PathWhiz

PathWhiz ID	Pathway	Meta Data
PW124419 View Pathway	drug action Nifedipine Homo sapiens Nifedipine, or BAY a 1040, is a first generation dihydropyridine L-type calcium channel blocker, similar to nicardipine. Nifedipine was developed by Bayer and first described in the literature, along with other dihydropyridines, in 1972. Since nifedipine's development, second and third generation dihydropyridines have been developed with slower onsets and longer durations of action. The most popular of the third generation dihydropyridines is amlodipine. Nifedipine was granted FDA approval on 31 December 1981. (DrugBank) Nifedipine blocks voltage gated L-type calcium channels in vascular smooth muscle and myocardial cells. This blockage prevents the entry of calcium ions into cells during depolarization, reducing peripheral arterial vascular resistance and dilating coronary arteries. These actions reduce blood pressure and increase the supply of oxygen to the heart, alleviating angina. (DrugBank) BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Dorsa Yahya Rayat Created On: January 06, 2021 at 13:05 Last Updated: January 06, 2021 at 13:05
PW000394 View Pathway	drug action Nifedipine Action Pathway Homo sapiens Nifedipine (also known as Adalat or Procardia) is a dihydropyridine calcium channel blocker that may be used for treatment of hypertension and exertion-related angina in the absence of vasospasm. Nifedipine binds the major channel in muscle cells: L-type calcium channels. Binding of Nifedipine on L-type calcium channels can change channels' confirmation to its inactive form, so that the channel couldn't faciltate the influx of calcium ions, which leads to decreased arterial smooth muscle contractility and subsequent vasoconstriction. Activated mysoin light chain kinase (MLCK) is required for muscle contraction since it can catalyze the phosphorylation of the regulatory light chain subunit of myosin. Without calcium ions in muscle cell, calmodulin couldn't form the calcium-bound calmodulin, which is required for binding and activating MLCK. Lack of initial influx of calcium can also reduce the level of contractile activity of muscle cells and results in vasodilation, which ultimately lead to overall decresing in blood pressure. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: August 22, 2013 at 10:45 Last Updated: August 22, 2013 at 10:45
PW127889 View Pathway	drug action Nifedipine Action Pathway (New) Homo sapiens Nifedipine is a dihydropyridine calcium channel blocker indicated for the management of several subtypes of angina pectoris, and hypertension. It can be found under the brand names Adalat, Afeditab CR, Nifediac, Nifedical, and Procardia. Nifedipine, or BAY a 1040, is a first generation dihydropyridine L-type calcium channel blocker, similar to nicardipine. Nifedipine was developed by Bayer and first described in the literature, along with other dihydropyridines, in 1972. Since nifedipine's development, second and third generation dihydropyridines have been developed with slower onsets and longer durations of action. Nifedipine blocks voltage gated L-type calcium channels in vascular smooth muscle and myocardial cells. This blockage prevents the entry of calcium ions into cells during depolarization, reducing peripheral arterial vascular resistance and dilating coronary arteries. The alpha-1C, alpha-1D, and beta-2 subunits are targeted. Nifedipine can be administered via oral capsules or tablets. These actions reduce blood pressure and increase the supply of oxygen to the heart, alleviating angina. Some side effects of using nifedipine may include headaches, dizziness, flushing, and palpitations. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Hayley Created On: June 16, 2023 at 09:27 Last Updated: June 16, 2023 at 09:27
PW145204 View Pathway	drug action Nifedipine Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 15:18 Last Updated: October 07, 2023 at 15:18
PW124482 View Pathway	metabolic Nifedipine Metabolic pathway Homo sapiens Nifedipine is predominantly metabolized by CYP3A4. Nifedipine is predominantly metabolized to 2,6-dimethyl-4-(2-nitrophenyl)-5-methoxycarbonyl-pyridine-3-carboxylic acid, and then further metabolized to 2-hydroxymethyl-pyridine carboxylic acid. Nifedipine is also minorly metabolized to dehydronifedipine. (DrugBank) BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Dorsa Yahya Rayat Created On: January 26, 2021 at 15:06 Last Updated: January 26, 2021 at 15:06
PW132386 View Pathway	metabolic Nifurtimox Drug Metabolism Homo sapiens Nifurtimox is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Nifurtimox 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 21:24 Last Updated: September 21, 2023 at 21:24
PW146456 View Pathway	drug action Nifurtimox Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 18:14 Last Updated: October 07, 2023 at 18:14
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