ApoA-I Milano

[1] The ApoA-I Milano mutation was found by University of Milan researchers after their 1974 investigation of a low HDL / high triglyceride phenotype exhibited by Valerio Dagnoli of Limone sul Garda, a small village in northern Italy.

[7] In the 1990s, researchers at the Cedars-Sinai Medical Center showed that injection of a synthetic version of the mutant ApoA-I into rabbits and mice could reverse vascular plaque buildup.

This trial was initiated by Steven Nissen of the Cleveland Clinic after prompting by Roger Newton of Esperion to examine the effects of the mutant protein using intravascular ultrasound imaging.

[8]: 2293 Due to its potential efficacy, it was speculated that development of synthetic ApoA-I Milano might be a key factor in eradicating coronary heart disease.

Clinically known as ETC-216, Pfizer did not move trials forward, probably because the complex protein is very expensive to produce and must be administered intravenously, limiting its application compared to oral medications.

[citation needed] On October 11, 2011, SemBioSys Genetics signed a multi-product commercialization and platform collaboration agreement with Tasly Pharmaceuticals of Tianjin (China).