(clopidogrel · DailyMed)
MOYOGEZ
ROSUVASTATIN & CLOPIDOGREL
What it does
Clopidogrel is a medication that helps prevent blood clots by making your blood less sticky.
Commonly used for: prevention of heart attacks, prevention of strokes, peripheral artery disease management
Read more in plain English ↓Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.
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Source: Pharmacy and Poisons Board · fetched 2026-01-28 21:51:50 · updated 2026-03-23 04:36:56
Drug Interactions
126Pharmacodynamic Warnings
Rosuvastatin appears in TABLE 1: Drugs that cause hepatotoxicity
Clopidogrel appears in TABLE 4: Drugs with antiplatelet effects
Severe (13)
Clopidogrel - decreases efficacy
Voriconazole is predicted to decrease the efficacy of clopidogrel. Avoid.
Clopidogrel - decreases efficacy
HIV-protease inhibitors (ritonavir) might decrease the efficacy of clopidogrel. Avoid.
Clopidogrel - decreases efficacy
Moclobemide is predicted to decrease the efficacy of clopidogrel. Avoid.
Clopidogrel - decreases efficacy
Ritonavirmightdecreasetheefficacyofclopidogrel.Avoid. oTheoretical
Rosuvastatin - increases exposure
Darolutamide is predicted to increase the exposure to statins (atorvastatin, fluvastatin, rosuvastatin). Avoid.
Moderate (28)
Pioglitazone - increases exposure
Clopidogrel increases the exposure to pioglitazone. Monitor blood glucose and adjust dose.
Rosuvastatin - increases exposure
Dronedarone slightly increases the exposure to statins (rosuvastatin). Adjust dose.
Rosuvastatin - increases exposure
Leflunomide is predicted to increase the exposure to statins (rosuvastatin). Adjust dose. Also see TABLE 1 p. 1517
Rosuvastatin - increases exposure
Roxadustat is predicted to increase the exposure to statins (atorvastatin, pravastatin, rosuvastatin, simvastatin). Monitor adverse effects and adjust dose.
Statins - increases exposure
Amiodarone is predicted to increase the exposure to statins (atorvastatin). Monitor and adjust dose.
Unknown (85)
Alitretinoin - increases exposure
Clopidogrel is predicted to increase the exposure to retinoids (alitretinoin). Adjust alitretinoin dose, p. 1382.
Anti-Androgens - increases exposure
Clopidogrel is predicted to increase the exposure to anti-androgens (apalutamide) and anti-androgens (apalutamide) are predicted to increase the exposure to the active metabolite of clopidogrel. Avoid
Apalutamide - increases exposure
Clopidogrel is predicted to increase the exposure to anti-androgens (apalutamide) and anti-androgens (apalutamide) are predicted to increase the exposure to the active metabolite of clopidogrel. Avoid
Apalutamide And Apalutamide Is Predicted To Increase The Https - increases exposure
Clopidogrelispredictedtoincreasetheexposureto apalutamideandapalutamideispredictedtoincreasethe https://www.facebook.c (Books-Courses-Medic
Clopidogrel - decreases efficacy
Fluconazoleispredictedtodecreasetheefficacyofclopidogrel. Avoid.rTheoretical
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: exact
About clopidogrel
Clopidogrel is a medication that helps prevent blood clots by making your blood less sticky.
What it treats
- prevention of heart attacks
- prevention of strokes
- peripheral artery disease management
How it works
Clopidogrel works by blocking platelets in your blood from sticking together, which helps to keep your blood flowing smoothly.
Who it's for
Clopidogrel is for individuals at risk of blood clots, such as those with heart conditions or a history of strokes.
Cautions
- • Avoid combining with other medications that also prevent blood clots.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
About rosuvastatin
Rosuvastatin is a medication that helps lower cholesterol levels in the blood.
What it treats
- high cholesterol (hyperlipidemia)
- prevention of heart disease
How it works
It works by blocking a substance your body needs to make cholesterol, thus reducing the amount of cholesterol in the blood.
Who it's for
This medication is for adults who need help managing their cholesterol levels.
Drug class
Statins
Cautions
- • Avoid using if you are taking medications that can harm the liver.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: Clopidogrel
BNF-referencedClopidogrel is an antiplatelet medication that belongs to the thienopyridine class. It is primarily used to prevent atherothrombotic events in patients at risk of myocardial infarction, stroke, and other cardiovascular complications. Clopidogrel is administered orally and is known for its ability to irreversibly inhibit platelet aggregation, thereby reducing the risk of clot formation. Its long duration of action and once-daily dosing make it a convenient option in clinical practice.
