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Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Stamulumab

Introduction

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Stamulumab (MYO-029[1]) is an experimental myostatin inhibiting drug developed by Wyeth Pharmaceuticals for the treatment of muscular dystrophy. MYO-029 was formulated and tested by Wyeth in Collegeville, PA.[2] Myostatin is a protein that inhibits the growth of muscle tissue, MYO-029 is a recombinant human antibody designed to bind to and inhibit the activity of myostatin.[3]

Stamulumab is a G1 immunoglobulin antibody which binds to myostatin and prevents it from binding to its target site, thus inhibiting the growth-limiting action of myostatin on muscle tissue. Research completed in 2002 found that Stamulumab might one day prove to be an effective treatment for Duchenne muscular dystrophy[4]

Phase 1 and 2 Trials

Phase 1 and 2 Trials

Related
  • ACVR2B is similar to Stamulumab but is not an antibody; rather, it provides a portion of the molecule to which myostatin would normally bind thus preventing the myostatin from binding with the actual molecule[7].
References

References

  1. ↑ Wyeth Product Pipeline, Wyeth, Website accessed April 22, 2007
  2. ↑ 2.0 2.1 NIH‘s ClinicalTrials.gov, Study Evaluating MYO-029 in Adult Muscular Dystrophy, record last updated January 24, 2007
  3. ↑ medicalnewstoday.com, Wyeth Initiates Clinical Trial with Investigational Muscular Dystrophy Therapy MYO-029, Article Date: 28 Feb 2005 – 7:00 PDT
  4. ↑ Blocking Myostatin Proves Beneficial in Mice with DMD, MDA Research News, 11/27/2002
  5. ↑ Wyeth Analyzing MYO-029 Results, Muscular Dystrophy Association announcement, December 4, 2006
  6. ↑ FSH Watch Newsletter, pg 11, FSH Society, Summer 2007
  7. ↑ New Myostatin Blocker Makes Mouse Muscles 60 Percent Larger, MDA Research News, January 6, 2006

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