SMP0000721
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3-Phosphoglycerate Dehydrogenase Deficiency
3-Phosphoglycerate dehydrogenase deficiency is a disorder of L-serine biosynthesis that is characterized by congenital microcephaly, psychomotor retardation, and seizures.The disorder is caused by homozygous or compound heterozygous or homozygous mutation in the gene encoding phosphoglycerate dehydrogenase on chromosome 1p12. Defects in the gene lead to a decrease of Glycine and Serine.
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Disease
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SMP0000179
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Dihydropyrimidine Dehydrogenase Deficiency (DHPD)
Dihydropyrimidine Dehydrogenase Deficiency (DHPD; Thymine-uraciluria) is a rare autosomal recessive disorder caused by a mutation in the DPYD gene which codes for dihydropyrimidine dehydrogenase. A deficiency in this enzyme results in accumulation of 5-hydroxymethyluracil, thymine, and uracil in urine. Symptoms include nystagmus, large liver, hypotonia, growth and mental retardation, and seizures.
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Disease
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SMP0000484
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Dimethylglycine Dehydrogenase Deficiency
Dimethylglycine dehydrogenase deficiency, also called DMGDH deficiency and dimethylglycinuria, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of glycine metabolism caused by a defective DMGDH gene. DMGDH codes for the mitochondrial protein dimethylglycine dehydrogenase which catalyzes the conversion of dimethylglycine into sarcosine. This disorder is characterized by a large accumulation of N,N-dimethylglycine (DMG) and creatinine kinase in serum, and DMG in the urine. Symptoms of the disorder include an unusual fish-like odour and muscle weakness. It is estimated that DMGDH deficiency affects 1 in 1 000 000 individuals.
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Disease
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SMP0000702
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Nepafenac Action Pathway
Nepafenac (also named nevanac or ilevro or amfenac amide) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to treat pain and inflammation that is associated with cataract surgery. Nepafenac 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. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of nepafenac.
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Drug Action
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- 11,12,15-THETA
- 11,12-DiHETrE
- 11,12-Epoxyeicosatrienoic acid
- 11,14,15-THETA
- 11-Dehydro-thromboxane B2
- 11-Epi-PGF2a
- 11H-14,15-EETA
- 12(R)-HETE
- 12(R)-HPETE
- 12(S)-HETE
- 12(S)-HPETE
- 12-KETE
- 12-Keto-leukotriene B4
- 14,15-DiHETrE
- 14,15-Epoxy-5,8,11-eicosatrien...
- 15(S)-HETE
- 15(S)-HPETE
- 15-Deoxy-d-12,14-PGJ2
- 15H-11,12-EETA
- 16(R)-HETE
- 19(S)-HETE
- 2,3-Dinor-8iso prostaglandin F...
- 2,3-Dinor-8iso prostaglandin F...
- 20-Carboxy-leukotriene B4
- 20-Hydroxy-leukotriene B4
- 20-Hydroxyeicosatetraenoic aci...
- 5,6-DHET
- 5,6-Epoxy-8,11,14-eicosatrieno...
- 5,6-Epoxytetraene
- 5-HETE
- 5-HPETE
- 5-KETE
- 6-Keto-prostaglandin F1a
- 6-Ketoprostaglandin E1
- 8(S)-HPETE
- 8,9-DiHETrE
- 8,9-Epoxyeicosatrienoic acid
- 8-HETE
- 8-Isoprostane
- Arachidonic acid
- Calcium
- Fe3+
- Glutathione
- Heme
- L-Glutamic acid
- Leukotriene A4
- Leukotriene B4
- Leukotriene C4
- Leukotriene D4
- LysoPC(14:0/0:0)
- Magnesium
- NADP
- NADPH
- Nepafenac
- Oxidized glutathione
- Oxygen
- PC(14:0/20:4(5Z,8Z,11Z,14Z))
- Prostaglandin A2
- Prostaglandin B2
- Prostaglandin D2
- Prostaglandin E2
- Prostaglandin F2a
- Prostaglandin G2
- Prostaglandin H2
- Prostaglandin I2
- Prostaglandin J2
- Prostaglandin-c2
- Thromboxane A2
- Thromboxane B2
- Water
- Zinc (II) ion
- δ-12-Prostaglandin J2
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SMP0000704
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Tolmetin Action Pathway
Tolmetin (also named Tolectin) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to reduce pain, swelling, tenderness, and stiffness. Tolmetin 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. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of tolmetin.
