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Plavix (Clopidogrel) tablets 300mg 10 tablets, 75mg 28 tablets, 75mg 100 tablets,

Plavix (Clopidogrel) tablets 300mg 10 tablets, 75mg 28 tablets, 75mg 100 tablets,


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  • Plavix (Clopidogrel) tablets 300mg 10 tablets, 75mg 28 tablets, 75mg 100 tablets, Plavix (Clopidogrel) tablets 300mg 10 tablets, 75mg 28 tablets, 75mg 100 tablets,

Plavix (Clopidogrel) tablets 300mg 10 tablets, 75mg 28 tablets, 75mg 100 tablets,

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Plavix (Clopidogrel) tablets Anti-aggregants 300mg 10 tablets, 75mg 28 tablets, 75mg 100 tablets,

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Pharmacological action 

Plavix – antiaggregants 


Clopidogrel is a prodrug, an active metabolite which is an inhibitor of platelet aggregation. The active metabolite of clopidogrel selectively inhibits the binding of ADP to P2Y12-receptor of platelets and the subsequent ADP-mediated activation of the complex GPIIb/IIIa, leading to platelet aggregation suppression. Due to the irreversible binding, platelets remain unresponsive to stimulation of the ADP for the remaining period of his life (approximately 7-10 days) and recovery of normal platelet function occurs at a rate corresponding with the refresh rate of platelets.

Platelet aggregation caused by agonists that is distinct from the ADP also inhibited by blockade of enhanced platelet activation released ADP.

Since the formation of the active metabolite occurs by means of enzymes of the P450 system, some of which may differ by the polymorphism or to also be inhibited by other drugs, not all patients may adequate inhibition of platelet aggregation.

The daily clopidogrel dose of 75 mg from the first day of admission showed a significant inhibition of ADP-induced platelet aggregation, which gradually increased over 3-7 days and then goes at a constant level (at equilibrium state). In steady state, platelet aggregation is inhibited on average by 40-60%. After stopping clopidogrel, platelet aggregation and bleeding time gradually return to baseline levels, on average, within 5 days.

Clopidogrel can prevent the development of atherothrombosis in all localizations of atherosclerotic vascular lesions, in particular lesions in the cerebral, coronary or peripheral arteries.

Clinical research ACTIVE-A showed that in patients with atrial fibrillation who had at least one risk factor for vascular complications, but was unable to take indirect anticoagulants, clopidogrel in combination with acetylsalicylic acid (ASA) (compared with an intake of only one ask) reduced the frequency of combined stroke, myocardial infarction, systemic embolism outside the CNS vessels or vascular death, largely due to the reduction in the risk of stroke.

The effectiveness of clopidogrel in combination with acetylsalicylic acid was detected early and persisted up to 5 years. Reducing the risk of major vascular complications in patients taking clopidogrel in combination with acetylsalicylic acid was mainly due to a larger decrease in the frequency of strokes. The risk of stroke of any severity in the clopidogrel in combination with ASA was reduced and there was a downward trend in the incidence of myocardial infarction in the group treated with clopidogrel in combination with ASA, but showed no significant differences in the frequency of thromboembolism vessels outside the Central nervous system or vascular death. In addition, clopidogrel in combination with ASA reduced the total number of days of hospitalization for cardiovascular reasons.


Suction. The single and repeated oral administration at a dose of 75 mg/day, clopidogrel is rapidly absorbed.

The average peak concentration of unchanged clopidogrel in plasma (approximately 2.2–2.5 ng/ml after ingestion of a single dose of 75 mg) are achieved after about 45 min after ingestion. According excretion of clopidogrel metabolites with the urine, its absorption is approximately 50%.

Distribution. In vitro clopidogrel and the main circulating inactive metabolite bind reversibly to plasma proteins (98% and 94%, respectively), and this is an unsaturated bond in a wide range of concentrations.

