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Pathways

PathWhiz ID Pathway Meta Data

PW146605

Pw146605 View Pathway
drug action

Bismuth subnitrate Drug Metabolism Action Pathway

Homo sapiens

PW146697

Pw146697 View Pathway
drug action

Bismuth subgallate Drug Metabolism Action Pathway

Homo sapiens

PW132592

Pw132592 View Pathway
metabolic

Bismuth subgallate Drug Metabolism

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

PW146064

Pw146064 View Pathway
drug action

Bismuth subcitrate potassium Drug Metabolism Action Pathway

Homo sapiens

PW132253

Pw132253 View Pathway
metabolic

Bismuth subcitrate potassium Drug Metabolism

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

PW145924

Pw145924 View Pathway
drug action

Bisacodyl Drug Metabolism Action Pathway

Homo sapiens

PW146961

Pw146961 View Pathway
drug action

Birch bark extract Drug Metabolism Action Pathway

Homo sapiens

PW251335

Pw251335 View Pathway
metabolic

Biphenyl degradation

Pseudoxanthomonas spadix
Biphenyl degradation in Pseudoxanthomonas spadix is a source of carbon and energy. Being hydrophobic biphenyl uptake in Pseudoxanthomonas spadix occurs via diffusion or through specific transport proteins or porins that facilitate passage of aromatic hydrocarbons. The process begins with the initial oxidation of biphenyl by biphenyl 2,3-dioxygenase, to formcis-2,3-Dihydro-2,3-dihydroxybiphenyl. Subsequent oxidation, reductions and hydrolysis result in the formation of 2-Oxopent-4-enoate, a precursor to the citrate cycle.

PW144917

Pw144917 View Pathway
drug action

Biperiden Drug Metabolism Action Pathway

Homo sapiens

PW127344

Pw127344 View Pathway
disease

Biotinidase Deficiency

Homo sapiens
Biotinidase deficiency (Multiple carboxylase deficiency) is an autosomal recessive disease caused by a mutation in the BTD gene which codes for biotinidase. A deficiency in this enzyme results in accumulation of ammonia and ketone bodies in blood; 3-hydroxyisovaleric acid in plasma, spinal fluid, and urine; hydroxypropionic acid, 2-hydroxybutyric acid, 3-Hydroxybutyric acid, and citric acid in spinal fluid; and 3-methylcrotonylglycine, hydroxypropionic acid, and L and D-lactic acid in urine. Symptoms, which can present from birth into adulthood include hypotonia, ketosis, hyperammonemia, motor retardation, coma, and seborrhoic skin rash. Treatment includes biotin.