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Drug Action
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- 11,12,15-THETA
- 11,12-DiHETrE
- 11,12-Epoxyeicosatrienoic acid
- 11,14,15-THETA
- 11-Dehydro-thromboxane B2
- 11-Epi-PGF2a
- 11H-14,15-EETA
- 12(R)-HETE
- 12(R)-HPETE
- 12(S)-HETE
- 12(S)-HPETE
- 12-KETE
- 12-Keto-leukotriene B4
- 14,15-DiHETrE
- 14,15-Epoxy-5,8,11-eicosatrien...
- 15(S)-HETE
- 15(S)-HPETE
- 15-Deoxy-d-12,14-PGJ2
- 15H-11,12-EETA
- 16(R)-HETE
- 19(S)-HETE
- 2,3-Dinor-8iso prostaglandin F...
- 2,3-Dinor-8iso prostaglandin F...
- 20-Carboxy-leukotriene B4
- 20-Hydroxy-leukotriene B4
- 20-Hydroxyeicosatetraenoic aci...
- 5,6-DHET
- 5,6-Epoxy-8,11,14-eicosatrieno...
- 5,6-Epoxytetraene
- 5-HETE
- 5-HPETE
- 5-KETE
- 6-Keto-prostaglandin F1a
- 6-Ketoprostaglandin E1
- 8(S)-HPETE
- 8,9-DiHETrE
- 8,9-Epoxyeicosatrienoic acid
- 8-HETE
- 8-Isoprostane
- Arachidonic acid
- Calcium
- Fe3+
- Glutathione
- Heme
- L-Glutamic acid
- Leukotriene A4
- Leukotriene B4
- Leukotriene C4
- Leukotriene D4
- LysoPC(14:0/0:0)
- Magnesium
- NADP
- NADPH
- Oxidized glutathione
- Oxygen
- PC(14:0/20:4(5Z,8Z,11Z,14Z))
- Prostaglandin A2
- Prostaglandin B2
- Prostaglandin D2
- Prostaglandin E2
- Prostaglandin F2a
- Prostaglandin G2
- Prostaglandin H2
- Prostaglandin I2
- Prostaglandin J2
- Prostaglandin-c2
- Thromboxane A2
- Thromboxane B2
- Tolmetin
- Water
- Zinc (II) ion
- δ-12-Prostaglandin J2
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SMP0000697
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Flurbiprofen Action Pathway
Flurbiprofen (also named Ansaid or Froben) is a nonsteroidal anti-inflammatory drugs. It is used for treatment of moderate pain. Flurbiprofen 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. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of flurbiprofen.
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Drug Action
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- 11,12,15-THETA
- 11,12-DiHETrE
- 11,12-Epoxyeicosatrienoic acid
- 11,14,15-THETA
- 11-Dehydro-thromboxane B2
- 11-Epi-PGF2a
- 11H-14,15-EETA
- 12(R)-HETE
- 12(R)-HPETE
- 12(S)-HETE
- 12(S)-HPETE
- 12-KETE
- 12-Keto-leukotriene B4
- 14,15-DiHETrE
- 14,15-Epoxy-5,8,11-eicosatrien...
- 15(S)-HETE
- 15(S)-HPETE
- 15-Deoxy-d-12,14-PGJ2
- 15H-11,12-EETA
- 16(R)-HETE
- 19(S)-HETE
- 2,3-Dinor-8iso prostaglandin F...
- 2,3-Dinor-8iso prostaglandin F...
- 20-Carboxy-leukotriene B4
- 20-Hydroxy-leukotriene B4
- 20-Hydroxyeicosatetraenoic aci...
- 5,6-DHET
- 5,6-Epoxy-8,11,14-eicosatrieno...
