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Pathways

PathWhiz ID Pathway Meta Data

PW145969

Pw145969 View Pathway
drug action

Trimebutine Drug Metabolism Action Pathway

Homo sapiens

PW145197

Pw145197 View Pathway
drug action

Trilostane Drug Metabolism Action Pathway

Homo sapiens

PW176156

Pw176156 View Pathway
metabolic

Trilaciclib Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Trilaciclib are predicted with biotransformer.

PW146914

Pw146914 View Pathway
drug action

Trilaciclib Drug Metabolism Action Pathway

Homo sapiens

PW144502

Pw144502 View Pathway
drug action

Trihexyphenidyl 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.

PW146424

Pw146424 View Pathway
drug action

Triheptanoin 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.