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Showing 571 - 580 of 49827 pathways
SMPDB ID Pathway Chemical Compounds Proteins

SMP0000604

Pw000580 View Pathway
Drug Metabolism

Cyclophosphamide Metabolism Pathway

Cyclophosphamide is an alkylating agent used in the treatment of certain cancers. Following absorption, cyclophosphamide is converted into 4-hydroxyphosphamide by a variety of cytochrome P450 isozymes in the liver. 4-Hydroxyphosphamide is more soluble than cyclophosphamide and is the primary form of the drug that is transported in blood. 4-Hydroxyphosphamide crosses the plasma membrane of the cancer cell and spontaneuosly forms aldophosphamide. This is a reversible reaction. Aldophosphamide can decompose into acrolein and phosphoramide mustard. Phosphoramide mustard is the active alkylating agent and forms alkyl adducts with DNA through a phosphoramide aziridinium intermediate. Alkylation of DNA causes DNA damage and eventually cell death.

SMP0000605

Pw000581 View Pathway
Drug Metabolism

Ifosfamide Metabolism Pathway

Ifosfamide is an alkylating agent used in the treatment of certain cancers. Following absorption, ifosfamide is converted into 4-hydroxyifosfamide by a variety of cytochrome P450 isozymes in the liver. 4-Hydroxyifosfamide crosses the plasma membrane of the cancer cell and spontaneuosly forms aldoifosfamide. This is a reversible reaction. Aldoifosfamide can decompose into acrolein and ifosforamide mustard. Ifosforamide mustard is the active alkylating agent and forms alkyl adducts with DNA through an ifosforamide aziridinium intermediate. Alkylation of DNA causes DNA damage and ultimately cell death.

SMP0000606

Pw000582 View Pathway
Drug Metabolism

Tamoxifen Metabolism Pathway

Tamoxifen is a selective estrogen modulator (SERM) used in the treatment of estrogen-sensitive breast cancer. Tamoxifen itself only has weak anti-estrogen effects and must be converted into more active metabolites to have therapeutic activity. Metabolism takes place in the liver and is carried out primarily by cytochrome P450 enzymes. Tamoxifen is hydroxylated by CYP2D6 and demethylated by CYP3A4 and CYP3A5, producing the active metabolites 4-hydroxytamoxifen and endoxifen. These metabolites inhibit estrogen binding to estrogen receptors in breast cancer cells, which in turn inhibit tumour growth.

SMP0000607

Pw000583 View Pathway
Drug Metabolism

Capecitabine Metabolism Pathway

Capecitabine is a fluoropyrimidine anticancer drug. After absorption, it is metabolized in the liver to the intermediate 5’-deoxy-5-fluorouridine, which is subsequently converted into 5-fluorouracil (5-FU) by intracellular thymidine phosphorylase. 5-FU exerts cytotoxic effects on the cell by direct incorporation into DNA and RNA as well as by inhibiting thymidylate synthase. Since thymidine phosphorylase is present at 3-10 fold higher concentration in cancer cells compared normal cells, capecitabine’s cytotoxic effect is selective for cancer cells.

SMP0000608

Pw000584 View Pathway
Drug Metabolism

Fluorouracil Metabolism Pathway

Fluorouracil (5-FU), sold under the brand name Adrucil among others, is a fluoropyrimidine anticancer drug. By injection into a vein, it is used to treat colon cancer, esophageal cancer, stomach cancer, pancreatic cancer, breast cancer, and cervical cancer. As a cream, it is used for actinic keratosis, basal cell carcinoma, and skin warts. Fluorouracil is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system . Fluorouracil exerts cytotoxic effects on the cell by direct incorporation into DNA and RNA as well as by inhibiting thymidylate synthase.

SMP0000609

Pw000585 View Pathway
Drug Metabolism

Mercaptopurine Metabolism Pathway

Mercaptopurine is a purine antimetabolite prodrug that exerts cytotoxic effects via three mechanisms: via incorporation of thiodeoxyguanosine triphosphate into DNA and thioguanosine triphosphate into RNA, inhibition of de novo synthesis of purine nucleotides, and inhibition of Ras-related C3 botulinum toxin substrate 1, which induces apoptosis of activated T cells. Mercaptopurine travels through the bloodstream and is transported into cells via nucleoside transporters. Mercaptopurine is then converted to thioguanosince diphosphate through a series of metabolic reactions that produces the metabolic intermediates, thioinosine 5’-monophosphate, thioxanthine monophosphate, and thioguanosine monophosphate. Thioguanosine diphosphate is then converted via a thiodeoxyguanosine diphosphate intermediate to thiodeoxyguanosine triphosphate, which is incorporated into DNA. Thioguanosine diphosphate is also converted to thioguanosine triphosphate which is incorporated into RNA. The thioguanosine triphosphate metabolite also inhibits Ras-related C3 botulinum toxin substrate 1, a plasma membrane-associated small GTPase that regulates cellular processes, inducing apoptosis in activated T cells. Finally, de novo synthesis of purine nucleotides is inhibited by the methyl-thioinosine 5’-monophosphate metabolite, which inhibits amidophosphoribosyl-transferase, the enzyme that catalyzes one of the first steps in this pathway.