Metabolism. Clopidogrel is extensively metabolized in the liver. In vitro and in vivo, clopidogrel is metabolized in two ways: first — using esterase and subsequent hydrolysis with the formation of active metabolite, a carboxylic acid derivative (85% of circulating metabolites), and the second way is via cytochrome P450. First, 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 clopidogrel — Colnago derivative of clopidogrel. In vitro, this pathway occurs by means of P450 isoenzymes CYP2C19, CYP1A2 and СУР2В6. Carbothiolic active metabolite of clopidogrel, which has been highlighted in studies in vitro, rapidly and irreversibly binds to receptors on platelets, blocking platelet aggregation.

Excretion. Within 120 h after ingestion by a human of 14C-labelled clopidogrel is about 50% of radioactivity excreted in the urine and approximately 46% of the radioactivity — with the kalovymi masses. After a single oral dose of 75 mg T1/2 of clopidogrel is approximately 6 h After a single dose and receiving repeated doses T1/2 of the main circulating inactive metabolite is 8 h.

Pharmacogenetics. Using the isoenzyme CYP2C19 is formed as an active metabolite, and intermediate metabolite 2-oxo-clopidogrel. Pharmacokinetics and the antiplatelet effect of the active metabolite of clopidogrel in the study of platelet aggregation ex vivo, varies depending on the genotype of isozyme СУР2С19.

The allele of CYP2C19*1 corresponds to fully functional metabolism while the CYP2C19 alleles*2 and CYP2C19*3 are non-functional. The alleles CYP2C19*2 иСУР2С19*3 a decrease metabolism the majority of Caucasian (85%) and Mongoloid race (99%). Other allele, which is associated with the absence or reduced metabolism are less common and include, but are not limited to alleles of gene CYP2C19*4, *5, *6, *7 and *8. Patients with low activity изоферментаСУР2С19 must have the two above mentioned alleles of the gene with loss of function.

The published frequency of occurrence of phenotypes of individuals with the low activity изоферментаСУР2С19 constitute in persons of Caucasian — 2%, those blacks — 4% Chinese — 14%.

To determine the existing patient genotype isoenzyme СУР2С19 there are appropriate tests. According to cross-sectional studies (40 healthy volunteers) and meta-analysis of six studies (335 healthy volunteers) taking clopidogrel, which included healthy volunteers with a very high, high, intermediate and low activity of isoenzyme СУР2С19, no substantial differences in active metabolite exposure and mean values of inhibition of platelet aggregation (IAT) (indutsirovannaya) in healthy volunteers with very high, high and intermediate СУР2С19 isozyme activity have been identified. In healthy volunteers with low activity of isoenzyme СУР2С19 exposure of the active metabolite decreased in comparison with healthy dobrovolcu with high activity of isoenzyme СУР2С19.

When healthy volunteers with low activity of isoenzyme СУР2С19 received a treatment regimen of 600 mg loading dose/150 mg maintenance dose (600/150 mg), exposure of the active metabolite was higher than when the regimens 300/75 mg. in addition, the IAT was similar to that in the groups of healthy volunteers treated with clopidogrel, with a higher intensity of metabolism via the isoenzyme CYP2C19 receiving treatment 300/75 mg. the dosing regimen of clopidogrel with low activity of isoenzyme CYP2C19.


The prevention of atherothrombotic events in:

  • adult patients with myocardial infarction (with prescription from a few days up to 35 days), ischemic stroke (with a prescription from 7 days to 6 months) or with diagnosed occlusive peripheral arterial disease;
  • adult patients with acute coronary syndrome without ST-segment elevation (unstable angina or myocardial infarction without Q wave), including patients who was held stenting in percutaneous coronary intervention (in combination with ASA); c ST-segment elevation (acute myocardial infarction) treatment is medication and the possibility of thrombolysis (in combination with ASA).
  • Prevention of atherothrombotic and thromboembolic complications, including stroke, atrial fibrillation (atrial fibrillation).

Patients with atrial fibrillation (atrial fibrillation) that have at least one risk factor for vascular complications, can not accept indirect anticoagulants and have a low risk of bleeding (in combination with ASA).


  • hypersensitivity to clopidogrel or any of the excipients of the drug;
  • severe liver failure;
  • severe bleeding, such as bleeding peptic ulcer or intracranial hemorrhage;
  • rare hereditary lactose intolerance, lactase deficiency and glucose-galactose malabsorption;
  • pregnancy and lactation (see “pregnancy and breastfeeding”);
  • children up to age 18 years (safety and efficacy not established).

