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

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 samples from dense deposit disease patients in vitro and complement activation in vivo.

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.