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Pathways

PathWhiz ID Pathway Meta Data

PW144508

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drug action

Tacrine Drug Metabolism Action Pathway

Homo sapiens

PW176494

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metabolic

Tacrine Predicted Metabolism Pathway

Homo sapiens
Metabolites of Tacrine are predicted with biotransformer.

PW126048

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drug action

Tacrolimus Action Pathway

Homo sapiens
Tacrolimus is a calcineurin inhibitor that is most often used as an immunosuppressive drug for organ transplant patients in order to reduce the activity of the immune system lowering the risk of organ rejection. Tacrolimus is administered orally or through a topical treatment which allows the drug to be absorbed into the bloodstream. Tacrolimus enters T-cells through the ABC or SLC transporters like ABCB1 and works by forming a complex with FKBP12 with inhibits calcineurin with leads to reduced T cell signal transduction and IL-2 transcription. IL-2 is an important mediator for T-cell activation, differentiation and migration which is through mTOR signalling. Lower IL-2 production and signal transduction leads to less activated immune cells leading to a weaker immune system. Tacrolimus also inhibits the transcription for genes encoding IL-3,4,5, GM-SCF, and TNF as well which are also involved in T cell activation. Organ transplant patients take tacrolimus after allogenic organ transplant for liver, kidney, heart, small bowel, pancreas, lung, trachea, skin, cornea and limb transplant.

PW144968

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drug action

Tacrolimus Drug Metabolism Action Pathway

Homo sapiens

PW126650

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drug action

Tadalafil Action Pathway (New)

Homo sapiens
Tadalafil is a phosphodiesterase-5 inhibitor used for the treatment of erectile dysfunction, similar to sildenafil; however, tadalafil has a longer duration of action. Sexual stimulation causes the release of nitric oxide (NO) from nerves and endothelial cells into the penis. NO activates the enzyme guanylate cyclase.2 The activation of this enzyme is followed by the synthesis of cyclic guanosine 3',5'-monophosphate (cGMP), activating a cascade of protein kinase-dependent phosphorylation events in smooth muscles, ultimately resulting in the dephosphorylation of myosin light chains within smooth muscle. This activity causes the relaxation of smooth muscle within blood vessels, resulting in the desired vasodilatory effect. Phosphodiesterase-5 breaks down cGMP to GMP. Tadalafil inhibits phosphodiesterase-5, preventing the breakdown of cGMP. This increases the concentration of cGMP, increasing the vasodilation and improving blood flow leading to penile erection. Tadalafil is usually administered orally. It is currently also in use as a therapeutic agent in cardiovascular conditions (e.g. pulmonary arterial hypertension) and being investigated for use in some cancers (as an antihyperplasic agent).

PW144926

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drug action

Tadalafil Drug Metabolism Action Pathway

Homo sapiens

PW176141

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metabolic

Tadalafil Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Tadalafil are predicted with biotransformer.

PW146419

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drug action

Tafamidis Drug Metabolism Action Pathway

Homo sapiens

PW145724

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drug action

Tafenoquine Drug Metabolism Action Pathway

Homo sapiens

PW176888

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drug action

Tafluprost Action Pathway

Homo sapiens
Tafluprost is a prostaglandin E1 analog that reduces the risk of NSAID-induced gastric ulcers. Tafluprost stimulates prostaglandin receptors on parietal cells in the stomach to reduce gastric acid secretion. Tafluprost activates prostaglandin EP3 receptors in parietal cells. Activation of this receptor triggers the Gi protein signaling cascade, inhibiting adenylate cyclase. Adenylate cyclase is responsible for converting ATP to cAMP, therefore, inhibition of adenylate cyclase reduces cytosolic cAMP concentration. cAMP is responsible for activating protein kinase A. With lower concentrations of cAMP, less protein kinase A is activated. Protein kinase A activates the proton pump in the luminal membrane of the parietal cell. The role of the proton pump is to secrete acid (H+) into the stomach lumen. With reduced protein kinase A activation, this decreases the activity of the proton pump, fewer H+ ions are pumped into the lumen, reducing the acidity and thus allowing stomach ulcers to heal and reducing the pain caused by the ulcers. Tafluprost may also promote ulcer healing by increasing mucus and bicarbonate secretion and thickening the mucosal bilayer so the mucosa can generate new cells.