With caution in the following conditions: moderate hepatic impairment, where a possible predisposition to bleeding (limited clinical experience); renal failure (limited clinical experience); trauma, surgery (see “Special instructions”); a disease in which there is a predisposition to the development of bleeding (especially gastrointestinal or intra-ocular); concurrent administration of NSAIDs, including selective COX-2 inhibitors; coadministration of warfarin, heparin, inhibitors of the glycoprotein IIb/IIIA; patients with genetically determined decrease in the function of isoenzyme СУР2С19 (there are published data indicating that patients with genetically determined decrease in the function of isoenzyme СУР2С19 are exposed to lower systemic exposure of the active metabolite of clopidogrel and have a less pronounced antiplatelet effect of the drug, in addition they may experience increased frequency of cardiovascular complications after myocardial infarction compared with patients with normal function of isoenzyme СУР2С19); a history of the indication of an allergic reaction to thienopyridine (e.g. tiklopidin, prasugrel the possibility of cross — Allergy); recent transient ischemic stroke or ischemic stroke in the acute period

Special instructions

In the treatment with clopidogrel, especially during the first weeks of treatment and/or after invasive cardiologic procedures/surgery, you need to keep a careful monitoring of patients in order to exclude signs of hemorrhage, including hidden.

In connection with the risk of bleeding and haematological adverse effects (see “Side effects”) in case of occurrence in the course of treatment of clinical symptoms, suspicious on a bleeding occurs, it is necessary to do clinical blood test to determine APTT, the number of platelets, indicators of functional activity of platelets and other necessary research.

Clopidogrel as well as other antiplatelet drugs should be used with caution in patients having an increased risk of bleeding associated with injuries, surgery or other pathological conditions and in patients receiving ASA, other NSAIDs, including COX-2 inhibitors, heparin or inhibitors of glycoprotein IIb/IIIa.

The combined use of clopidogrel with warfarin may intensify the bleeding (see “Interactions”), therefore caution should be exercised when coadministration of clopidogrel and warfarin.

If a patient needs to undergo planned surgery, and no need for antiplatelet effect, that for 5-7 days before surgery, clopidogrel should be discontinued.

Clopidogrel prolongs bleeding time and should be used with caution in patients with diseases predisposing to the development of bleeding (particularly gastrointestinal and intraocular). Drugs that can cause damage to the mucosa of the gastrointestinal tract(NSAIDs, including ASA) in patients receiving clopidogrel should be used with caution.

Patients should be alerted to the fact that when taking clopidogrel (one or in combination with ASA) to stop bleeding may take more time, and that in case they have unusual (for localization or duration) bleeding, they should report this to your doctor. Before any upcoming surgery and before taking any new drug, patients should inform the doctor (including the dentist) of clopidogrel.

Very rarely following use of clopidogrel (sometimes even short) was the development of TTP, which is characterized by thrombocytopenia and microangiopathic hemolytic anemia, accompanied by neurological disorders, impaired renal function and fever. TTP is a potentially life-threatening condition requiring immediate treatment, including plasmapheresis.

It has been shown that in patients with recent transient ischemic stroke or stroke, have high risk of recurrent ischemic complications, the combination of ASA and clopidogrel increases the risk of large bleeding. Therefore, such combined treatment should be conducted with caution and only in case of clinical evidence of benefits from its use.

Reported cases of acquired haemophilia while taking clopidogrel. In case of confirmed isolated APTT increase, accompanied or not accompanied by the development of bleeding, should consider the possibility of development of acquired hemophilia. Patients with a confirmed diagnosis of acquired haemophilia should be observed and treated by specialists in this disease and to stop taking clopidogrel.

Patients will be interviewed on the subject of Allergy to thienopyridines (such as tiklopidin, prasugrel) in history, as it was reported the existence of cross-Allergy between thienopyridine and clopidogrel.

During treatment necessary to monitor the functional state of the liver. In severe lesions of the liver, be aware of the risk of the development of the hemorrhagic diathesis. Clopidogrel is not recommended for acute stroke with less prescription 7 days (because there are no data on its use in this condition).

