Revision as of 17:56, 19 April 2017 edit72.244.116.122 (talk) Updates to trialsTag: Visual edit← Previous edit | Revision as of 09:49, 2 May 2017 edit undoRjwilmsi (talk | contribs)Extended confirmed users, Pending changes reviewers, Rollbackers932,094 editsm →Blisibimod: Journal cites, added 1 PMC using AWB (12156)Next edit → | ||
Line 18: | Line 18: | ||
=== Blisibimod === | === Blisibimod === | ||
*] is a selective peptibody antagonist of ] (BAFF). BAFF is critical to the development, maintenance and survival of B-cells, but is known to be up-regulated in ].<ref>{{Cite journal|last1=Groom|first1=J|last2=Kalled|first2=SL|last3=Cutler|first3=AH|last4=Olson|first4=C|last5=Woodcock|first5=SA|last6=Schneider|first6=P|last7=Tschopp|first7=J|last8=Cachero|first8=TG|last9=Batten|first9=M|last10=Wheway|first10=J|last11=Mauri|first11=D|last12=Cavill|first12=D|last13=Gordon|first13=TP|last14=Mackay|first14=CR|last15=Mackay|first15=F|title=Association of BAFF/BLyS overexpression and altered B cell differentiation with Sjögren's syndrome|pmid=11781351|doi=10.1172/JCI14121|volume=109|issue=1|date=Jan 2002|journal=J Clin Invest|pages=59–68}}</ref><ref>{{cite web|last1=Petri|first1=Michelle|last2=Stohl|first2=William|last3=Chatham|first3=Winn|last4=McCune|first4=Joseph|last5=Chevrier|first5=Marc|last6=Ryel|first6=Jeff|last7=Recta|first7=Virginia|last8=Zhong|first8=John|last9=Freimuth|first9=William|title=ARTHRITIS & RHEUMATISM Vol. 58, No. 8, August 2008, pp 2453–2459 DOI 10.1002/art.23678 © 2008, American College of Rheumatology Association of Plasma B Lymphocyte Stimulator Levels and Disease Activity in Systemic Lupus Erythematosus|url=http://deepblue.lib.umich.edu/bitstream/handle/2027.42/60900/23678_ftp.pdf?sequence=1|website=Deepblue|publisher=American College of Rheumatology|accessdate=August 11, 2014}}</ref><ref>{{Cite journal|last1=Zhang|first1=J|last2=Roschke|first2=K|last3=Baker|first3=KP|last4=Wang|first4=Z|last5=Alarcon|first5=GS|last6=Fessler|first6=BJ|last7=Bastian|first7=H|last8=Kimberly|first8=RP|last9=Zhou|first9=T|title=Cutting edge: a role for B lymphocyte stimulator in systemic lupus erythematosus|journal=Journal of immunology (Baltimore, Md. : 1950)|volume=166|issue=1|pages=6–10|publisher=J Immunol|pmid=11123269|year=2001|doi=10.4049/jimmunol.166.1.6}}</ref> It is primarily expressed by ], ] and ].<ref>{{cite web|title=Product Candidates|url=http://www.anthera.com/products_a623.htm|website=Anthera Pharmaceuticals, Inc.|publisher=Anthera Pharmaceuticals, Inc.|accessdate=August 11, 2014}}</ref> Blisibimod binds to BAFF and inhibits the interaction of BAFF with its receptors.<ref>{{Cite journal|last1=Hsu|first1=H|last2=Khare|first2=SD|last3=Lee|first3=F|last4=Miner|first4=K|last5=Hu|first5=YL|last6=Stolina|first6=M|last7=Hawkins|first7=N|last8=Chen|first8=Q|last9=Ho|first9=SY|last10=Min|first10=H|last11=Xiong|first11=F|last12=Boone|first12=T|last13=Zack|first13=DJ|title=A novel modality of BAFF-specific inhibitor AMG623 peptibody reduces B-cell number and improves outcomes in murine models of autoimmune disease|publisher=Clinical and Experimentla Rheumatology|pmid=22325420|volume=30|issue=2|journal=Clin Exp Rheumatol|pages=197–201}}</ref> Blisibimod is currently being evaluated in IgA nephropathy . | *] is a selective peptibody antagonist of ] (BAFF). BAFF is critical to the development, maintenance and survival of B-cells, but is known to be up-regulated in ].