Celldex Receives Positive Data of Dense Deposit Disease Drug

Researchers believe that control of the complement abnormalities will be confirmed with further clinical testing in children with earlier stage disease, and that CDX-1135 may be able to restore kidney function and provide long-term disease control.

Celldex Therapeutics, in collaboration with University of Iowa in the US, has received positive in vitro and in vivo animal efficacy data for dense deposit disease drug CDX-1135.

CDX-1135 is a soluble, recombinant human complement receptor type 1 that inhibits the classical, lectin and alternative complement pathways, at both the early (C3) and late (C5) activation steps.

Celldex's previous clinical trial with CDX-1135, involving over 500 patients in other indications, had shown a good safety profile and potent inhibition of complement pathways.

University of Iowa researchers demonstrated that in a mouse model, CDX-1135 controlled the activation of AP complement in serum