Pathways

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.

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)

Nimodipine (also known as Nimotop or Periplum) is a dihydropyridine calcium channel blocker that may not be used for treatment of hypertension. Compared to other DHP CCBs, nimodipine is more active in the cerebral vasculature than in the periphery. This may be due to its high lipophilicity and ability to penetrate the blood brain barrier. This unique property of nimodipine led to clinical studies for its use to improve neurological outcomes in patients following subarachnoid hemorrhage from ruptured intracranial aneurysms. While it has been approved as adjunct treatment for this indication, the exact mechanism by which it exerts these effects is unclear. Nimodipine has little effect on cardiac myocytes and conduction cells at therapeutic sub-toxic concentrations. Nimodipine binds the major channel in muscle cells: L-type calcium channels. Binding of Nimodipine 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.

Nimodipine is a calcium channel blocker used to improve neurological outcomes in patients with subarachnoid hemorrhage due to a ruptured intracranial aneurysm. It can be found under the brand names Nimotop and Nymalize. 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. 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. It targets the alpha-1C, alpha-1D, alpha-1E, alpha-1S, beta-1, beta-2, beta-3, and beta-4 subunits.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. Nimodipine can be administered as an oral capsule, tablet, solution, or as an intravenous injection. Some side effects of using nimodipine may include blurred vision, chest pain, lightheadedness, and swelling.

Metabolites of Nimodipine are predicted with biotransformer.

Nintedanib is a versatile triple angiokinase inhibitor used in the treatment of several conditions. It's indicated for idiopathic pulmonary fibrosis (IPF), systemic sclerosis-associated interstitial lung disease, and chronic fibrosing interstitial lung diseases with a progressive phenotype, where it helps slow down the decline in pulmonary function. Additionally, in combination with docetaxel, nintedanib is employed for non-small cell lung cancer (NSCLC) treatment, specifically for patients who have not responded to first-line chemotherapy options. This drug offers valuable therapeutic options for these challenging medical conditions.