JP2012100675A - 免疫エフェクター活性を有する葉酸受容体アルファ陽性細胞に内部移行する抗体 - Google Patents
免疫エフェクター活性を有する葉酸受容体アルファ陽性細胞に内部移行する抗体 Download PDFInfo
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Abstract
【解決手段】FRAを発現する細胞に特異的に結合し、二者択一でこの細胞に内部移行し、抗体依存性細胞傷害作用などの免疫エフェクター活性を誘導する能力を有するモノクローナルおよびポリクローナル抗体。また、該抗体をコードするヌクレオチド、該抗体を発現する細胞、該抗体を用いて癌細胞を検出、治療する方法。
【選択図】図2
Description
1987年、Miottiらは、ヒト卵巣癌細胞の抗原を認識する、3種類の新しいモノクローナル抗体について報告した(Miotti et al.(1987)Int.J.Cancer 39(3):297−303)。このうちの1つがMOv18と命名されており、これは絨毛癌細胞表面の38kDaタンパク質を認識する。MOv18はマウスIgG1κ抗体であり、卵巣癌細胞株IGROV1の特異的細胞溶解を媒介する。Albertiら((1990)Biochem.Biophys.Res.Commun.171(3):1051−1055)は、MOv18により認識される抗原はGPI結合タンパク質であることを示した。その後、これはヒト葉酸結合タンパク質として特定された(Coney et al.(1991)Cancer Res.51(22):6125−6132)。Tomassettiらは、MOv18が、IGROV1細胞にある前記葉酸結合タンパク質の可溶型とGPIアンカー型を認識することを示した(Tomassetti et al.(1993)FEBS Lett.317(1−2):143−146)。その後の研究では、マウスMOv18の可変領域をヒトIgG1(κ)の定常領域と結合させ、キメラ化MOv18抗体を作製した。前記キメラ化抗体は、10〜100倍低い抗体濃度で、IGROV1細胞のより多く、より特異的な溶解を媒介した(Coney et al.(1994)Cancer Res.54(9):2448−2455)。
本発明の抗体には、タイプIgA、IgG、IgE、IgD、IgM(およびそのサブタイプ)を含む、すべてのアイソタイプの完全な免疫グロブリンを含む。前記免疫グロブリンの軽鎖はκまたはλである。
Claims (47)
- (a)葉酸受容体アルファ(FRA)に特異的に結合し、さらに(b)選択的に免疫エフェクター活性を誘発するか、或いはFRA提示細胞に内部移行する、インアウト抗葉酸受容体アルファ抗体。
- 請求項1記載の抗体において、前記抗体は少なくとも約1×10−7Mの親和性でFRAに結合するものである。
- 請求項1記載の抗体において、前記抗体は少なくとも約1×10−8Mの親和性でFRAに結合するものである。
- 請求項1記載の抗体において、前記抗体は少なくとも約1×10−9Mの親和性でFRAに結合するものである。
- 請求項1記載の抗体において、前記抗体は少なくとも約1×10−10Mの親和性でFRAに結合するものである。
- 請求項1記載の抗体において、前記抗体はキメラ抗体である。
- 請求項6記載の抗体において、前記キメラ抗体はヒト−マウスキメラ抗体である。
- 請求項1記載の抗体において、前記抗体はヒト化抗体である。
- 請求項1記載の抗体において、前記抗体は完全ヒト抗体である。
- 請求項1記載の抗体において、前記抗体は化学治療物質に結合される。
- 請求項10記載の抗体において、前記化学治療物質は放射性核種である。
- 請求項1記載の抗体において、FRAは配列ID番号2のアミノ酸配列を有するものである。
- 請求項1記載の抗体において、FRAは配列ID番号1の前記ヌクレオチド配列によってコードされるものである。
- 請求項1記載の抗体において、前記免疫エフェクター活性は抗体依存性細胞傷害作用である。
- 請求項1記載の抗体の重鎖をコードするポリヌクレオチド。
- 請求項1記載の抗体の軽鎖をコードするポリヌクレオチド。
- 請求項1記載の抗体の重鎖および軽鎖をコードするポリヌクレオチド。
- 請求項1記載の抗体を有する薬学的組成物。
- 請求項18記載の医薬品において、前記抗体は化学治療物質と結合される。
- 請求項19記載の医薬品において、前記化学治療物質は放射性核種である。
- 請求項1記載の抗体の重鎖をコードするポリヌクレオチドを有するベクター。
- 請求項1記載の抗体の軽鎖をコードするポリヌクレオチドを有するベクター。
- 請求項1記載の抗体の重鎖と請求項1記載の抗体の軽鎖とをコードするポリヌクレオチドを有するベクター。
- 請求項1記載の抗体の重鎖をコードするポリヌクレオチドと、請求項1記載の抗体の軽鎖をコードするポリヌクレオチドとを有する発現細胞。
- 請求項23記載の前記ベクターを有する発現細胞。
- 請求項25記載の発現細胞において、前記細胞は哺乳類細胞である。
- 請求項24記載の発現細胞において、前記細胞は哺乳類細胞である。
- 請求項1記載の抗体を産生する細胞。
- 請求項28記載の細胞において、前記細胞はハイブリドーマである。
