Pathways

Carbamoyl Phosphate Synthetase Deficiency, also called hyperammonemia due to carbamoyl phosphate synthetase 1 deficiency, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of the urea cycle caused by a defective CPS1 gene. The CPS1 gene codes for the protein carbamoyl phosphate synthetase I, which plays a role in the urea cycle. This disorder is characterized by a large accumulation of ammonia in the blood. Symptoms of the disorder include unusual movements, seizures, unusual sleeping or coma. Treatment with citrulline or arginine, which maintains a regular rate of protein creation. It is estimated that carbamoyl phosphate synthetase deficiency affects 1 in 800,000 individuals in Japan.

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

Carbamazepine is an oral drug used as an antiepileptic, analgesic and mood stabilizer drug. It is used to treat conditions including simple and complex partial seizures, generalized tonic-clonic seizures, trigeminal neuralgia, acute mania or mixed episodes in bipolar I disorder. Carbamazepine acts in neurons where it inhibits voltage gated sodium channels in the pre synaptic neurons. In neurons, voltage gated sodium channels allow sodium to come into the neuron triggering the depolarization phase. the potassium channels are responsible for the repolarization phase to bring the neuron back to resting potential. The action potentials created travel down the axon of the neuron and at the nerve terminal, calcium channels open, allowing calcium to enter the cell. Calcium entry causes synaptic vesicles containing neurotransmitters like glutamate to fuse with the membrane and expel the neurotransmitter into the synapse. Glutamate binds to AMPA and NMDA receptor on the post synaptic neurons where they cause excitation of the neuron. By blocking the voltage gated sodium channels, carbamazepine prevents the depolarization phase, inhibiting action potential generation and the release of excitatory neurotransmitter like glutamate. Pre and post synaptic neuronal firing are therefore reduced. Carbamazepine works as a “use-dependent” block. This means that it preferentially binds to channels that are being opened. In neurons that are repetitively firing, their sodium channels are being opened more often, and as a result, carbamazepine is able to produce a greater block in these neurons. This property of carbamazepine is essential in treating conditions like seizures, trigeminal neuralgia and mania which caused by excessive neuronal activity. Side effects of carbamazepine include dizziness, drowsiness, ataxia, nausea, vomiting, water retention, hyponatremia, severe bone marrow depression, hypersensitivity reactions and gastrointestinal and cardiovascular dysfunctions.

Carbamazepine is a drug used in the treatment of epilepsy, bipolar disorder, trigeminal neuralgia, and other psychiatric disorders. Carbamazepine is almost entirely metabolized in the liver, with the primary metabolic pathway being conversion to 10,11-epoxycarbamazepine. Ring hydroxylation to 2-hydroxycarbamazepine and 3-hydroxycarbamazepine represent a minor metabolic route, presumably though a carbamazepine 2,3-epoxide intermediate. Potential bioactivation occurs via CYP3A4-mediated secondary oxidation of 2-hydroxycarbamazepine to the potentially reactive carbamazepine iminoquinone and of 3-hydroxycarbamazepine to form other reactive metabolites. Radicals can also be formed from metabolism of 3-hydroxycarbamazepine by myeloperoxidase. Oxcarbazepine, an anticonvulsant used primarily in the treatment of epilepsy, is converted to 10,11-dihydroxycarbamazepine via 10-hydroxycarbazepine.

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

Captopril is a potent, competitive inhibitor of angiotensin-converting enzyme (ACE), the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Captopril may be used in the treatment of hypertension. (DrugBank) Major metabolites are captopril-cysteine disulfide and the disulfide dimer of captopril. Metabolites are produced by Cytochrome P450 3A4 in the liver and may undergo reversible interconversion. These metabolites are excreted via the Organic anion transporter 1 (OAT1).