Loader

Pathways

PathWhiz ID Pathway Meta Data

PW128620

Pw128620 View Pathway
drug action

Nomifensine Dopamine Reuptake Inhibitor Action Pathway

Homo sapiens
Nomifensine, formerly known as Merital capsules, is a dopamine reuptake inhibitor drug that was removed from the market in 1986 for increased incidence of hemolytic anemia. The drug was originally used to treat depression. Nomifensine stimulates the nervous system through the reuptake of norepinephrine and dopamine, which prolongs their duration in the synapse so that they can bind more readily to the receptors. The mechanism is not fully understood, but may be similar to other dopamine reuptake inhibitors where Nomifensine would cross the blood-brain barrier through diffusion. Dopamine is synthesized in the ventral tegmental area of the brain from tyrosine being synthesized into L-dopa by the enzyme Tyrosine 3-monooxygenase . L-Dopa is then synthesized into dopamine with the enzyme aromatic-L-amino-acid decarboxylase. Dopamine then travels to the prefrontal cortex, which is released into the synapse when the neuron is stimulated and fires. Nomifensine binds to the sodium-dependent dopamine transporter, preventing dopamine from re-entering the presynaptic neuron. The dopamine then binds to Dopamine D4 receptors on the postsynaptic membrane. The dopamine D4 receptor activates the Gi protein cascade which inhibits adenylate cyclase. This prevents adenylate cyclase from catalyzing ATP into cAMP.

PW147062

Pw147062 View Pathway
metabolic

Nomifensine Drug Metabolism Pathway

Homo sapiens

PW122015

Pw122015 View Pathway
disease

Non-Ketotic Hyperglycinemia

Rattus norvegicus
Non Ketotic Hyperglycinemeia (Glycine encephalopathy; Glycine cleavage system deficiency; NKH) is caused by mutations in several genes in the mitochondrial glycine cleavage system. These include the genes encoding P protein (GLDC), T protein (GCST), and, in one case, the H protein (GCSH). Most patients with GCE (Glycine Encephalopathy, or NKH) have a defect in the GLDC gene.The enzyme system for cleavage of glycine (glycine cleavage system), which is confined to the mitochondria, is composed of 4 protein components: P protein (a pyridoxal phosphate-dependent glycine decarboxylase), H protein (a lipoic acid-containing protein), T protein (a tetrahydrofolate-requiring enzyme), and L protein (a lipoamide dehydrogenase). NKH is characterized by accumulation of glycine in plasma, spinal fluid and urine. Symptoms include seizures, respiratory distress, mental retardation, chorea, visual impairment and hydrocephalus.

PW121790

Pw121790 View Pathway
disease

Non-Ketotic Hyperglycinemia

Mus musculus
Non Ketotic Hyperglycinemeia (Glycine encephalopathy; Glycine cleavage system deficiency; NKH) is caused by mutations in several genes in the mitochondrial glycine cleavage system. These include the genes encoding P protein (GLDC), T protein (GCST), and, in one case, the H protein (GCSH). Most patients with GCE (Glycine Encephalopathy, or NKH) have a defect in the GLDC gene.The enzyme system for cleavage of glycine (glycine cleavage system), which is confined to the mitochondria, is composed of 4 protein components: P protein (a pyridoxal phosphate-dependent glycine decarboxylase), H protein (a lipoic acid-containing protein), T protein (a tetrahydrofolate-requiring enzyme), and L protein (a lipoamide dehydrogenase). NKH is characterized by accumulation of glycine in plasma, spinal fluid and urine. Symptoms include seizures, respiratory distress, mental retardation, chorea, visual impairment and hydrocephalus.

PW127144

Pw127144 View Pathway
disease

Non-Ketotic Hyperglycinemia

Homo sapiens
Non Ketotic Hyperglycinemeia (Glycine encephalopathy; Glycine cleavage system deficiency; NKH) is caused by mutations in several genes in the mitochondrial glycine cleavage system. These include the genes encoding P protein (GLDC), T protein (GCST), and, in one case, the H protein (GCSH). Most patients with GCE (Glycine Encephalopathy, or NKH) have a defect in the GLDC gene.The enzyme system for cleavage of glycine (glycine cleavage system), which is confined to the mitochondria, is composed of 4 protein components: P protein (a pyridoxal phosphate-dependent glycine decarboxylase), H protein (a lipoic acid-containing protein), T protein (a tetrahydrofolate-requiring enzyme), and L protein (a lipoamide dehydrogenase). NKH is characterized by accumulation of glycine in plasma, spinal fluid and urine. Symptoms include seizures, respiratory distress, mental retardation, chorea, visual impairment and hydrocephalus.

PW000209

Pw000209 View Pathway
disease

Non-Ketotic Hyperglycinemia

Homo sapiens
Non Ketotic Hyperglycinemeia (Glycine encephalopathy; Glycine cleavage system deficiency; NKH) is caused by mutations in several genes in the mitochondrial glycine cleavage system. These include the genes encoding P protein (GLDC), T protein (GCST), and, in one case, the H protein (GCSH). Most patients with GCE (Glycine Encephalopathy, or NKH) have a defect in the GLDC gene.The enzyme system for cleavage of glycine (glycine cleavage system), which is confined to the mitochondria, is composed of 4 protein components: P protein (a pyridoxal phosphate-dependent glycine decarboxylase), H protein (a lipoic acid-containing protein), T protein (a tetrahydrofolate-requiring enzyme), and L protein (a lipoamide dehydrogenase). NKH is characterized by accumulation of glycine in plasma, spinal fluid and urine. Symptoms include seizures, respiratory distress, mental retardation, chorea, visual impairment and hydrocephalus.

PW145808

Pw145808 View Pathway
drug action

Nonoxynol-9 Drug Metabolism Action Pathway

Homo sapiens

PW128139

Pw128139 View Pathway
drug action

Norelgestromin Action Pathway

Homo sapiens
Norelgestromin is a synthetic progestational hormone indicated in women to prevent pregnancy. This drug is also used in menopausal hormonal therapy. This drug is administered as a contraceptive pill or as a transdermal patch. This drug is also available in combination with ethinyl estradiol as a vaginal ring. Norelgestromin acts on the hypothalamic–pituitary–gonadal axis (HPG axis) where it binds to the progesterone receptor. This binding inhibits the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. GnRH secretion is required to activate a luteinizing hormone (LH) surge that leads to ovulation. By its inhibition, the absence of LH results in no release of a viable egg from the ovaries. The thickening of the mucus interferes with sperm migration into the uterus for fertilization.

PW132526

Pw132526 View Pathway
metabolic

Norelgestromin Drug Metabolism

Homo sapiens
Norelgestromin is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Norelgestromin passes through the liver and is then excreted from the body mainly through the kidney.

PW145754

Pw145754 View Pathway
drug action

Norelgestromin Drug Metabolism Action Pathway

Homo sapiens