Loader

Pathways

PathWhiz ID Pathway Meta Data

PW144774

Pw144774 View Pathway
drug action

Verapamil Drug Metabolism Action Pathway

Homo sapiens

PW146916

Pw146916 View Pathway
drug action

Vericiguat Drug Metabolism Action Pathway

Homo sapiens

PW145685

Pw145685 View Pathway
drug action

Vernakalant Drug Metabolism Action Pathway

Homo sapiens

PW132454

Pw132454 View Pathway
metabolic

Verteporfin Drug Metabolism

Homo sapiens
Verteporfin is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Verteporfin passes through the liver and is then excreted from the body mainly through the kidney.

PW144584

Pw144584 View Pathway
drug action

Verteporfin Drug Metabolism Action Pathway

Homo sapiens

PW000516

Pw000516 View Pathway
disease

Very-Long-Chain Acyl-CoA Dehydrogenase Deficiency (VLCAD)

Homo sapiens
Very long-chain acyl-CoA dehydrogenase deficiency (VLCAD), also called ACADL and VLCAD, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder, which is caused by a defective very long-chain specific acyl-CoA dehydrogenase. Very long-chain specific acyl-CoA dehydrogenase breakdown certain fats to energy. This disorder is characterized by a large accumulation of fatty acids such as L-Palmitoylcarnitine in the mitochondria. Symptoms of the disorder include muscle weakness, lethargy (lack of energy) and hypoglycemia (low blood sugar). Treatment with diet modifications such as consuming supplemental calories is suggested. It is estimated that very long-chain acyl-CoA dehydrogenase deficiency affects 1 in 40,000 to 120,000 individuals.

PW122085

Pw122085 View Pathway
disease

Very-Long-Chain Acyl-CoA Dehydrogenase Deficiency (VLCAD)

Rattus norvegicus
Very long-chain acyl-CoA dehydrogenase deficiency (VLCAD), also called ACADL and VLCAD, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder, which is caused by a defective very long-chain specific acyl-CoA dehydrogenase. Very long-chain specific acyl-CoA dehydrogenase breakdown certain fats to energy. This disorder is characterized by a large accumulation of fatty acids such as L-Palmitoylcarnitine in the mitochondria. Symptoms of the disorder include muscle weakness, lethargy (lack of energy) and hypoglycemia (low blood sugar). Treatment with diet modifications such as consuming supplemental calories is suggested. It is estimated that very long-chain acyl-CoA dehydrogenase deficiency affects 1 in 40,000 to 120,000 individuals.

PW121861

Pw121861 View Pathway
disease

Very-Long-Chain Acyl-CoA Dehydrogenase Deficiency (VLCAD)

Mus musculus
Very long-chain acyl-CoA dehydrogenase deficiency (VLCAD), also called ACADL and VLCAD, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder, which is caused by a defective very long-chain specific acyl-CoA dehydrogenase. Very long-chain specific acyl-CoA dehydrogenase breakdown certain fats to energy. This disorder is characterized by a large accumulation of fatty acids such as L-Palmitoylcarnitine in the mitochondria. Symptoms of the disorder include muscle weakness, lethargy (lack of energy) and hypoglycemia (low blood sugar). Treatment with diet modifications such as consuming supplemental calories is suggested. It is estimated that very long-chain acyl-CoA dehydrogenase deficiency affects 1 in 40,000 to 120,000 individuals.

PW127308

Pw127308 View Pathway
disease

Very-Long-Chain Acyl-CoA Dehydrogenase Deficiency (VLCAD)

Homo sapiens
Very long-chain acyl-CoA dehydrogenase deficiency (VLCAD), also called ACADL and VLCAD, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder, which is caused by a defective very long-chain specific acyl-CoA dehydrogenase. Very long-chain specific acyl-CoA dehydrogenase breakdown certain fats to energy. This disorder is characterized by a large accumulation of fatty acids such as L-Palmitoylcarnitine in the mitochondria. Symptoms of the disorder include muscle weakness, lethargy (lack of energy) and hypoglycemia (low blood sugar). Treatment with diet modifications such as consuming supplemental calories is suggested. It is estimated that very long-chain acyl-CoA dehydrogenase deficiency affects 1 in 40,000 to 120,000 individuals.

PW002502

Pw002502 View Pathway
signaling

VHL Pathway

Homo sapiens