Pathways

Lornoxicam (also named Chlortenoxicam or Xefocam) is a nonsteroidal anti-inflammatory drug. It can be used to treat moderate pain such as pain relieving. It can also treat swelling and fever reducing. Lornoxicam can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of Lornoxicam.

Lornoxicam is an NSAID indicated in the treatment of mild to moderate pain, as well as rheumatoid arthritis and osteoarthritis. It has analgesic, anti-inflammatory, and antipyretic properties. It targets the prostaglandin G/H synthase-1 (COX-1) and prostaglandin G/H synthase-2 (COX-2) in the cyclooxygenase pathway. The cyclooxygenase pathway begins in the cytosol with phospholipids being converted into arachidonic acid by the action of phospholipase A2. The rest of the pathway occurs on the endoplasmic reticulum membrane, where prostaglandin G/H synthase 1 & 2 convert arachidonic acid into prostaglandin H2. Prostaglandin H2 can either be converted into thromboxane A2 via thromboxane A synthase, prostacyclin/prostaglandin I2 via prostacyclin synthase, or prostaglandin E2 via prostaglandin E synthase. COX-2 is an inducible enzyme that is responsible for prostaglandin synthesis during inflammation. It leads to the formation of prostaglandin E2 which is responsible for contributing to the inflammatory response by activating immune cells and for increasing pain sensation by acting on pain fibers. Lornoxicam inhibits the action of COX-1 and COX-2 on the endoplasmic reticulum membrane. This reduces the formation of prostaglandin H2 and therefore, prostaglandin E2 (PGE2). The low concentration of prostaglandin E2 attenuates the effect it has on stimulating immune cells and pain fibers, consequently reducing inflammation and pain. Inflammatory and infectious diseases trigger fever. Cytokines are produced in the central nervous system (CNS) during an inflammatory response. These cytokines induce COX-2 production that increases the synthesis of prostaglandin, specifically prostaglandin E2 which adjusts hypothalamic temperature control by increasing heat production. Because lornoxicam decreases PGE2 in the CNS, it has an antipyretic effect. This drug is administered as an oral tablet.

Metabolites of Lornoxicam are predicted with biotransformer.

Lorpiprazole is a serotonin antagonist and reuptake inhibitor thus, its activity is performed by antagonizing the 5-HT2A and the 5-HT2C serotoninergic receptors as well as the alpha1 and alpha2 adrenergic receptors, H1 histaminergic receptors and at high doses, inhibiting the SERT serotonin transporter

Losartan is metabolized to an aldehyde intermediate, E-3179, which is further metabolized to a carboxylic acid, E-3174, by cytochrome P450s like CYP2C9. Losartan can also be hydroxylated to an inactive metabolite, P1. Approximately 14% of losartan is metabolized to E-3174. Losartan can be metabolized by CYP3A4, CYP2C9, and CYP2C10. Losartan can also be glucuronidated by UGT1A1, UGT1A3, UGT1A10, UGT2B7, and UGT 2B17. (DrugBank)

Losartan, sometimes called Cozaar, is a medication used to treat hypertension, also know as hypertension. It works by preventing the mechanism of action that causes blood vessels to tighten. It acts as an angiotensin II receptor blocker, or an ARB. This means that it works by inhibiting the activation of angiotensin through the angiotensin II receptor. This prevents the subsequent activation of cytochrome P450 11B2, which in turn creates aldosterone. For this reason, Losartan can be used in the treatment of diabetes, as it can help prevent damage to the kidneys. Losartan has side effects such as headaches, dizziness, sleep disruptions, and diarrhea,

Losartan (also named Cozaar) is an active metabolite of angiotensin II receptor blockers (ARBs). Losartan competes with angiotensin II to bind type-1 angiotensin II receptor (AT1) in many tissues (e.g. vascular smooth muscle, the adrenal glands, etc.) to prevent increasing sodium, water reabsorption and peripheral resistance (that will lead to increasing blood pressure) via aldosterone secretion that is caused by angiotensin II. Therefore, action of losartan binding to AT1 will result in decreasing blood pressure. For more information on the effects of aldosterone on electrolyte and water excretion, refer to the description of the \spironolactone\:http://pathman.smpdb.ca/pathways/SMP00134/pathway or \triamterene\:http://pathman.smpdb.ca/pathways/SMP00132/pathway pathway, which describes the mechanism of direct aldosterone antagonists. Losartan is an effective agent for reducing blood pressure and may be used to treat essential hypertension and heart failure.