agonists other than ADP is also inhibited by blocking enhanced platelet activation by the released ADP. Because formation of the active metabolite occurs via cytochrome P450 isoenzymes, some of which may be polymorphic or may be inhibited by other drugs, adequate platelet suppression is not possible in all patients.

When clopidogrel is taken daily at a dose of 75 mg, significant suppression of ADP-induced platelet aggregation is noted from the first day of administration, which gradually increases over 3-7 days and then reaches a constant level (when an equilibrium state is reached). In the equilibrium state, platelet aggregation is suppressed by an average of 40-60%. After stopping clopidogrel administration, platelet aggregation and bleeding time gradually return to baseline within an average of 5 days.

When studying the pharmacodynamics of clopidogrel, less inhibition of ADP-induced platelet aggregation was observed in women. However, no differences were found between men and women in prolongation of bleeding time.

Clopidogrel is able to prevent the development of atherothrombosis in any localization of atherosclerotic vascular lesions, in particular, in lesions of the cerebral, coronary or peripheral arteries.

In patients with recent myocardial infarction, ischemic stroke and/or diagnosed peripheral arterial occlusive disease, administration of clopidogrel at a dose of 75 mg daily significantly reduces the risk of vascular complications (myocardial infarction, stroke, cardiovascular mortality)

. In acute coronary syndrome without ST-segment elevation on ECG (unstable angina pectoris, myocardial infarction) the use of clopidogrel (loading dose of 300 mg once and then 75 mg/day) in combination with acetylsalicylic acid 75-325 mg/day and other standard therapy significantly and independently of other treatments reduces risk of vascular complications.

. In ST-segment elevation myocardial infarction on ECG, administration of clopidogrel (loading dose of 300 mg once during the first 12 hours of the disease, then 75 mg/day) in combination with acetylsalicylic acid (loading dose of 150-325 mg, then 75-162 mg/day) fibrinolytic therapy and, when indicated, heparin, reduces the incidence of infarct-related coronary artery occlusion (according to coronary angiography at discharge from hospital), recurrent myocardial infarction and fatal outcomes. In patients who did not undergo coronary angiography at discharge, clopidogrel administration according to the specified scheme reduces the rate of fatal outcomes and recurrent myocardial infarction until day 8 of the disease or until discharge from the hospital.

In general, in myocardial infarction, regardless of ECG changes (ST-segment elevation, ST-segment depression, or first-time complete left bundle branch block), clopidogrel at a dose of 75 mg/day combined with acetylsalicylic acid 162 mg/day reduces overall mortality and cumulative recurrent myocardial infarction, ischemic stroke and fatal outcomes.

. In patients with atrial fibrillation who have at least one risk factor for vascular complications and are not taking indirect anticoagulants for any reason, clopidogrel at 75 mg/day in combination with acetylsalicylic acid (compared with taking acetylsalicylic acid alone) reduces the cumulative incidence of stroke, myocardial infarction, systemic thromboembolism outside the central nervous system, and cardiovascular mortality, primarily by reducing the risk of nonfatal stroke. This effect of clopidogrel has been observed in studies lasting up to 5 years.

Pharmacokinetics

Eabsorption

Clopidogrel is rapidly absorbed at a single and course oral dose of 75 mg daily. Thus the mean maximum concentration (Cmax) of unchanged clopidogrel in plasma is very low (approximately 2.2-2.5 ng/ml after a single oral dose of 75 mg) is reached approximately 45 minutes after intake. According to the urinary excretion of clopidogrel metabolites, its absorption is approximately 50%.

The concentration of the unchanged substance in plasma decreases rapidly and does not reach the limit of measurement (0.025 µg/L) within 2 hours after administration.

Distribution

In vitro clopidogrel and its main circulating inactive metabolite are reversibly bound to plasma proteins (98% and 94%, respectively) and this binding is unsaturated in a wide concentration range.

Metabolism

As a prodrug, clopidogrel is extensively metabolized in the liver. The active metabolite is not detected in the blood.

