PathWhiz

PathWhiz ID	Pathway	Meta Data
PW123791 View Pathway	disease nihao Acinetobacter baylyi (strain ATCC 33305 / BD413 / ADP1) BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: qijie Created On: February 07, 2020 at 22:54 Last Updated: February 07, 2020 at 22:54
PW145603 View Pathway	drug action Nilotinib Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 16:11 Last Updated: October 07, 2023 at 16:11
PW032595 View Pathway	drug action Nilotinib Inhibition of BCR-ABL Action Pathway Homo sapiens Nilotinib is a tyrosine kinase inhibitor used to treat chronic myelogenous leukemia (CML), a cancer characterized by increased and unregulated growth of white blood cells in the bone marrow and the accumulation of these cells in the blood. The cause of CML pathophysiology is the BCR-ABL fusion protein - the result of a genetic abnormality known as the Philadelphia chromosome in which Abelson Murine Leukemia viral oncogene homolog 1 (ABL1) translocates within the Breakpoint Cluster Region (BCR) gene on chromosome 22. BCR-ABL is a cytoplasm-targeted constitutively active tyrosine kinase that activates several oncogenic pathways which promote increased cell proliferation and survival including the MAPK/ERK Pathway, the JAK-STAT Pathway, and the PI3K/Akt pathway. Nilotinib is considered a second generation BCR-ABL inhibitor (Imatinib being the progenitor) that inhibits BCR-ABL activity by binding a highly conserved ATP binding site to effectively lock the tyrosine kinase in an inactive conformation. As a result, phosphate is unable to be transferred from ATP to activate oncogenic signalling cascades. For greater detail, refer to the pathway titled BCR-ABL Action in CML Pathogenesis. Nilotinib is able to bind ABL with greater affinity than Imatinib (20-fold to 30-fold increase). It is therefore administered to patients with Imatinib resistance. Notably, Nilotinib is ineffective against the T315I mutation in BCR-ABL, and further research is necessary. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Carin Li Created On: August 16, 2017 at 00:36 Last Updated: August 16, 2017 at 00:36
PW176275 View Pathway	metabolic Nilotinib Predicted Metabolism Pathway Homo sapiens Metabolites of Nilotinib are predicted with biotransformer. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Omolola Created On: December 04, 2023 at 14:31 Last Updated: December 04, 2023 at 14:31
PW132413 View Pathway	metabolic Nilutamide Drug Metabolism Homo sapiens Nilutamide is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Nilutamide passes through the liver and is then excreted from the body mainly through the kidney. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: September 21, 2023 at 21:35 Last Updated: September 21, 2023 at 21:35
PW144778 View Pathway	drug action Nilutamide Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 14:24 Last Updated: October 07, 2023 at 14:24
PW127927 View Pathway	drug action Nilvadipine Action Pathway Homo sapiens Nilvadipine is a calcium channel blocker used to manage arterial hypertension. For the management of vasospastic angina, chronic stable angina and hypertension. Nilvadipine is similar to other dihydropyridines including amlodipine, felodipine, isradipine, and nicardipine. Nilvadipine is used to treat Prinzmetal's angina, hypertension, and other vascular disorders such as Raynaud's phenomenon. By blocking the calcium channels, Nifedipine inhibits the spasm of the coronary artery and dilates the systemic arteries, results in an increase of myocardial oxygen supply and a decrease in systemic blood pressure. Nilvadipine inhibits the influx of extracellular calcium through myocardial and vascular membrane pores by physically plugging the channel. The decrease in intracellular calcium inhibits the contractile processes of 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. Nilvadipine targets the alpha-1C, alpha-2/delta-1, and beta-2 subunits of the channel, and it is administered as on oral tablet. Possible side effects of using nilvadipine may include headache, dizziness, fatigue, and flushing. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Hayley Created On: June 20, 2023 at 09:17 Last Updated: June 20, 2023 at 09:17
PW145753 View Pathway	drug action Nilvadipine Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 16:33 Last Updated: October 07, 2023 at 16:33
PW145570 View Pathway	drug action Nimesulide Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 16:06 Last Updated: October 07, 2023 at 16:06
PW124420 View Pathway	drug action Nimodipine Homo sapiens Nimodipine is a 1,4-dihydropyridine calcium channel blocker. It acts primarily on vascular smooth muscle cells by stabilizing voltage-gated L-type calcium channels in their inactive conformation. By inhibiting the influx of calcium in smooth muscle cells, nimodipine prevents calcium-dependent smooth muscle contraction and subsequent vasoconstriction. Compared to other calcium channel blocking agents, nimodipine exhibits greater effects on cerebral circulation than on peripheral circulation. Nimodipine is used to as an adjunct to improve the neurologic outcome following subarachnoid hemorrhage from ruptured intracranial aneurysm. (DrugBank) Although the precise mechanism of action is not known, nimodipine blocks intracellular influx of calcium through voltage-dependent and receptor-operated slow calcium channels across the membranes of myocardial, vascular smooth muscle, and neuronal cells. By specifically binding to L-type voltage-gated calcium channels, nimodipine inhibits the calcium ion transfer, resulting in the inhibition of vascular smooth muscle contraction. Evidence suggests that the dilation of small cerebral resistance vessels, with a resultant increase in collateral circulation, and/or a direct effect involving the prevention of calcium overload in neurons may be responsible for nimodipine's clinical effect in patients with subarachnoid hemorrhage. (DrugBank) BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Dorsa Yahya Rayat Created On: January 06, 2021 at 13:12 Last Updated: January 06, 2021 at 13:12