Esperion Therapeutics

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Esperion Therapeutics, Inc.
Public
Traded as NASDAQESPR
Industry Pharmaceutical
Founded 2008 (2008)
Founder
  • Dr. Roger Newton
Headquarters Ann Arbor, MI
Key people
Timothy M. Mayleben (President & CEO)
  • Decrease(US$26.1 million)loss (2013)
  • (US$11.7 million)loss (2012)
Total assets
  • IncreaseUS$78.3 million (2013)
  • US$7.31 million (2012)
Website Esperion.com
Footnotes / references
financial information[1]:F-3,4

Esperion Therapeutics, Inc. is a public, American pharmaceutical company focused on the development of a first-in-class, orally available, small molecule designed to significantly lower elevated levels of LDL-C - with the reduced potential for muscle-related side effects associated with statin use. The company is headquartered in Ann Arbor, MI.

History

Pfizer acquired the original Esperion in 2004 for US$1.3 billion as a defensive move to prevent ETC-216 from falling into competitors' hands.[2]:165 Two years later, in 2006, Pfizer decided to kill the Esperion organization and development of ETC-216. In May 2008, Dr. Roger Newton, Esperion's founder and chief scientific officer, who co-discovered the statin marketed as Lipitor® — the most commonly prescribed LDL-C lowering therapy in the world and best-selling drug in the pharmaceutical industry’s history, raised sufficient capital to acquire rights to ETC-1002 and Esperion from Pfizer, thereby leading to a second independent period for the company.[2]:165[3][4] In June 2013, Esperion became a public company again through an initial public offering.[5] As of April 2014, Esperion was traded on NASDAQ under the symbol "ESPR".[6]

Product Candidates

ETC-1002

ETC-1002 is an innovative, first-in-class, orally available, once-daily LDL-C lowering small molecule designed to lower elevated levels of LDL-C and to avoid side effects associated with existing LDL-C lowering therapies. ETC-1002 is absorbed rapidly in the small intestine and enters the liver through cell surface receptors different from those transporters that selectively take up statins.

Once in the liver, ETC-1002 inhibits ACL. Pre-clinical studies show that in the liver, ETC-1002 is converted to a derivative coenzyme, or ETC-1002-CoA, which directly inhibits ACL, a key enzyme that supplies substrate for cholesterol and fatty acid synthesis in the liver.

To date, Esperion has studied ETC-1002 in ten completed clinical trials and treated approximately 726 patients with ETC-1002 across completed Phase 1 and 2 studies.

References

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  4. Lua error in package.lua at line 80: module 'strict' not found.Closed access
  5. Lua error in package.lua at line 80: module 'strict' not found.open access publication - free to read
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Further reading

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