In vitro and in vivo clopidogrel is metabolized in two ways:

through esterases and subsequent hydrolysis to form an inactive carboxylic acid derivative (85% of circulating metabolites);
through the cytochrome P450 system. Initially, clopidogrel is metabolized to 2-oxo-clopidogrel, which is an intermediate metabolite. Subsequent metabolism of 2-oxo-clopidogrel leads to the formation of the active metabolite of clopidogrel – thiol derivative of clopidogrel. In vitro metabolism through this pathway occurs via the cytochrome P450 isoenzymes CYP3A4, CYP2C19, CYP1A2, and CYP2B6. The active thiol metabolite of clopidogrel, which has been isolated in in vitro studies, binds rapidly and irreversibly to platelet receptors under in vivo conditions, blocking platelet aggregation.

The Cmax of the active metabolite clopidogrel after a loading dose of 300 mg is twice the Cmax after a maintenance dose of clopidogrel 75 mg for 4 days. When clopidogrel 300 mg is taken, the TCmax is approximately 30-60 min.

After repeated oral administration of clopidogrel at a dose of 75 mg per day, the Cmax of the main inactive metabolite is approximately 3 mg/L, the TCmax of the inactive metabolite is reached in 1 hour.

Elimation

In 120 hours after human oral administration of 14C-labeled clopidogrel, approximately 50% of the radioactivity is excreted in the urine and approximately 46% of the radioactivity in the feces.

The elimination half-life (T1/2) of the main circulating inactive metabolite (carboxylic acid derivative) is 8 hours after a single dose and repeated doses.

Pharmacogenetics

A few polymorphic isoenzymes of the cytochrome P450 system are involved in the activation of clopidogrel. CYP2C19 isoenzyme is involved in the formation of both the active metabolite and the intermediate metabolite, 2-oxo-clopidogrel. Pharmacokinetics and antiaggregant effect of the active metabolite clopidogrel studied by ex vivo platelet aggregation differ depending on the genotype of CYP2C19 isoenzyme.

The CYP2C19*1 gene allele is responsible for normally functioning metabolism, whereas the CYP2C19*2 and CYP2C19*3 gene alleles are nonfunctional. These alleles are responsible for reduced metabolism in about 85% of Caucasoid races and in 99% of Mongoloid races. Other alleles associated with no or reduced metabolism are CYP2C19*4, *5, *6, *7, and *8, but these are rare in the general population. Patients with low CYP2C19 isoenzyme activity, must have the above two loss-of-function gene alleles.

The published incidence of phenotypes of individuals with low CYP2C19 isoenzyme activity in Caucasoid individuals is 2%, in non-Hispanic individuals 4%, and in Chinese individuals 14%.

Tests exist to determine a patient’s CYP2C19 genotype; these tests can be used as an adjunctive tool in determining treatment tactics.

A cross-sectional study involving 40 healthy volunteers (10 volunteers each with very fast, extensive, intermediate, and delayed metabolism) examined the pharmacokinetics and antiaggregant effects of clopidogrel when used in two regimens:

300 mg once followed by a dose of 75 mg daily for 5 days and
600 mg once followed by a dose of 150 mg daily for 5 days (until equilibrium is reached)

There were no significant differences in active metabolite exposure and mean platelet aggregation inhibition (IAT) between the very fast, extensive, and intermediate metabolism groups of volunteers. Volunteers with reduced metabolic rate had 63-71% lower exposure to the active metabolite compared to volunteers extensively metabolizing clopidogrel.

When the drug was administered on a 300 mg once / 75 mg daily regimen, platelet response (when stimulated by 5 μm ADP) was reduced in volunteers with delayed clopidogrel metabolism: IAT was 24% (after 24 hours) and 37% (Day 5). In comparison, volunteers with extensive metabolism had an IAT of 39% (after 24 hours) and 60% (Day 5).

When clopidogrel was administered at 600 mg once / 150 mg daily in volunteers with decreased clopidogrel metabolic rate, the effects of the drug were more pronounced than when the drug was used at 300 mg once / 75 mg daily: IAT was 32% (after 24 hours) and 61% (Day 5), which was comparable to IAT in groups of volunteers with other clopidogrel metabolic rates who received the drug at the 300 mg / 75 mg regimen. A suitable dosing regimen for the patient population with a reduced clopidogrel metabolic rate has not been established in clinical trials.

