A Phase I, Multi-Center, Open-Label, Dosimetry Study of I-131-CLR1404 in Patients With Relapsed or Refractory Advanced Solid Tumors Who Have Failed Standard Therapy or for Whom No Standard Therapy Exists

The purpose of the study is to investigate the safety, biodistribution, radiation dosimetry and pharmacokinetics of I-131-CLR1404.

Start Date01 Jun 2009

Sponsor / Collaborator

Cellectar, Inc.

EUCTR2006-001990-32-GB / Not yet recruitingPhase 3

A Randomized, Open-Label, Phase 3 Trial of NOV-002 in Combination with Paclitaxel and Carboplatin vs. Paclitaxel and Carboplatin Alone for the Treatment of Advanced Non-Small-Cell Lung Cancer (NSCLC)

Start Date07 Mar 2007

Sponsor / Collaborator

Novelos Therapeutics, Inc.

EUCTR2006-001990-32-IT / Not yet recruitingNot Applicable

A Randomized, Open-Label, Phase 3 Trial of NOV-002 in Combination withPaclitaxel and Carboplatin vs. Paclitaxel and Carboplatin Alone for theTreatment of Advanced Non-Small-Cell Lung Cancer (NSCLC) - ND

Start Date22 Nov 2006

Sponsor / Collaborator

Novelos Therapeutics, Inc.

100 Clinical Results associated with Novelos Therapeutics, Inc.

0 Patents (Medical) associated with Novelos Therapeutics, Inc.

Literatures (Medical) associated with Novelos Therapeutics, Inc.

20 May 2014·Journal of Clinical Oncology

A novel “diapeutic” molecular imaging agent for combined oncologic diagnosis and therapy in a broad spectrum of human cancers: Preliminary clinical experience with CLR1404.

Author: Titz, Benny ; Kuo, John S. ; Grudzinski, Joe ; Pickhardt, Perry J. ; Lee, Matthew ; Jaskowiak, Christine ; Weichert, Jamey ; Banash, Maria ; Hall, Lance T. ; Longino, Marc ; Pinchuk, Anatoly

11000 Background: Extensive preclinical investigation into CLR1404, an akylphosphocholine analog, has demonstrated highly selective uptake and prolonged retention within a variety of human cancer p...

20 Jan 2014·Journal of Clinical Oncology

Phospholipid ether analogs for the detection of colorectal cancers.

Author: Hall, Lance T. ; Deming, Dustin A. ; Albrecht, Dawn ; Halberg, Richard B. ; Clipson, Linda ; Grudzinski, Joe ; Weichert, Jamey ; Matkowskyj, Kristina ; Pazoles, Christopher J. ; Washington, Mary Kay ; Maher, Molly ; Lubner, Sam Joseph ; Leystra, Alyssa A.

486 Background: The treatment of pts with localized colorectal cancer (CRC) depends on the resection of the primary tumor with adequate margins and sufficient lymph node sampling. A novel imaging agent that accumulates in CRCs and regional lymph nodes is needed. Novelos, Inc. has developed a new phospholipid ether analog therapeutic and diagnostic platform. Molecules from this platform have shown to preferentially accumulate in multiple cancer types. CLR1502 is a near-infrared fluorescent labeled phospholipid ether analog, whereas 124/131I-CLR1404 is under clinical investigation as a PET tracer or a therapeutic agent imaged by SPECT. We investigated the use of CLR1502 for the detection of intestinal cancers in a murine model and 131I-CLR1404 in human metastatic CRC. Methods: Mice with loss of APC and a constitutively active PI3K in the distal small intestine and colon develop multiple intestinal tumors ranging from benign adenomas to locally advanced adenocarcinomas. These mice were injected intravenously with CLR1502. At necropsy 96 hours after injection, the intestine was removed and tumors were analyzed using a Spectrum IVIS Caliper Life Science Imager and Fluobeam Handheld Imager. The intensity of the fluorescent signal was correlated with the histological characteristics for each individual intestinal tumor. In addition, SPECT imaging with 131I-CLR404 was performed as part of a clinical trial in patients with advanced solid tumors. Results: Colon adenocarcinomas demonstrated increased accumulation of CLR1502 compared to non-invasive lesions (total radiant efficiency: 1.76E+10 vs 3.27E+9 respectively, p=0.027). Metastatic spread to the mesentery and mesenteric lymph nodes was detected with near-infrared fluorescent imaging. Similarly, 131I-CLR1404 was shown to accumulate in metastatic tumors in a patient with colorectal adenocarcinoma. Conclusions: CLR1502 and 124/131I-CLR1404 hold great promise for enhancing our ability to treat CRC. CLR1502 may enhance our ability to properly resect CRCs through better localization of the primary tumor and improve staging through the identification of involved lymph nodes. 124/131I-CLR1404 has the advantage of detecting distant disease.

