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Pathways

PathWhiz ID Pathway Meta Data

PW176141

Pw176141 View Pathway
metabolic

Tadalafil Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Tadalafil are predicted with biotransformer.

PW146419

Pw146419 View Pathway
drug action

Tafamidis Drug Metabolism Action Pathway

Homo sapiens

PW145724

Pw145724 View Pathway
drug action

Tafenoquine Drug Metabolism Action Pathway

Homo sapiens

PW176888

Pw176888 View Pathway
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.

PW145843

Pw145843 View Pathway
drug action

Tafluprost Drug Metabolism Action Pathway

Homo sapiens

PW058511

Pw058511 View Pathway
drug action

Talastine H1-Antihistamine Action

Homo sapiens
Talastine is a first-generation alkylamine H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.

PW132539

Pw132539 View Pathway
metabolic

Talazoparib Drug Metabolism

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

PW146446

Pw146446 View Pathway
drug action

Talazoparib Drug Metabolism Action Pathway

Homo sapiens

PW127729

Pw127729 View Pathway
drug action

Talbutal Action Pathway

Homo sapiens
Talbutal, also called 5-allyl-5-sec-butylbarbituric acid, is a barbiturate with a short to intermediate duration of action. It is a nonselective central nervous system (CNS) depressant. As with other barbiturates, talbutal is capable of producing all levels of CNS mood alteration from excitation to mild sedation, hypnosis, and deep coma. Barbiturates may also induce anesthesia at sufficiently high therapeutic doses. Talbutal binds to GABAA receptors at a distinct binding site associated with a Cl- ionopore of the receptor. Upon binding, talbutal increases the duration of time for which the Cl- ionopore is open, leading to prolonged inhibitory effect of GABA at the postsynaptic thalamic neuron. Talbutal is a potentiator of the GABA(A) alpha-1 through alpha-6 subunits. Some side effects of using Talbutal may include drowsiness, loss or coordination, nausea, and insomnia.

PW132536

Pw132536 View Pathway
metabolic

Talbutal Drug Metabolism

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