Similarly, a meta-analysis of six studies that included data from 335 healthy volunteers who received clopidogrel and were at equilibrium concentration reached showed that intermediate metabolizers had a 28% reduction in active metabolite exposure and weak metabolizers had a 72% reduction. Compared to extensive metabolizers, platelet aggregation inhibition was reduced by 5.9% and 21.4% in intermediate and weak metabolizers, respectively.

The effect of CYP2C19 genotype on clinical outcomes in patients receiving clopidogrel has not been evaluated in prospective randomized controlled trials. Existing data from retrospective analyses of clinical trials for which patient genotyping results are available do not have sufficient power to assess differences in clinical outcomes in weak clopidogrel metabolizers compared with extensive and intermediate metabolizers.

Separate patient groups

Elderly persons

There were no differences in platelet aggregation and bleeding time in elderly volunteers (over 75 years of age) when compared with younger volunteers. No dose adjustment of clopidogrel in elderly persons is required

Age under 18 years

The pharmacokinetics of clopidogrel in children has not been studied.

Kidney function impairment

. After repeated doses of clopidogrel at a dose of 75 mg/day in patients with severe chronic renal impairment (creatinine clearance (CK) 5-15 ml/min), inhibition of ADP-induced platelet aggregation was 25% lower than in healthy volunteers, but no prolongation of bleeding time was observed.

Hepatic impairment

After administration of clopidogrel at a dose of 75 mg daily for 10 days in patients with severe liver injury, inhibition of ADP-induced platelet aggregation did not differ from that in healthy volunteers. The mean bleeding time in patients with severe liver injury and in healthy volunteers was comparable.

Raciality

The prevalence of CYP2C19 isoenzyme gene alleles responsible for intermediate or reduced metabolism differs among racial groups. The available literature is insufficient to assess the value of CYP2C19 isoenzyme genotyping for predicting the development of ischemic complications.

Indications
Indications
Prevention of thrombosis, Prevention of heart attacks and strokes
Prevention of atherothrombotic complications in adult patients with
myocardial infarction (several days to 35 days old),
ischemic stroke (from 7 days to 6 months)
diagnosed peripheral artery occlusive disease
acute coronary syndrome:
without ST-segment elevation (unstable angina, myocardial infarction without Q-wave), including patients who have had stenting for percutaneous coronary intervention (in combination with acetylsalicylic acid);
with ST-segment elevation (acute myocardial infarction) with drug treatment and the possibility of thrombolysis (in combination with acetylsalicylic acid).
Prevention of atherothrombotic and thromboembolic complications (including stroke) in atrial fibrillation (atrial fibrillation) in adult patients with at least one risk factor for vascular complications, contraindications to indirect anticoagulants and low risk of bleeding (in combination with acetylsalicylic acid).

Active ingredient
Active ingredient
Clopidogrel

Composition
Composition
Component Quantity, mg
75 mg 150 mg 300 mg
Active substance
Clopidogrel hydrosulfate
(in terms of clopidogrel) 97.875
(75.0) 195.75
(150.0) 391.50
(300.0) (300.0)
Excipients
Mannitol 36.125 72.25 52.00
Crospovidone 20.00 40.00 52.00
Microcrystalline cellulose 67.00 134.00 79.50
Hyprolose (low-substituted) 4.00 8.00 8.00
Macrogol 6000 8.00 16.00 20.00
Colloidal Silicon Dioxide 3.00 6.00 6.00
Zinc stearate 12.00 24.00 32.00

Film Cover
Opadray Pink* 7.44 – –
Opadray White** – 14.88 19.23
Carnauba wax traces/td>
traces traces
* Opadray pink contains: BP lactose monohydrate – 39.5%, BP hypromellose – 39.25%; BP titanium dioxide (E171) – 10%, USP triacetin – 10%, iron oxide red dye BP (E172)) – 1.25%
** Opadray white contains: lactose monohydrate BP – 40%, hypromellose BP – 40%, titanium dioxide BP (E171) – 10%, triacetin USP – 10%

How to take, the dosage
How to take, the dosage
Clopidogrel should be taken orally regardless of meals

