(Company Web Page, Niiki Pharma, JAN 8, 2012, View Source;a=NKP-1339Mechanism&a=NKP-1339ClinicalTrial&a=NKP-1339Companion&a=NKP-1339Projected&a=NKP-1339Commercial&a=NKP-1339Intellectual&a=NKP-1339ScientificPresentations&a=NKP-2235Compound&a=NKP-2235Mechanism&a=NKP-2235ClinicalTrial&a=NKP-2235Companion&a=NKP-2235Projected&a=NKP-2235Commercial&a=NKP-2235Intellectual [SID:1234506957])

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Neoprobe Corporation Becomes Navidea Biopharmaceuticals

On January 5, 2012 Neoprobe Corporation (NEOP) reported that it has completed its corporate name change to Navidea Biopharmaceuticals, Inc. (NYSE Amex: NAVB) (Press release, Navidea Biopharmaceuticals, JAN 5, 2012, View Source;p=irol-newsArticle&ID=1645017 [SID:1234510715]). The Company will begin trading under the ticker symbol, NAVB, on the NYSE Amex at market open today. The CUSIP number for NAVB common stock has also been changed to 63937X103.

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The Navidea name and logo represent the Company’s dedication to "NAVigating IDEAs" that translate cutting edge innovation and precision diagnostics technology into novel products to advance patient care.

Navidea’s website is expected to be launched in the coming days and may be found at www.navidea.com.

GSK Exercises Option to License ChemoCentryx’s CCR1 Inhibitor, CCX354, for theTreatment of Rheumatoid Arthritis

On January 5, 2012 ChemoCentryx, Inc.reported that GlaxoSmithKline (GSK) has exercised its option to obtain an exclusive license for further development and worldwide commercialization of the investigational medicine CCX354, a potent and selective inhibitor of CCR1, a chemokine receptor that drives the recruitment of inflammatory cells into the joints of patients with rheumatoid arthritis (RA) (Press release, ChemoCentryx, JAN 5, 2012, View Source [SID:SID1234515181]). ChemoCentryx recently reported positive results from a Phase II clinical trial with CCX354 which investigated the safety, tolerability, clinical and biological activity of this compound in patients with RA.
Under the terms of the collaboration, ChemoCentryx will receive an option exercise fee of $25 million and will be eligible for further regulatory and sales milestone payments. Subject to successful development and commercialization of CCX354, ChemoCentryx will also receive double-digit royalties on net sales. GSK will now be solely responsible for funding further clinical development and commercialization for CCX354 worldwide.

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"This announcement is a key milestone for ChemoCentryx that further validates our ability to advance new medicines from drug discovery through clinical development," said Thomas J. Schall, Ph.D., President and Chief Executive Officer of ChemoCentryx. "Furthermore, the exercise fee associated with this agreement provides additional financial flexibility to our already strong balance sheet. GSK’s continued enthusiasm and interest in our programs expands our relationship and highlights our belief in the tremendous potential of our innovative products. GSK’s global reach and financial commitment will be invaluable to the advancement of CCX354 through the rest of its development."

This transaction represents the second product licensing opportunity resulting from the original collaboration with ChemoCentryx through GSK’s Centre of Excellence for External Drug Discovery (CEEDD). GSK previously exercised its option to license ChemoCentryx’s CCX282-B (Traficet-EN), now designated GSK1605786 (also called GSK’786), a novel, orally active CCR9 inhibitor, for the treatment of inflammatory bowel disease, in January 2010.

About CCX354 and Rheumatoid Arthritis (RA)
CCX354 is a potent and selective antagonist of CCR1, a chemokine receptor that drives the recruitment of certain inflammatory cells including populations of monocytes, macrophages and T cells into the joints of patients with RA. By selectively blocking the CCR1 receptor, CCX354 is designed to reduce the infiltration of inflammatory cells into the joints of RA patients, thus inhibiting the inflammation, swelling, pain and associated joint destruction while minimizing the potential for off-target effects. RA is estimated to affect more than two million people in the U.S. and is a leading cause of morbidity, disability and reduced work ability. The exact cause of RA is unknown, but is believed to reflect the body’s immune system attack on the synovium, the tissue that lines the joints. Despite available treatments, there remains a significant unmet medical need for better therapies for RA.

