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Human Monoclonal Antibody Fragments Binding to Insulin-like Growth Factors I and II with Picomolar Affinity

  1. Author:
    Zhao, Q.
    Feng, Y.
    Zhu, Z. Y.
    Dimitrov, D. S.

  2. Author Address

    [Zhao, Q; Feng, Y; Zhu, ZY; Dimitrov, DS] NCI, Prot Interact Grp, Ctr Canc Res Nanobiol Program, NIH, Frederick, MD 21702 USA.;Dimitrov, DS (reprint author), NCI, Prot Interact Grp, Ctr Canc Res Nanobiol Program, NIH, Bldg 469,Rm 150B, Frederick, MD 21702 USA;dimiter.dimitrov@nih.gov
    1. Year: 2011
    2. Date: Sep
  2. Journal: Molecular Cancer Therapeutics
    1. 10
    2. 9
    3. Pages: 1677-1685
  4. Type of Article: Article
  5. ISSN: 1535-7163
  1. Abstract:

    The type 1 insulin-like growth factor receptor (IGF1R) and its ligands (IGF-I and IGF-II) have been implicated in a variety of physiologic processes and in diseases such as cancer. In addition to IGF1R, IGF-II also activates the insulin receptor (IR) isoform A, and therefore, antibodies against IGF-II can inhibit cell proliferation mediated by the signaling through both IGF1R and IR triggered by IGF-II. We identified a new human monoclonal antibody (mAb), m708.2, which is bound to IGF-I and IGF-II but not to insulin. m708.2 potently inhibited signal transduction mediated by the interaction of IGF-I or IGF-II with the IGF1R and IGF-II with the IR. It also inhibited the growth of the breast cancer cell line MCF-7. An affinity-matured derivative of m708.2, m708.5, bound to IGF-I with equilibrium dissociation constant, K(D)-200 pmol/L and to IGF-II with K(D)-60 pmol/L. m708.5 inhibited signal transduction mediated by IGF-I and IGF-II and cancer cell growth more potently than m708.2. These results suggest that m708.5 could have potential as a candidate therapeutic for cancers driven by the IGF-I and IGF-II interactions with IGF1R and IR. Mol Cancer Ther; 10(9); 1677-85. (C)2011 AACR.

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External Sources

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  2. DOI: 10.1158/1535-7163.mct-11-0281
  3. View record in Web of Science®
  4. WOS: 000294668900015

Library Notes

  1. Fiscal Year: FY2011-2012
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