Pathways

Cerebrotendinous Xanthomatosis, also called CTX, is a rare inborn error of metabolism (IEM) which results from a genetic mutation. More specifically, it is the result of a mutated CYP27A1 gene. This said gene is responsible for encoding sterol 27-hydroxylase. The importance of this enzyme if the following, the said enzyme is responsible for the catalysis during the oxidation of several compounds. In particular, the said enzyme interacts with sterol intermediates, and 7-alpha,12-alpha-triol, among others. CTX is rare and can be thought of as an inherited lipid-storage disease. It causes the widespread deposition of two main compounds (cholesterol and cholestanol) throughout essentially every single tissue in the body. Including, the brain and lungs, to the detriment of the affected. Symptoms of CTX are neurological dysfunction, premature atherosclerosis, and cataracts.

Cerebrotendinous Xanthomatosis, also called CTX, is a rare inborn error of metabolism (IEM) which results from a genetic mutation. More specifically, it is the result of a mutated CYP27A1 gene. This said gene is responsible for encoding sterol 27-hydroxylase. The importance of this enzyme if the following, the said enzyme is responsible for the catalysis during the oxidation of several compounds. In particular, the said enzyme interacts with sterol intermediates, and 7-alpha,12-alpha-triol, among others. CTX is rare and can be thought of as an inherited lipid-storage disease. It causes the widespread deposition of two main compounds (cholesterol and cholestanol) throughout essentially every single tissue in the body. Including, the brain and lungs, to the detriment of the affected. Symptoms of CTX are neurological dysfunction, premature atherosclerosis, and cataracts.

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

Statins are a class of medications that lower lipid levels and are administered to reduce illness and mortality in people who are at high risk of cardiovascular disease. Cerivastatin is an orally-administered synthetic statin that reduces levels of total cholesterol, low-density lipoprotein (LDL)-cholesterol, triglyceride, and very-low-density lipoprotein (VLDL)-cholesterol. It also increases levels of high-density lipoprotein (HDL)-cholesterol. It has since been withdrawn from the canadian market due to multiple reports of fatal Rhabdomyolysis. It reduces cholesterol biosynthesis due to the result of a prolonged duration of HMG-CoA reductase inhibition. Reported side effects of cerivastatin include constipation, flatulence, dyspepsia (indigestion), abdominal pain, headache, and myalgia (muscle pain) with possible adverse effects of fatal Rhabdomyolysis and liver concerns. The primary therapeutic mechanism of action of statins is the inhibition of the rate-limiting enzyme 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase in hepatocytes. HMG-CoA reductase catalyzes the conversion of HMG-CoA into mevalonic acid, a precursor for cholesterol biosynthesis. Statins bind reversibly to the active site of HMG-CoA reductase and the subsequent structural change in the enzyme effectively disables it. Due to the resulting decrease in intracellular sterol levels, the ER membrane protein INSIG no longer binds to SREBP cleavage-activating protein (SCAP) which is, itself, bound to the transcription factor sterol regulatory element-binding protein (SREBP). Freed from INSIG, SCAP escorts SREBP to the Golgi apparatus from the ER as cargo in COPII vesicles. At the Golgi membrane, two proteases, S1P and S2P, sequentially cleave the SCAP-SREBP complex, releasing the mature form of SREBP into the cytoplasm. SREBP then translocates to the nucleus where it is actively transported into the nucleoplasm by binding directly to importin beta in the absence of importin alpha. SREBP binds to the sterol regulatory element (SRE) present in the promoter region of genes involved in cholesterol uptake and cholesterol synthesis, including the gene encoding low-density lipoprotein (LDL) receptor (LDL-R). As a result, LDL-R gene transcription increases which then leads to an increased synthesis of the LDL-R protein. LDL-R localizes to the endoplasmic reticulum for transport and exocytosis to the cell surface. The elevated amount of LDL-R results in the binding of more circulating free LDL cholesterol and subsequent internalization via endocytosis. Lysosomal degradation of the internalized LDL cholesterol elevates cellular cholesterol levels to maintain homeostasis.

Cerivastatin inhibits cholesterol synthesis via the mevalonate pathway by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. HMG-CoA reductase is the enzyme responsible for the conversion of HMG-CoA to mevalonic acid, the rate-limiting step of cholesterol synthesis by this pathway. Cerivastatin bears a chemical resemblance to the reduced HMG-CoA reaction intermediate that is formed during catalysis. Cerivastatin, like fluvastatin, atorvastatin and rosuvastatin, is one of the synthetically derived statins. Cholesterol biosynthesis accounts for approximately 80% of cholesterol in the body; thus, inhibiting this process can significantly lower cholesterol levels.

Metabolites of Cerivastatin are predicted with biotransformer.

Certoparin is a heparin with a low molecular weight (LMWH), it prevents and treats venous thromboembolism. Certoparin can interact with herbs and supplements, it is best to avoid those with anticoagulant and antiplatelet activity such as garlic, ginger, bilberry, danshen, piracetam and ginkgo biloba.