Resalis’ objective is to therapeutically support the body’s biology to tackle obesity and fatty liver disease and achieve long-lasting effects.
Metabolic syndromes are complex diseases regulated via multiple cellular pathways. MicroRNA miR-22 orchestrates multiple pro-lipogenic programs modulating both direct and indirect gene targets. Resalis has applied a cutting-edge locked nucleic acid (LNA) technology to design RES-010 so that it is tailored to target miR-22. The LNA approach also provides increased stability to RES-010 without affecting its bioavailability.
RES-010 inhibits miR-22 to:
- Restore regulation of lipid biosynthesis
- Promote metabolic rewiring towards higher energy expenditure
- Transform white adipose tissue into brown adipose tissue
- Reduce and prevent hepatic steatosis, fibrosis, and inflammation
- Induce weight loss
Binding and inhibition of miR-22 by RES-010 could ultimately improve a patient’s quality of life.
RES-010 boosts the cellular “heat engine”
UCP1 is a protein in the inner mitochondrial membrane that enables cells to release energy as heat rather than storing it as ATP. In adipocytes, UCP1 activation:
- Converts stored fat into heat, increasing calorie burning
- Raises metabolic activity, so cells consume more fuel
- Shifts the balance from fat storage toward fat burning, supporting a healthier energy balance
RES-010 markedly increases UCP1 expression, demonstrating its ability to “switch on” the cell’s heat-making machinery and boost adipocyte energy consumption.
Video description
4-D immunofluorescence microscopy imaging of organoids derived from obese human adipose tissue, showing lipid droplets in red, nuclei in blue, the mitochondrial outer membrane in yellow, and UCP1 in green. Organoids were treated with RES-010, with NaCl serving as the negative control.
