Propionate kinase 2

Biotin is mainly required as a coenzyme for carboxylation reactions and the main examples are carboxylation of-i) pyruvate to oxaloacetate (first step of gluconeogenesis); ii) Acetyl co A to Malonyl co A (first step of fatty acid synthesis) and iii) Propionyl co A to D-Methyl malonyl co A (in the conversion of propionyl co A to Succinyl co A to gain entry to TCA cycle). In biotin deficiency, out of the given options, defective fatty acid synthesis is the most suited option because of the impaired conversion of acetyl co A to malonyl co A.

If OAA is converted to PEP by mitochondrial PEPCK, it is transported to the cytosol where it is a direct substrate for gluconeogenesis and nothing further is required. Transamination of OAA to aspartate allows the aspartate to be transported to the cytosol where the reverse transamination occurs yielding cytosolic OAA. This transamination reaction requires continuous transport of glutamate into, and 2-oxoglutatrate (α-ketoglutarate) out of, the mitochondrion. Therefore, this process is limited by the availability of these other substrates. Either of these latter two reactions will predominate when the substrate for gluconeogenesis is lactate. Whether mitochondrial decarboxylation or transamination occurs is a function of the availability of PEPCK or transamination intermediates.

Dexamethasone has also been used during pregnancy as an off-label prenatal treatment for the symptoms of congenital adrenal hyperplasia (CAH) in female fetuses. CAH causes a variety of physical abnormalities, notably ambiguous genitalia in girls. Early prenatal CAH treatment has been shown to reduce some CAH symptoms, but it does not treat the underlying congenital disorder . This use is controversial: it is inadequately studied, only around one in ten of the foetuses of women treated are at risk of the condition, and serious adverse events have been documented. [21] Experimental use of dexamethasone in pregnancy for foetal CAH treatment was discontinued in Sweden when one in five cases suffered adverse events. [22]

Teva Pharmaceuticals claims two companies are violating patents on Copaxone, glatiramer acetate for Multiple Sclerosis (MS). The original suit against Momenta Pharmaceuticals and Sandoz now has expanded to include ten patents, three of which run past the expected generic drug entry of 2014…so when generics will appear is now an open question. Copaxone, approved as an orphan drug, is Teva’s flagship product, with sales of over $680 million a year. In addition to being in clinical trials for various combinations, dosage rates, and administration strategies in the mitigation of MS, the drug is now also being studied for macular degeneration and Crohn’s Disease.

Propionate kinase 2

propionate kinase 2

Teva Pharmaceuticals claims two companies are violating patents on Copaxone, glatiramer acetate for Multiple Sclerosis (MS). The original suit against Momenta Pharmaceuticals and Sandoz now has expanded to include ten patents, three of which run past the expected generic drug entry of 2014…so when generics will appear is now an open question. Copaxone, approved as an orphan drug, is Teva’s flagship product, with sales of over $680 million a year. In addition to being in clinical trials for various combinations, dosage rates, and administration strategies in the mitigation of MS, the drug is now also being studied for macular degeneration and Crohn’s Disease.

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