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Pathways

PathWhiz ID Pathway Meta Data

PW123412

Pw123412 View Pathway
metabolic

PreQ0 Metabolism

Pseudomonas aeruginosa
PreQ0 or 7-cyano-7-carbaguanine is biosynthesized by degrading GTP. GTP first interacts with water through a GTP cyclohydrolase resulting in the release of a formate, a hydrogen ion and a 7,8-dihydroneopterin 3'-triphosphate. The latter compound then interacts with water through a 6-carboxy-5,6,7,8-tetrahydropterin synthase resulting in a acetaldehyde, triphosphate, 2 hydrogen ion and 6-carboxy-5,6,7,8-tetrahydropterin. The latter compound then reacts spontaneously with a hydrogen ion resulting in the release of a ammonium molecule and a 7-carboxy-7-deazaguanine. This compound then interacts with ATP and ammonium through 7-cyano-7-deazaguanine synthase resulting in the release of water, phosphate, ADP, hydrogen ion and a 7-cyano-7-carbaguanine. The degradation of 7-cyano-7-deazaguanine can lead to produce a preQ1 or a queuine by reacting with 3 hydrogen ions and 2 NADPH through a 7-cyano-7-deazaguanine reductase. PreQ1 then interacts with a guanine 34 in tRNA through a tRNA-guanine transglycosylase resulting in a release of a guanine and a 7-aminomethyl-7-deazaguanosine 34 in tRNA. This nucleic acid then interacts with SAM through a S-adenosylmethionine tRNA ribosyltransferase-isomerase resulting in a release of a hydrogen ion, L-methionine, adenine and an epoxyqueuosine

PW001893

Pw001893 View Pathway
metabolic

PreQ0 Metabolism

Escherichia coli
PreQ0 or 7-cyano-7-carbaguanine is biosynthesized by degrading GTP. GTP first interacts with water through a GTP cyclohydrolase resulting in the release of a formate, a hydrogen ion and a 7,8-dihydroneopterin 3'-triphosphate. The latter compound then interacts with water through a 6-carboxy-5,6,7,8-tetrahydropterin synthase resulting in a acetaldehyde, triphosphate, 2 hydrogen ion and 6-carboxy-5,6,7,8-tetrahydropterin. The latter compound then reacts spontaneously with a hydrogen ion resulting in the release of a ammonium molecule and a 7-carboxy-7-deazaguanine. This compound then interacts with ATP and ammonium through 7-cyano-7-deazaguanine synthase resulting in the release of water, phosphate, ADP, hydrogen ion and a 7-cyano-7-carbaguanine. The degradation of 7-cyano-7-deazaguanine can lead to produce a preQ1 or a queuine by reacting with 3 hydrogen ions and 2 NADPH through a 7-cyano-7-deazaguanine reductase. PreQ1 then interacts with a guanine 34 in tRNA through a tRNA-guanine transglycosylase resulting in a release of a guanine and a 7-aminomethyl-7-deazaguanosine 34 in tRNA. This nucleic acid then interacts with SAM through a S-adenosylmethionine tRNA ribosyltransferase-isomerase resulting in a release of a hydrogen ion, L-methionine, adenine and an epoxyqueuosine

PW145630

Pw145630 View Pathway
drug action

Pretomanid Drug Metabolism Action Pathway

Homo sapiens

PW176354

Pw176354 View Pathway
metabolic

Pretomanid Predicted Metabolism Pathway

Homo sapiens
Metabolites of sildenafil are predicted with biotransformer.

PW126541

Pw126541 View Pathway
drug action

Prilocaine

Homo sapiens
Prilocaine is an local anesthetic that is similar to lidocaine often used most commonly for dental procedures. Prilocaine acts by binding to the intracellular surface of the sodium channels which blocks the influx of sodium into the cell. Due to this block of sodium ions this prevents the generation and propagation of action potential. This reverses when the drug diffuses out of the cell and is excreted from the body, allowing the sodium channel to function as it normally would and continue to generate action potential. Prilocaine is metabolized by the liver and kidney and is excreted by the kidney.

PW000407

Pw000407 View Pathway
drug action

Prilocaine Action Pathway

Homo sapiens
Prilocaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Prilocaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore prilocaine preferentially inhibits neurons that are actively firing.

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.