LEIDEN, the Netherlands, Aug. 17, 2016 (GLOBE NEWSWIRE) -- ProQR Therapeutics N.V. (Nasdaq:PRQR), a company dedicated to changing lives through the creation of transformative RNA medicines for the treatment of severe orphan diseases such as cystic fibrosis (CF) and Leber's congenital amaurosis Type 10 (LCA10), today announced results for the second quarter of 2016.
“We continue to make good progress with our three different development programs, all RNA oligonucleotides for serious genetic diseases. For QR-010 for patients with CF due to the ?F508 mutation, we will present top-level results from clinical proof-of-concept study, PQ-010-002 later this year during the North American Cystic Fibrosis Conference (NACFC)", said Daniel de Boer, Chief Executive Officer of ProQR. “For QR-110 for patients with LCA10, we presented strong pre-clinical proof-of-concept data at the Association for Research in Vision and Ophthalmology (ARVO) conference. We plan to move this program towards the clinic this year. For QR-313 for dystrophic epidermolysis bullosa (DEB) patients due to mutations in Exon 73, we continue to strengthen the pre-clinical proof-of-concept in important clinically relevant models. In addition to our three molecules in development, we are strengthening our pipeline of RNA oligonucleotides for severe genetic diseases through our innovation unit.”
“We continue to make good progress with our three different development programs, all RNA oligonucleotides for serious genetic diseases. For QR-010 for patients with CF due to the ?F508 mutation, we will present top-level results from clinical proof-of-concept study, PQ-010-002 later this year during the North American Cystic Fibrosis Conference (NACFC)", said Daniel de Boer, Chief Executive Officer of ProQR. “For QR-110 for patients with LCA10, we presented strong pre-clinical proof-of-concept data at the Association for Research in Vision and Ophthalmology (ARVO) conference. We plan to move this program towards the clinic this year. For QR-313 for dystrophic epidermolysis bullosa (DEB) patients due to mutations in Exon 73, we continue to strengthen the pre-clinical proof-of-concept in important clinically relevant models. In addition to our three molecules in development, we are strengthening our pipeline of RNA oligonucleotides for severe genetic diseases through our innovation unit.”
