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PathWhiz ID Pathway Meta Data

PW145051

Pw145051 View Pathway
drug action

Naratriptan Drug Metabolism Action Pathway

Homo sapiens

PW128609

Pw128609 View Pathway
drug action

Naratriptan Mechanism of Action Action Pathway

Homo sapiens
Triptans are a class of medications used in the treatment of migraine headaches. Triptans act as antimigraine agents by selectively binding to the serotonin receptors 5-HT1B and 5-HT1D. Triptan binding to the vascular 5-HT1B receptors leads to vasoconstriction of the cranial arteries, which painfully dilate during a migraine attack. Naratriptan is a selective 5-HT1B/1D receptor agonist and leads to vasoconstriction in the basilar artery and the blood vessels of the dura mater. It decreases peripheral nociception either by selective cranial vasoconstriction or an effect on trigeminovascular nerves. The blocking effect of sumatriptan indicated a peripheral effect on trigeminal vascular nerves in neurogenically mediated plasma extravasation. Naratriptan has only a weak affinity for 5-HT1A, 5-HT5A, and 5-HT7 receptors and no significant affinity or pharmacological activity at 5-HT2, 5-HT3 or 5-HT4 receptor subtypes or at alpha1-, alpha2-, or beta-adrenergic, dopamine1,; dopamine2; muscarinic, or benzodiazepine receptors. Three distinct pharmacological actions have been implicated in the antimigraine effect of the triptans: (1) stimulation of presynaptic 5-HT1D receptors, which serves to inhibit both dural vasodilation and inflammation; (2) direct inhibition of trigeminal nuclei cell excitability via 5-HT1B/1D receptor agonism in the brainstem and (3) vasoconstriction of meningeal, dural, cerebral or pial vessels as a result of vascular 5-HT1B receptor agonism.

PW176101

Pw176101 View Pathway
metabolic

Naratriptan Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Naratriptan are predicted with biotransformer.

PW127396

Pw127396 View Pathway
drug action

Natamycin Action Pathway

Homo sapiens
Natamycin is a macrolide antifungal used to treat fungal infections of the eye. Natamycin is an antifungal drug for topical ophthalmic administration. It possesses in vitro activity against a variety of yeast and filamentous fungi, including Candida, Aspergillus, Cephalosporium, Fusarium and Penicillium. Natamycin inhibits fungal growth by binding to ergosterol in the plasma membrane, preventing ergosterol-dependent fusion of vacuoles and membrane fusion and fission. This differs from the mechanism of most other polyene antibiotics, which tend to work by altering fungal membrane permeability instead.

PW132613

Pw132613 View Pathway
metabolic

Natamycin Drug Metabolism

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

PW144932

Pw144932 View Pathway
drug action

Natamycin Drug Metabolism Action Pathway

Homo sapiens

PW000432

Pw000432 View Pathway
drug action

Nateglinide Action Pathway

Homo sapiens
Nateglinide is a non-sulfonylurea insulin secretagogue used in the treatment of type 2 diabetes. As the name of the drug class suggests, nateglinide acts on pancreatic beta-cells to stimulate insulin secretion. Under physiological conditions, insulin secretion from beta-cells is mediated by elevated glucose concentration in the blood. Glucose enters the cell via GLUT2 (SLC2A2) transporters. Once inside the cell, glucose is metabolized to produce ATP. High concentration of ATP will inhibit ATP-dependent potassium channels (ABCC8), which depolarizes the cell. Depolarization causes opening of voltage-gated calcium channels, allowing calcium to enter cell. High intracellular calcium subsequently stimulate vesicle exocytosis and insulin secretion. Nateglinide stimulate insulin secretion in a glucose-sensitive manner by inhibiting ATP-dependent potassium channels. As a result, there tends to be a lesser likelihood of hypoglycemia with nateglinide therapy compared to sulfonylureas.

PW127988

Pw127988 View Pathway
drug action

Nateglinide Action Pathway (New)

Homo sapiens
Nateglinide is an antihyperglycemic agent, a meglitinide one. It is used in the treatment of non insulin dependent diabetes mellitus (NIDDM). This drug had the function to increase the insulin release by the pancreas to the blood. It does this by inhibiting the ATP-sensitive potassium channels in a glucose-dependent manner. This drug does not act on the insulin level without the presence of glucose, which differentiates it from sulfonylurea drugs. The mechanism of action starts with the need for functioning beta cells in the pancreas and glucose in the blood. Since the release of insulin is controlled by the beta cells membrane potential, the binding of the drug to the ATP-binding cassette subfamily C member 8 causes its closing. This results in the depolarization of the cell and the opening of the L-type calcium channels. In consequence, the increased concentration of calcium results in the stimulation of the calcium-dependent exocytosis of insulin granules. An overdose of this drug may result in the development of hypoglycemic symptoms. Nateglinide is administered as an oral tablet.

PW144842

Pw144842 View Pathway
drug action

Nateglinide Drug Metabolism Action Pathway

Homo sapiens

PW124604

Pw124604 View Pathway
metabolic

Nateglinide Metabolic Pathway

Homo sapiens
Hepatic, via cytochrome P450 isoenzymes CYP2C9 (70%) and CYP3A4 (30%). Metabolism is via hydroxylation followed by glucuronidation. The major metabolites have less antidiabetic activity than nateglinide, but the isoprene minor metabolite has antidiabetic activity comparable to that of nateglinide. (DrugBank)