* Ares Serono Group, of Geneva, got a boost from research on Rebif (interferon beta-1a), which was shown to significantly delay disability progression of multiple sclerosis in patients at high risk of progression. The data were reported in an abstract from the PRISMS study, at the European Neurological Society's annual meeting in Nice, France. PRISMS stands for Prevention of Relapses and Disability by Interferon beta, Subcutaneously in Multiple Sclerosis. Earlier this year, Serono filed a biologics license application with the FDA for approval of Rebif. (See BioWorld Today, March 4, 1998, p. 1.)
* DuPont Merck Pharmaceutical Co., of Wilmington, Del., said Phase III trial results show its investigational ultrasound contrast agent, DMP 115, enhances ultrasound images of the primary pumping chamber of the heart. In almost 90 percent of more than 200 patients with sub-optimal baseline ultrasound images, the agent enhanced images of the left ventricular cavity.
* Immune Response Corp., of Carlsbad, Calif., said an independent Data and Safety Monitoring Board has completed an interim analysis of the 2,500-patient pivotal Phase III trial using Remune, an HIV vaccine, and recommended the study continue as currently being conducted. In addition to the Phase III trial, the company is conducting a trial to further examine the effects of Remune in subjects concurrently treated with highly active antiviral drug therapy. Remune is inactivated HIV combined with a mineral oil-based adjuvant and is designed to stimulate a patient's own immune defenses to fight the virus. Through purification, the killed HIV loses glycoprotein (gp) 120, an envelope protein that helps the virus infect cells. (See BioWorld Today, May 1, 1998, p. 1.)
* Targeted Genetics Corp., of Seatttle, said its gene therapy for cystic fibrosis, tgAAV-CFTR, showed safe, dose-dependent and effective gene transfer in a 10-patient Phase I trial. AAV stands for adeno-associated viral vectors, and CFTR refers to the cystic fibrosis transmembrane conductance regulator. The treatment involves transferring to lung cells the gene encoding CFTR, which is missing or mutated in cystic fibrosis patients.