Browsing Pathways
Showing 41 -
50 of 605359 pathways
SMPDB ID | Pathway Name and Description | Pathway Class | Chemical Compounds | Proteins |
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SMP0000651View Pathway |
Artemether Metabolism PathwayArtemether is a semisynthetic derivative of artemisinin, a phytoconstituent that acts as a short-acting antimalarial agent and is used to treat uncomplicated Plasmodium falciparum malaria. Artemisinin derivatives kill parasites more rapidly than conventional antimalarial drugs, and are active against both the sexual and asexual stages of the parasite cycle. However due to their short half-life (and to prevent resistance development) artemisinin compounds are often combined with long-acting antimalarial drugs. Artemeter is administered orally and as an oil-based intramuscular injection. The antimalarial activity of artemether and other artemisinin derivatives is a result of the peroxide bridge found in the active metabolite dihydroartemisinin. Dihydroartemisinin is formed from the rapid demethylation of artmether via CYP3A4 and CYP3A5. It then undergoes glucuronidation catalyzed by the UDP-glucuronosyltransferases UGT1A9 and UGT2B7 into inactive metabolites that are eliminated in the bile.
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SMP0000593View Pathway |
Enalapril Metabolism PathwayEnalapril (trade name: Vasotec) 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. Enalapril is a prodrug which, following oral administration, undergoes biotransformation in vivo into its active form enalaprilat 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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SMP0000595View Pathway |
Moexipril Metabolism PathwayMoexipril (trade name: Univasc) 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. Moexipril is a prodrug which, following oral administration, undergoes biotransformation in vivo into its active form moexiprilat 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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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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SMP0000646View Pathway |
Fluoxetine Metabolism PathwayFluoxetine is a selective serotonin reuptake inhibitor that exerts antidepressive effects by selectively inhibiting serotonin reuptake in the brain. It does so by competing for the same binding site as serotonin on the the sodium-dependent serotonin transporter (SLC6A4). This increases the concentrations of serotonin in the synaptic cleft and reverses the state of low concentration seen in depression. Higher concentration of serotonin has also been shown to have long-term neuromodulatory effects. Binding of serotonin to certain serotonin receptors activate adenylate cyclase, which produces cAMP. cAMP activates protein kinase A which activates cAMP-responsive binding protein 1 (CREB-1). CREB-1 enters the nucleus and affects transcription of brain-derived neurotrophic factor (BDNF). BDNF subsequently stimulates neurogenesis, which may contribute to the long-term reversal of depression.
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SMP0000607View Pathway |
Capecitabine Metabolism PathwayCapecitabine 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.
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SMP0000632View Pathway |
Prednisolone Metabolism PathwayPrednisolone is a synthetic glucocorticoid that is used clinically for its anti-inflammatory properties. Prednisolone diffuses passively across the cell membrane, where it binds to glucocorticoid receptors in the cytoplasm. Upon binding, the glucocorticoid receptor (GR) dissociates from heat shock protein 90, and translocate into the nucleus. In the nucleus, GR dimers can bind to glucocorticoid response element (GRE) in the promoter region of anti-inflammatory genes, which activates their transcription. GRs also inhibit transcription of inflammatory mediators by binding to negative GRE (nGRE). GRs further interact with the transcription factors cAMP-responsive element binding protein and NF-kappa-B, and inihibit their activation of inflammatory gene transcription. GRs also recruit histone deacetylase 2 to inflammatory gene loci on DNA, which leads to DNA condensation and suppression of gene expression.
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SMP0000627View Pathway |
Citalopram Metabolism PathwayCitalopram is a selective serotonin reuptake inhibitor that exerts antidepressive effects by selectively inhibiting serotonin reuptake in the brain. It does so by competing for the same binding site as serotonin on the the sodium-dependent serotonin transporter (SLC6A4). This increases the concentrations of serotonin in the synaptic cleft and reverses the state of low concentration seen in depression. Higher concentration of serotonin has also been shown to have long-term neuromodulatory effects. Binding of serotonin to certain serotonin receptors activate adenylate cyclase, which produces cAMP. cAMP activates protein kinase A which activates cAMP-responsive binding protein 1 (CREB-1). CREB-1 enters the nucleus and affects transcription of brain-derived neurotrophic factor (BDNF). BDNF subsequently stimulates neurogenesis, which may contribute to the long-term reversal of depression.
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SMP0000612View Pathway |
Esomeprazole Metabolism Pathway (Old)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.
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SMP0000614View Pathway |
Lansoprazole Metabolism Pathway (old)Lansoprazole, sold as Prevacid, is a proton pump inhibitor (PPI) class drug that suppresses the final step in gastric acid production. In this pathway, lansoprazole is taken orally and is oxidized in the stomach to form the active metabolite of lansoprazole. 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. Lansoprazole 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.
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Showing 41 -
50 of 62 pathways