<ref>{{Cite journal|last1=Groom|first1=J|last2=Kalled|first2=SL|last3=Cutler|first3=AH|last4=Olson|first4=C|last5=Woodcock|first5=SA|last6=Schneider|first6=P|last7=Tschopp|first7=J|last8=Cachero|first8=TG|last9=Batten|first9=M|last10=Wheway|first10=J|last11=Mauri|first11=D|last12=Cavill|first12=D|last13=Gordon|first13=TP|last14=Mackay|first14=CR|last15=Mackay|first15=F|title=Association of BAFF/BLyS overexpression and altered B cell differentiation with Sjögren's syndrome|pmid=11781351|doi=10.1172/JCI14121|volume=109|issue=1|date=Jan 2002|journal=J Clin Invest|pages=59–68|pmc=150825}}</ref><ref>{{cite web|last1=Petri|first1=Michelle|last2=Stohl|first2=William|last3=Chatham|first3=Winn|last4=McCune|first4=Joseph|last5=Chevrier|first5=Marc|last6=Ryel|first6=Jeff|last7=Recta|first7=Virginia|last8=Zhong|first8=John|last9=Freimuth|first9=William|title=ARTHRITIS & RHEUMATISM Vol. 58, No. 8, August 2008, pp 2453–2459 DOI 10.1002/art.23678 © 2008, American College of Rheumatology Association of Plasma B Lymphocyte Stimulator Levels and Disease Activity in Systemic Lupus Erythematosus|url=http://deepblue.lib.umich.edu/bitstream/handle/2027.42/60900/23678_ftp.pdf?sequence=1|website=Deepblue|publisher=American College of Rheumatology|accessdate=August 11, 2014}}</ref><ref>{{Cite journal|last1=Zhang|first1=J|last2=Roschke|first2=K|last3=Baker|first3=KP|last4=Wang|first4=Z|last5=Alarcon|first5=GS|last6=Fessler|first6=BJ|last7=Bastian|first7=H|last8=Kimberly|first8=RP|last9=Zhou|first9=T|title=Cutting edge: a role for B lymphocyte stimulator in systemic lupus erythematosus|journal=Journal of immunology (Baltimore, Md. : 1950)|volume=166|issue=1|pages=6–10|publisher=J Immunol|pmid=11123269|year=2001|doi=10.4049/jimmunol.166.1.6}}</ref> It is primarily expressed by ], ] and ].<ref>{{cite web|title=Product Candidates|url=http://www.anthera.com/products_a623.htm|website=Anthera Pharmaceuticals, Inc.|publisher=Anthera Pharmaceuticals, Inc.|accessdate=August 11, 2014}}</ref> Blisibimod binds to BAFF and inhibits the interaction of BAFF with its receptors.<ref>{{Cite journal|last1=Hsu|first1=H|last2=Khare|first2=SD|last3=Lee|first3=F|last4=Miner|first4=K|last5=Hu|first5=YL|last6=Stolina|first6=M|last7=Hawkins|first7=N|last8=Chen|first8=Q|last9=Ho|first9=SY|last10=Min|first10=H|last11=Xiong|first11=F|last12=Boone|first12=T|last13=Zack|first13=DJ|title=A novel modality of BAFF-specific inhibitor AMG623 peptibody reduces B-cell number and improves outcomes in murine models of autoimmune disease|publisher=Clinical and Experimentla Rheumatology|pmid=22325420|volume=30|issue=2|journal=Clin Exp Rheumatol|pages=197–201}}</ref> Blisibimod is currently being evaluated in IgA nephropathy . | ||
=== Sollpura === | === Sollpura === |
Revision as of 09:49, 2 May 2017
A major contributor to this article appears to have a close connection with its subject. It may require cleanup to comply with Misplaced Pages's content policies, particularly neutral point of view. Please discuss further on the talk page. (January 2017) (Learn how and when to remove this message) |
Company type | Public |
---|---|
Traded as | Nasdaq: ANTH |
Industry | Pharmaceuticals |
Founded | 2004 |
Headquarters | Hayward, California, U.S. |
Key people | Craig Thompson (President and CEO) |
Website | Anthera.com |
Anthera Pharmaceuticals, Inc. is a biopharmaceutical company focused on developing and commercializing products to treat serious conditions associated with cystic fibrosis, inflammation and autoimmune diseases. Liprotamase (Sollpura), Anthera’s leading drug candidate which is being developed for exocrine pancreatic insufficiency (EPI) is currently in Phase 3 clinical trials, and A-623 (Blisibimod) for the treatment of IgA nephropathy is currently in Phase 2 clinical trial.
