Pathways

Pirenzepine is a drug that targets antimuscarinic agents in order to treat ulcers, this is done through inhibiting gastic secretions in order to allow the ulver to heal. Pirenzepine belongs to antispasmodics and anticholinergics group, that are used to relieve cramping or spasming of the gastrointestinal tract. It can be used along with antacids to treat peptic ulcers, it can also be used to prevent nausea, vomiting and motion sickness. Pirenzepine acts on muscarinic acetylcholine receptor M1 antagonizing it and eliciting inhibition of adenylate cyclase, breakdown of phosphoinositides and modulation of potassium channels.

Pirenzepine (also known as Gastrozepin) is a selective antagonist (antimuscarinic) that will inhibit the muscarinic acetylcholine receptor M3 inside the stomach. Binding of pirenzepine on the receptor will decrease the level of exertion of gastric acid secretion, and also it can reduce muscle spasms. Therefore, pirenzipine can be used for treating peptic ulcers, prevent motion sickness, vomiting and nausea.

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

Pirbuterol is a beta-2 adrenergic agonist that has a preferential effect. It is a short acting, inhaled drug that causes bronchial smooth muscle relaxation through stimulation of adenylyl cyclase. It is used as a bronchodilator for the treatment of asthma and relief from bronchospasm. The result of taking this drug is relaxation of the bronchial smooth muscles causing bronchodilaton and increased airflow. Once pirbuterol is administered and it binds to the beta-2 adrenergic receptor, the G protein signalling cascade begins. The alpha and beta/gamma subunits of the G protein separate and GDP is replaced with GTP on the alpha subunit. This alpha subunit then activates adenylyl cyclase which converts ATP to cAMP. cAMP then activates protein kinase A (PKA) which in turn phosphorylates targets and inhibits MLCK through decreased calcium levels causing muscle relaxation. PKA can phosphorylate certain Gq-coupled receptors as well as phospholipase C (PLC) and thereby inhibit G protein-coupled receptor (GPCR) -PLC-mediated phosphoinositide (PI) generation, and thus calcium flux. PKA phosphorylates the inositol 1,4,5-trisphosphate (IP3) receptor to reduce its affinity for IP3 and further limit calcium mobilization. PKA phosphorylates myosin light chain kinase (MLCK) and decreases its affinity to calcium calmodulin, thus reducing activity and myosin light chain (MLC) phosphorylation. PKA also phosphorylates KCa++ channels in ASM, increasing their open-state probability (and therefore K+ efflux) and promoting hyperpolarization. Since myosine light chain kinase is not activated, Serine/threonine-protein phosphatase continues to dephosphorylate myosin LC-P, and more cannot be synthesized so myosin remains unbound from actin causing muscle relaxation. This relaxation of the smooth muscles in the lungs causes the bronchial airways to relax which causes bronchodilation, making it easier to breathe. Pirbuterol is administered via respiratory inhalation. Some side effects of using pibuterol may include tremor, nervousness, dizziness, weakness, headache, and upset stomach.

Metabolites of Piracetam are predicted with biotransformer.

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