Interaction
Interaction
Orderal anticoagulants
The simultaneous use of clopidogrel and oral anticoagulants may increase the intensity of bleeding, in connection with this combination is not recommended. Clopidogrel at a dose of 75 mg per day does not affect warfarin pharmacokinetics and does not change the International Normalized Ratio (INR) in patients taking warfarin for a long time. However, concomitant administration of warfarin with clopidogrel may increase the risk of bleeding due to the independent effect of these drugs on hemostasis (see “Cautions”).
Glycoprotein IIb/IIIa inhibitors
The administration of glycoprotein IIb/IIIa inhibitors together with clopidogrel requires caution in patients with increased risk of bleeding (for trauma and surgery or other pathological conditions) (see “Special Precautions”).
Acetylsalicylic acid
Acetylsalicylic acid does not alter the effect of clopidogrel inhibiting ADP-induced platelet aggregation, but clopidogrel potentiates the effect of acetylsalicylic acid on collagen-induced platelet aggregation. However, concomitant administration of acetylsalicylic acid at 500 mg twice daily for 1 day with clopidogrel did not significantly increase bleeding time caused by clopidogrel administration. There is a possible pharmacodynamic interaction between clopidogrel and acetylsalicylic acid, which leads to an increased risk of bleeding. Therefore, although in clinical trials patients received combined therapy with clopidogrel and acetylsalicylic acid for up to one year, caution should be exercised when using them concomitantly.
Heparin
In a clinical study conducted with healthy volunteers, no change in heparin dose was required when taking clopidogrel and its anticoagulant effect was not altered. Concomitant use of heparin did not change the inhibitory effect of clopidogrel on platelet aggregation. There is a possible pharmacodynamic interaction between clopidogrel and heparin, which may increase the risk of bleeding, so the simultaneous use of these drugs requires caution.
Trombolytics
The safety of concomitant use of clopidogrel, fibrin-specific or fibrin-nonspecific thrombolytics and heparin has been studied in patients with acute myocardial infarction. The frequency of clinically significant bleeding was similar to that observed when thrombolytics and heparin were used together with acetylsalicylic acid.
Non-steroidal anti-inflammatory drugs (NSAIDs)
The simultaneous use of clopidogrel with NSAIDs may increase the risk of bleeding. In a clinical study involving healthy volunteers, concomitant use of clopidogrel and naproxen increased hidden blood loss through the gastrointestinal tract. However, due to the lack of studies on the interaction of clopidogrel with other NSAIDs, it remains unknown whether there is an increased risk of gastrointestinal bleeding when clopidogrel is taken together with other NSAIDs. Therefore, the use of NSAIDs, including COX-2 inhibitors, in combination with clopidogrel should be used with caution (see “Precautions”).
Selective serotonin reuptake inhibitors (SSRIs)
Because SSRIs impair platelet activation and increase the risk of bleeding, concomitant use of SSRIs with clopidogrel should be performed with caution.
CYP2C19 inhibitors
Because clopidogrel is metabolized to its active metabolite partially by CYP2C19, use of drugs that inhibit this system may result in lower levels of the active metabolite of clopidogrel and decreased clinical effectiveness. The clinical significance of this interaction remains unknown, but as a precautionary measure, it is recommended to avoid concomitant administration of clopidogrel with drugs that inhibit CYP2C19 (omeprazole, esomeprazole, fluvoxamine, fluoxetine, moclobemide, voriconazole, fluconazole, ticlopidine, ciprofloxacin, cimetidine, carbamazepine, oxcarbazepine, chloramphenicol).
Proton pump inhibitors
Omeprazole at a dose of 80 mg once daily taken simultaneously with clopidogrel or at 12-hour intervals after clopidogrel reduces exposure to the active metabolite by 45% after a loading dose and by 40% after a maintenance dose. This reduction results in a 39% and 21% reduction in platelet aggregation inhibition, respectively. Esomeprazole is assumed to have a similar effect on clopidogrel activity. In observational and controlled clinical studies, conflicting data have been obtained regarding the clinical significance of this interaction (as assessed by the risk of major cardiovascular complications). As a precautionary measure, it is not recommended to use clopidogrel together with omeprazole and esomeprozole.
If it is necessary to prescribe proton pump inhibitors concomitantly with clopidogrel, the drug with the lowest CYP2C19 inhibition (pantaprazole or lanzoprazole) should be used. When concomitant use with pathoprazole at a dose of 80 mg once daily, plasma concentration of the active metabolite clopidogrel is decreased by 20% after loading dose and by 14% after maintenance dose of clopidogrel. At the same time inhibition of platelet aggregation decreases by 20% after loading dose and by 14% after maintenance dose of clopidogrel. At the same time, inhibition of platelet aggregation decreases by 15% and 11%, respectively
Another combination therapy
. Since clopidogrel is metabolized to form its active metabolite partially by the CYP2C19 system, the use of drugs that inhibit this system (e.g., omeprazole) may lead to decreased levels of the active metabolite clopidogrel and reduce its clinical effectiveness. Simultaneous use of drugs that inhibit the CYP2C19 system is not recommended. If proton pump inhibitors are to be taken concomitantly with clopidogrel, the proton pump inhibitor with the least CYP2C19 isoenzyme inhibition, such as pantoprazole, should be used.
A number of clinical studies have been conducted with clopidogrel and other concomitantly administered drugs to examine possible pharmacodynamic and pharmacokinetic interactions and have shown that:
when using clopidogrel concomitantly with atenolol, nifedepine, or both drugs simultaneously, no clinically significant pharmacodynamic interactions were observed;