Indications
- Prevention of atherothrombotic events in patients with acute coronary syndrome
- Secondary prevention of ischaemic stroke
- Prevention of atherothrombotic events in peripheral arterial disease
Mechanism of action
Clopidogrel is activated through a two-step metabolic process to form an active thiol-containing metabolite. This metabolite irreversibly binds to the P2Y12 ADP receptors on platelets, preventing ADP from activating the GPIIb/IIIa complex, which is crucial for platelet aggregation. As a result, clopidogrel inhibits platelet aggregation for the lifespan of the platelets (approximately 7 to 10 days). The inhibition of the P2Y12 receptor reduces platelet activation and aggregation not just from ADP, but also from other agonists.
Pharmacodynamics
Clopidogrel is a prodrug that serves as a potent antiplatelet agent, effectively reducing the risk of myocardial infarction and stroke. Its pharmacological effects are long-lasting, allowing for once-daily dosing. Clopidogrel exhibits a broad therapeutic window, and its dosage ranges from 75 mg to 300 mg per day, depending on the clinical scenario. Its action helps maintain blood flow and prevent occlusive vascular events.
Pharmacokinetics
Clopidogrel is well absorbed in the gastrointestinal tract, with peak plasma concentrations occurring within 1 to 2 hours after oral administration. It undergoes extensive hepatic metabolism, primarily through CYP450 enzymes, which convert it into its active form. The elimination half-life of clopidogrel is approximately 6 hours, but the antiplatelet effect lasts much longer due to the irreversible nature of its action on platelets. It is primarily excreted through urine, with a majority of the dose eliminated as inactive metabolites.
Contra-indications
- Active bleeding
Adverse effects
- Confusion
- Fever
- Gynaecomastia
- Hallucination
- Hepatic disorders
- Hypotension
- Myalgia
- Neutropenia
- Severe cutaneous adverse reactions (SCARs)
- Stomatitis
- Taste altered
- Ulcerative colitis
- Vasculitis
- Vertigo
- Wound haemorrhage
Interactions
- Voriconazole + clopidogrel: Severe (decreases efficacy)
- HIV protease inhibitors + clopidogrel: Severe (decreases efficacy)
- Moclobemide + clopidogrel: Severe (decreases efficacy)
- Ritonavir + clopidogrel: Severe (decreases efficacy)
- Clopidogrel + pioglitazone: Moderate (increases exposure)
- Clopidogrel + treprostinil: Moderate (increases exposure)
- Clopidogrel + apalutamide: Unknown (increases exposure)
- Clopidogrel + enzalutamide: Unknown (increases exposure)
- Fluconazole + clopidogrel: Unknown (decreases efficacy)
- Clopidogrel + anti-androgens: Unknown (increases exposure)
Precautions
- Caution with history of hypersensitivity reactions to thienopyridines
- Caution in moderate hepatic impairment
- Caution in renal impairment
- Discontinue 7 days before elective surgery if antiplatelet effect not desirable
- Patients at risk of increased bleeding from trauma, surgery, or other pathological conditions
Pregnancy
Manufacturer advises avoid-no information available.
Breast-feeding
Manufacturer advises avoid.
Storage
Store in a cool, dry place, away from direct sunlight.
Formulations
- Clopidogrel 75 mg tablet
- Clopidogrel 300 mg tablet
- Clopidogrel oral suspension
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Clinical monograph: Rosuvastatin
BNF-referencedRosuvastatin is a synthetic statin medication used primarily as an antilipemic agent to lower cholesterol levels in the blood. It is particularly effective in reducing low-density lipoprotein cholesterol (LDL-C) and triglycerides while increasing high-density lipoprotein cholesterol (HDL-C). Rosuvastatin works by inhibiting the enzyme HMG-CoA reductase, leading to decreased hepatic cholesterol synthesis and increased clearance of LDL from the bloodstream. This mechanism contributes to its role in managing hyperlipidaemia and reducing cardiovascular risk.
Mechanism of action
Rosuvastatin acts as a competitive inhibitor of HMG-CoA reductase, the enzyme responsible for converting HMG-CoA to mevalonate, a crucial step in cholesterol biosynthesis. By inhibiting this enzyme, rosuvastatin decreases hepatic cholesterol levels, which in turn upregulates the expression of hepatic LDL receptors, enhancing the uptake of LDL cholesterol from the circulation. Additionally, it reduces the hepatic synthesis of very low-density lipoprotein (VLDL). Beyond its lipid-lowering effects, rosuvastatin exhibits pleiotropic effects, improving endothelial function, stabilizing atherosclerotic plaques, reducing oxidative stress and inflammation, and inhibiting thrombogenic responses.