- FRAに特異的に結合するインアウト抗体を作製する方法であって、請求項28記載の細胞を培養する工程と、成長培地から前記抗体を回収する工程とを有する方法。
- FRA陽性細胞の成長を阻害する方法であって、前記細胞を有する対象にインアウト抗FRA抗体を投与する工程を有する方法。
- 請求項31記載の方法において、前記インアウト抗FRA抗体は生体分子に結合されるものである。
- 請求項31記載の方法において、前記FRA陽性細胞は異型細胞である。
- 請求項31記載の方法において、前記対象はヒトである。
- 請求項31記載の方法において、前記抗体は化学治療物質と結合される。
- 請求項35記載の方法において、前記化学治療物質は放射性核種である。
- 請求項31記載の方法において、この方法は、さらに、細胞傷害性薬を前記被験者に投与する工程を有するものである。
- 請求項31記載の方法において、この方法は、さらに、細胞増殖抑制物質を前記被験者に投与する工程を有するものである。
- 請求項31記載の方法において、この方法は、さらに、化学治療物質を前記被験者に投与する工程を有するものである。
- 請求項31記載の方法において、前記抗体は非複合型抗体として投与されるものである。
- 請求項31記載の方法において、前記抗体は非複合型抗体と化学治療物質に結合した抗体との混合物として投与されるものである。
- キットであって、FRAに特異的に結合する抗体において、この抗体は選択的に免疫エフェクター活性を誘発するか、或いはFRA提示細胞に内部移行するものである前記抗体と、対象のFRA提示細胞の成長を阻害する方法において前記キットを使用するための使用説明書とを有する、キット。
- 請求項42のキットにおいて、このキットは、さらに、少なくとも1つの化学治療物質を有するものである。
- 請求項42のキットにおいて、このキットは、さらに、少なくとも1つの診断薬を有するものである。
- 請求項42のキットにおいて、このキットは、さらに、前記抗体を前記被験者に投与する方法と使用説明書を有するものである。
- キットであって、インアウト抗FRA抗体と、インビトロまたはインビボでFRA提示細胞の有無を同定する方法において前記キットを使用するための使用説明書とを有する、キット。
- 請求項46のキットにおいて、このキットは、さらに、少なくとも1つの診断薬を有するものである。
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US67418505P | 2005-04-22 | 2005-04-22 | |
US60/674,185 | 2005-04-22 |
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EP (2) | EP2172487A1 (ja) |
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Publication number | Priority date | Publication date | Assignee | Title |
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WO2020129838A1 (ja) * | 2018-12-17 | 2020-06-25 | 株式会社カネカ | 特定抗原特異的抗体を産生する細胞のスクリーニング方法 |
JP7426661B2 (ja) | 2018-12-17 | 2024-02-02 | 株式会社カネカ | 特定抗原特異的抗体を産生する細胞のスクリーニング方法 |
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JP2009521206A (ja) | 2009-06-04 |
EP1879922A2 (en) | 2008-01-23 |
EP2172487A1 (en) | 2010-04-07 |
WO2006116592A9 (en) | 2007-03-22 |
US20120171200A1 (en) | 2012-07-05 |
US20060239910A1 (en) | 2006-10-26 |
CA2607444C (en) | 2015-03-10 |
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CA2607444A1 (en) | 2006-11-02 |
AU2006241099A1 (en) | 2006-11-02 |
WO2006116592A2 (en) | 2006-11-02 |
US8124083B2 (en) | 2012-02-28 |
US9144614B2 (en) | 2015-09-29 |
WO2006116592A3 (en) | 2007-04-19 |
US10253106B2 (en) | 2019-04-09 |
AU2006241099B2 (en) | 2012-04-19 |
US20160058885A1 (en) | 2016-03-03 |
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