15 Apr 2013·Cancer Research

Abstract 2738: PIK3CA and APC mutations are synergistic in the development of intestinal cancers.

Author: Nettekoven, Laura ; Pazoles, Christopher ; Albrecht, Dawn ; Clipson, Linda ; Deming, Dustin ; Weichert, Jamey ; Washington, Mary Kay ; Bacher, Jeff ; Kohns, Chelsie ; Halberg, Richard ; Leystra, Alyssa

AbstractBackground: Human colorectal cancers are known to possess multiple mutations, though how these mutations interact in tumor development and progression has not been thoroughly investigated. We have previously described the FC PIK3ca* murine colon cancer model which expresses a constitutively activated phosphoinositide-3 kinase (PI3K) in the intestinal epithelium. The expression of this dominantly active form of PI3K results in hyperplasia and invasive mucinous adenocarcinomas in the proximal colon. These cancers form via a non-canonical mechanism without aberrations in Wnt signaling. Since the Adenomatous Polyposis Coli (APC) gene is mutated in the vast majority of human colon cancers and often occurs concurrently with PIK3CA mutations, we sought to better understand the interaction between APC and PIK3CA mutations in the mammalian intestine using novel murine models.Methods: B6 females carrying a transgene encoding for a chimeric protein with the iSH2 domain of the p85 subunit of PI3K fused to the N-terminus of p110 (PIK3ca*) were crossed to B6 males carrying the Min allele of Apc (ApcMin/+). The resulting B6 PIK3ca* ApcMin/+ mice were then crossed to mice carrying a transgene in which the fatty acid binding protein promoter is fused to Cre recombinase (FC). (FVB x B6)F1 FC PIK3ca* ApcMin/+ progeny express this constitutively active form of PI3K in epithelial cells of the distal small bowel and colon, as well as having lost one allele of Apc. An additional novel model system was developed to induce mutations in the cells of the mid to distal colon using a minimally invasive technique to instil adenovirus expressing the Cre recombinase. These tumors could then be monitored over time with colonoscopy with biopsies taken for histological and molecular analyses.Results: FC PIK3ca* ApcMin/+ mice develop multiple small intestinal and colon tumors, including invasive adenocarcinomas with lymphatic and mesenteric metastases. Tumor multiplicity and size were increased. Moreover, the tumors appeared less differentiated and were more invasive as compared to those in controls. Advanced adenomas and adenocarcinomas were easily detectible with a novel near-infrared phospholipid ether analog, CLR1502, that selectively accumulates in tumors. In the proximal colon, mucinous adenocarcinomas that were initiated by the dominant active PI3K rarely exhibited nuclear β-catenin and when observed, this localization was limited to select areas. This indicates that in these tumors loss of APC in these cells was a late event and can be a source of clonal outgrowth. The tumors that form in this model are microsatellite stable. Interestingly this synergy appears to be independent of PI3K mediated regulation of GSK-3β and β-catenin signaling.Conclusion: Expression of a dominant active PI3K synergizes with loss of APC activity resulting in dramatic changes in tumor multiplicity, size, morphology, and invasiveness.Citation Format: Dustin Deming, Alyssa Leystra, Laura Nettekoven, Chelsie Kohns, Linda Clipson, Dawn Albrecht, Jeff Bacher, Mary Kay Washington, Christopher Pazoles, Jamey Weichert, Richard Halberg. PIK3CA and APC mutations are synergistic in the development of intestinal cancers. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2738. doi:10.1158/1538-7445.AM2013-2738

100 Deals associated with Novelos Therapeutics, Inc.

100 Translational Medicine associated with Novelos Therapeutics, Inc.

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