Pharmacodynamics
Rosuvastatin effectively lowers total cholesterol, LDL-C, apolipoprotein B (apoB), and triglycerides while raising HDL-C levels. High levels of LDL-C and triglycerides, along with low HDL-C, are associated with an increased risk of atherosclerosis and cardiovascular disease (CVD). By improving the total cholesterol to HDL-C ratio, rosuvastatin reduces the risk of cardiovascular morbidity and mortality. Statins, including rosuvastatin, are considered cost-effective in managing CVD due to their significant impact on reducing LDL levels and overall cardiovascular risk.
Pharmacokinetics
Rosuvastatin is rapidly absorbed after oral administration, with peak plasma concentrations typically occurring within 3 to 5 hours. It has a bioavailability of approximately 20%, and its absorption is not significantly affected by food. The drug is primarily metabolized in the liver, and about 90% of the administered dose is excreted in the faeces, with the remainder eliminated via urine. The half-life of rosuvastatin is approximately 19 hours, allowing for once-daily dosing. Renal impairment may
Contra-indications
- Active liver disease
- Pregnancy
- Known hypersensitivity to rosuvastatin or any excipients
Adverse effects
- Muscle weakness
- Myopathy
- Rhabdomyolysis
- Abnormal liver function tests
- Gastrointestinal disturbances
- Headache
- Dizziness
- Allergic reactions including angioedema
Interactions
- Ciclosporin increases exposure
- Darolutamide increases exposure
- Letermovir increases exposure
- Tedizolid increases exposure
- Voxilaprevir with sofosbuvir and velpatasvir markedly increases exposure
- Dronedarone moderately increases exposure
- Leflunomide moderately increases exposure
- Roxadustat moderately increases exposure
- Apalutamide decreases exposure
- Eslicarbazepine decreases exposure
Precautions
- Monitor liver function tests prior to and during treatment
- Use with caution in patients with a history of muscle disorders
- Caution in patients with renal impairment
- Consider alternative therapy for patients with a history of statin intolerance
Pregnancy
Manufacturer advises against use during pregnancy due to potential harm to the fetus.
Breast-feeding
Manufacturer advises avoiding use during breastfeeding, as small amounts may be present in breast milk.
Storage
Store in a cool, dry place below 30°C. Protect from light.
Formulations
- Tablets: 5 mg, 10 mg, 20 mg, 40 mg
- Oral suspension
- Oral solution
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: Clopidogrel
PubChem CID 60606Molecular formula: C16H16ClNO2S
Mechanism of action
Clopidogrel is activated via a 2 steps reaction to an active thiol-containing metabolite. This active form is a platelet inhibitor that irreversibly binds to P2Y<sub>12</sub> ADP receptors on platelets. This binding prevents ADP binding to P2Y<sub>12</sub> receptors, activation of the glycoprotein GPIIb/IIIa complex, and platelet aggregation. Clopidogrel must be metabolized by CYP450 enzymes to produce the active metabolite that inhibits platelet aggregation. The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible. Consequently, platelets exposed to clopidogrel's active metabolite are affected for the remainder of their lifespan (about 7 to 10 days). Platelet aggregation induced by agonists other than ADP is also inhibited by blocking the amplification of platelet activation by released ADP. The P2Y12 receptor plays a crucial role in the regulation of platelet activation by several agonists, which is irreversibly antagonized by the active metabolite of clopidogrel, a widely used anti-thrombotic drug. In this study, we investigated whether reduction of platelet reactivity leads to reduced inflammatory responses using a rat model of erosive arthritis. We evaluated the effect of clopidogrel on inflammation in Lewis rats in a peptidoglycan polysaccharide (PG-PS)-induced arthritis model with four groups of rats: 1) untreated, 2) clopidogrel-treated, 3) PG-PS-induced, and 4) PG-PS-induced and clopidogrel-treated. There were significant differences between the PG-PS+clopidogrel group when compared to the PG-PS group including: increased joint diameter and clinical manifestations of inflammation, elevated plasma levels of pro-inflammatory cytokines (IL-1 beta, interferon (IFN) gamma, and IL-6), an elevated neutrophil blood count and an increased circulating platelet count. Plasma levels of IL-10 were significantly lower in the PG-PS+clopidogrel group compared to the PG-PS group. Plasma levels of platelet factor 4 (PF4) were elevated in both the PG-PS and the PG-PS+clopidogrel groups, however PF4 levels showed no difference upon clopidogrel treatment, suggesting that the pro- inflammatory effect of clopidogrel may be due to its action on cells other than platelets. Histology indicated an increase in leukocyte infiltration at the inflammatory area of the joint, increased pannus formation, blood vessel proliferation, subsynovial fibrosis and cartilage erosion upon treatment with clopidogrel in PG-PS-induced arthritis animals. In summary, animals treated with clopidogrel showed a pro-inflammatory effect in the PG-PS-induced arthritis animal model, which might not be mediated by platelets.