Effects on ability to drive and use machines. Plavix® has no significant influence on the abilities required for driving or operating mechanisms.


Active substance: clopidogrel hydrosulfate in the form II97,875 mg (calculated as clopidogrel — 75 mg);

Auxiliary substances: mannitol — 68,925 mg, macrogol 6000 — 34 mg; ICC (low water content — 90 µm) — 31 mg; hyprolose nizkosoleva — 12,9 mg; hydrogenated castor oil and 3.3 mg; 

Shell film: Opadry pink (lactose monohydrate, hypromellose, titanium dioxide (E171), triacetin, colorant iron oxide red (E172) — 7,5 mg; Carnauba wax traces

Method of application and doses

Inside, regardless of meals.

Adults and the elderly with normal CYP2C19 isozyme activity

Myocardial infarction, ischemic stroke or diagnosed with occlusive peripheral arterial disease. The drug is taken for 75 mg 1 time per day.

Acute coronary syndrome without ST-segment elevation (unstable angina, myocardial infarction without the Q wave). Treatment with clopidogrel should be initiated with a single oral loading dose of 300 mg, and then continue to the dose 75 mg 1 times per day (in combination with ASA in doses of 75-325 mg/day). Since the use of higher doses of ASA are associated with an increased risk of bleeding recommended in this indication the dose of ASA should not exceed 100mg. the Optimal duration of treatment is not officially defined. These clinical studies support the drug up to 12 months, and the maximum favorable effect was observed for the 3rd months of treatment.

Acute coronary syndrome with ST-segment elevation (acute myocardial infarction with ST-segment elevation). Clopidogrel should be taken once a day at a dose of 75 mg with the initial one-time admission loading dose of clopidogrel 300 mg in combination with ASA in combination with thrombolytic drugs with or without combination with thrombolytic drugs. In patients older than 75 years, treatment with clopidogrel should be started without taking a loading dose. Combination therapy is started as early as possible after the onset of symptoms and continued for at least 4 weeks. The efficacy of the combination of clopidogrel and ASA in this indication more than 4 weeks has not been studied.

Atrial fibrillation (a-FIB). Clopidogrel should be taken 1 time a day at a dose of 75 mg In combination with clopidogrel should be started and then continue taking the ASA (75-100 mg/day).

Skip taking the next dose

1. If it’s been less than 12 hours after the pass reception of the next dose, then you should immediately take the missed dose and the next dose taken at the usual time.

2. If it has been more than 12 hours after the pass reception of the next dose, the patient should take the next dose at the usual time (should not take a double dose).

Patients with genetically reduced CYP2C19 isozyme activity

Low activity of isoenzyme CYP2C19 is associated with a decrease in the antiplatelet action of clopidogrel. The mode of application of higher doses (600 mg loading dose, then 150 mg 1 time / day) in patients with low activity of isoenzyme CYP2C19 increases the antiplatelet effect of clopidogrel (see “Pharmacokinetics”). Currently, however, in clinical studies, taking into account clinical outcomes, not the optimum dosing regimen of clopidogrel for patients with its reduced metabolism due to genetically determined low activity of isoenzyme СУР2С19.

Special groups of patients

The elderly. The volunteers of advanced age (over 75 years) when compared with young volunteers has not been received differences in platelet aggregation and bleeding time. No dose adjustment is required for elderly.

Children. No experience with the drug in children.

Patients with impaired renal function. After repeated taking clopidogrel at a dose of 75 mg/sutu patients with severe renal (Cl creatinine from 5 to 15 ml/min), inhibition of ADP-induced platelet aggregation (25%) was lower compared with that in healthy volunteers, however, the prolongation of bleeding time was similar to that in healthy volunteers who received clopidogrel at a dose of 75 mg/day. In addition, all patients had good tolerance of the drug.

Patients with impaired liver function. After daily within 10 days of receiving clopidogrel at a daily dose of 75 mg in patients with severe liver ingibirovaniya-induced platelet aggregation was similar to that in healthy volunteers. The average time of bleeding was also comparable in both groups.

