Children’s Hospital of Boston and Fate Therapeutics Sign IP Deal

The biotech company Fate Therapeutics has announced an IP agreement that involves technology licensed primarily from Children’s Hospital of Boston as well as technology developed at Massachusetts General Hospital, also of Boston. Based in San Diego and known for what it calls its "adult stem cell biology engine", Fate Therapeutics has entered into a number of IP agreements in recent months, and this is the seventh in a series of licensing deals between Fate and various research or academic institutions. Although the precise details were not disclosed, the latest agreement involves technology for supporting hematopoietic stem cell development. Dr. Len Zon, director of the stem cell program at Children’s Hospital and a co-founder of Fate Therapeutics, develped the technology.

Fate Therapeutics had previously licensed technology from Mass General which was developed by Dr. David Scadden, another co-founder of Fate Therapeutics who also co-founded and co-directs the Harvard Stem Cell Institute and who is also currently director of the Center for Regenerative Medicine at Mass General Hospital. According to Seema Basu, senior business strategy and licensing manager with the Office of Corporate Sponsored Research and Licensing at Mass General Hospital, "Depending on how the clinical development pans out, they could have different applications. There are many steps to that system’s biology, and they all complement each other. A lot will pan out once Fate does more clinical development. We’re excited that a therapeutic company is trying to take this technology into clinical development."

Founded in 2007, Fate Therapeutics was originally organized from research that had been conducted at Mass General, Stanford University, Harvard University, the University of Washington and The Scripps Research Institute. Although the company’s primary focus is adult stem cells, it is also developing iPS (induced pluripotent stem) cell technology. While iPS cells are not, in the technically strict sense of the term, "adult stem cells" – because iPS cells are derived from adult somatic cells (which are merely ordinary, mature, differentiated cells and are not stem cells) – the more important point is that iPS cells, like adult stem cells, are also not derived from embryonic stem cells even though iPS cells exhibit the same pluripotency as embryonic stem cells.

According to Fate president and CEO Paul Grayson, "Over the past two years, Fate Therapeutics has amassed extensive intellectual property assets as a foundation for our adult stem cell biology engine. The agreement we signed today with Children’s Hospital and the technologies associated with it continue to expand our engine and accelerate the company’s core mission to develop small molecules and biologics that modulate adult stem cells for regenerative medicine."

As the name implies, the company uses small molecules and biologics to guide and direct the "fate" – i.e., the ultimate direction and differentiation type – of cell development. Such techniques apply not only to adult stem cells but also to mature adult somatic (non-stem cell) cells which can be modulated and reprogrammed back to a more primitive state in which the cells exhibit a pluripotency similar to that of embryonic stem cells. As stated on the company’s website, "Fate Therapeutics is focusing on adult stem cells and induced pluripotent stem (iPS) cells. Adult stem cells naturally exist in tissues or organs and are responsible for maintaining and repairing the tissue in which they are found. iPS cells are stem cells created from fully mature differentiated cells, like a skin cell, and promise to be of great use for drug discovery and development and personalized cell replacement therapies."

As also stated on their website, "Fate’s scientific founders have identified and characterized key stem cell pathways, such as Wnt, Hedgehog and Notch, which are known to regulate cell fate and play key roles in tissue repair and regeneration and iPS cell creation." By harnessing the molecular mechanisms of such cellular pathways, Fate is developing therapeutic programs that have clinical applications not only across the broad spectrum of regenerative medicine, such as in the treatment of traumatic injury and degenerative diseases, but also in other fields such as metastatic cancer and hematological diseases. In a company statement, Fate therapeutics announced that, "The discovery of a number of conserved mechanisms from developmental biology and tissue repair has led to the identification of small molecules and biologics that can direct stem cell proliferation and function. Fate is developing these small molecule and biologic stem cell modulators to modulate the activity of adult stem cells to stimulate healing or block cancer growth."

Shortly after Fate’s founding in 2007, Dr. Sheng Ding, associate professor of chemistry and cell biology at The Scripps Research Institute who is also one of Fate’s co-founders, explained that Fate Therapeutics "is really about a collection of small molecules and protein therapeutics for modulating stem cell fate in vivo. That’s a totally different approach", he says, from other stem cell companies that "are using cells, and are primarily focused on cell-based therapies."

In April of this year, Fate Therapeutics and the Boston-based company Stemgent announced a strategic alliance, known as Catalyst, which is "a collaborative one-of-a-kind program to provide pharmaceutical and biotechnology companies with the most advanced induced pluripotent stem (iPS) cell technology platform for drug discovery and development", as described on the website of Fate Therapeutics. The novel technology utilizes protein-based reprogramming methods developed by Dr. Sheng Ding which constitute "a technique that effectively eliminates any risk of genetic modification" and which is free of oncogenic and viral reprogramming factors.

(Please see the related news article on this website, entitled, "First Patient Treated in Clinical Trial for Hematopoietic Stem Cells", dated May 27, 2009).

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