The Science
Tapping into Nature’s Original Survival System
Mitochondria are more than powerplants, they are ancient bacterial symbionts that still follow the rules of their single-celled ancestors. When stressed, mitochondria quickly adapt, mutate, and influence cellular behavior.
In healthy tissues, mitochondria self-regulate, removing damaged cells before they become a problem.
Heart cancer is so rare because its mitochondria are constrained by strict quality control mechanisms. (See the heart cancer paradox)
In organs like lung, breast, colon, prostate and others, cellular control breaks down leading to treatment-resistant cancers, chronic inflammation, and immune suppression. Pathways long targeted by cancer researchers are all controlled by mitochondria (HIF-1a, NRF1/2, PGC-1a/b, PI3K, FOXO1/3, P53, NF-kB, MYC, RAS, ATF4/5, SIRT1-7, HATs/HDACs and the list goes on).
ICM targets a primitive electrical signaling system to help restore the cell’s ability to regulate its fate.
Through a novel mechanism that alters mitochondrial electrical signaling and electron flow, we can:
• Reduce treatment resistance in Chagas, cancer and other diseases.
• Trigger immune responses that eliminate diseased cells.
• Enhance mitochondrial quality control, stopping disease at its source.
Accumulation of Dysfunctional Mitochondria Allow Diseases to Thrive
Mitochondria sometimes survive when they shouldn’t.
• Overriding DNA and “rewiring” cell signaling
• Resisting apoptosis | Fueling oxidative stress | Altering cell metabolism
When dysfunctional mitochondria accumulate, diseases thrive.
Dysfunctional mitochondria contribute to many treatment failures.
We’re pioneering clinical development of compounds that target and modulate mitochondrial signaling and health.
Our approach selectively diverts electron flow in chronically hyperpolarized mitochondria.
Mitoflashes are bursts of mitochondrial electrical activity regulating adaptation, survival, and cell fate.
High mitoflash activity signifies local electrical bursts within dysfunctional mitochondria.
We control cell fate by correcting mitochondrial signaling.
