PHILLIPSBURG, N.J., July 1, 2013 (GLOBE NEWSWIRE) -- Celldex Therapeutics, Inc. (Nasdaq:CLDX) today reported that the first patient has been dosed in the Company's pilot study of CDX-1135 (a soluble form of human complement receptor type 1) in dense deposit disease (DDD). DDD is an ultra-rare, progressive kidney disease that ultimately results in kidney failure in the majority of affected individuals. DDD is caused by dysregulation of the C3 Convertase, a major early component of the alternative pathway of complement. CDX-1135 has been shown to inhibit complement activation and has yielded promising results in an animal model of DDD and in a single patient with DDD that was treated under a compassionate use protocol. The open-label study will enroll up to five patients (ages four and older) from clinical centers across the United States to determine the CDX-1135 dose level required to normalize alternative complement activity on an individual patient basis. Potential effects on renal function will also be assessed. Patients will initially be treated at the University of Iowa under the leadership of Richard J.H. Smith, MD and Carla M. Nester, MD. If selected complement levels normalize on therapy, patients may be able to return to their local treatment center to continue in the study. Dr. Smith, a widely recognized expert in DDD, is Professor of Otolaryngology and Internal Medicine and the Director of the Molecular Otolaryngology and Renal Research Laboratories (MORL) at the University of Iowa. MORL maintains the largest DDD patient database in the world. Dr. Nester, also a member of MORL, is an Assistant Professor at the University of Iowa, trained in adult and pediatric nephrology. "CDX-1135 is a much needed and exciting entrant to the dense deposit disease field," said Dr. Smith. "There are currently no treatments and nearly half of all patients progress to end-stage renal disease within 10 years of presentation, often spending the rest of their lives on dialysis. In a mouse model of dense deposit disease, CDX-1135 has been shown to control the abnormal complement activity and to reduce deposits in the kidneys. Short term use of CDX-1135 in a patient with dense deposit disease and end-stage renal disease was well-tolerated and normalized the activity of the alternative complement pathway. We are optimistic that if we can control complement activation earlier in the disease course and at a critical step in the complement pathway, CDX-1135 may be able to restore kidney function and provide long term disease control—a long-awaited outcome for patients, their families and physicians."