NewGen Therapeutics Announces the Acquisition of Three Targeted Oncology Programs

On December 19, 2011 NewGen Therapeutics reported the acquisition of three novel oncology development programs from Kanion USA, Inc. (Hayward, CA) and Kanion Pharmaceutical Co., Ltd. (Lianyungang, China) (Press release NewGen Therapeutics, DEC 19, 2011, View Source [SID:1234501416]). Under an agreement between the companies, NewGen has received exclusive global rights, excluding China, for the development, manufacture and commercialization of three separate small molecule therapeutic programs targeting pan-erbB, EGFR/Her-2, and PARP, respectively. NewGen intends to continue pre-clinical development of the oral lead molecules currently identified within each program, and seek partners for their clinical development and marketing. In return, Kanion Pharmaceutical has taken a minority equity position in privately financed NewGen, and will continue development of the compounds for China markets. The two companies also plan to share data on the compounds’ development. Further financial details were not disclosed.
"Targeted therapeutics should result in higher response rates, more efficient drug development, and an increased likelihood of clinical success," said Harry Pedersen, NewGen Therapeutics President and Chief Executive Officer. "Acquiring the rights to these late pre-clinical programs gives NewGen a strong pipeline and multiple partnering opportunities with molecules that can help advance our mission to make a difference in the treatment of cancer."
The three oncology programs acquired by NewGen Therapeutics include:
Pan-ErbB inhibitor: NewGen’s pan-ErbB inhibitor lead compound (NT-113) is an investigational, orally active, irreversible inhibitor of ErbB1 (EGFR), ErbB2 (Her-2) and the ErbB4 (Her-4). Compounds identified in this program permanently inactivate the ErbB kinases to affect downstream signal transduction events and cell cycle pathways such as cell division, ultimately resulting in decreased cell proliferation.
EGFR/Her-2 Dual Inhibitor: NewGen’s ERFR/Her-2 dual inhibitor lead compound (NT- 004) is an investigational, orally active inhibitor of ErbB1 (EGFR) and ErbB2 (Her-2). The EGFR and Her-2 receptors are both involved in cell proliferation, differentiation and apoptosis (programmed cell death). Their inhibition may play a critical role in the prevention of tumor growth and metasteses. Overexpression of EGFR and Her-2 is associated with poor prognosis and advanced-stage cancers.
PARP Inhibitor: NewGen’s PARP [poly (ADP-ribose) polymerase] inhibitor lead compound (NT-125) is an investigational, orally active inhibitor of PARP, a DNA nicksensor that signals the presence of DNA damage and facilitates DNA repair. PARP has been gaining significant interest as a therapeutic target for cancer, as investigators have reported impressive phase 2 clinical efficacy in BRCA-positive breast and ovarian cancer patients treated with PARP inhibitors. Inhibition of PARP increases the activity of DNA damaging agents including alkylators, platinums, topoisomerase inhibitors and radiation by inhibiting DNA repair. In addition, tumors with DNA repair defects, such as those arising from BRCA and PTEN mutations, appear to be very sensitive to single agent PARP inhibition. Many tumors have defects in DNA repair pathways. Mutations in the BRCA1 and BRCA2 genes have been demonstrated to be synthetic lethal in tumor models and in patients. Tumor cells with BRCA1 or BRCA2 mutations have a deficiency in the repair of DNA double strand breaks (DSBs) by the homologous recombination (HR) pathway.

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7th Annual European Antibody Congress 2011

Using both Fc mutants and wild type Chinese hamster ovary (CHO) cells as a model, iDD biotech generated anti CD19 antibodies displaying different levels of fucosylation as demonstrated by MALDI-TOF mass spectrometry based glycoprofiling (Poster, 7th Annual European Antibody Congress 2011, November 29–December 1, 2011, Geneva, Switzerland, iDD biotech, NOV 29, 2011, View Source [SID:1234502456]). The downmodulation of the fucose level also led to the construction of antiCD19 MAbs with a strongly enhanced ADCC effector function.

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