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Pathways

PathWhiz ID Pathway Meta Data

PW144557

Pw144557 View Pathway
drug action

Trifluridine Drug Metabolism Action Pathway

Homo sapiens

PW176178

Pw176178 View Pathway
metabolic

Trifluridine Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Trifluridine are predicted with biotransformer.

PW128148

Pw128148 View Pathway
drug action

Triflusal Action Pathway

Homo sapiens
Triflusal is a 2-acetoxy-4-trifluorobenzoic acid chemically related to acetylsalicylic acid. This drug has antithrombotic effects by inhibiting irreversibly the cycloxygenase-1 (COX-1) in the platelets. It is indicated as prophylaxis of thromboembolic disorders (prevention of strokes and myocardial infarction). Trifusal binds to the prostaglandin G/H synthase 1, this inhibits the production of thromboxane-B2 in cells. It also acts on many other cellular targets like NF kappa B, which is a gene expression regulatory factor for cycloxygenase-a and cytokines. In addition, this drug induces the production of nitric oxide by binding as an agonist to the nitric oxide synthase. The high level of nitric oxide results in vasodilatation. Trifusal is administered as an oral tablet.

PW128147

Pw128147 View Pathway
drug action

Triflusal Action Pathway (new)

Homo sapiens
Triflusal is a chemically related molecule similar to aspirin, used to treat thromboembolic diseases due to the antithrombotic effects. Triflusal is administered orally and acts as an antithrombotic anticoagulant that irreversibly inhibits cyclooxygenase-1(COX-1) also known as prostaglandin g/h synthase 1. By inhibiting COX-1 this prevents the formation of thromboxane B2 in platelets, unlike aspirin, it does not act on arachidonic acid in endothelial cells. The drug is metabolized into 2-hydroxy-4-trifluoromethyl benzoic acid, which also appears to have antiplatelet properties. Due to the anticoagulant and antiplatelet nature, herbs and supplements with similar activity should be avoided such as garlic, ginger, bilberry, danshen, piracetam and ginkgo biloba.

PW145839

Pw145839 View Pathway
drug action

Triflusal Drug Metabolism Action Pathway

Homo sapiens

PW121865

Pw121865 View Pathway
disease

Trifunctional Protein Deficiency

Mus musculus
Trifunctional protein deficiency is a condition caused by mutations in the genes HADHA and HADHB. The enzyme affected is required to metabolize long-chain fatty acids, which makes a patients ability to convert fats to energy very difficult. This is exacerbated by periods without food. The symptoms associated with this disorder differ depending on when they appear in a patient. In infancy, symptoms would include lethargy, hypoglycaemia and hypotonia. Infants are also at higher risk for sudden death and heart problems. Later onset trifunctional protein deficiency symptoms also include hypotonia, but also include breakdown of muscle tissue and peripheral neuropathy. Treatment includes a low-fat, high-carbohydrate diet and avoiding fasting, as this can induce symptoms of this condition.

PW122089

Pw122089 View Pathway
disease

Trifunctional Protein Deficiency

Rattus norvegicus
Trifunctional protein deficiency is a condition caused by mutations in the genes HADHA and HADHB. The enzyme affected is required to metabolize long-chain fatty acids, which makes a patients ability to convert fats to energy very difficult. This is exacerbated by periods without food. The symptoms associated with this disorder differ depending on when they appear in a patient. In infancy, symptoms would include lethargy, hypoglycaemia and hypotonia. Infants are also at higher risk for sudden death and heart problems. Later onset trifunctional protein deficiency symptoms also include hypotonia, but also include breakdown of muscle tissue and peripheral neuropathy. Treatment includes a low-fat, high-carbohydrate diet and avoiding fasting, as this can induce symptoms of this condition.

PW000521

Pw000521 View Pathway
disease

Trifunctional Protein Deficiency

Homo sapiens
Trifunctional protein deficiency is a condition caused by mutations in the genes HADHA and HADHB. The enzyme affected is required to metabolize long-chain fatty acids, which makes a patients ability to convert fats to energy very difficult. This is exacerbated by periods without food. The symptoms associated with this disorder differ depending on when they appear in a patient. In infancy, symptoms would include lethargy, hypoglycaemia and hypotonia. Infants are also at higher risk for sudden death and heart problems. Later onset trifunctional protein deficiency symptoms also include hypotonia, but also include breakdown of muscle tissue and peripheral neuropathy. Treatment includes a low-fat, high-carbohydrate diet and avoiding fasting, as this can induce symptoms of this condition.

PW127311

Pw127311 View Pathway
disease

Trifunctional Protein Deficiency

Homo sapiens
Trifunctional protein deficiency is a condition caused by mutations in the genes HADHA and HADHB. The enzyme affected is required to metabolize long-chain fatty acids, which makes a patients ability to convert fats to energy very difficult. This is exacerbated by periods without food. The symptoms associated with this disorder differ depending on when they appear in a patient. In infancy, symptoms would include lethargy, hypoglycaemia and hypotonia. Infants are also at higher risk for sudden death and heart problems. Later onset trifunctional protein deficiency symptoms also include hypotonia, but also include breakdown of muscle tissue and peripheral neuropathy. Treatment includes a low-fat, high-carbohydrate diet and avoiding fasting, as this can induce symptoms of this condition.

PW146424

Pw146424 View Pathway
drug action

Triheptanoin Drug Metabolism Action Pathway

Homo sapiens