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Pathways

PathWhiz ID Pathway Meta Data

PW000684

Pw000684 View Pathway
drug action

Salsalate Action Pathway

Homo sapiens
Salsalate (also named Salflex, Disalcid or Salsitab) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to treat pain, fever and inflammation. Salsalate 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 salsalate.

PW128184

Pw128184 View Pathway
drug action

Salsalate Action Pathway (New)

Homo sapiens
Salsalate (also named Salflex, Disalcid, or Salsitab) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to treat pain, fever, and inflammation. Salsalate can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 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. Salsalate 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 salsalate decreases PGE2 in the CNS, it has an antipyretic effect. Antipyretic effects increase peripheral blood flow, vasodilation, and subsequent heat dissipation. This drug is administered as an oral tablet.

PW145412

Pw145412 View Pathway
drug action

Salsalate Drug Metabolism Action Pathway

Homo sapiens

PW002061

Pw002061 View Pathway
metabolic

Salvage Pathways of Pyrimidine Deoxyribonucleotides

Escherichia coli
The pathway begins with the introduction of deoxycytidine into the cytosol, either through a nupG symporter or a nupC symporter. Once inside it is deaminated when reacting with a water molecule, a hydrogen ion and a deoxycytidine deaminase resulting in the release of an ammonium and a deoxyuridine. Deoxyuridine can also be imported through a nupG symporter or a nupC symporter. Deoxyuridine can react with an ATP through a deoxyuridine kinase resulting in the release of a ADP , a hydrogen ion and a dUMP. Deoxyuridine can also react with a phosphate through a uracil phosphorylase resulting in the release of a uracil and a deoxy-alpha-D-ribose 1-phosphate. This compound in turn reacts with a thymine through a thymidine phosphorylase resulting in the release of a phosphate and a thymidine. Thymidine in turn reacts with an ATP through a thymidine kinase resulting in a release of an ADP, a hydrogen ion and a dTMP

PW064702

Pw064702 View Pathway
physiological

samar

Homo sapiens
using Immunofluorescence for breast cancer

PW064703

Pw064703 View Pathway
drug action

samar94

Homo sapiens

PW132184

Pw132184 View Pathway
metabolic

Samarium (153Sm) lexidronam Drug Metabolism

Homo sapiens
Samarium (153Sm) lexidronam is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Samarium (153Sm) lexidronam passes through the liver and is then excreted from the body mainly through the kidney.

PW145637

Pw145637 View Pathway
drug action

Samarium (153Sm) lexidronam Drug Metabolism Action Pathway

Homo sapiens

PW131154

Pw131154 View Pathway
metabolic

Sambucus nigra flower Drug Metabolism

Homo sapiens

PW127915

Pw127915 View Pathway
drug action

Samidorphan Action Pathway

Homo sapiens
Samidorphan, also known as Lybalvi, is a novel opioid-system modulator, it is similar to naltrexone. It functions primarily as a μ-opioid receptor antagonist and is used primarily in combination with antipsychotics to reduce their metabolic dysfunction-associated adverse effects. Samidorphan was first approved by the FDA in May 2021. It is used in combination with olanzapine, an antipsychotic, for the treatment of bipolar disorder and for the treatment of schizophrenia in adults. It is demonstrated that the addition of samidorphan to olanzapine helps mitigate the metabolic-related adverse effects of olanzapine; presumably, this is due to opioid receptor signaling, though the exact mechanism remains to be determined. Samidorphan functions primarily as a μ-opioid receptor antagonist and as a κ/δ-opioid receptor partial agonist. Since it is an opioid antagonist, this drug can potentiate opioid withdrawal. Samidorphan acts as an antagonist at the μ-opioid, a partial agonist at both the κ- and δ-opioid receptors in vitro. Samidorphan inhibits the exchange of GTP for GDP which is required to activate the G-protein complex. This prevents the Gi subunit of the mu opioid receptor from inhibiting adenylate cyclase, which can therefore continue to catalyze ATP into cAMP. cAMP increases the excitability in spinal cord pain transmission neurons which allows the patient to feel pain rather than the analgesic effects of opioids. The inhibition of Mu-type opioid receptors also prevents the Gi subunit of the mu opioid receptor from activating the inwardly rectifying potassium channel increasing K+ conductance which would cause hyperpolarization. Samidorphan also prevents the gamma subunit of the mu opioid receptor from inhibiting the N-type calcium channels on the neuron. This allows calcium to enter the neuron and depolarize. The inhibition of mu-opioid receptors prevents hyperpolarization in the neuron, allowing it to fire at a normal rate. The neuron is able to depolarize and the high concentration of calcium releases GABA into the synapse which binds to GABA receptors. GABA receptors inhibits dopamine cell firing in the pain transmission neurons. This prevents the analgesic and depressive effects of opioids, preventing opioid overdose. GABA also inhibits dopamine cell firing in the reward pathway which is the main cause of addiction to opioids and other drugs.