NEEDHAM, Mass.--(BUSINESS WIRE)--Celldex Therapeutics, Inc. (Nasdaq: CLDX) today announced key in vivo efficacy data for its CDX-1135 program from a collaboration with Drs. Richard Smith and Carla Nester at the University of Iowa. The data were presented August 20, 2011 at the Fourth Dense Deposit Disease Focus Group in conjunction with the 13th European Meeting on Complement in Human Disease in Leiden, Netherlands. Dr. Smith presented in vitro and in vivo results, including data from animal models of Dense Deposit Disease (DDD) showing reversal of kidney damage after therapy with CDX-1135. CDX-1135 is a soluble, recombinant human Complement Receptor Type 1 (sCR1) that inhibits the classical, lectin and alternative complement pathways, both at the early (C3) and late (C5) activation steps in these pathways. Celldex’s previous clinical experience with CDX-1135 in over 500 patients in other indications has shown a good safety profile and potent inhibition of complement pathways.
