That may change as research from the Mount Sinai Health System and the City of Hope continues to progress.
“There is nothing like this available to patients right now.”
This enzyme normally maintains quiescence in adult human beta cells, essentially putting the brakes on beta cell proliferation.
By inhibiting DYRK1A, harmineremovesthese brakes, allowing beta cells to proliferate.
GLP1 receptor agonists work in conjunction with harmine to further stimulate beta cell proliferation.
The combination therapy has been shown to normalize glucose levels in diabetic mouse models, outperforming either drug alone.
In addition, the therapy improved the beta cells' function and survival along with increasing their number.
It is now planning to initiate first-in-human trials with next-generation DYRK1A inhibitors next year.
They plan to test inducers of beta cell regeneration together with immunomodulators that regulate the immune system.
Their goal is for the combination to allow new beta cells to thrive and improve insulin levels.
