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Inotek Pharmaceuticals Announces Presentation of Phase 2 Clinical,Data for INO-1001 at ACC Demonstrating PARP Inhibition and,Anti-inflammatory Activity in Plasma of Patients Undergoing Primary,Percutaneous Coronary Intervention

BEVERLY, Mass.--(BUSINESS WIRE)--Mar 27, 2007 - Inotek Pharmaceuticals Corporation announced today the presentation of positive Phase 2 clinical data demonstrating the safety of INO-1001 as well as the potential for INO-1001 as a preventative agent for cardiac reperfusion injury. The study was conducted in subjects with acute ST-elevated myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention. The presentation was made in a poster session at the American College of Cardiology (ACC) 56th Annual Scientific Session in New Orleans, Louisiana. INO-1001 is an inhibitor of poly(ADP-Ribose) polymerase (PARP), a nuclear enzyme that directs the repair of damaged DNA via the activation and recruitment of DNA repair enzymes and is being studied as a treatment for certain acute cardiovascular conditions and cancer. Additionally, PARP inhibition shows promise in inflammatory disorders. PARP's role in the inflammatory response may result from its ability to potentiate the activity of key inflammatory transcription factors (NF-kappaB and AP-1).

"Whereas advances in pharmacologic and mechanical reperfusion therapy have improved the outcomes of patients with STEMI, reperfusion injury, which is associated with severe damage to the cardiac tissue, is a significant complication that has no current safe and effective treatment options," commented Dr. Andrew Salzman, Inotek's President and CEO. "These Phase 2 data provide further support for our PARP inhibitor program in cardiovascular disease. These results combined with existing preclinical data suggest that INO-1001 produces significant PARP inhibition and has the potential to protect cardiac tissue from damage."

Researchers from the Brigham and Women's TIMI Study Group and Inotek Pharmaceuticals reported that plasma from patients treated with INO-1001 suppressed ex vivo PARP activation. This effect was observed up to 24 hours following drug admi
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