Hydrogels have gained significant attention as ideal delivery vehicles for protein drugs. However, the use of hydrogels for protein delivery has been restricted because their porous structures inevitably cause a premature leakage of encapsulated proteins. Here, we report a simple yet effective approach to regulate the protein release kinetics of hydrogels through the creation of microstructures, which serve as a reservoir, releasing their payloads in a controlled manner. Microstructured dextran hydrogels enable burst-free sustained release of PEGylated interferon over 3 months without compromising its bioactivity. These hydrogels substantially extend the circulation half-life of PEGylated interferon, allowing for less frequent dosing in a humanized mouse model of hepatitis C. The present approach opens up possibilities for the development of sustained protein delivery systems for a broad range of pharmaceutical and biomedical applications.
Copyright © 2015 Elsevier Ltd. All rights reserved.

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Never in Mitosis (NIMA) Related Kinase 2 (NEK2) plays a key role in regulating mitotic processes, including centrosome duplication and separation, microtubule stabilization, kinetochore attachment and spindle assembly checkpoint. NEK2 is aberrantly overexpressed in a wide variety of human cancers and has been implicated in various aspects of malignant transformation, including tumorigenesis, drug resistance and tumor progression. The close relationship between NEK2 and cancer has made it an attractive target for anticancer therapeutic development; however, the mechanisms of how NEK2 coordinates altered signaling to malignant transformation remains unclear. In this paper, we discuss the functional roles of NEK2 in cancer development; highlight some of the significant NEK2 signaling in cancer, and summarize recent advances in the development of NEK2 inhibitors.

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On March 28, 2016 OXiGENE, Inc. (Nasdaq:OXGN), a biopharmaceutical company developing vascular disrupting agents (VDAs) for the treatment of cancer, reported financial results for 2015 (Press release, OXiGENE, MAR 28, 2016, View Source [SID:1234510064]).

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For the year ended December 31, 2015, OXiGENE reported a net loss of $13.7 million compared to a net loss of $12.6 million for the year ended December 31, 2014. R&D expenses increased to $9.1 million in 2015 compared to $7.4 million in 2014, while general and administrative expenses decreased to $4.6 million in 2015 compared to $5.2 million in 2014.

At December 31, 2015, OXiGENE had cash of $27.3 million.

"During the second half of 2015 the Company worked to define and optimize a clinical plan that would most efficiently advance the development of CA4P, our lead investigational drug. We built our plan on results from a phase 2 clinical trial completed in 2014 in which CA4P, a novel vascular disrupting agent, dramatically improved platinum-resistant ovarian cancer treatment outcomes when combined with the approved anti-angiogenic agent bevacizumab (Avastin)," stated William D. Schwieterman, M.D., OXiGENE’s President and Chief Executive Officer. "As we begin 2016 our progress continues. The FDA recently approved our protocol for FOCUS, a phase 2/3 clinical trial designed to provide us with data to support the registration of CA4P as a new drug for the treatment of platinum-resistant ovarian cancer, and we remain on track to enroll patients in this study before mid-year. I am pleased that our year-end cash balance is expected to provide us with a sufficient runway to collect and present important data from FOCUS and other programs we have on-going."

About OXiGENE

On March 28, 2016 CASI Pharmaceuticals, Inc. (Nasdaq: CASI), a biopharmaceutical company dedicated to innovative therapeutics addressing cancer and other unmet medical needs, reported financial results for the three and 12 months ended December 31, 2015 (Filing, Q4/Annual, EntreMed, 2015, MAR 28, 2016, View Source [SID:1234510065]).

The Company reported a net loss of ($1.7 million), or ($0.05) per share, for the three months ended December 31, 2015. This compares with a net loss of ($1.6 million), or ($0.05) per share for the fourth quarter of 2014. The increase in net loss can be attributed to costs associated with enrolling patients in our Phase 2 Trial for ENMD-2076 in fibrolamellar carcinoma (FLC) during the fourth quarter of 2015, as well as increasing costs associated with expanding our China operations.

The net loss for the year ended December 31, 2015 was ($7.2 million), or ($0.22) per share, compared with a net loss of ($26.2) million or ($0.92) per share for 2014. The reported net loss for 2014 included a non-cash expense of $19.7 million for acquired in-process research and development associated with the September 2014 successful in-license of the rights for greater China of MARQIBO, ZEVALIN and EVOMELA from Spectrum Pharmaceuticals. The Company secured these rights primarily with equity and no cash up front. Excluding this non-cash expense, the net loss for 2014 would have been ($6.5 million), or ($0.23) per share.

