Pathways

Metabolites of Tiaprofenic acid are predicted with biotransformer.

Ticagrelor also known via brand names Brilinta or Brilique, is a platelet inhibitor used to prevent infarction, stroke or cardiovascular death. Once administered orally it travels to the bloodstream and acts on platelets' P2Y receptors which inhibits the formation of thromboses. An activated P2Y receptor couples with guanine nucleotide-binding protein subunit i2 that inhibits adenylyl cyclase. By inhibiting adenylyl cyclase, it stops the formation of cAMP, leading to a stop of calcium efflux causing platelet aggregation and activation. Grapefruit products should be avoided as it inhibits the CYP3A4 metabolism of ticagrelor and cause an increase in the drug which may lead to an overdose. Herbs and supplements with anticoagulant and antiplatelet activity should be avoided such as garlic, ginger, bilberry, danshen, piracetam and ginkgo biloba. St. John's Wort induces the CYP3A4 metabolism of the drug and will reduce its efficacy and concentration.

Metabolites of Ticagrelor are predicted with biotransformer.

Metabolites of Ticarcillin are predicted with biotransformer.

Ticlopidine, marketed as Ticlid, is an antiplatelet drug that targets the P2Y12 receptor of platelets. Ticlopidine is taken orally - evidence shows that food increases its absorption. It is a prodrug that must be metabolically activated before it can be effective. It first enters the liver and enters the endoplasmic reticulum where it is metabolized to form the active metabolite. First, it is catalyzed by cytochromes P450 2C19, 2B6 and 1A2 into 2-oxoclopidogrel. Secondly, it is processed by cytochromes P450 2B6, 2C9, 2C19, 3A4, 3A5, and serum paraoxonase/arylesterase 1 into the active metabolite of clopidogrel. The active metabolite of clopidogrel then enters the blood stream, where it binds irreversibly to the P2Y purinoreceptor 12 on the surface of platelet cells, preventing ADP from binding to and activating it. Clopidogrel prevents the activation of the Gi protein associated with the P2Y12 receptor from inactivating adenylate cyclase in the platelet, leading to a buildup of cAMP. This cAMP then activates calcium efflux pumps, preventing calcium buildup in the platelet, which would cause activation, and later, aggregation. By blocking the ADP receptor that is involved in GPIIb/IIIa receptor activation leading to platelet aggregation, ticlopidine is an effective platelet aggregation inhibitor (especially for patients unable to take aspirin) and is used in the prevention of conditions associated with thrombi, such as stroke and transient ischemic attacks. Note that the FDA has labelled ticlopidine with a black-box warning of neutropenia, aplastic anemia, thrombotic thrombocytopenia purpura, and agranulocytosis: clinicians must monitor patients taking this drug. Ticlopidine is metabolized extensively by the liver.

Ticlopidine, marketed as Ticlid, is an antiplatelet drug that targets the P2Y12 receptor of platelets. Ticlopidine is taken orally and is a prodrug that must be metabolically activated before it can be effective. It first enters the liver and enters the endoplasmic reticulum where it is metabolized to form the active metabolite. First, it is catalyzed by cytochromes P450 2C19, 2B6 and 1A2 into 2-oxoclopidogrel. Secondly, it is processed by cytochromes P450 2B6, 2C9, 2C19, 3A4, 3A5, and serum paraoxonase/arylesterase 1 into the active metabolite of clopidogrel. The active metabolite of clopidogrel then enters the blood stream, where it binds irreversibly to the P2Y purinoreceptor 12 on the surface of platelet cells, preventing ADP from binding to and activating it. Clopidogrel prevents the activation of the Gi protein associated with the P2Y12 receptor from inactivating adenylate cyclase in the platelet, leading to a buildup of cAMP. This cAMP then activates calcium efflux pumps, preventing calcium buildup in the platelet, which would cause activation, and later, aggregation.