Pharmacokinetic parameters of digoxin or theophylline were not changed when they were used together with clopidogrel;
antacids did not decrease the absorption of clopidogrel;

It is unlikely that clopidogrel can affect the metabolism of other drugs, such as phenytoin and tolbutamide, as well as NSAIDs, which are metabolized through the CYP2C9 isoenzyme.
.Angiotensin-converting enzyme (ACE) inhibitors, diuretics, beta-adrenoblockers, “slow” calcium channel blockers, hypolipidemic drugs, hypoglycemic agents (including insulin), coronary vasodilators, antiepileptic drugs, drugs of hormone replacement therapy and glycoprotein IIb/IIIa inhibitors – no clinically significant adverse interactions were found in the clinical studies.
.

Special Instructions
Special Instructions
During treatment with clopidogrel, especially during the first weeks of treatment and/or after invasive cardiac procedures/surgery, patients should be closely monitored for signs of bleeding, including hidden bleeding.

Contraindications
Contraindications
High sensitivity to clopidogrel or any of the excipients of the drug.
Severe hepatic impairment.
Active bleeding, such as bleeding from a peptic ulcer or intracranial hemorrhage.
Hereditary galactose intolerance, lactase deficiency and glucose-galactose malabsorption.
Pregnancy and lactation (see “Pregnancy and lactation”).
Children under 18 years of age (safety and effectiveness of use not established).
With caution
Clopidogrel should be taken with caution:
moderate hepatic impairment (Child-Pugh score 7-9) with possible predisposition to bleeding (limited clinical experience with use);
mild to moderate chronic renal failure (creatinine clearance 60-30 ml/min) (limited clinical experience);
injuries, surgical interventions (see “Special Indications. “
disorders with a predisposition to bleeding (especially gastrointestinal or intraocular);
concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs), including selective cyclooxygenase-2 (COX-2) inhibitors;)
concomitant use of oral anticoagulants, heparin glycoprotein IIb/IIIa inhibitors, selective serotonin reuptake inhibitors (SSRIs) and thrombolytics;
in genetically determined decreased CYP2C19 isoenzyme function.
. There is literature data indicating that patients with genetically determined decreased CYP2C19 isoenzyme function have less systemic exposure to the active metabolite clopidogrel and less antiplatelet activity, and may have more frequent cardiovascular complications after myocardial infarction compared to patients with normal CYP2C19 isoenzyme function;
when there is a history of allergic or hematological reactions to other thienopyridines (such as ticlopidine, prasugrelu) due to the possibility of cross-allergic or hematological reactions (see
.

