SAN RAFAEL, Calif., Oct. 20, 2013 (GLOBE NEWSWIRE) -- BioMarin Pharmaceutical Inc. (Nasdaq:BMRN) today announced that five poster presentations on BMN 673 will be featured at the 2013 AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics in Boston from October 19-23, 2013. The five pre-clinical and clinical data abstracts include:
- Stereospecific Trapping of PARP-DNA Complexes by BMN 673 and Comparison with Olaparib and Rucarparib (Abstract A257) to be presented on Sunday, October 20, 2013 from 12:30 – 3:00 PM.
- Inhibition of PBMC PARP activity with the novel PARP 1/2 inhibitor BMN 673 in patients with advanced solid tumors (Abstract A220) to be presented on Sunday, October 20, 2013 from 12:30 – 3:00 PM.
- Preclinical evaluation of BMN 673 in combination with temozolomide (TMZ) in various tumor types including small cell lung cancer (SCLC) cells (Abstract B93) to be presented on Monday, October 21, 2013 from 12:30 PM - 3:00 PM
- Pediatric Preclinical Testing Program (PPTP) evaluation of BMN 673, an inhibitor of Poly-ADP Ribose Polymerase (PARP), alone and with Temozolomide (TMZ) (Abstract C206) to be presented Tuesday, October 22, 2013 from 12:30 PM - 3:00 PM
- Update on first-in-human trial of novel oral PARP inhibitor BMN 673 in patients with solid tumors (Abstract C295) to be presented on Tuesday, October 22 from 12:30-3:00.
Junko Murai and Yves Pommier from the National Cancer Institute, will present Stereospecific trapping of PARP-DNA complexes by BMN 673 and comparison with olaparib and rucaparib. The research as reported on the poster concluded that BMN 673 was approximately 100-fold more potent than olaparib and rucaparib at trapping PARP, making it the most potent clinical PARP inhibitor to date with the highest efficiency at trapping PARP-DNA complexes.
PARP-DNA trapping helps explain why PARP inhibitors show different potency in killing tumor cells, even when they are similar in inhibiting enzymatic activity in PARP. While reducing the level of PARP enzymatic activity seems to be important, trapping PARP onto DNA is lethal to the cancer cell if not repaired. Tumor cells defective in DNA repair function are more sensitive to PARP inhibitors than normal cells with full DNA repair capability. The research concluded that PARP inhibitors should be evaluated on both catalytic PARP inhibition and PARP-DNA trapping to fully understand the impact.