- 5,6-Epoxytetraene
- 5-HETE
- 5-HPETE
- 5-KETE
- 6-Keto-prostaglandin F1a
- 6-Ketoprostaglandin E1
- 8(S)-HPETE
- 8,9-DiHETrE
- 8,9-Epoxyeicosatrienoic acid
- 8-HETE
- 8-Isoprostane
- Arachidonic acid
- Calcium
- Fe3+
- Flurbiprofen
- Glutathione
- Heme
- L-Glutamic acid
- Leukotriene A4
- Leukotriene B4
- Leukotriene C4
- Leukotriene D4
- LysoPC(14:0/0:0)
- Magnesium
- NADP
- NADPH
- Oxidized glutathione
- Oxygen
- PC(14:0/20:4(5Z,8Z,11Z,14Z))
- Prostaglandin A2
- Prostaglandin B2
- Prostaglandin D2
- Prostaglandin E2
- Prostaglandin F2a
- Prostaglandin G2
- Prostaglandin H2
- Prostaglandin I2
- Prostaglandin J2
- Prostaglandin-c2
- Thromboxane A2
- Thromboxane B2
- Water
- Zinc (II) ion
- δ-12-Prostaglandin J2
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SMP0000709
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Salicylic Acid Action Pathway
Salicylic acid (also named rutranex or salonil) is a nonsteroidal anti-inflammatory drug. Salicylic acid is also an important active metabolite of aspirin (acetylsalicylic acid). It can be used to reduce pain and fever. Salicylic acid 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. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of Salicylic acid.
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Drug Action
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- 11,12,15-THETA
- 11,12-DiHETrE
- 11,12-Epoxyeicosatrienoic acid
- 11,14,15-THETA
- 11-Dehydro-thromboxane B2
- 11-Epi-PGF2a
- 11H-14,15-EETA
- 12(R)-HETE
- 12(R)-HPETE
- 12(S)-HETE
- 12(S)-HPETE
- 12-KETE
- 12-Keto-leukotriene B4
- 14,15-DiHETrE
- 14,15-Epoxy-5,8,11-eicosatrien...
- 15(S)-HETE
- 15(S)-HPETE
- 15-Deoxy-d-12,14-PGJ2
- 15H-11,12-EETA
- 16(R)-HETE
- 19(S)-HETE
- 2,3-Dinor-8iso prostaglandin F...
- 2,3-Dinor-8iso prostaglandin F...
- 20-Carboxy-leukotriene B4
- 20-Hydroxy-leukotriene B4
- 20-Hydroxyeicosatetraenoic aci...
- 5,6-DHET
- 5,6-Epoxy-8,11,14-eicosatrieno...
- 5,6-Epoxytetraene
- 5-HETE
- 5-HPETE
- 5-KETE
- 6-Keto-prostaglandin F1a
- 6-Ketoprostaglandin E1
- 8(S)-HPETE
- 8,9-DiHETrE
- 8,9-Epoxyeicosatrienoic acid
- 8-HETE
- 8-Isoprostane
- Arachidonic acid
- Calcium
- Fe3+
- Glutathione
- Heme
- L-Glutamic acid
- Leukotriene A4
- Leukotriene B4
- Leukotriene C4
- Leukotriene D4
- LysoPC(14:0/0:0)
- Magnesium
- NADP
- NADPH
- Oxidized glutathione
- Oxygen
- PC(14:0/20:4(5Z,8Z,11Z,14Z))
- Prostaglandin A2
- Prostaglandin B2
- Prostaglandin D2
- Prostaglandin E2
- Prostaglandin F2a
- Prostaglandin G2
- Prostaglandin H2
- Prostaglandin I2
- Prostaglandin J2
- Prostaglandin-c2
- Salicylic acid
- Thromboxane A2
- Thromboxane B2
- Water
- Zinc (II) ion
- δ-12-Prostaglandin J2
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SMP0059868
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Ketotifen H1-Antihistamine Action
Ketotifen is a first-generation piperidine H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.
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Drug Action
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SMP0058956
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Meclizine H1-Antihistamine Action
Meclizine (Meclozine) is a first-generation piperazine H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.
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Drug Action
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SMP0060195
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Loratadine H1-Antihistamine Action
Loratadine is a second-generation tricyclic H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.
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Drug Action
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