stamulumab
{{Short description|Monoclonal antibody}}
{{Drugbox
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 470470459
| type = mab
| mab_type = mab
| source = u
| target = myostatin
| tradename =
| routes_of_administration = injection only
| CAS_number_Ref = {{cascite|changed|??}}
| CAS_number = 705287-60-1
| ATC_prefix = none
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = V43X8G4797
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = D05917
| ChemSpiderID_Ref = {{chemspidercite|changed|chemspider}}
| ChemSpiderID = none
| C=6330 | H=9748 | N=1672 | O=1668 | S=48
}}
Stamulumab (MYO-029[http://www.wyeth.com/research/pipeline Wyeth Product Pipeline] {{Webarchive|url=https://web.archive.org/web/20070509163323/http://www.wyeth.com/research/pipeline |date=2007-05-09 }}, Wyeth, Website accessed April 22, 2007) 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.{{Cite web|title=Study Evaluating MYO-029 in Adult Muscular Dystrophy
| date = 24 June 2007
|url=https://clinicaltrials.gov/ct2/show/NCT00104078|access-date=2023-02-19|website=clinicaltrials.gov|language=en}} 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.{{Cite press release
| archive-url= https://web.archive.org/web/20050315140242/https://www.medicalnewstoday.com/medicalnews.php?newsid=20441
| archive-date= 15 March 2005
|url=https://www.medicalnewstoday.com/medicalnews.php?newsid=20441
| url-status=unfit
| title= Wyeth Initiates Clinical Trial with Investigational Muscular Dystrophy Therapy MYO-029
| date = 28 February 2005
|access-date=2023-02-19|website=www.medicalnewstoday.com|language=en}}
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.{{Cite web
| archive-url= https://web.archive.org/web/20021222005143/http://www.mdausa.org/news/021127micedmd.html
| archive-date= 22 December 2002
| url-status=dead
| title=Blocking Myostatin Proves Beneficial in Mice with DMD
| date = 27 November 2002
|url=http://www.mdausa.org/news/021127micedmd.html|access-date=2023-02-19|website=MDA Research News}}
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.[http://www.mda.org/research/061204myo_029_nov06.html Wyeth Analyzing MYO-029 Results] {{Webarchive|url=https://archive.today/20130415094420/http://www.mda.org/research/061204myo_029_nov06.html |date=2013-04-15 }}, Muscular Dystrophy Association announcement, December 4, 2006[http://www.fshsociety.org/fsh/FSHSociety_FSHWatchNewsletterSummer2007.pdf FSH Watch Newsletter] {{Webarchive|url=https://web.archive.org/web/20080309013417/http://www.fshsociety.org/fsh/FSHSociety_FSHWatchNewsletterSummer2007.pdf|date=2008-03-09}}, pg 11, FSH Society, Summer 2007 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".{{Cite magazine|last=Madrigal|first=Alexis
| date = 24 January 2008
|title=Pharma Company Responds to WiSci on Muscle-Building Drug|language=en-US|magazine=Wired|url=https://www.wired.com/2008/01/pharma-company/|access-date=2023-02-19|issn=1059-1028}} The publication appeared in Annals of Neurology in May 2008.{{cite journal | vauthors = Wagner KR, Fleckenstein JL, Amato AA, Barohn RJ, Bushby K, Escolar DM, Flanigan KM, Pestronk A, Tawil R, Wolfe GI, Eagle M, Florence JM, King WM, Pandya S, Straub V, Juneau P, Meyers K, Csimma C, Araujo T, Allen R, Parsons SA, Wozney JM, Lavallie ER, Mendell JR | display-authors = 6 | title = A phase I/IItrial of MYO-029 in adult subjects with muscular dystrophy | journal = Annals of Neurology | volume = 63 | issue = 5 | pages = 561–71 | date = May 2008 | pmid = 18335515 | doi = 10.1002/ana.21338 | s2cid = 9934165 | doi-access = free }}
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.{{Cite web|url=http://www.mda.org/research/080311md_myo-029.html
| date = 11 March 2008
|title=Wyeth Won't Develop MYO-029 for MD|access-date=2008-11-03|archive-date=2012-09-06|archive-url=https://archive.today/20120906121040/http://www.mda.org/research/080311md_myo-029.html|url-status=dead}}
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.{{Cite web
| archive-date= 11 January 2006
| archive-url=https://web.archive.org/web/20060111050055/http://www.mdausa.org/research/060106myostatin_blocker.html
|url=http://www.mdausa.org/research/060106myostatin_blocker.html
| url-status= dead
|access-date=2023-02-19
| title=New Myostatin Blocker Makes Mouse Muscles 60 Percent Larger
|website=MDA Research News
| date= 6 January 2006}}
References
{{Monoclonals for bone, musculoskeletal, circulatory, and neurologic systems}}
{{Muscular Dystrophy}}
{{TGFβ receptor superfamily modulators}}
Category:Drugs developed by Wyeth