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Pathways

PathWhiz ID Pathway Meta Data

PW146633

Pw146633 View Pathway
drug action

Sultopride Drug Metabolism Action Pathway

Homo sapiens

PW176407

Pw176407 View Pathway
metabolic

Sultopride Predicted Metabolism Pathway

Homo sapiens
Metabolites of Sultopride are predicted with biotransformer.

PW144781

Pw144781 View Pathway
drug action

Sumatriptan Drug Metabolism Action Pathway

Homo sapiens

PW128601

Pw128601 View Pathway
drug action

Sumatriptan Mechanism of Action Action Pathway

Homo sapiens
Triptans are a class of medications used in the treatment of migraine headaches. Triptans act as antimigraine agents by selectively binding to the serotonin receptors 5-HT1B and 5-HT1D. Triptan binding to the vascular 5-HT1B receptors leads to vasoconstriction of the cranial arteries, which painfully dilate during a migraine attack. Sumatriptan is a 5-HT1B/1D receptor agonist and leads to vasoconstriction in the basilar artery and the blood vessels of the dura mater. It decreases peripheral nociception either by selective cranial vasoconstriction or an effect on trigeminovascular nerves. The blocking effect of sumatriptan indicated a peripheral effect on trigeminal vascular nerves in neurogenically mediated plasma extravasation. Sumatriptan inhibits the presynaptic terminal of the trigeminal nucleus caudalis, which leads to the reversal of facial allodynia. Triptans decrease transmission of the pain impulses to the trigeminal nucleus caudalis and reduce inflammatory mediators from trigeminal nerves, therefore reducing calcitonin gene-related peptide-mediated vasodilation. Migraine pain is associated with middle cerebral artery dilatation, which leads to a lower velocity of regional cerebral blood flow. Sumatriptan reverses the dilatation of MCA, which suggests that the 5-HT receptor system has a role in the pathogenesis of a migraine.

PW128477

Pw128477 View Pathway
drug action

Sunitinib Action Pathway

Homo sapiens
Sunitinib is a chemotherapeutic agent and receptor tyrosine kinase inhibitor utilized in the treatment of renal cell carcinoma (RCC) and imatinib-resistant gastrointestinal stromal tumor (GIST). Approved by the US FDA on January 26, 2006, it's administered orally and operates as a multi-targeted small-molecule receptor tyrosine kinase (RTK) inhibitor. Its actions encompass inhibiting key signaling pathways by targeting various RTKs, including platelet-derived growth factor receptors (PDGF-R), vascular endothelial growth factor receptors (VEGF-R), and KIT (CD117) in GIST cases. Sunitinib also affects RET, CSF-1R, and flt3 RTKs. Indicated conditions for sunitinib include advanced RCC, adjuvant treatment post-nephrectomy for high-risk recurrent RCC, and well-differentiated pancreatic neuroendocrine tumors (pNET) with unresectable locally advanced or metastatic disease. Its mechanism entails inhibiting RTKs implicated in cancer progression, tumor growth, and angiogenesis. This inhibition encompasses PDGFRa, PDGFRb, VEGFR1, VEGFR2, VEGFR3, KIT, FLT3, CSF-1R, and RET receptors. The primary metabolite mirrors sunitinib's potency in relevant assays.

PW145351

Pw145351 View Pathway
drug action

Sunitinib Drug Metabolism Action Pathway

Homo sapiens

PW002053

Pw002053 View Pathway
metabolic

Superoxide Radicals Degradation

Escherichia coli
In gram-negative bacteria, cytoplasmic and periplasmic isozymes of superoxide dismutase (SOD) is their defense system against superoxide anion (O2-). In E.coli, there are several SOD isozymes which are manganese-cofactored (MnSOD), iron-cofactored (FeSOD) and copper, zinc-cofactored (CuZnSOD) in perplasm, and they can be generated by autooxidation of dihydromenaquinone in the cytoplasmic membrane. In E.coli, MnSOD and FeSOD have similar structure and kinetic, but CuZnSOD is monomeric. FeSOD is the only SOD in E.coli under anaerobic conditions. MnSOD is induced by environmental stress condition as well as aerobic growth. CuZnSOD is induced in stationary phase. SOD will catalyze the superoxide anion to form oxygen and H2O2. With increasing concentration of H2O2, catalase such as cryptic adenine deaminase is induced in E.coli to degrade H2O2 into water and oxygen.

PW123543

Pw123543 View Pathway
metabolic

Superoxide Radicals Degradation

Pseudomonas aeruginosa
In gram-negative bacteria, cytoplasmic and periplasmic isozymes of superoxide dismutase (SOD) is their defense system against superoxide anion (O2-). In E.coli, there are several SOD isozymes which are manganese-cofactored (MnSOD), iron-cofactored (FeSOD) and copper, zinc-cofactored (CuZnSOD) in perplasm, and they can be generated by autooxidation of dihydromenaquinone in the cytoplasmic membrane. In E.coli, MnSOD and FeSOD have similar structure and kinetic, but CuZnSOD is monomeric. FeSOD is the only SOD in E.coli under anaerobic conditions. MnSOD is induced by environmental stress condition as well as aerobic growth. CuZnSOD is induced in stationary phase. SOD will catalyze the superoxide anion to form oxygen and H2O2. With increasing concentration of H2O2, catalase such as cryptic adenine deaminase is induced in E.coli to degrade H2O2 into water and oxygen.

PW000258

Pw000258 View Pathway
drug action

Suprofen Action Pathway

Homo sapiens
Suprofen (also named Profenal and Maldocil) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to relieve pain (analgesic) and reduce fever (antipyretic). Suprofen is also a type of ophthalmic anti-inflammatory medicines which may be used to help prevent eye constrict for pupil during surgery. Suprofen 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. Since prostaglandin is the messenger molecules in the process of inflammation; hence, inhibition of prostaglandin synthesis can reduce the pain and inflammation (e.g. in the eyes).

PW144973

Pw144973 View Pathway
drug action

Suprofen Drug Metabolism Action Pathway

Homo sapiens