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Enoxaparin.
smpdb.ca/view/SMP0000272Drug actionEnoxaparin's action is antithrombin-dependent. The drug binds to antithrombin III to reduce thrombin inhibition in the plasma. … The drug increases the inactivation of coagulation factors IXa, Xa and XIIa. This increases the antithrombin effects.
Enzymes: Antithrombin-IIIArdeparin Action Pathway
smpdb.ca/view/SMP0000275Drug actionArdeparin binds and increases antithrombin III activity and inactivates thrombin, factor Xa and coagulation factors XIIa, XIa, plasmin and kallikrein to prevent clot formation. … These properties increase ardeparin's bioavailability and give a more predictable anticoagulant activity.
Enzymes: Antithrombin-IIITirofiban Action Pathway (new)
smpdb.ca/view/SMP0126470Drug actionIt is administered intravenously and acts as an antagonist of the platelet glycoprotein IIb/IIIa receptor, this receptor is responsible for platelet aggregation in order to form a thrombus, without this
Enzymes: Integrin alpha-IIbCarnitine Palmitoyl Transferase Deficiency II
smpdb.ca/view/SMP0000541DiseaseThe most common cause of hereditary myoglobinuria is the myopathic form of CPT II deficiency and affects men more than women. … There are three forms of CPT II deficiency: (1) lethal neonatal form, (2) severe infantile hepatocardiomuscular form, and (3) the myopathic form.
Drugs: Adenosine phosphate · NADH · ATP · Levocarnitine · Magnesium cation · Flavin adenine dinucleotide +2 moreCarnitine Palmitoyl Transferase Deficiency II
smpdb.ca/view/SMP0125742DiseaseThe most common cause of hereditary myoglobinuria is the myopathic form of CPT II deficiency and affects men more than women. … There are three forms of CPT II deficiency: (1) lethal neonatal form, (2) severe infantile hepatocardiomuscular form, and (3) the myopathic form.
Drugs: Adenosine phosphate · NADH · ATP · Levocarnitine · Magnesium cation · Flavin adenine dinucleotide +2 moreCongenital Bile Acid Synthesis Defect Type II
smpdb.ca/view/SMP0000314DiseaseChenodeoxycholic acid and cholic acid are decreased in plasma and urine. … Symptoms of this disease include cholestatic jaundice, atypical oxo and allo bile acids in urine and serum, liver failure, and steatosis.
Chondrodysplasia Punctata II, X-Linked Dominant (CDPX2)
smpdb.ca/view/SMP0000388DiseaseSymptoms include alopecia, dysmorphism, hyperkeratosis, ichthyosis, kyphoscoliosis, limb abnormalities and deformities, and mental retardation. … A defect in this enzyme causes accumulation of 8-dehydrocholesterol and 8(9)cholestenol in the plasma.
Drugs: Cholecalciferol · ATP · Magnesium cation · Iron · Dimethylallyl Diphosphate · Formic acid +8 moreCongenital Bile Acid Synthesis Defect Type II
smpdb.ca/view/SMP0125689DiseaseChenodeoxycholic acid and cholic acid are decreased in plasma and urine. … Symptoms of this disease include cholestatic jaundice, atypical oxo and allo bile acids in urine and serum, liver failure, and steatosis.
Chondrodysplasia Punctata II, X-Linked Dominant (CDPX2)
smpdb.ca/view/SMP0125639DiseaseSymptoms include alopecia, dysmorphism, hyperkeratosis, ichthyosis, kyphoscoliosis, limb abnormalities and deformities, and mental retardation. … A defect in this enzyme causes accumulation of 8-dehydrocholesterol and 8(9)cholestenol in the plasma.
Drugs: Cholecalciferol · ATP · Magnesium cation · Iron · Dimethylallyl Diphosphate · Formic acid +8 morePorphyrin Metabolism
smpdb.ca/view/SMP0000024MetabolicIn the next reaction, a second methylene group (located between rings III and IV of the porphyrin ring) is reduced by the enzyme known as biliverdin reductase, producing bilirubin. … This step is mediated by two enzymes: uroporphyrinogen synthase and uroporphyrinogen III cosynthase. Hydroxymethylbilane can also be non-enzymatically cyclized to form uroporphyrinogen I.
Enzymes: Uroporphyrinogen-III synthase, Coproporphyrinogen-III oxidase, mitochondrial