SMP0000610

Pw000586 View Pathway
Drug Metabolism

Clopidogrel Metabolism Pathway

Clopidogrel, marketed as Plavix, is an antiplatelet drug that targets the P2Y12 receptor of platelets. Clopidogrel is taken orally as a prodrug, and must be metabolically activated before it can be effective. It first enters the liver and enters the endoplasmic reticulum where it is metabolized to form the active metabolite. First, it is catalyzed by cytochromes P450 2C19, 2B6 and 1A2 into 2-oxoclopidogrel. Secondly, it is processed by cytochromes P450 2B6, 2C9, 2C19, 3A4, 3A5, and serum paraoxonase/arylesterase 1 into the active metabolite of clopidogrel. The active metabolite of clopidogrel then enters the blood stream, where it binds irreversibly to the P2Y purinoreceptor 12 on the surface of platelet cells, preventing ADP from binding to and activating it. Clopidogrel prevents the activation of the Gi protein associated with the P2Y12 receptor from inactivating adenylate cyclase in the platelet, leading to a buildup of cAMP. This cAMP then activates calcium efflux pumps, preventing calcium buildup in the platelet, which would cause activation, and later, aggregation.

SMP0000611

Pw000587 View Pathway
Drug Metabolism

Ticlopidine Metabolism Pathway

Ticlopidine, marketed as Ticlid, is an antiplatelet drug that targets the P2Y12 receptor of platelets. Ticlopidine is taken orally and is a prodrug that must be metabolically activated before it can be effective. It first enters the liver and enters the endoplasmic reticulum where it is metabolized to form the active metabolite. First, it is catalyzed by cytochromes P450 2C19, 2B6 and 1A2 into 2-oxoclopidogrel. Secondly, it is processed by cytochromes P450 2B6, 2C9, 2C19, 3A4, 3A5, and serum paraoxonase/arylesterase 1 into the active metabolite of clopidogrel. The active metabolite of clopidogrel then enters the blood stream, where it binds irreversibly to the P2Y purinoreceptor 12 on the surface of platelet cells, preventing ADP from binding to and activating it. Clopidogrel prevents the activation of the Gi protein associated with the P2Y12 receptor from inactivating adenylate cyclase in the platelet, leading to a buildup of cAMP. This cAMP then activates calcium efflux pumps, preventing calcium buildup in the platelet, which would cause activation, and later, aggregation.

SMP0000612

Pw000588 View Pathway
Drug Metabolism

Esomeprazole Metabolism Pathway

Esomeprazole, sold as Nexium, is a proton pump inhibitor (PPI) class drug that suppresses the final step in gastric acid production. In this pathway, esomeprazole is taken orally and is oxidized in the stomach to form the active metabolite of esomeprazole. This active metabolite then binds covalently to the potassium-transporting ATPase protein subunits, found at the secretory surface of the gastric parietal cell, preventing any stimulus. Because the drug binds covalently, its effects are dose-dependent and last much longer than similar drugs that bind to the protein non-covalently. This is because additional ATPase enzymes must be created to replace the ones covalently bound by pantoprazole. Esomeprazole is used to manage gastroesophageal reflux disease, to prevent stomach ulcers, and can be used to help treat the effects of a H. pylori infection.

SMP0000613

Pw000589 View Pathway
Drug Metabolism

Omeprazole Metabolism Pathway

Omeprazole, sold as Prilosec. Losec and Zegerid, is a proton pump inhibitor (PPI) class drug that suppresses the final step in gastric acid production, and was the first proton pump inhibitor to e developed. In this pathway, omeprazole is taken orally and is oxidized in the stomach to form the active metabolite of omeprazole. This active metabolite then binds covalently to the potassium-transporting ATPase protein subunits, found at the secretory surface of the gastric parietal cell, preventing any stimulus. Because the drug binds covalently, its effects are dose-dependent and last much longer than similar drugs that bind to the protein non-covalently. This is because additional ATPase enzymes must be created to replace the ones covalently bound by pantoprazole. Omeprazole is used to manage gastroesophageal reflux disease, to prevent stomach ulcers, and can be used to help treat the effects of a H. pylori infection.
Showing 571 - 580 of 49827 pathways