Diabetes is a chronic metabolic disorder resulting from a failure to manage glucose levels in the blood appropriately. In Type 2 Diabetes Mellitus (T2DM), a loss of insulin sensitivity keeps increasing the stressful demand on beta-cells in the pancreas to produce insulin, until these cells ultimately degenerate. In Type 1 Diabetes Mellitus (T1DM), beta-cells are directly attacked. The elevated glucose levels make diabetes a major cardiovascular risk factor and cause of blindness, kidney failure, heart attacks, stroke and lower limb amputation. The number of patients with diabetes has risen from 108 million in 1980 to 422 million in 2014, making diabetes the largest pandemic to hit our societies in the coming years.
Current diabetes treatments on the market and in development all treat symptoms only, without addressing fundamentally the underlying beta-cell degeneration which keeps progressing at a steady rate. Hence, the key patient need in diabetes is durability, i.e. how to prevent the increase in dose and addition of multiple therapies. Most diabetes companies have beta-cell health as a core pillar in their R&D strategy, but none have such projects close to clinical development.
reMYND’s lead diabetes program ReS39 sustains and even doubles the endogenous insulin production capacity of the pancreas by restoring beta-cell function in as well T1DM as T2DM animal models through restraining the formation of oxidative stress. Hence, ReS39 provides as well fast symptomatic relief as durability in T2DM. And in T1DM, provided sufficient beta-cells remain to be re-functionalised. In addition, ReS39 reduces liver weight and its triglyceride content, making it also relevant for NASH.
As for beta-cell in diabetes, the program has a similar protective effect on dopamine producing neurons in Parkinson’s disease (PD), the most common motor disorder, typically affecting the aged 65+ population. PD is caused by degeneration of dopaminergic neurons required for appropriate control of motoric functions. It is expected that the number of patients suffering from Parkinson’s disease will double in the next ten years, reflecting the aging of the population. With the exception of cell transplants and gene therapy programs there have been no breakthroughs in the field since the seventies. ReS39 targets alpha-synuclein driven neuronal degeneration, a process involving oxidative stress which fundamentally underlies dopaminergic degeneration in PD. The program therefore has the potential to delay or, as we observed in our animal models, even stop neuronal degeneration allowing patients to sustain dopaminergic signaling.
Currently the preclinical candidate is being profiled.