I founded Fairbanks Pharmaceuticals to develop potential novel diabetes therapies based on my National Institutes of Health (NIH)-funded research over a period of 35 years. Fairbanks is currently funded by a Phase II SBIR grant from the National Institute of Diabetes and Digestive Diseases (NIDDK) at NIH.
NIH is the most important agency of the federal government dedicated to funding biomedical research that leads to better health for Americans. Since this research is often lengthy and labor intensive, consistent funding that keeps up with inflation is essential for a vibrant research effort that maximizes the benefit of NIH-funded research.
On March 5th, 2019, I joined two other Massachusetts-based biomedical researchers to visit our congressional representatives as part of the Federation of American Societies for Experimental Biology (FASEB)’s Capitol Hill Day to discuss how critical this funding is for health.
We first met with staff from Representatives Joe Kennedy and Katherine Clark, who were already familiar with, and big supporters of both the NIH and National Science Foundation (NSF). In our meetings we discussed funding increases for NIH and NSF and the specific opportunities and needs based on FASEB analysis.
We also visited the office of Representative Lori Trahan, whose district includes Concord, MA, where Fairbanks is located. Meeting with her staff members we explained our request that Representative Trahan support the recommended budget increases for NIH and NSF. I mentioned that our SBIR grant has helped us create three jobs in Massachusetts while allowing us to further evaluate our diabetes therapy. We were assured of strong support from the entire Massachusetts House delegation.
Our final visits were with staff from the offices of Senators Ed Markey and Elizabeth Warren.. At each office we found the same unwavering support for biomedical and basic science research funded by both NIH and NSF. We were impressed by and appreciative of the expertise on biomedical topics and specifically diseases like diabetes displayed by the staff we met. They were also sympathetic to the need for the continued level support necessary to attract the next generation of scientists into research as well as to continue progress on longer term research efforts.
The opportunity to speak with the Massachusetts delegation about the benefits of biomedical research was both enjoyable and productive. I look forward to continuing this discussion in the home districts over the coming year.
The Challenge is a proposal- and presentation-based competition for small companies in the T1 and T2 space that are making real progress towards better outcomes for those diagnosed. It offers the chance to win in-kind awards and receive early and later-stage validation of their ideas and products specific to Type 1 and Type 2 diabetes.
The transcription factor Arx is required to form pancreatic islet alpha cells while the factor Pax4 is required to specify beta cells. Reducing Arx expression in alpha cells is sufficient to turn them into beta cells.Fairbanks scientists have collaborated on new research published in Endocrinology showing that activin directly suppressed Arx and increased Pax4 expression, consistent with our hypothesis that increased activin signaling promotes alpha to beta cell transdifferentiation.
Since FSTL3 knockout mice have increased activin signaling, these new results suggest that the enhanced beta cell formation in FSTL3 knockout mice could be due to activin-assisted transdifferentiation from alpha cells. More research is needed to determine if this process occurs naturally and amenable to intervention as a basis for developing novel diabetes treatments.
Fairbanks Pharmaceuticals scientists collaborated on a recently published study in which the hormone activin was applied to human islets from donors who had type 2 diabetes. In untreated islets, glucose failed to stimulate insulin secretion as one would expect in diabetes. But in the activin treated islets, elevated glucose stimulated insulin release to levels seen in normal islets in the absence of activin.
This is important because of another part of this study in which gene expression was compared between normal and diabetic islets. Activin production is very high in normal islets but reduced by 50% in diabetic islets. Critically, the activin inhibitor, FSTL3, is expressed at 8-fold greater levels in diabetic islets compared to normal. This means that functional activin (activin not inhibited by FSTL3) is much lower in diabetic islets. This suggests that one defect in diabetic islets is loss of activin signaling and when that activin is restored, insulin release returns to normal.
Fairbanks Pharmaceuticals is developing technology that will inhibit the action of FSTL3. Therefore, the newly published research suggests that this technology could have important therapeutic effects in patients with diabetes to enhance insulin release and restore more normal glucose control.
Fairbanks Pharmaceuticals received an award from the Massachusetts Life Science Center to hire an intern starting in July 2015. Alfredo (Eddie) Mesiti, a 2014 graduate from the University of Massachusetts-Amherst with an undergraduate degree in Microbiology, was selected to fill this role.
Eddie is currently completing a Masters Degree in Applied Molecular Biotechnology. This internship will help him in his degree program while amplifying progress in pursuing our research agenda. Welcome Aboard Eddie!
On November 25th, 2014, Fairbanks Pharmaceuticals opened its research laboratory in Springfield, Massachusetts.
The space is located at 3601 Main St within recently renovated open lab space that has a wealth of shared facilities available to Fairbanks scientists.
In our first two weeks we have been screening libraries to identify candidate compounds that we can then test for effectiveness in treating diabetes in animal models. Its been a hectic start but now we are ready to focus on our research and hopefully make excellent progress.
In order to determine the function of Follistatin Like-3 we created knockout mice in which the gene that codes for this protein was disabled. Mice without FSTL3 had larger pancreatic islets and improved glucose control suggesting that loss of FSTL3 might be beneficial for patients with diabetes. We continued our analysis of these mice and found that the increased number of insulin producing beta cells was not due to increased proliferation of the existing beta cell population.
Our current research is focused on whether loss of FSTL3 stimulates a process where other cell types in the pancreas, such as alpha cells, change their fate and become beta cells, a process known as transdifferentiation or reprogramming. Regardless of the actual mechanism, however, Fairbanks Pharmaceuticals is focused on development of new diabetes therapies based on altering FSTL3 function.