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Replies to post #179501 on Avid Bioservices Inc (CDMO)
June 12, 2014
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....Quizartinib is also being studied in newly diagnosed patients in combination with chemotherapy as well as maintenance following a hematopoietic stem cell transplantation (HSCT). In addition to quizartinib, Ambit's clinical pipeline includes AC410, an oral JAK2 inhibitor, and CEP-32496, a BRAF inhibitor licensed to Teva Pharmaceutical Industries Ltd. Ambit's preclinical portfolio includes a proprietary CSF1R inhibitor program.
http://www.bizjournals.com/sanfrancisco/prnewswire/press_releases/California/2014/06/12/LA46577
CSF1R inhibition delays cervical and mammary tumor growth in murine models by attenuating the turnover of tumor-associated macrophages and enhancing infiltration by CD8+ T cells
Dec 4, 2013
Abstract
Increased numbers of tumor-infiltrating macrophages correlate with poor disease outcome in patients affected by several types of cancer, including breast and prostate carcinomas. The colony stimulating factor 1 receptor (CSF1R) signaling pathway drives the recruitment of tumor-associated macrophages (TAMs) to the neoplastic microenvironment and promotes the differentiation of TAMs toward a pro-tumorigenic phenotype. Twelve clinical trials are currently evaluating agents that target the CSF1/CSF1R signaling pathway as a treatment against multiple malignancies, including breast carcinoma, leukemia, and glioblastoma. The blockade of CSF1R signaling has been shown to greatly decrease the number of macrophages in a tissue-specific manner. However, additional mechanistic insights are needed in order to understand how macrophages are depleted and the global effects of CSF1R inhibition on other tumor-infiltrating immune cells. Using BLZ945, a highly selective small molecule inhibitor of CSF1R, we show that CSF1R inhibition attenuates the turnover rate of TAMs while increasing the number of CD8+ T cells that infiltrate cervical and breast carcinomas. Specifically, we find that BLZ945 decreased the growth of malignant cells in the mouse mammary tumor virus-driven polyomavirus middle T antigen (MMTV-PyMT) model of mammary carcinogenesis. Furthermore, we show that BLZ945 prevents tumor progression in the keratin 14-expressing human papillomavirus type 16 (K14-HPV-16) transgenic model of cervical carcinogenesis. Our results demonstrate that TAMs undergo a constant turnover in a CSF1R-dependent manner, and suggest that continuous inhibition of the CSF1R pathway may be essential to maintain efficacious macrophage depletion as an anticancer therapy.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902121/
March 14, 2014 - ties to David Parkinson...
David Mott ex-Ambit Director re: Ambit Biosciences Raises Over $49 Million in Series D Financing
Elliott Sigal(ex-BMS), M.D., Ph.D., New Enterprise Associates
Now.. Ambit BOD at 9 total -- including Mark Foletta - ex-BMS
"Don't you work at the hospital?" Elliott Sigal asked the young woman in front of him in the cafeteria line. He had seen Ruth Leff at work and around the University of Chicago's International House, where they both lived. At the time, he was a medical student and she was studying for her master's in art history.
The introductory line was "pretty non-original," Sigal admits. "But extremely effective." The Sigals have been together for 40 years.
Family has been a major influence in Sigal's life. His father, who worked at Eli Lilly, always encouraged his son to pursue his interests at the highest level, which is how Sigal came to earn a PhD in industrial engineering at Purdue University. "My mother's struggle with cancer caused me to reflect on where my career would go next," he said. He entered the Pritzker School of Medicine determined to pursue interdisciplinary research that might someday be life changing for other families.
Sigal put his training to work in research and development in the pharmaceutical field, ultimately serving as executive vice president and chief scientific officer at Bristol-Myers Squibb from 2004 to 2013. Under his leadership, more than 12 new medicines were brought to market. Among these was the first checkpoint inhibitor for cancer immunotherapy. Up until then, combining the science of immunology with cancer drug development was not well accepted. His team developed an industry-leading pipeline of immunotherapies for cancer and helped transform the way cancer drugs are now developed.
"Even though it's profound when it works, immunotherapy works on fewer patients than we would like to see," said Sigal, whose parents both died from cancer at young ages. "I dedicated my post-Bristol-Myers Squibb career to helping researchers take this to the next level."
To that end, the Sigals endowed UChicago's first fellowship in cancer immunotherapy this year. The inaugural Elliott Sigal, MD'81, Fellow is Jonathan Trujillo, MD, PhD, whose research seeks to identify tumor-intrinsic oncogene pathways that mediate cancer immune evasion and resistance to immunotherapies. Trujillo is a member of the UChicago laboratory of Thomas Gajewski, AB'84, PhD'89, MD'91, a pioneer in the field of cancer immunotherapy. The couple also established the Elliott Sigal, MD'81, Immuno-Oncology Lectureship.
Sigal's current focus is on mentoring the next generation of biotechnology innovators. He co-chairs the Amgen Scientific Advisory Board and advises health care investors at New Enterprise Associates.
"The University of Chicago is at the forefront of cancer immunotherapy," Sigal said. "UChicago Medicine has made major contributions to this area in the past and we should expect great things in the future.
"I am grateful for my time at the University," Sigal said. "The willingness to think outside the box and the deep emphasis on working on what is best for patients have always stayed with me."
https://givetomedicine.uchicago.edu/donor-stories/two-disciplines-one-goal
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