PINK1 is a master regulator of mitochondrial quality control that is directly linked to certain forms of Parkinson’s Disease. Patients who are homozygous for mutant forms of PINK1 or PINK1-pathway members Parkin or Fbxo7 develop early onset Parkinson’s Disease. What makes PINK1 so unusual? For one thing, it’s unstable and inactive under most conditions; it only becomes catalytically active in the presence of a depolarized mitochondrion. Second, it is the only known kinase that can phosphorylNew ate ubiquitin, which it does to drive the degradation of various mitochondrial proteins and even whole mitochondria, depending on the extent of the depolarization. Mitokinin is focused on boosting the activity of this critical kinase, but only when its active. Mitokinin’s drugs do not interfere with PINK1’s endogenous regulation; rather, they make it work harder once it has achieved its active conformation.


PINK1 Regulates Mitochondrial Quality Control


Drugging PINK1–Our “Light Touch” Approach

Our therapeutic approach allows PINK1’s endogenous regulation to remain in place, and amplifies PINK1 activity only when PINK1 is catalytically active


PINK1: Therapeutic Opportunity

Mitochondrial dysfunction has been implicated in the pathophysiology of many diseases. Researchers have uncovered a protective role for PINK1 in several of them, including:

  • Parkinson’s Disease (Many Labs; Top Genetically Validated Target)
  • Diabetic cardiomyopathy (Liang Lab, NYIT)
  • Diabetic Kidney Disease (Kanwar Lab, Northwestern)
  • Cardiac hypertrophy (Dorn Lab, Washington University)