Semma Therapeutics raised $44 million of Series A funding led by MPM Capital, Fidelity Biosciences, ARCH Venture Partners, and Medtronic. The company is developing stem cell therapy for the treatment of type 1 diabetes. Furthermore, the company has entered into an undisclosed agreement with Novartis.
The scientific founder of Semma is Douglas Melton, a father of two children with type 1 diabetes and a member of the National Academy of Sciences. Douglas Melton has thrown himself into this field for 15 years, and has done what any father would want to do. In 2001 when George Bush cut federal funding of embryonic stem cell research, he used private donations to support other researchers.
In 2008, Melton identified a combination of three transcription factors that reprograms adult exocrine pancreatic cells into insulin secreting cells[1]. In 2013, Melton reported the discovery of betatrophin, a hormone that controls pancreatic β cell proliferation[2]. In 2014, Melton reported a step-by-step procedure which generates pancreatic β cells from human pluripotent stem cells (hPSC) in a dish[3].
Semma intends to transplant these stem cell-derived β cells (SC-β) into patients to mimic natural pancreatic β cells. SC-β cells showed good comparability to β cells within islets and responded to increased glucose by secreting increased insulin.
There is at least one other company, ViaCyte, which is developing diabetes stem cell therapy as well. In August 2014, JDRF and ViaCyte initiated the first ever clinical trial (NCT02239354) of a stem cell therapy for the treatment of type 1 diabetes. ViaCyte’s product candidate, VC-01, consists of pancreatic progenitor cells, called PEC-01 cells, which are derived from human embryonic stem cells. When implanted under the skin, the PEC-01 cells are specifically designed to differentiate into β cells.
Mitchell Finer, chief scientific officer of BlueBird Bio, will join Semma as a director. From 2008 to 2010, Finer served as chief development officer of Novocell (now ViaCyte).
[1] Nature. 2008, 455(7213), 627-632.
[2] Cell. 2013, 153(4), 747-758.
[3] Cell. 2014, 159(2), 428-439.
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