Scientific Development

Scientific Development

General Vision

Family of molecules with therapeutic potential for diabetes, hypertension, dyslipidemia, overweight, hepatic steatosis and NASH.

Metabolic Syndrome is a group of symptoms that increase the risk of developing cardiovascular diseases and other pathologies, such as type 2 diabetes.

These include obesity, insulin resistance, glucose intolerance, dyslipidemia (primarily increased cholesterol and triglycerides in the blood), hepatic steatosis, NASH or high blood pressure.

Metabolic syndrome is increasing worldwide, which requires the search for new therapeutic alternatives to control it.

The family of molecules developed in SJT is being evaluated to treat simultaneously various factors associated with the metabolic syndrome. The tests have shown very encouraging results to date for the treatment of type 2 diabetes, hypertension, dyslipidemia, obesity, and hepatic steatosis.

Development Phases

Encouraging results obtained in each of the development stages.

The project is currently in pre-clinical development phase.

The synthesis and purification of the compounds has been optimized, achieving a high process efficiency, with a simple synthesis (only 3-4 steps) and high purity in the final product (> 99%).

The solubility of the compounds has been increased by obtaining hydrochlorides.

The compounds have a safe toxicity profile and a pharmacokinetic profile that assures the bioavailability to ensure their therapeutic function.

The following therapeutic activities have been validated in animal models:

  • Decreased of blood glucose levels in a high-fat diet obesity induced model DIO mice.
  • Decreased of insulin resistance in hyperinsulinemic DIO mice.
  • Decreased of blood pressure in spontaneous hypertension SHR rats.
  • Decreased levels of plasma cholesterol in SHR rats.
  • Decreased overweight in obese DIO mice.
  • Decreased of lipid content in liver, associated to hepatic steatosis in DIO mice.
  • Decreased of steatosis and hepatic inflammation in DIO NASH mice.