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Pathways

PathWhiz ID Pathway Meta Data

PW127757

Pw127757 View Pathway
drug action

Sulodexide Action Pathway

Homo sapiens
Sulodexide mixture of glycosaminoglycans (GAGs), dermatan sulfate (DS) and fast-moving heparin. Its mechanism of action inhibits coagulation by inhibiting antithrombin III thus stopping the conversion of prothrombin and thrombin. Doing that also inhibits the conversion of fibrinogen to fibrin halting the clotting factor. Sulodexide is administered via oral, intravenous or intramuscular, it is mainly metabolized by the liver. It is eliminated through renal, fecal and bile routes, and sometimes adverse effects occur that relate to the gastrointestinal system. Some other adverse reaction to sulodexide despite being fairly well tolerated includes diarrhea, epigastralgia, dyspepsia, heartburn and dizziness. Some allergic reactions can cause skin rash but these occurrences are rare.

PW144516

Pw144516 View Pathway
drug action

Sulpiride Drug Metabolism Action Pathway

Homo sapiens

PW128078

Pw128078 View Pathway
drug action

Sulpiride Mechanism of Action Action Pathway

Homo sapiens
Sulpiride is a substituted benzamide derivative and a selective dopamine D2 antagonist indicated to treat acute and chronic schizophrenia. Sulpiride is a selective dopamine D2 and D3 receptor antagonist.

PW146496

Pw146496 View Pathway
drug action

Sultamicillin Drug Metabolism Action Pathway

Homo sapiens

PW145830

Pw145830 View Pathway
drug action

Sulthiame Drug Metabolism Action Pathway

Homo sapiens

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.