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Tafamidis, sold under the brand names Vyndaqel and Vyndamax, [5] is a medication used to delay disease progression in adults with certain forms of transthyretin amyloidosis. It can be used to treat both hereditary forms, familial amyloid cardiomyopathy and familial amyloid polyneuropathy , as well as wild-type transthyretin amyloidosis , which ...
In late 2011, the European Medicines Agency approved the transthyretin kinetic stabilizer Tafamidis or Vyndaqel discovered by Jeffery W. Kelly and developed by FoldRx pharmaceuticals (acquired by Pfizer in 2010) for the treatment of FAP based on clinical trial data. Tafamidis (20 mg once daily) slowed the progression of FAP over a 36-month ...
The product is approved only in Europe. Prior to Vyndaqel, liver transplantation was the only treatment option for FAP, and few patients could afford this expensive and difficult process. Vyndaqel ...
(Reuters) -Alnylam Pharmaceuticals said on Monday it would not pursue expanded use of its drug to treat a potentially fatal heart disease in the U.S. after the Food and Drug Administration ...
In 2011, the European Medicines Agency approved tafamidis (Vyndaqel) for the amelioration of FAP. [6] Tafamidis kinetically stabilizes the TTR tetramer, preventing tetramer dissociation required for TTR amyloidogenesis and degradation of the autonomic nervous system [27] and/or the peripheral nervous system and/or the heart. [21]
Pfizer Inc said on Monday that its drug tafamidis reduced the risk of death for patients with a rare and fatal heart disease by around 30 percent, boosting the prospects of what could be a billion ...
In another key category, our Vyndaqel family of products achieved continuing momentum with 90% year-over-year growth in the U.S. and 32% operational growth in international markets.
Recently the European Medicines Agency approved the use of Tafamidis or Vyndaqel (a kinetic stabilizer of tetrameric transthyretin) for the treatment of transthyretin amyloid diseases. This suggests that the process of amyloid fibril formation (and not the fibrils themselves) causes the degeneration of post-mitotic tissue in human amyloid ...