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Stamulumab

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Subject: Muscular dystrophy, Facioscapulohumeral muscular dystrophy, Wyeth, Rinucumab, Evinacumab
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Stamulumab

Stamulumab?
Monoclonal antibody
Type Whole antibody
Source Human
Target myostatin
Clinical data
Routes of
administration
injection only
Identifiers
CAS Registry Number  N
ATC code None
UNII  Y
KEGG  Y
Chemical data
Formula C6330H9748N1672O1668S48
Molecular mass 137.5 kDa
 N   

Stamulumab (MYO-029[1]) is an experimental myostatin inhibiting drug developed by Wyeth Pharmaceuticals for the treatment of muscular dystrophy (MD). Stamulumab was formulated and tested by Wyeth in Collegeville, Pennsylvania.[2] Myostatin is a protein that inhibits the growth of muscle tissue, stamulumab 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

Wyeth undertook a Phase 1 and 2 clinical trial in 2005 and 2006 of stamulumab. The multiple ascending dose trial (36 patients per cohort) contained some measures of efficacy. The trial's participants included people afflicted with Facioscapulohumeral muscular dystrophy, Becker's muscular dystrophy, and Limb-girdle muscular dystrophy. Through 2007 Wyeth had been analyzing the results but the hoped-for news and/or a publication in 2007 did not occur.[2][5][6] In January 24, 2008, Wyeth announced that the study had been accepted by a peer-reviewed journal and publication was expected "in the next few months".[7] The publication appeared in Annals of Neurology in May 2008. [8]

On 11 March 2008 it was announced that Wyeth would not develop the drug further for MD, but would continue to explore myostatin inhibition along with other strategies.[9]

See also

  • ACVR2B represents an alternative approach to inhibiting myostatin. Not belonging to the antibody class of molecules, the ACVR2B protein drug is rather mimicking myostatin's endogenous binding partner, therefore competing for its binding affinity. [10]

References

  1. ^ Wyeth Product Pipeline, Wyeth, Website accessed April 22, 2007
  2. ^ a b 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, 27 November 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. ^ Pharma Company Responds to WiSci on Muscle-Building Drug, Wired Science, Alexis Madrigal, January 24, 2008, 2008, 4:26:27 PM
  8. ^ A phase I/IItrial of MYO-029 in adult subjects with muscular dystrophy., Ann Neurol. 2008 May;63(5):561-71.
  9. ^ Wyeth Won't Develop MYO-029 for MD
  10. ^ New Myostatin Blocker Makes Mouse Muscles 60 Percent Larger, MDA Research News, January 6, 2006
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