Products
Blisibimod
- Blisibimod is a selective peptibody antagonist of B-cell activating factor (BAFF). BAFF is critical to the development, maintenance and survival of B-cells, but is known to be up-regulated in autoimmune diseases. It is primarily expressed by macrophages, monocytes and dendritic cells. Blisibimod binds to BAFF and inhibits the interaction of BAFF with its receptors. Blisibimod is currently being evaluated in IgA nephropathy .
Sollpura
July 2014, Anthera acquired Sollpura (Liprotamase) from Eli Lilly and Company. Sollpura is an investigational pancreatic enzyme replacement therapy (PERT) that uses three biotechnology-derived digestive enzymes intended to treat patients with endocrine pancreatic insufficiency as a result of cystic fibrosis and other diseases.
References
- "Overview". Anthera Pharmaceuticals,Inc. Retrieved August 11, 2014.
- "Management Team". Anthera Pharmaceuticals, Inc. Anthera Pharmaceuticals, Inc. Retrieved August 11, 2014.
- Groom, J; Kalled, SL; Cutler, AH; Olson, C; Woodcock, SA; Schneider, P; Tschopp, J; Cachero, TG; Batten, M; Wheway, J; Mauri, D; Cavill, D; Gordon, TP; Mackay, CR; Mackay, F (Jan 2002). "Association of BAFF/BLyS overexpression and altered B cell differentiation with Sjögren's syndrome". J Clin Invest. 109 (1): 59–68. doi:10.1172/JCI14121. PMC 150825. PMID 11781351.
- Petri, Michelle; Stohl, William; Chatham, Winn; McCune, Joseph; Chevrier, Marc; Ryel, Jeff; Recta, Virginia; Zhong, John; Freimuth, William. "ARTHRITIS & RHEUMATISM Vol. 58, No. 8, August 2008, pp 2453–2459 DOI 10.1002/art.23678 © 2008, American College of Rheumatology Association of Plasma B Lymphocyte Stimulator Levels and Disease Activity in Systemic Lupus Erythematosus" (PDF). Deepblue. American College of Rheumatology. Retrieved August 11, 2014.
- Zhang, J; Roschke, K; Baker, KP; Wang, Z; Alarcon, GS; Fessler, BJ; Bastian, H; Kimberly, RP; Zhou, T (2001). "Cutting edge: a role for B lymphocyte stimulator in systemic lupus erythematosus". Journal of immunology (Baltimore, Md. : 1950). 166 (1). J Immunol: 6–10. doi:10.4049/jimmunol.166.1.6. PMID 11123269.
- "Product Candidates". Anthera Pharmaceuticals, Inc. Anthera Pharmaceuticals, Inc. Retrieved August 11, 2014.
- Hsu, H; Khare, SD; Lee, F; Miner, K; Hu, YL; Stolina, M; Hawkins, N; Chen, Q; Ho, SY; Min, H; Xiong, F; Boone, T; Zack, DJ. "A novel modality of BAFF-specific inhibitor AMG623 peptibody reduces B-cell number and improves outcomes in murine models of autoimmune disease". Clin Exp Rheumatol. 30 (2). Clinical and Experimentla Rheumatology: 197–201. PMID 22325420.
- "Anthera Pharmaceuticals Announces Acquisition of Sollpura® (liprotamase) for Exocrine Pancreatic Insufficiency From Eli Lilly and Company". Anthera Pharmaceuticals, Inc. Anthera Pharmaceuticals. Retrieved August 11, 2014.
- "Anthera Pharmaceuticals Announces Acquisition of Sollpura® (liprotamase) for Exocrine Pancreatic Insufficiency From Eli Lilly and Company". Anthera Pharmaceuticals, Inc. Anthera Pharmaceuticals. Retrieved August 11, 2014.