Browsing Pathways
Showing 51 -
60 of 605359 pathways
SMPDB ID | Pathway Name and Description | Pathway Class | Chemical Compounds | Proteins |
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SMP0000648View Pathway |
Sorafenib Metabolism Pathway (old)Sorafenib is a drug that belongs to the antineoplastics drug class, which is the drug class relating to the treatment of cancer, specifically renal, hepatic and thyroid cancers. This drug works by stopping cancerous tumour progress and stopping therapy replication pf potentially malignant cells. It does this by inhibiting protein synthesis, as we will explore in the pathway. Sorafenib is administered orally, in a tablet form taken twice daily without food. Once ingested, sorafenib finds itself in the endoplasmic reticulum membrane , where it inhibits cytochrome P450 2B6, cytochrome P450 2C8, cytochrome P450 2C9 and UDP-glucuronosyltransferase 1-1. Sorafenib is also catalyzed, with the help uridine diphosphate glucuronic acid and the enzyme UDP-glucuronosyltransferase 1-9 to sorafenib b-D-glucuronide with a by-product of uridine 5’-diphosphate. Sorafenib also undergoes a transformation without the use of catalytic enzymes and becomes sorafenib metabolite M4 and subsequently becomes sorafenib metabolite M5. In another reaction, sorafenib teams up with water and oxygen, using cytochrome P450 3A4 to create sorafenib N-oxide and hydrogen peroxide. Sorafenib N-oxide then undergoes two more reactions, one where it becomes sorafenib N-oxide glucuronide, and another where it becomes sorafenib metabolite M1. Sorafenib metabolite M1 is also attached to another reaction, as sorafenib creates sorafenib metabolite M3, sorafenib metabolite M1 is also created from this metabolite.
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SMP0000598View Pathway |
Spirapril Metabolism PathwaySpirapril (trade name: Renormax) belongs to the class of drugs known as angiotensin-converting enzyme (ACE) inhibitors and is used primarily to lower high blood pressure (hypertension). This drug can also be used in the treatment of congestive heart failure and type II diabetes. Spirapril is a prodrug which, following oral administration, undergoes biotransformation in vivo into its active form spiraprilat via cleavage of its ester group by the liver. Angiotensin-converting enzyme (ACE) is a component of the body's renin–angiotensin–aldosterone system (RAAS) and cleaves inactive angiotensin I into the active vasoconstrictor angiotensin II. ACE (or kininase II) also degrades the potent vasodilator bradykinin. Consequently, ACE inhibitors decrease angiotensin II concentrations and increase bradykinin concentrations resulting in blood vessel dilation and thereby lowering blood pressure.
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SMP0000606View Pathway |
Tamoxifen Metabolism PathwayTamoxifen 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.
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SMP0000732View Pathway |
Temocapril Metabolism PathwayTemocapril (trade name: Acecol) belongs to the class of drugs known as angiotensin-converting enzyme (ACE) inhibitors and is used primarily to lower high blood pressure (hypertension). This drug can also be used in the treatment of congestive heart failure and type II diabetes. Temocapril is a prodrug which, following oral administration, undergoes biotransformation in vivo into its active form temocaprilat via cleavage of its ester group by the liver. Angiotensin-converting enzyme (ACE) is a component of the body's renin–angiotensin–aldosterone system (RAAS) and cleaves inactive angiotensin I into the active vasoconstrictor angiotensin II. ACE (or kininase II) also degrades the potent vasodilator bradykinin. Consequently, ACE inhibitors decrease angiotensin II concentrations and increase bradykinin concentrations resulting in blood vessel dilation and thereby lowering blood pressure.
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SMP0000602View Pathway |
Teniposide Metabolism PathwayTeniposide is a type of chemotherapy drug, derived from the epipodophyllotoxin form the American Mayapple plant. Teniposide is related to etoposide, another anti-cancer drug. It works in a similar way, inhibiting topoisomerase II. This causes single- and double-stranded DNA breaks. These breaks cause cell growth to stop and prevents cancer cells from entering mitosis. It is administered through an intravenous infusion. It is used to treat many cancers such as lymphoma, leukemia (acute lymphocytic), and neuroblastoma.
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SMP0000630View Pathway |
Tenofovir Metabolism PathwayTenofovir is a nucleotide analogue used in the treatment of HIV and chronic hepatitis B. It is taken up into the cell and is subsequently phosphorylated first by adenylate kinases and then by nucleoside diphosphate kinases into tenofovir diphosphate. Tenofovir diphosphate is an analogue of deoxyadenosine triphosphate (dATP) and competes with dATP for binding to the viral DNA polymerase and subsequent incorporation into the growing DNA strand. Once incorporated into the DNA, tenofovir causes chain termination, thus preventing viral replication.
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SMP0000647View Pathway |
Thioguanine Metabolism Pathway (old)Thioguanine is a purine antimetabolite prodrug closely related to mercaptopurine and similarly inhibits purine metabolism. The thioguanine pathway is shown as a part of the mercaptopurine pathway. Thioguanine exerts cytotoxic effects via incorporation of thiodeoxyguanosine triphosphate into DNA and thioguanosine triphosphate into RNA and inhibition of Ras-related C3 botulinum toxin substrate 1, which induces apoptosis of activated T cells. Once in a cell, thioguanine is converted to thioguanosine monophosphate by hypoxanthine-guanine phosphoribosyltransferase. Thioguanosine monophosphate is then phosphorylated to thioguanosine diphosphate, which is converted via a thiodeoxyguanosine diphosphate intermediate to thiodeoxyguanosine triphosphate. Thiodeoxyguanosine triphosphate is incorporated into DNA causing cytotoxicity. 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.
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SMP0000611View Pathway |
Ticlopidine Metabolism PathwayTiclopidine, 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.
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SMP0000637View Pathway |
Tramadol Metabolism PathwayTramadol (also named Ultram) is a class of opioid pain medication that used for treating pain. Metabolism of tramadol mainly happened in liver cell. The N-demethylation of tramadol is catalyzed by the cytochrome CYP3A4 and CYP2B6 to form N-Desmethyltramadol, which further metabolized to N,N-Didesmethyltramadol through CYP3A4 and CYP2B6 and to N,O-Didesmethyltramadol through CYP2D6. The O-demethylation of tramadol is catalyzed by the cytochrome CYP2D6 to form O-Desmethyltramadol, which further metabolized to O-Desmethyltramadol glucuronide through UDP-glucuronosyltransferase 2B7 and UDP-glucuronosyltransferase 1-8. O-Desmethyltramadol can also be metabolized to N,O-Didesmethyltramadol through CYP2D6.
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SMP0000599View Pathway |
Trandolapril Metabolism PathwayTrandolapril (trade name: Mavik) belongs to the class of drugs known as angiotensin-converting enzyme (ACE) inhibitors and is used primarily to lower high blood pressure (hypertension). This drug can also be used in the treatment of congestive heart failure and type II diabetes. Trandolapril is a prodrug which, following oral administration, undergoes biotransformation in vivo into its active form trandolaprilat via cleavage of its ester group by the liver. Angiotensin-converting enzyme (ACE) is a component of the body's renin–angiotensin–aldosterone system (RAAS) and cleaves inactive angiotensin I into the active vasoconstrictor angiotensin II. ACE (or kininase II) also degrades the potent vasodilator bradykinin. Consequently, ACE inhibitors decrease angiotensin II concentrations and increase bradykinin concentrations resulting in blood vessel dilation and thereby lowering blood pressure.
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Showing 51 -
60 of 62 pathways