Patients of different ethnicity. The prevalence of gene alleles of the CYP2C19 isoenzyme responsible for the intermediate and reduced metabolism of clopidogrel to its active metabolite, varies in different ethnic groups (see”Pharmacogenetics”). Limited data are available for representatives of the Mongoloid race to assess the impact of the isoenzyme CYP2C19 genotype on clinical outcome events.

Patients, male and female. In a small study comparing the pharmacodynamic properties of clopidogrel in men and women, women were observed less inhibition of ADP-induced platelet aggregation, but the difference in prolongation of bleeding time was not. In a large controlled study CAPRIE (clopidogrel in comparison with ASA in patients with risk of ischemic complications), the frequency of clinical outcomes and other side effects and deviations from normal clinical laboratory parameters was similar in men and women.

Side effects

From the nervous system: rare — headache, dizziness, paresthesia; rare — vertigo.

By the blood: often — dyspepsia, abdominal pain, diarrhea; infrequently — nausea, gastritis, bloating, constipation, vomiting, gastric ulcer, duodenal ulcer.

The skin and subcutaneous tissue: often — rash, itching.

The blood and lymphatic system: rarely — increased bleeding time, reduced platelet count in the peripheral blood, a leukopenia, a decrease in the number of neutrophils in peripheral blood eosinophilia.

Post-marketing experience with the drug

The blood and lymphatic system: unspecified frequency — cases of serious bleeding, predominantly subcutaneous, muscular-skeletal, eye bleeding (conjunctival, tissue and the retina of the eye), bleeding from the airway (hemoptysis, pulmonary bleeding), nasal bleeding, hematuria and bleeding from postoperative wounds and cases of bleeding with fatal outcome (especially intracranial hemorrhage, gastrointestinal bleeding and retroperitoneal hemorrhage), agranulocytosis, granulocytopenia, aplastic anemia/pancytopenia, thrombotic thrombocytopenic purpura (TTP), acquired hemophilia A.

The immune system: unspecified frequency — anaphylactoid reactions, serum sickness, cross-Allergy with other thienopyridine (such as tiklopidin, prasugrel — see “Special instructions”).

Psychiatric disorders: unknown frequency — confusion, hallucinations.

From the nervous system: unspecified frequency — violation of taste perception.

From the vessel: unknown frequency — vasculitis, decrease in blood pressure.

The respiratory system, chest and mediastinum disorders: unknown frequency — bronchospasm, interstitial pneumonia, eosinophilic pneumonia.

Gastrointestinal: unknown frequency — colitis (including ulcerative or lymphocytic ), pancreatitis, stomatitis.

The liver and biliary tract disorders: unknown frequency — hepatitis (non-infectious), acute liver failure.

The skin and subcutaneous tissue: unknown frequency — maculopapular erythematous or exfoliative rash, urticaria, pruritus, angioedema, bullous dermatitis (erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis), drug hypersensitivity syndrome, drug rash with eosinophilia and systemic manifestations (DRESS syndrome), eczema, flat lichen.

From the musculoskeletal and connective tissue: unknown frequency — arthralgia (joint pain), arthritis, myalgia.

The kidneys and urinary tract: unknown frequency — glomerular disease (e.g. glomerulonephritis).

General disorders injection site: unknown frequency fever.

Laboratory and instrumental data: unknown frequency of abnormal laboratory parameters of liver function, increasing the concentration of creatinine in the blood.

Drug interactions

Warfarin: although clopidogrel at a dose of 75 mg/day did not change the pharmacokinetics of warfarin (substrate of CYP2C9 isoenzyme) or INR in patients receiving long-term treatment with warfarin, concomitant use of clopidogrel increases the risk of bleeding in connection with an independent extra effect on blood clotting. Therefore, care should be taken while taking warfarin and clopidogrel.

Blockers IIb/IIIa receptor: assigning blockers IIb/IIIa receptor in conjunction with clopidogrel requires caution in patients with an increased risk of bleeding (trauma and surgical interventions or other pathological conditions) (see “Special instructions”).

