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CLDX reports 3rd quarter results


Celldex Reports Third Quarter 2012 Financial Results
Business WirePress Release: Celldex Therapeutics, Inc. – 2 hours 49 minutes ago



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NEEDHAM, Mass.--(BUSINESS WIRE)--

Celldex Therapeutics, Inc. (CLDX) today reported financial results for the third quarter ended September 30, 2012. Celldex reported a net loss of $15.0 million, or $0.25 per share, for the third quarter of 2012 compared to a net loss of $11.8 million, or $0.27 per share, for the third quarter of 2011. For the nine months ended September 30, 2012, Celldex reported a net loss of $42.3 million, or $0.75 per share, compared to a net loss of $32.1 million, or $0.85 per share, for the nine months ended September 30, 2011.

Anthony Marucci, President and Chief Executive Officer of Celldex Therapeutics commented, “In the third quarter, Celldex continued to advance our two lead programs, rapidly opening clinical sites for the Phase 3 ACT IV study and the Phase 2 ReACT study of rindopepimut in glioblastoma and preparing for an end-of-Phase 2 meeting with the Food and Drug Administration to discuss future development of CDX-011 in breast cancer. We look forward to presenting updates from these programs at the Society for Neuro-Oncology Annual Meeting in November and the San Antonio Breast Cancer Symposium in December. Further, by year-end, we anticipate completing accrual in the solid tumor arm of the Phase 1 study of CDX-1127. We will also initiate a Phase 2 pilot study of CDX-1135 in dense deposit disease. These events, coupled with ongoing activity in a number of other programs, will set the stage for a series of future significant milestones in 2013 and beyond.”

At September 30, 2012, Celldex reported cash, cash equivalents and marketable securities of $77.6 million, which the Company believes will be sufficient to meet estimated working capital requirements and fund planned program development into 2014. The decrease of $1.1 million from June 30, 2012 is due primarily to planned, increased operational expenses during the quarter related to ongoing studies of rindopepimut (CDX-110), including the pivotal ACT IV study in patients with newly diagnosed EGFRvIII-positive glioblastoma and the Phase 2 ReACT study in patients with recurrent EGFRvIII-positive glioblastoma. The cash outflows for these expenses were offset by the issuance of 2.0 million shares during the quarter through our Cantor ATM facility that raised net proceeds to Celldex of $10.9 million.

Third Quarter and Recent Highlights

Celldex continued to advance the CDX-011 program, including requesting and preparing for an end-of-Phase 2 meeting with the Food and Drug Administration to discuss future clinical and regulatory development for this program. In May of 2012, Celldex presented positive, topline results from the Phase 2b EMERGE study of CDX-011 in patients with advanced, refractory breast cancer. Preliminary results suggested that CDX-011 induced impressive response rates compared to currently available therapies in patient subsets with advanced, refractory breast cancers with high GPNMB expression (expression in =25% of tumor cells) and in patients with triple negative breast cancer. Mature data from the EMERGE study will be presented at the San Antonio Breast Cancer Symposium in December.
Celldex continued its major initiative to open clinical sites to support enrollment in the Phase 3 ACT IV study and the Phase 2 ReACT study of rindopepimut in glioblastoma. In total, there are now more than 150 clinical sites around the world that have been selected to participate in the ACT IV study and, to date, 105 of these sites are actively screening patients. The ReACT study is also well positioned, with 25 study sites selected to participate and 21 actively screening to date.
Celldex presented positive results from its Phase 1 study of CDX-1401 in solid tumors at the Society for Immunotherapy of Cancer (SITC) Annual Meeting on October 26, 2012. The study evaluated the safety, immunogenicity and clinical activity of escalating doses of CDX-1401 plus resiquimod and/or Poly ICLC (HiltonolTM) in 45 patients with advanced malignancies that had progressed after any available curative and/or salvage therapies. 60% of patients had confirmed NY-ESO-1 expression in archived tumor sample. Thirteen patients maintained stable disease for up to 13.4 months with a median of 6.7 months. Treatment was well-tolerated and there were no dose limiting toxicities. Humoral responses were elicited in both NY-ESO-1 positive and negative patients. NY-ESO-1-specific T cell responses were absent or low at baseline, but increased post-vaccination in 53% of evaluable patients, including both CD4 and/or CD8 T cell responses. Robust immune responses were observed with CDX-1401 with resiquimod and Poly ICLC alone and in combination. The study has identified a well-tolerated and immunogenic regimen and we expect that a study sponsored by the Cancer Immunotherapy Trials Network will be initiated in 2013.
Celldex received a new Small Business Innovation Research (SBIR) contract award totaling approximately $200,000 from the National Cancer Institute to develop the combination of two immune modulators, CDX-301 (Flt3L) and CDX-1127 (an antibody that activates CD27) for use during radiotherapy.
Celldex recently completed patient accrual and treatment in the CDX-301 healthy volunteer study and expects to present preliminary results from this Phase 1 study at the American Society of Hematology (ASH) Annual Meeting in December 2012.

Anticipated Milestones

Celldex expects to:

Present updated overall survival data from the rindopepimut Phase 2 ACT III, ACT II and ACTIVATE studies at the Society for Neuro-Oncology (SNO) meeting in November 2012.
Present more mature data from the EMERGE Phase 2b study at the San Antonio Breast Cancer Symposium in December 2012.
Complete Phase 1 accrual of the solid tumor arm of the CDX-1127 study in the fourth quarter of 2012.
Initiate a Phase 2 pilot study of CDX-1135 in dense deposit disease (DDD), an orphan kidney disease in children and young adults, by year-end 2012. DDD is caused by uncontrolled activation of the alternative pathway of complement, which leads to progressive kidney damage and failure. CDX-1135 has been shown to inhibit the complement cascade at both the C3 and C5 levels and has shown clear biologic activity in DDD animal models and in earlier human clinical trials.
Participate in four upcoming financial conferences, the Brean Capital 2012 Life Sciences Summit and the Lazard Capital Markets 9th Annual Healthcare Conference in November and the 2012 dbAccess BioFEST Conference and the Oppenheimer Annual Healthcare Conference in December.


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