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.

DDD is a rare but devastating disease where C3 activation leads to progressive kidney damage in children. There is currently no treatment for patients with DDD and about half progress to end-stage renal disease within 10 years. Because DDD recurs in virtually all patients who receive a kidney transplant, transplantation is not a viable option for these patients.

DDD is caused by uncontrolled activation of the alternative pathway (AP) of complement, which leads to the consumption of the circulating complement component C3, deposition of C3 in the kidneys, and subsequent damage to kidney function. Dr. Smith demonstrated that CDX-1135 can control the activation of AP complement in serum samples from DDD patients in vitro. In a mouse model of DDD, Dr. Smith showed that administration of CDX-1135 can control complement activation in vivo, preventing the damaging deposition of C3 in the kidneys.

“The results in mice are remarkable,” stated Dr. Smith, “as no other interventions have shown control of the C3-based damage to the kidney.” Initial experience in a patient with DDD treated by Drs. Smith and Nester showed control of the complement abnormalities. This patient was already in renal failure requiring dialysis and so reversal of disease was not expected. Drs. Smith and Nester hope that control of the complement abnormalities will be confirmed with further clinical testing in children with earlier stage disease, where C3 consumption and deposition plays an important role in disease progression, and CDX-1135 may be able to restore kidney function and provide long term disease control. Dr. Nester noted that “currently available complement inhibitors are only active against the C5 component of complement and are predicted to have little effect in DDD patients.”

Dr. Thomas Davis, Chief Medical Officer of Celldex, added, “Celldex is excited to explore the potential role of CDX-1135 in C3 mediated disease, and we plan to begin clinical studies in 2012. We believe that blocking both C3 and C5 will provide more profound and complete disease control in children with DDD. We are also excited about the potential utility of CDX-1135 in other complement mediated disorders.”

About Celldex Therapeutics, Inc.

Celldex Therapeutics is the first antibody-based combination immunotherapy company. Celldex has a pipeline of drug candidates in development for the treatment of cancer and other difficult-to-treat diseases based on its antibody focused Precision Targeted Immunotherapy (PTI) Platform. The PTI Platform is a complementary portfolio of monoclonal antibodies, antibody-targeted vaccines and immunomodulators used in optimal combinations to create novel disease-specific drug candidates. For more information, please visit http://www.celldextherapeutics.com.

Safe Harbor Statement Under the Private Securities Litigation Reform Act of 1995: This release contains “forward-looking statements” made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995, including those related to the Company’s strategic focus and the future development and commercialization (by Celldex and others) of rindopepimut (CDX-110), CDX-1307, CDX-011, CDX-1135 (formerly TP10), CDX-1401, CDX-1127, Belinostat and other products. Forward-looking statements reflect management's current knowledge, assumptions, judgment and expectations regarding future performance or events. Although management believes that the expectations reflected in such statements are reasonable, they give no assurance that such expectations will prove to be correct and you should be aware that actual results could differ materially from those contained in the forward-looking statements. Forward-looking statements are subject to a number of risks and uncertainties, including, but not limited to, our ability to obtain additional capital on acceptable terms, or at all, including the additional capital which will be necessary to complete the clinical trials that we plan to initiate in 2011; our ability to adapt APC Targeting TechnologyTM to develop new, safe and effective vaccines against oncology and infectious disease indications; our ability to successfully complete product research and further development of our programs; the uncertainties inherent in clinical testing; our limited experience in bringing programs through Phase 3 clinical trials; our ability to manage research and development efforts for multiple products at varying stages of development; the timing, cost and uncertainty of obtaining regulatory approvals; the failure of the market for the Company's programs to continue to develop; our limited cash reserves and our ability to obtain additional capital on acceptable terms, or at all; our ability to protect the Company’s intellectual property; the loss of any executive officers or key personnel or consultants; competition; changes in the regulatory landscape or the imposition of regulations that affect the Company’s products; and other risks detailed from time to time in the Company's filings with the Securities and Exchange Commission, including the Company's Form 10-K for the fiscal year ended December 31, 2010, and its Forms 10-Q and 8-K.

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