Pharmacodynamics
Clopidogrel is a prodrug of a platelet inhibitor used to reduce the risk of myocardial infarction and stroke. It has a long duration of action as it is taken once daily and a large therapeutic window as it is given in doses of 75-300mg daily.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
Molecular reference: Rosuvastatin
PubChem CID 446157Molecular formula: C22H28FN3O6S
Mechanism of action
Rosuvastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Rosuvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low density lipoprotein (LDL) receptors which increases hepatic uptake of LDL. Rosuvastatin also inhibits hepatic synthesis of very low density lipoprotein (VLDL). The overall effect is a decrease in plasma LDL and VLDL. In vitro and in vivo animal studies also demonstrate that rosuvastatin exerts vasculoprotective effects independent of its lipid-lowering properties, also known as the pleiotropic effects of statins. This includes improvement in endothelial function, enhanced stability of atherosclerotic plaques, reduced oxidative stress and inflammation, and inhibition of the thrombogenic response. Statins have also been found to bind allosterically to β2 integrin function-associated antigen-1 (LFA-1), which plays an important role in leukocyte trafficking and in T cell activation. Rosuvastatin exerts an anti-inflammatory effect on rat mesenteric microvascular endothelium by attenuating leukocyte rolling, adherence and transmigration. The drug also modulates nitric oxide synthase (NOS) expression and reduces ischemic-reperfusion injuries in rat hearts. Rosuvastatin increases the bioavailability of nitric oxide by upregulating NOS and by increasing the stability of NOS through post-transcriptional polyadenylation. It is unclear as to how rosuvastatin brings about these effects though they may be due to decreased concentrations of mevalonic acid. Crestor is a selective and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate, a precursor of cholesterol. In vivo studies in animals, and in vitro studies in cultured animal and human cells have shown rosuvastatin to have a high uptake into, and selectivity for, action in the liver, the target organ for cholesterol lowering. In in vivo and in vitro studies, rosuvastatin produces its lipid-modifying effects in two ways. First, it increases the number of hepatic LDL receptors on the cell-surface to enhance uptake and catabolism of LDL. Second, rosuvastatin inhibits hepatic synthesis of VLDL, which reduces the total number of VLDL and LDL particles.
Pharmacodynamics
Rosuvastatin is a synthetic, enantiomerically pure antilipemic agent. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and trigleride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, rosuvastatin reduces the risk of cardiovascular morbidity and mortality. Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD. Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality. Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack. Evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within 5 years) statins cause a 20%-22% relative reduction in major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks. **Skeletal Muscle Effects** Cases of myopathy and rhabdomyolysis with acute renal failure secondary to myoglobinuria have been reported with HMG-CoA reductase inhibitors, including rosuvastatin. These risks can occur at any dose level, but are increased at the highest dose (40 mg). Rosuvastatin should be prescribed with caution in patients with predisposing factors for myopathy (e.g., age ≥ 65 years, inadequately treated hypothyroidism, renal impairment). The risk of myopathy during treatment with rosuvastatin may be increased with concurrent administration of some other lipid-lowering therapies (such as [fenofibrate] or [niacin]), [gemfibrozil], [cyclosporine], [atazanavir]/[ritonavir], [lopinavir]/ritonavir, or [simeprevir]. Cases of myopathy, including rhabdomyolysis, have been reported with HMG-CoA reductase inhibitors, including rosuvastatin, coadministered with [colchicine], and caution should therefore be exercised when prescribing these two medications together. Real-world data from observational studies has suggested that 10-15% of people taking statins may experience muscle aches at some point during treatment. **Liver Enzyme Abnormalities** Increases in serum transaminases have been reported with HMG-CoA reductase inhibitors, including rosuvastatin. In most cases, the elevations were transient and resolved or improved on continued therapy or after a brief interruption in therapy. There were two cases of jaundice, for which a relationship to rosuvastatin therapy could not be determined, which resolved after discontinuation of therapy. There were no cases of liver failure or irreversible liver disease in these trials. **Endocrine Effects** Increases in HbA1c and fasting serum glucose levels have been reported with HMG-CoA reductase inhibitors, including rosuvastatin calcium tablets. Based on clinical trial data with rosuvastatin, in some instances these increases may exceed the threshold for the diagnosis of diabetes mellitus. An in vitro study found that [atorvastatin], [pravastatin], [rosuvastatin], and [pitavastatin] exhibited a dose-dependent cytotoxic effect on human pancreas islet β cells, with reductions in cell viability of 32, 41, 34 and 29%, respectively, versus control]. Moreover, insulin secretion rates wer
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
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