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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.

PW145839

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drug action

Triflusal Drug Metabolism Action Pathway

Homo sapiens

PW128147

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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.

PW128148

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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.

PW176178

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metabolic

Trifluridine Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Trifluridine are predicted with biotransformer.

PW144557

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drug action

Trifluridine Drug Metabolism Action Pathway

Homo sapiens

PW127471

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drug action

Trifluridine Action Pathway

Homo sapiens
Trifluridine is a fluorinated pyrimidine nucleoside that is structurally related to idoxuridine and an active antiviral agent in ophthalmic solutions that is mainly used in the treatment of primary keratoxonjunctivitis and recurrent epithelial keratitis due to herpes simplex virus. It displays effective antiviral activity against Herpes simplex virus type 1 and 2. The mechanism of action of trifluridine as an antiviral agent has not been fully elucidated, but appears to involve the inhibition of viral replication. Trifluridine gets incorporated into viral DNA during replication in replacement of thymidine, which leads to the formation of defective proteins and an increased mutation rate. Less Viral DNA is transported into the nucleus, therefore, less viral DNA is integrated into the host DNA. Less viral proteins produced, fewer viruses can form. Trifluridine also mediates antineoplastic activities via this mechanism; following uptake into cancer cells, trifluridine is rapidly phosphorylated by thymidine kinase to its active monophosphate form. It is further phosphorylated into trifluridine triphosphate, which is readily incorporated into the DNA of tumour cells in place of thymidine bases to perturb DNA function, DNA synthesis, and tumour cell proliferation.

PW128151

Pw128151 View Pathway
drug action

Triflupromazine Serotonin Antagonist Action Pathway

Homo sapiens
Triflupromazine is a member of a class of drugs called phenothiazines, which are dopamine D1/D2 receptor antagonists. Triflupromazine is used particularly to control violent behavior during acute episodes of psychotic disorders. It can also be used to control severe nausea and vomiting, severe hiccups, and moderate to severe pain in some hospitalized patients. Triflupromazine acts on the central nervous system. The mechanism of the anti-emetic effect is due predominantly to blockage of the dopamine D2 neurotransmitter receptors in the chemoreceptor trigger zone (CTZ) and vomiting centre. Triflupromazine blocks the neurotransmitter dopamine and the vagus nerve in the gastrointestinal tract. Triflupromazine also binds the muscarinic acetylcholine receptors (M1 and M2) and the tryptamine D receptors (5HT2B). Dopamine hypothesis states that dopamine abnormalities in the mesolimbic and prefrontal brain regions exist in schizophrenia.

PW128090

Pw128090 View Pathway
drug action

Triflupromazine Mechanism of Action Action Pathway

Homo sapiens
Triflupromazine is a member of a class of drugs called phenothiazines, which are dopamine D1/D2 receptor antagonists. Triflupromazine is used particularly to control violent behavior during acute episodes of psychotic disorders. It can also be used to control severe nausea and vomiting, severe hiccups, and moderate to severe pain in some hospitalized patients. Triflupromazine acts on the central nervous system. The mechanism of the anti-emetic effect is due predominantly to blockage of the dopamine D2 neurotransmitter receptors in the chemoreceptor trigger zone (CTZ) and vomiting centre. Triflupromazine blocks the neurotransmitter dopamine and the vagus nerve in the gastrointestinal tract. Triflupromazine also binds the muscarinic acetylcholine receptors (M1 and M2) and the tryptamine D receptors (5HT2B). Dopamine hypothesis states that dopamine abnormalities in the mesolimbic and prefrontal brain regions exist in schizophrenia.

PW144628

Pw144628 View Pathway
drug action

Triflupromazine Drug Metabolism Action Pathway

Homo sapiens