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Pathways

PathWhiz ID Pathway Meta Data

PW144861

Pw144861 View Pathway
drug action

Prilocaine Drug Metabolism Action Pathway

Homo sapiens

PW127442

Pw127442 View Pathway
drug action

Primaquine Action Pathway

Plasmodium falciparum
Primaquine is an minoquinoline antimalarial is a radical cure and prevent relapse of vivax and ovale malarias following treatment with a blood schizontocide. It has also been used to prevent transmission of falciparum malaria by those returning to areas where there is a potential for re-introduction of malaria. It is the essential co-drug with chloroquine in treating all cases of malaria. In the blood, malaria parasites break down a part of the red blood cells known as haemoglobin. When this happens haemoglobin is divided into two parts; haem and globin. Haem is toxic to the malaria parasite. To prevent it from being damaged, the malaria parasite produces an chemical which converts the toxic haem into a non-toxic product. Primaquine acts by interfering with a part of the parasite (mitochondria) that is responsible for supplying it with energy. Without energy the parasite dies. Primaquine's mechanism of action is not well understood. It may be acting by generating reactive oxygen species or by interfering with the electron transport in the parasite. Also, although its mechanism of action is unclear, primaquine may bind to and alter the properties of protozoal DNA.

PW145178

Pw145178 View Pathway
drug action

Primaquine Drug Metabolism Action Pathway

Homo sapiens

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.