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Stamulumab

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Stamulumab
Monoclonal antibody
TypeWhole antibody
SourceHuman
Targetmyostatin
Clinical data
Routes of
administration		injection only
ATC code
  • none
Identifiers
CAS Number
ChemSpider
  • none
UNII
KEGG
Chemical and physical data
FormulaC6330H9748N1672O1668S48
Molar mass137500.53 g·mol−1
 ☒NcheckY (what is this?)  (verify)

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

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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] On 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

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  • 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

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  1. ^ Wyeth Product Pipeline Archived 2007-05-09 at the Wayback Machine, Wyeth, Website accessed April 22, 2007
  2. ^ a b "Study Evaluating MYO-029 in Adult Muscular Dystrophy". clinicaltrials.gov. 24 June 2007. Retrieved 2023-02-19.
  3. ^ "Wyeth Initiates Clinical Trial with Investigational Muscular Dystrophy Therapy MYO-029". www.medicalnewstoday.com (Press release). 28 February 2005. Archived from the original on 15 March 2005. Retrieved 2023-02-19.{{cite press release}}: CS1 maint: unfit URL (link)
  4. ^ "Blocking Myostatin Proves Beneficial in Mice with DMD". MDA Research News. 27 November 2002. Archived from the original on 22 December 2002. Retrieved 2023-02-19.
  5. ^ Wyeth Analyzing MYO-029 Results Archived 2013-04-15 at archive.today, Muscular Dystrophy Association announcement, December 4, 2006
  6. ^ FSH Watch Newsletter Archived 2008-03-09 at the Wayback Machine, pg 11, FSH Society, Summer 2007
  7. ^ Madrigal, Alexis (24 January 2008). "Pharma Company Responds to WiSci on Muscle-Building Drug". Wired. ISSN 1059-1028. Retrieved 2023-02-19.
  8. ^ Wagner KR, Fleckenstein JL, Amato AA, Barohn RJ, Bushby K, Escolar DM, et al. (May 2008). "A phase I/IItrial of MYO-029 in adult subjects with muscular dystrophy". Annals of Neurology. 63 (5): 561–71. doi:10.1002/ana.21338. PMID 18335515. S2CID 9934165.
  9. ^ "Wyeth Won't Develop MYO-029 for MD". 11 March 2008. Archived from the original on 2012-09-06. Retrieved 2008-11-03.
  10. ^ "New Myostatin Blocker Makes Mouse Muscles 60 Percent Larger". MDA Research News. 6 January 2006. Archived from the original on 11 January 2006. Retrieved 2023-02-19.
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