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Pathways

PathWhiz ID Pathway Meta Data

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

PW127991

Pw127991 View Pathway
drug action

Trihexyphenidyl Action Pathway

Homo sapiens
Trihexyphenidyl is an antispasmodic drug used as an adjunct drug in the management of parkinsonism and as a treatment for extrapyramidal symptoms caused by drugs affecting the central nervous system (CNS). Trihexyphenidyl is a non-selective muscarinic acetylcholine receptor antagonist but binds with higher affinity to the M1 subtype. In vivo studies have shown that trihexyphenidyl demonstrates higher affinity for central muscarinic receptors located in the cerebral cortex and lower affinity for those located peripherally. Other studies suggest that trihexyphenidyl may modify nicotinic acetylcholine receptor neurotransmission, leading indirectly to enhanced dopamine release in the striatum. Although the anticholinergic has proven to be useful in the treatment of symptoms associated with Parkinson’s disease or other movement disorders, its mechanism of action has yet to be fully elucidated. The precise mechanism of action of trihexyphenidyl remains inadequately comprehended; it appears to act on the parasympathetic nervous system by inhibiting efferent impulses directly. Structures innervated by the parasympathetic system, such as the salivary glands, eyes, and smooth muscles (directly and indirectly), are affected, even at smaller doses. Possible side effects of using Trihexyphenidyl may include dry mouth, constipation, nausea, and vomiting. Trihexyphenidyl is administered as an oral tablet.

PW144502

Pw144502 View Pathway
drug action

Trihexyphenidyl Drug Metabolism Action Pathway

Homo sapiens