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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/11/15 22:20:13」(JST)

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Efalizumab (trade name Raptiva, Genentech, Merck Serono) is a formerly available medication designed to treat autoimmune diseases, originally marketed to treat psoriasis. As implied by the suffix -zumab, it is a recombinant humanized monoclonal antibody administered once weekly by subcutaneous injection. Efalizumab binds to the CD11a subunit of lymphocyte function-associated antigen 1 and acts as an immunosuppressant by inhibiting lymphocyte activation and cell migration out of blood vessels into tissues. Efalizumab was associated with fatal brain infections and was withdrawn from the market in 2009.^[1]

Known side effects include bacterial sepsis, viral meningitis, invasive fungal disease and progressive multifocal leukoencephalopathy (PML), a brain infection caused by reactivation of latent JC virus infection.^[2]^[3] Four cases of PML were reported in plaque psoriasis patients, an incidence of approximately one in 500 treated patients.^[1]

Due to the risk of PML, the European Medicines Agency and the FDA recommended suspension from the market in the European Union and the United States, respectively.^[4] In April 2009, Genentech Inc. announced a phased voluntary withdrawal of Raptiva from the U.S. market.^[1]^[5]

References[edit]

^ ^a ^b ^c Major, E. (2010). "Progressive multifocal leukoencephalopathy in patients on immunomodulatory therapies". Annual review of medicine 61 (1): 35–47. doi:10.1146/annurev.med.080708.082655. PMID 19719397. edit
^ "Efalizumab FDA Warning". Retrieved 7 December 2008.
^ Berger, J. R.; Houff, S. A.; Major, E. O. (2009). "Monoclonal antibodies and progressive multifocal leukoencephalopathy". MAbs 1 (6): 583–589. doi:10.4161/mabs.1.6.9884. PMC 2791316. PMID 20073129. edit
^ "EMEA press release regarding suspension" (PDF). Retrieved 20 February 2009.
^ "Genentech Announces Voluntary Withdrawal of Raptiva from the U.S. Market" (Press release). Genentech, Inc. 8 April 2009. Retrieved 9 April 2009.

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UpToDate Contents

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1. 乾癬の治療 treatment of psoriasis
2. Secondary immunodeficiency induced by biologic therapies
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4. 炎症の病因における白血球内皮細胞接着 leukocyte endothelial adhesion in the pathogenesis of inflammation
5. 円形脱毛症のマネージメント management of alopecia areata

English Journal

Cerebellar manifestation of PML under fumarate and after efalizumab treatment of psoriasis.

Stoppe M1, Thomä E, Liebert UG, Major EO, Hoffmann KT, Claßen J, Then Bergh F.
Journal of neurology.J Neurol.2014 Mar 18. [Epub ahead of print]
PMID 24638202

Monoclonal gammopathy of undetermined significance (MGUS) in patients with psoriasis may be associated with long-term treatment with efalizumab, but not with anti-TNF-α treatments or ustekinumab.

Vilarrasa E1, Puig L.
Journal of the European Academy of Dermatology and Venereology : JEADV.J Eur Acad Dermatol Venereol.2014 Mar 5. doi: 10.1111/jdv.12409. [Epub ahead of print]
PMID 24593678

T-cell trafficking and anti-adhesion strategies in inflammatory bowel disease: current and future prospects.

Mosli MH1, Rivera-Nieves J, Feagan BG.Author information 1Department of Medicine, University of Western Ontario, 100 Perth Dr, London, ON, N6A 5K8, Canada.AbstractThe medical management of idiopathic inflammatory bowel disease (IBD) has historically been based upon the use of broad-spectrum anti-inflammatory drugs such as corticosteroids and thiopurines. Recently, the identification of novel mechanisms central to the pathophysiology of IBD has provided more specific targets, including inhibition of leukocyte trafficking to the gut. In this article, we discuss the molecular biology of intestinal leukocyte trafficking and review the emerging therapies that target this process, including vedolizumab, natalizumab, etrolizumab, PF-547659, alicaforsen, efalizumab, and emerging members of this class.
Drugs.Drugs.2014 Mar;74(3):297-311. doi: 10.1007/s40265-013-0176-2.
The medical management of idiopathic inflammatory bowel disease (IBD) has historically been based upon the use of broad-spectrum anti-inflammatory drugs such as corticosteroids and thiopurines. Recently, the identification of novel mechanisms central to the pathophysiology of IBD has provided more s
PMID 24452878

Japanese Journal

Efalizumab modulates T cell function both in vivo and in vitro

Journal of dermatological science 60(3), 159-166, 2010-12-01
NAID 10027840949

次世代の生物学的製剤(第11回)エファリズマブ

分子リウマチ治療 3(4), 204-206, 2010-11
NAID 40017367202

T細胞表面分子を標的とする生物学的製剤抗BLyS抗体(ベリムマブ)および抗LFA-1α鎖抗体(エファリズマブ) (生物学的製剤の免疫薬理と臨床--変貌する関節リウマチ治療ストラテジー) -- (主要な生物学的製剤の構造,免疫薬理学的特徴と有用性のエビデンス)

日本臨床 65(7), 1239-1242, 2007-07
NAID 40015531779

Related Pictures

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★リンクテーブル★

リンク元	「mab」「エファリズマブ」「エファリツマブ」

「mab」

Efalizumab ^?
Monoclonal antibody
Type	Whole antibody
Source	Humanized (from mouse)
Target	CD11a
Clinical data
Trade names	Raptiva
AHFS/Drugs.com	monograph
Pregnancy cat.	?
Legal status	?
Routes	subcutaneous injection
Identifiers
CAS number	214745-43-4
ATC code	L04AA21
DrugBank	DB00095
UNII	XX2MN88N5D
ChEMBL	CHEMBL1201575
Chemical data
Formula	?
Physical data
Melt. point	66 °C (151 °F)
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