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Pathways

PathWhiz ID Pathway Meta Data

PW128387

Pw128387 View Pathway
drug action

Sulfisoxazole Action Pathway

Escherichia coli (strain K12)
Sulfisoxazole is a short-acting antibiotic from the sulfonamide drug class. It has activity against a wide range of gram-negative and gram-positive organisms. This drug is indicated in the treatment of many infections: urinary tract infections, meningococcal meningitis, acute otitis media, trachoma, nocardiosis, chancroid, toxoplasmosis, malaria, and many others. This drug is bacteriostatic; it inhibits the replication of bacteria by inhibiting the dihydropteroate synthase. This enzyme is responsible for one of the reactions to synthesize folic acid in bacteria by the condensation of the pteridine with para-aminobenzoic acid (PABA). This drug stops the replication of the bacteria (bacteriostatic). Sulfisoxazole is administered as an oral tablet.

PW144392

Pw144392 View Pathway
drug action

Sulfisoxazole Drug Metabolism Action Pathway

Homo sapiens

PW122077

Pw122077 View Pathway
disease

Sulfite Oxidase Deficiency

Rattus norvegicus
Sulfite oxidase deficiency (SOD) is a disorder, an autosomal recessive disease. In classic SOD, it is usually identified a few days after the birth of an affected individual, and is recognizable through characteristic dysmorphic features, seizures, and other signs of progressive encephalopathy. Patients also have ocular lenses that are dislocated, and usually die within a few months of being born. In late- onset SOD, the disorder is identified only in the later months, usually 6-18 months, of the child’s life by a delay or regression of neurological progress. This disorder is very rare, but the actual prevalence is not known. It can be diagnosed through a sulfite test strip in urine or by a skin fibroblast culture, which will indicate an absence of sulfite oxidase.

PW121853

Pw121853 View Pathway
disease

Sulfite Oxidase Deficiency

Mus musculus
Sulfite oxidase deficiency (SOD) is a disorder, an autosomal recessive disease. In classic SOD, it is usually identified a few days after the birth of an affected individual, and is recognizable through characteristic dysmorphic features, seizures, and other signs of progressive encephalopathy. Patients also have ocular lenses that are dislocated, and usually die within a few months of being born. In late- onset SOD, the disorder is identified only in the later months, usually 6-18 months, of the child’s life by a delay or regression of neurological progress. This disorder is very rare, but the actual prevalence is not known. It can be diagnosed through a sulfite test strip in urine or by a skin fibroblast culture, which will indicate an absence of sulfite oxidase.

PW127276

Pw127276 View Pathway
disease

Sulfite Oxidase Deficiency

Homo sapiens
Sulfite oxidase deficiency (SOD) is a disorder, an autosomal recessive disease. In classic SOD, it is usually identified a few days after the birth of an affected individual, and is recognizable through characteristic dysmorphic features, seizures, and other signs of progressive encephalopathy. Patients also have ocular lenses that are dislocated, and usually die within a few months of being born. In late- onset SOD, the disorder is identified only in the later months, usually 6-18 months, of the child’s life by a delay or regression of neurological progress. This disorder is very rare, but the actual prevalence is not known. It can be diagnosed through a sulfite test strip in urine or by a skin fibroblast culture, which will indicate an absence of sulfite oxidase.

PW000508

Pw000508 View Pathway
disease

Sulfite Oxidase Deficiency

Homo sapiens
Sulfite oxidase deficiency (SOD) is a disorder, an autosomal recessive disease. In classic SOD, it is usually identified a few days after the birth of an affected individual, and is recognizable through characteristic dysmorphic features, seizures, and other signs of progressive encephalopathy. Patients also have ocular lenses that are dislocated, and usually die within a few months of being born. In late- onset SOD, the disorder is identified only in the later months, usually 6-18 months, of the child’s life by a delay or regression of neurological progress. This disorder is very rare, but the actual prevalence is not known. It can be diagnosed through a sulfite test strip in urine or by a skin fibroblast culture, which will indicate an absence of sulfite oxidase.

PW128466

Pw128466 View Pathway
drug action

Sulfoxone Action Pathway

Mycobacterium leprae
Sulfoxone, also known as aldesulfone sodium, is a sulfonamide antibiotic with bacteriostatic activity. It is indicated in the treatment of leprosy and dermatitis herpetiformis. Leprosy is caused by Mycobacterium leprae. Sulfoxone inhibits the growth of the bacteria by inhibiting competitively the dihydropteroate synthase enzyme. This results in the inability to bind the substrate, para-aminobenzoic acid (PABA) resulting in the inability of the bacteria to do the synthesis of folic acid. Without folic acid, the bacteria can not grow because it can not produce DNA anymore. Right now this drug has been discontinued. It is administered as an oral tablet.

PW145233

Pw145233 View Pathway
drug action

Sulfoxone Drug Metabolism Action Pathway

Homo sapiens

PW176425

Pw176425 View Pathway
metabolic

Sulfoxone Predicted Metabolism Pathway

Homo sapiens
Metabolites of Sulfoxone are predicted with biotransformer.

PW146234

Pw146234 View Pathway
drug action

Sulfur hexafluoride Drug Metabolism Action Pathway

Homo sapiens