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Pathways

PathWhiz ID Pathway Meta Data

PW176527

Pw176527 View Pathway
metabolic

Primaquine Predicted Metabolism Pathway

Homo sapiens
Metabolites of Primaquine are predicted with biotransformer.

PW121878

Pw121878 View Pathway
disease

Primary Hyperoxaluria II, PH2

Mus musculus
Primary hyperolaria type 2 (PH2) is a rare condition resulting from glyoxylate reductase/hydroxypyruvate reductase (GR/HPR) enzyme deficiency. PH2 results in calcium oxalate (also known as oxalic acid) deposits and end-stage renal disease. These deposits may cause kidney damage or failure.

PW127340

Pw127340 View Pathway
disease

Primary Hyperoxaluria II, PH2

Homo sapiens
Primary hyperolaria type 2 (PH2) is a rare condition resulting from glyoxylate reductase/hydroxypyruvate reductase (GR/HPR) enzyme deficiency. PH2 results in calcium oxalate (also known as oxalic acid) deposits and end-stage renal disease. These deposits may cause kidney damage or failure.

PW122102

Pw122102 View Pathway
disease

Primary Hyperoxaluria II, PH2

Rattus norvegicus
Primary hyperolaria type 2 (PH2) is a rare condition resulting from glyoxylate reductase/hydroxypyruvate reductase (GR/HPR) enzyme deficiency. PH2 results in calcium oxalate (also known as oxalic acid) deposits and end-stage renal disease. These deposits may cause kidney damage or failure.

PW000534

Pw000534 View Pathway
disease

Primary Hyperoxaluria II, PH2

Homo sapiens
Primary hyperolaria type 2 (PH2) is a rare condition resulting from glyoxylate reductase/hydroxypyruvate reductase (GR/HPR) enzyme deficiency. PH2 results in calcium oxalate (also known as oxalic acid) deposits and end-stage renal disease. These deposits may cause kidney damage or failure.

PW122024

Pw122024 View Pathway
disease

Primary Hyperoxaluria Type I

Rattus norvegicus
Type I primary hyperoxaluria (Glycolicaciduria) is caused by mutation in the gene encoding alanine-glyoxylate aminotransferase (AGXT). AGXT normally catalyzes the reaction from L-serine and pyruvate to 3-hydroxypyruvate and L-alanine and the reaction from L-alanine and glyoxylate to pyruvate and glycine. A defect in AGXT results in accumulation of glycolic acid, glyoxylic acid, and oxalate in urine. Symptoms include hematuria, myocarditis, nephrocalcinosis, peripheral neuropathy, and renal failure.

PW000057

Pw000057 View Pathway
disease

Primary Hyperoxaluria Type I

Homo sapiens
Type I primary hyperoxaluria (Glycolicaciduria) is caused by mutation in the gene encoding alanine-glyoxylate aminotransferase (AGXT). AGXT normally catalyzes the reaction from L-serine and pyruvate to 3-hydroxypyruvate and L-alanine and the reaction from L-alanine and glyoxylate to pyruvate and glycine. A defect in AGXT results in accumulation of glycolic acid, glyoxylic acid, and oxalate in urine. Symptoms include hematuria, myocarditis, nephrocalcinosis, peripheral neuropathy, and renal failure.

PW127316

Pw127316 View Pathway
disease

Primary Hyperoxaluria Type I

Homo sapiens
Type I primary hyperoxaluria (Glycolicaciduria) is caused by mutation in the gene encoding alanine-glyoxylate aminotransferase (AGXT). AGXT normally catalyzes the reaction from L-serine and pyruvate to 3-hydroxypyruvate and L-alanine and the reaction from L-alanine and glyoxylate to pyruvate and glycine. A defect in AGXT results in accumulation of glycolic acid, glyoxylic acid, and oxalate in urine. Symptoms include hematuria, myocarditis, nephrocalcinosis, peripheral neuropathy, and renal failure.

PW121799

Pw121799 View Pathway
disease

Primary Hyperoxaluria Type I

Mus musculus
Type I primary hyperoxaluria (Glycolicaciduria) is caused by mutation in the gene encoding alanine-glyoxylate aminotransferase (AGXT). AGXT normally catalyzes the reaction from L-serine and pyruvate to 3-hydroxypyruvate and L-alanine and the reaction from L-alanine and glyoxylate to pyruvate and glycine. A defect in AGXT results in accumulation of glycolic acid, glyoxylic acid, and oxalate in urine. Symptoms include hematuria, myocarditis, nephrocalcinosis, peripheral neuropathy, and renal failure.

PW127749

Pw127749 View Pathway
drug action

Primidone Action Pathway

Homo sapiens
Primidone is an antiepileptic used to treat grand mal, psychomotor, and focal epileptic seizures. Primidone alters sodium and calcium channel transport, reducing the frequency of nerve firing, which may be responsible for its effect on convulsions and essential tremor. Primidone and its metabolites, phenobarbital and phenylethylmalonamide (PEMA), are active anticonvulsants. Primidone does not directly interact with GABA-A receptors or chloride channels but phenobarbital does. Primidone alters transmembrane sodium and calcium channel transport, reducing the frequency of nerve firing, which may be responsible for the primidone’s effect on convulsions and essential tremor. Primidone is metabolized to phenobarbitol and phenylethylmalonamide (PEMA). This metabolism is largely mediated by CYP2C9, CYP2C19, and CYP2E1. The major metabolite, phenobarbital, is also a potent anticonvulsant in its own right and likely contributes to primidone's effects in many forms of epilepsy. According to Brenner's Pharmacology textbook, Primidone also increases GABA-mediated chloride flux: thereby hyperpolarizing the membrane potential. Some side effects of using primidone may include tiredness, dizziness, nausea, and double vision.