The ASC does not alter the effect of clopidogrel inhibition of ADP-induced platelet aggregation, but clopidogrel potentiates the effect of ASA on kollageninducyruemuyu platelet aggregation. However, simultaneous with clopidogrel receiving ASA in dose 500 mg 2 times a day for 1 day did not cause an additional increase in bleeding time caused by clopidogrel. Between clopidogrel and ASA is possible pharmacodynamic interaction, which leads to increased risk of bleeding. Therefore, during their concomitant use caution, although in clinical studies, patients received combined therapy with clopidogrel and ASA is up to one year.

Heparin: in clinical trials conducted with the participation of healthy individuals, while clopidogrel did not require changing the dose of heparin and did not change its anticoagulant effects. Coadministration of heparin did not change the antiplatelet effect of clopidogrel. Between the drug plavix® and heparin is possible pharmacodynamic interaction, which may increase the risk of bleeding, so the simultaneous use of these drugs requires caution.

Thrombolytics: the safety of joint use of clopidogrel, fibrinoliticeski or fibrinoliticeski thrombolytic drugs and heparin was studied in patients with acute myocardial infarction. The frequency of clinically significant bleeding was similar to that observed in the case of a joint application means of the thrombolytic and heparin with ASA.

NSAIDs: in a clinical study involving healthy volunteers, the combined use of clopidogrel and naproxen increased the hidden blood loss through the gastrointestinal tract. However, due to the lack of research on the interaction of clopidogrel with other NSAIDs, it is currently unknown whether the increased risk of gastrointestinal bleeding when taking clopidogrel with other NSAIDs. Therefore, the appointment of NSAIDs, including COX-2 inhibitors in combination with clopidogrel should be undertaken with caution (see “Special instructions”).

Other drug interactions. Since clopidogrel is metabolized to the formation of its active metabolite partly with the help of isozyme CYP2C19, use of drugs inhibiting this isoenzyme, may result in lower levels of the active metabolite of clopidogrel. The clinical significance of this interaction is not established.

Avoid concurrent use with clopidogrel strong or moderate inhibitors of the isoenzyme CYP2C19 (e.g. omeprazole or esomeprazole see “Pharmacokinetics” subsection of the “Pharmacogenetics”; “Special instructions”). If the proton pump inhibitors should be taken concurrently with clopidogrel, use proton pump inhibitors with the least inhibition of CYP2C19 isoenzyme, such as pantoprazole or lansoprazole.

Conducted a series of clinical trials with clopidogrel and other, simultaneously used drugs, with the aim of exploring the possible pharmacodynamic and pharmacokinetic interactions, which showed that:

– the use of clopidogrel in conjunction with atenolol, nifedipine or their combination clinically significant pharmacodynamic interactions were observed;

– concurrent use of phenobarbital, cimetidine or estrogen had no significant influence on the pharmacodynamics of clopidogrel;

– the pharmacokinetic parameters of digoxin or theophylline were not changed in their joint application with clopidogrel;

– antacids did not reduce the absorption of clopidogrel;

– phenytoin and tolbutamide can be safely used in conjunction with clopidogrel (CAPRIE study). It is unlikely that clopidogrel may affect the metabolism of other drugs, such as phenytoin and tolbutamide and the NSAIDs, which are metabolized through CYP2C9 isoenzyme of the cytochrome P450 family.

– ACE inhibitors, diuretics, beta-blockers, CCB, hypolipidemic funds, coronary vasodilators, hypoglycemic drugs (including insulin), antiepileptic means, means hormone replacement therapy and blockers of GPIIb/IIIa receptor: in clinical studies, no clinically significant undesirable interactions.


Symptoms: overdose of clopidogrel may increase bleeding time with subsequent complications in the form of development of hemorrhage.

Treatment: at the onset of bleeding requires the implementation of appropriate remedial measures. If you need a fast correction of the lengthening of bleeding time, it is recommended that the platelet transfusion. The antidote clopidogrel is not installed.

Storage conditions

At temperatures above 30 °C.

Shelf life

3 years

Additional Information

SKU ml5192
Manufacturer Sanofi
The purpose of the medication Anti-aggregants
Weight kg. 0.05

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