Nov. 5, 2009 (PR Newswire) --
NOVATO, Calif., Nov. 5 /PRNewswire-FirstCall/ -- BioMarin Pharmaceutical Inc. (Nasdaq: BMRN) announced today that the United States Patent and Trademark Office has issued a patent covering the approved administration of Kuvan® (sapropterin dihydrochloride) with food for the treatment of phenylketonuria (PKU). The patent expires in 2024.
"We believe that the food effect patent, based on the discovery that food increases the bioavailability of Kuvan, along with our patents for once daily dosing and stable tablet formulation, will create significant barriers to therapeutically equivalent generic competition from entering the market for approximately ten years beyond orphan drug exclusivity," said Jean-Jacques Bienaime, Chief Executive Officer of BioMarin. "We remain committed to serving the PKU community with initiatives such as implementation of an outcomes study in the second quarter of next year and the ongoing development of a blood Phe monitor. We also look forward to results from various investigator-sponsored trials that, if positive, will strengthen the value proposition for the use of Kuvan."
About Kuvan
Kuvan® (sapropterin dihydrochloride) Tablets are indicated in the United States to reduce blood phenylalanine (Phe) levels in patients with hyperphenylalaninemia (HPA) due to tetrahydrobiopterin- (BH4-) responsive phenylketonuria (PKU). Kuvan is to be used in conjunction with a Phe-restricted diet. The active ingredient in Kuvan, sapropterin dihydrochloride, is the synthetic form of 6R-BH4 (tetrahydrobiopterin), a naturally occurring enzyme cofactor that works in conjunction with phenylalanine hydroxylase (PAH) to metabolize Phe.
Kuvan has received orphan drug designation from both the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMEA). Kuvan has received seven years of orphan exclusivity in the United States and ten years of market exclusivity in the E.U.
About PKU
PKU, a genetic disorder affecting approximately 50,000 diagnosed patients in the developed world, is caused by a deficiency of the enzyme phenylalanine hydroxylase. PAH is required for the metabolism of phenylalanine, an essential amino acid found in most protein-containing foods. If the active enzyme is not present in sufficient quantities, Phe accumulates to abnormally high levels in the blood and becomes toxic to the brain, resulting in a variety of complications including severe mental retardation and brain damage, mental illness, seizures, tremors, and limited cognitive ability. As a result of newborn screening efforts implemented in the 1960s and early 1970s, virtually all PKU patients under the age of 40 in developed countries have been diagnosed at birth. To learn more about PKU, please visit www.PKU.com.
