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Pathways

PathWhiz ID Pathway Meta Data

PW000115

Pw000115 View Pathway
disease

Leigh Syndrome

Homo sapiens
Leigh Syndrome, also called Leigh Disease or infantile subacute necrotizing encephalopathy, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder that is caused by a mutation of any one of 75 different genes. Disruptions of the complexes I or IV are the most common reasons for Leigh syndrome. Complex IV is crucial in the electron transfer steps of oxidative phosphorylation, which is needed to provide energy to the mitochondria. This disorder is characterized by a large accumulation of lactate in the body. Symptoms of the disorder include diarrhea, dysphagia and vomiting. There is no cure for Leigh syndrome and the loss motor skills degenerate rapidly. It is estimated that Leigh syndrome affects 1 in 40,000 individuals.

PW002397

Pw002397 View Pathway
metabolic

Leloir Pathway

Saccharomyces cerevisiae
The pathway starts with the isomerization of Beta-D-galactose into Alpha-D-galactose through a galactose mutarotase. Alpha-D-galactose is then phosphorylated through an ATP dependent galactokinase resulting in the release of ADP, a hydrogen ion and alpha-D-galactose 1-phosphate. The latter compound reacts with UDP glucose which is the result of UTP reacting with alpha-D-glucose through a uridinephosphoglucose pyrophosphorylase. The reaction between alpha-D-galactose 1-phosphate and UDP glucose results in the release of glucose 1-phosphate and UDP-alpha-D-galactose. Glucose 1-phosphate can be further isomerized into glucose 6-phosphate, while UDP-alpha-D-galactose can be reverted into UDP glucose through a UDP-epimerase.

PW132552

Pw132552 View Pathway
metabolic

Lemborexant Drug Metabolism

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

PW146474

Pw146474 View Pathway
drug action

Lemborexant Drug Metabolism Action Pathway

Homo sapiens

PW144602

Pw144602 View Pathway
drug action

Lenalidomide Drug Metabolism Action Pathway

Homo sapiens

PW176334

Pw176334 View Pathway
metabolic

Lenalidomide Predicted Metabolism Pathway

Homo sapiens
Metabolites of sildenafil are predicted with biotransformer.

PW128523

Pw128523 View Pathway
drug action

Lenvatinib Action Pathway

Homo sapiens
Lenvatinib is a receptor tyrosine kinase (RTK) inhibitor used in the treatment of various cancers. It primarily targets the kinase activities of vascular endothelial growth factor (VEGF) receptors, including VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (FLT4). Lenvatinib also inhibits other RTKs, such as fibroblast growth factor receptors (FGFR1, 2, 3, and 4), the platelet-derived growth factor receptor alpha (PDGFRα), KIT, and RET, all of which play crucial roles in processes like angiogenesis, tumor growth, and cancer progression. Its approved indications include metastatic thyroid cancer, advanced renal cell carcinoma in combination with everolimus, and unresectable hepatocellular carcinoma. Lenvatinib offers a targeted therapeutic approach for patients with limited treatment options.

PW132436

Pw132436 View Pathway
metabolic

Lenvatinib Drug Metabolism

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

PW145958

Pw145958 View Pathway
drug action

Lenvatinib Drug Metabolism Action Pathway

Homo sapiens

PW000300

Pw000300 View Pathway
drug action

Lepirudin Action Pathway

Homo sapiens
Lepirudin (also known as Refludan) is an anticoagulant that can be used for inhibiting thrombin (prothrombin) irreversibly. Binding of thrombin can prevent formation of clot as well as thrombus. Lepirudin can also reduce thrombocytopenia and break up clot.