As of December 31, 2015, CASI had cash and cash equivalents of $5.1 million. In January 2016, the Company completed an initial closing of a strategic financing and received net proceeds of $10.2 million.

Sara B. Capitelli, CASI’s Vice President, Finance and Principal Accounting Officer, commented, "Our research and development expenses for the fourth quarter increased over the prior year due to clinical trial costs associated with the initiation of our FLC trial in November 2015 and higher costs associated with our growing China operations during 2015. The decrease in general and administrative expenses compared with the previous year primarily reflects higher costs incurred in 2014 associated with our in-license of Spectrum products in 2014. We are continuing to execute our clinical development plans in the U.S. and China, and expect operating expenses to increase in 2016."

Further information regarding the Company, including its Annual Report on Form 10-K for the year ended December 31, 2015, can be found at www.casipharmaceuticals.com.

Ken K. Ren, Ph.D., Chief Executive Officer, commented, "Our financial results for the fourth quarter and year ended December 31, 2015 were as anticipated. In January 2016, we received $10.2 million net proceeds in an initial closing of a strategic financing which included common stock priced at $1.19 per share, the proceeds of which will support our product pipeline and advance our clinical and regulatory activities. Our import drug registration activities for MARQIBO, ZEVALIN and EVOMELA in China are ongoing, including the filing of our import registration trial application with CFDA for MARQIBO in January 2016. Our partner, Spectrum Pharmaceuticals, recently received FDA approval for EVOMELA which now allows us to advance the CFDA registration process towards an import registration trial and market approval in China. We continue to advance the clinical development of our lead proprietary drug candidate, ENMD-2076. Our Phase 2 trial in FLC is progressing well with 60% of patients already recruited for stage one of our 2-stage trial, and our Phase 2 trials in ovarian clear cell carcinoma, triple negative breast cancer and soft tissue sarcoma continue to progress along with correlative biomarker analysis. We continue to carefully manage our expenses, while achieving interim milestones towards our mission to become a fully-integrated pharmaceutical company with a rich product pipeline."

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DNA structural lesions are prevalent in sporadic colorectal cancer. Therefore, we proposed that gene variants that predispose to DNA double-strand breaks (DSBs) would be found in patients with familial colorectal carcinomas of an undefined genetic basis (UFCRC).
We collected primary T cells from 25 patients with UFCRC and matched patients without colorectal cancer (controls) and assayed for DSBs. We performed exome sequence analyses of germline DNA from 20 patients with UFCRC and 5 undiagnosed patients with polyposis. The prevalence of identified variants in genes linked to DNA integrity was compared with that of individuals without a family history of cancer. The effects of representative variants found to be associated with UFCRC was confirmed in functional assays with HCT116 cells.
Primary T cells from most patients with UFCRC had increased levels of the DSB marker γ(phosphorylated)histone2AX (γH2AX) after treatment with DNA damaging agents, compared with T cells from controls (P < .001). Exome sequence analysis identified a mean 1.4 rare variants per patient that were predicted to disrupt functions of genes relevant to DSBs. Controls (from public databases) had a much lower frequency of variants in the same genes (P < .001). Knockdown of representative variant genes in HCT116 CRC cells increased γH2AX. A detailed analysis of immortalized patient-derived B cells that contained variants in the Werner syndrome, RecQ helicase-like gene (WRN, encoding T705I), and excision repair cross-complementation group 6 (ERCC6, encoding N180Y) showed reduced levels of these proteins and increased DSBs, compared with B cells from controls. This phenotype was rescued by exogenous expression of WRN or ERCC6. Direct analysis of the recombinant variant proteins confirmed defective enzymatic activities.
These results provide evidence that defects in suppression of DSBs underlie some cases of UFCRC; these can be identified by assays of circulating lymphocytes. We specifically associated UFCRC with variants in WRN and ERCC6 that reduce the capacity for repair of DNA DSBs. These observations could lead to a simple screening strategy for UFCRC, and provide insight into the pathogenic mechanisms of colorectal carcinogenesis.
Copyright © 2015 AGA Institute. Published by Elsevier Inc. All rights reserved.

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