Side effects
Side effects
The frequency of side effects is defined according to the WHO classification:
very common > 1/10 (more than 10%)
frequent from >1/100 to < 1/10
frequently from > 1/1000 to < 1/100
frequently from >1/10000 to < 1/1000
very rarely < 1/10000
unknown frequency (the incidence of an adverse reaction cannot be determined from the available data).
Blood and lymphatic system disorders
Infrequent: thrombocytopenia, leukopenia, eosinophilia.
Rare: neutropenia, including severe.
very rarely: thrombotic thrombocytopenic purpura (see section “Special Indications”), aplastic anemia, pancytopenia, agranulocytosis, severe thrombocytopenia, granulocytopenia, anemia. frequency unknown – acquired hemophilia.
Immune system disorders
Very rare: anaphylactoid reactions, serum sickness, cross-allergic and hematological reactions with other thienopyridines (such as ticlopidine, prasugrel).
Mental disorders
Very rare: hallucinations, confusion.
Nervous system disorders
Infrequent: intracranial hemorrhage (including fatal), headache, paresthesia, dizziness.
very rarely: disorders of taste perception.
Visual disorders
Infrequent: ocular hemorrhages (conjunctival, tissue and retina).
Hearing and labyrinth disorders
Rarely: vertigo.
Vascular disorders
Often: hematoma.
Very rare: serious bleeding from a surgical wound, vasculitis, decreased blood pressure.
Respiratory system, chest and mediastinum disorders
Often: nasal bleeding.
very rarely: bronchospasm, interstitial pneumonitis, pulmonary bleeding, hemoptysis, eosinophilic pneumonia.
Gastrointestinal disorders
Very common: gastrointestinal bleeding, diarrhea, abdominal pain, dyspepsia.
Infrequent: gastric and 12 duodenal ulcer, vomiting, nausea, constipation, abdominal bloating.
Rare: retroperitoneal hemorrhage.
Very rare: gastrointestinal bleeding and retroperitoneal hemorrhage with fatal outcome, pancreatitis, colitis (including ulcerative colitis or lymphocytic colitis), stomatitis.
Liver and biliary tract disorders
very rarely: acute hepatic failure, hepatitis, abnormal liver function parameters.
Skin and subcutaneous tissue disorders
Often: “bruising” (localized subcutaneous hemorrhages).
Infrequent: rash, itching, purpura (fine-pointed capillary hemorrhages in the skin, under the skin or in the mucous membranes).
Unknown frequency: Maculopapular or erythematous rash, urticaria, pruritus, angioedema, bullous dermatitis (toxic epidermal necrolysis, Stevens-Johnson syndrome, erythema multiforme), drug hypersensitivity syndrome, drug rash with eosinophilia and systemic manifestations (DRESS syndrome), eczema, red squamous lichen.
Muscular and connective tissue disorders
very rarely: haemorrhage in muscles and joints (haemarthrosis), arthritis, arthralgia, myalgia.
Remorbid: renal and urinary tract disorders
Infrequent: hematuria.
very rarely: glomerulonephritis.
General disorders and disorders at the site of administration
Often: bleeding from the site of vascular puncture.
Very rarely: fever.
Laboratory and instrumental data
Infrequent: prolongation of bleeding time, decreased neutrophil count, decreased platelet count in peripheral blood, impaired liver function tests, increased plasma creatinine concentration
.

Overdose
Overdose
Symptoms
Clopidogrel overdose may lead to prolonged bleeding time and subsequent hemorrhagic complications.
The treatment
Symptomatic. An antidote for clopidogrel has not been established. If rapid correction of prolonged bleeding time is necessary, platelet transfusions are recommended.

Pregnancy use
Pregnancy use
As a precautionary measure, administration of clopidogrel during pregnancy is not recommended due to the lack of clinical data on its administration in pregnant women, although animal studies have shown no adverse effects on pregnancy, embryonic development, delivery and postnatal development. Breastfeeding should be discontinued in case of treatment with clopidogrel, since it has been shown in studies in rats that clopidogrel and/or its metabolites are excreted into breast milk. Whether or not clopidogrel passes into human breast milk is not known.

Similarities
Similarities
Clopidogrel, Zilt, Egithromb, Lopirel, Plagril, Clopidex, Clopidogrel-SZ

Additional information
Weight 0.022 kg
Shelf life
3 years.
Conditions of storage
Store in a dry place protected from light at a temperature not exceeding 25C. Keep out of reach of children.
Manufacturer
Novalek Pharmaceuticals Pvt. Ltd.
Medication form
pills
Brand
#Н/Д