Celldex Reports Third Quarter 2012 Financial Results NEEDHAM, Mass.--(BUSINESS WIRE)

Reports Third Quarter 2012 Financial Results

NEEDHAM, Mass.--(BUSINESS WIRE)--November 1, 2012--Celldex Therapeutics,

Inc. (NASDAQ: 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

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

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

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

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