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Pathways

PathWhiz ID Pathway Meta Data

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.

PW124549

Pw124549 View Pathway
drug action

Lepirudin Mechanism of Action Action Pathway

Homo sapiens
Lepirudin is a synthetic peptide thrombin inhibitor that binds reversibly to the catalytic site and anion-binding exosite inhibiting the cleavage of fibrinogen into fibrin. Lepirudin is used to treat heparin-induced thrombocytopenia as well as to prevent thrombosis. It is used in patients that are undergoing percutaneous coronary intervention or who have a risk in acute coronary syndromes caused by unstable angina or non-ST segment elevation. Thrombin is an important proteinase as it cleaves fibrinogen into fibrin monomers which help form the thrombus that forms the clot at the site of vascular injury. Because Lepirudin inhibits thrombin, clotting cannot form which is ideal for heart surgeries and some heart conditions. Lepirudin should be monitored as it inhibits clotting so other injuries won't clot and it also can cause blood stagnation. Monitoring changes in hematocrit and blood pressure is extremely important when taking this drug. It is normally administered intravenously so that it is delivered to the site of action right away and can be controlled more easily. Production of lepirudin by Bayer Pharmaceuticals has been stopped in 2012.

PW127920

Pw127920 View Pathway
drug action

Lercanidipine Action Pathway

Homo sapiens
Lercanidipine is a calcium channel blocker of the dihydropyridine class for the management of hypertension. It can be found under the brand name Zanidip. Lercanidipine, a dihydropyridine calcium-channel blocker, is used alone or with an angiotensin-converting enzyme inhibitor, to treat hypertension, chronic stable angina pectoris, and Prinzmetal's variant angina. Lercanidipine is similar to other peripheral vasodilators. Lercanidipine inhibits the influx of extra cellular calcium across the myocardial and vascular smooth muscle cell membranes possibly by deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum. The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload. Possible side effects of using lercanidipine may include headaches, palpitations, flushing, and oedema.

PW144646

Pw144646 View Pathway
drug action

Lercanidipine Drug Metabolism Action Pathway

Homo sapiens

PW000078

Pw000078 View Pathway
disease

Lesch-Nyhan Syndrome (LNS)

Homo sapiens
Lesch-Nyhan Syndrome is a syndrome identified through its neurological, behavioural metabolic impact. It is characterized by a mental deficit and self-mutilation, accompanied with an overproduction of uric acid. A mutation of the HPRT1 gene are responsible for this condition, as they cause the enzyme hypoxanthine phosphoribosyltransferase 1 to be present in extremely low levels or absent altogether. This causes an overproduction of uric acid as the purines are not recycled, but only broken down. This gene is also connected to dopamine production, which a lack of causes smooth muscle function to suffer, resulting in dystonia, ballismus and chorea. Patients are usually unable to walk, and the connection between a lack of hypoxanthine phosphoribosyltransferase 1 and the behavioural abnormalities associated with this condition are unknown.

PW121987

Pw121987 View Pathway
disease

Lesch-Nyhan Syndrome (LNS)

Rattus norvegicus
Lesch-Nyhan Syndrome is a syndrome identified through its neurological, behavioural metabolic impact. It is characterized by a mental deficit and self-mutilation, accompanied with an overproduction of uric acid. A mutation of the HPRT1 gene are responsible for this condition, as they cause the enzyme hypoxanthine phosphoribosyltransferase 1 to be present in extremely low levels or absent altogether. This causes an overproduction of uric acid as the purines are not recycled, but only broken down. This gene is also connected to dopamine production, which a lack of causes smooth muscle function to suffer, resulting in dystonia, ballismus and chorea. Patients are usually unable to walk, and the connection between a lack of hypoxanthine phosphoribosyltransferase 1 and the behavioural abnormalities associated with this condition are unknown.

PW121762

Pw121762 View Pathway
disease

Lesch-Nyhan Syndrome (LNS)

Mus musculus
Lesch-Nyhan Syndrome is a syndrome identified through its neurological, behavioural metabolic impact. It is characterized by a mental deficit and self-mutilation, accompanied with an overproduction of uric acid. A mutation of the HPRT1 gene are responsible for this condition, as they cause the enzyme hypoxanthine phosphoribosyltransferase 1 to be present in extremely low levels or absent altogether. This causes an overproduction of uric acid as the purines are not recycled, but only broken down. This gene is also connected to dopamine production, which a lack of causes smooth muscle function to suffer, resulting in dystonia, ballismus and chorea. Patients are usually unable to walk, and the connection between a lack of hypoxanthine phosphoribosyltransferase 1 and the behavioural abnormalities associated with this condition are unknown.

PW127291

Pw127291 View Pathway
disease

Lesch-Nyhan Syndrome (LNS)

Homo sapiens
Lesch-Nyhan Syndrome is a syndrome identified through its neurological, behavioural metabolic impact. It is characterized by a mental deficit and self-mutilation, accompanied with an overproduction of uric acid. A mutation of the HPRT1 gene are responsible for this condition, as they cause the enzyme hypoxanthine phosphoribosyltransferase 1 to be present in extremely low levels or absent altogether. This causes an overproduction of uric acid as the purines are not recycled, but only broken down. This gene is also connected to dopamine production, which a lack of causes smooth muscle function to suffer, resulting in dystonia, ballismus and chorea. Patients are usually unable to walk, and the connection between a lack of hypoxanthine phosphoribosyltransferase 1 and the behavioural abnormalities associated with this condition are unknown.