Anti-CD22 antigen binding molecules to treat lung cancer and prostate cancer
Patent Number: US20140248278
Executive Summary:
General Description:
In the United States, lung cancer is the most common cause of cancer-death in both men and women. Despite refinements in platinum-based chemotherapy and several newly approved targeted agents, the median overall survival of patients with advanced, unresectable, NSCLC is only 8-11 months. MAbs and tyrosine kinase inhibitors (TKIs) that inhibit signaling from epidermal growth factor receptor (EGFR) and vascular endothelial cell growth factor (VEGF) provide clinical benefit to some NSCLC patients. Still, the EGFR inhibitor erlotinib is effective in only a small subset of patients and they inevitably develop resistance; the VEGF-targeted mAb bevacizumab adds only incrementally to progression-free survival. New therapeutic approaches are essential if significant advances are to be made in the treatment of NSCLC. The present invention is based, in part, on the discovery of CD22 as a target on NSCLC. Several anti-CD22 monoclonal antibodies (mAb) have been found to bind to lung and prostate cancer including those developed for the treatment of non-Hodgkin's lymphoma (NHL). Once anti-CD22 mAb, HB22.7, effectively binds NSCLC, it mediates specific in vitro and in vivo killing. It has heretofore been thought that CD22 was exclusively expressed on B-cells. The observation that CD22 is expressed on NSCLC and prostate cancers identifies an unexplored mechanism of tumorigenesis and moreover provides a method for CD22 antigen-targeted therapy for lung cancer and prostate cancer where there are few if any tumor-specific targets.
The present invention provides methods of preventing, reducing, delaying or inhibiting the proliferation and/or growth of a lung cancer cell and a prostate cancer cell. In some embodiments, the methods comprise contacting the lung cancer cell or prostate with an antigen binding molecule that binds to CD22 expressed on the surface of the lung cancer cell. The invention also provides methods of preventing, reducing, delaying or inhibiting the proliferation and/or growth and/or metastasis of a lung cancer or a prostate cancer in a subject in need thereof.
Patent Status:
Publications:
1. CD22 antigen is broadly expressed on lung cancer cells and is a target for antibody-based therapy. Tuscano JM, Kato J, Pearson D, Xiong C, Newell L, Ma Y, Gandara DR, O'Donnell RT. Cancer Res. 2012 Nov 1;72(21):5556-65. doi: 10.1158/0008-5472.CAN-12-0173. Epub 2012 Sep 17.
2. Phosphatase inhibition augments anti-CD22-mediated signaling and cytotoxicity in non-hodgkin's lymphoma cells. O'Donnell RT, Pearson D, McKnight HC, Ma YP, Tuscano JM. Leuk Res. 2009 Jul;33(7):964-9. doi: 10.1016/j.leukres.2009.01.026. Epub 2009 Feb 23.
3. The HB22.7 Anti-CD22 monoclonal antibody enhances bortezomib-mediated lymphomacidal activity in a sequence dependent manner. Martin SM, Churchill E, McKnight H, Mahaffey CM, Ma Y, O'Donnell RT, Tuscano JM. J Hematol Oncol. 2011 Dec 1;4:49. doi: 10.1186/1756-8722-4-49.
4. Dose, timing, schedule, and the choice of targeted epitope alter the efficacy of anti-CD22 immunotherapy in mice bearing human lymphoma xenografts. O'Donnell RT, Ma Y, McKnight HC, Pearson D, Tuscano JM. Cancer Immunol Immunother. 2009 Dec;58(12):2051-8. doi: 10.1007/s00262-009-0713-8. Epub 2009 May 13.
Inventor Bio: Joseph M. Tuscano and Robert T. O'Donnell
http://www.ucdmc.ucdavis.edu/publish/providerbio/internalmedicine/76
http://www.ucdmc.ucdavis.edu/publish/providerbio/search/201
Executive Summary:
- Invention Type: Therapeutic
- Patent Status: Priority date: June 8th, 2011, Filing date: June 8th, 2012, Publication date: September 4th, 2014
- Patent Link: https://www.google.com/patents/US20140248278
- Research Institute: University of California, Davis
- Disease Focus: Metastatic lung cancer, prostate cancer and other cancer types that over-expresses CD22
- Basis of Invention: This invention provides methods for preventing, reducing, delaying or inhibiting the proliferation and/or growth and/or metastasis of lung cancers and prostate cancer that express or overexpress CD22
- How it works: This method works by contacting the lung cancer cell or prostate cancer cell with an antigen binding molecule that binds to CD22 expressed on the surface of the cancer cell
- Inventors: Joseph Tuscano, Robert O'Donnell
- Development Stage: Pre-clinical, in vitro and in vivo assays data available
- Novelty:
- Validated the over-expression of CD22 in lung cancer and prostate cancer
- Proved the human chimera antibody or antibody fragment can effectively inhibit the CD22 over-expressing lung and prostate cancer cell growth in vitro and in vivo
- Clinical Applications:
- This invention provides methods for preventing, reducing, delaying or inhibiting the proliferation and/or growth and/or metastasis of lung cancers and prostate cancers that express or overexpress CD22.
General Description:
In the United States, lung cancer is the most common cause of cancer-death in both men and women. Despite refinements in platinum-based chemotherapy and several newly approved targeted agents, the median overall survival of patients with advanced, unresectable, NSCLC is only 8-11 months. MAbs and tyrosine kinase inhibitors (TKIs) that inhibit signaling from epidermal growth factor receptor (EGFR) and vascular endothelial cell growth factor (VEGF) provide clinical benefit to some NSCLC patients. Still, the EGFR inhibitor erlotinib is effective in only a small subset of patients and they inevitably develop resistance; the VEGF-targeted mAb bevacizumab adds only incrementally to progression-free survival. New therapeutic approaches are essential if significant advances are to be made in the treatment of NSCLC. The present invention is based, in part, on the discovery of CD22 as a target on NSCLC. Several anti-CD22 monoclonal antibodies (mAb) have been found to bind to lung and prostate cancer including those developed for the treatment of non-Hodgkin's lymphoma (NHL). Once anti-CD22 mAb, HB22.7, effectively binds NSCLC, it mediates specific in vitro and in vivo killing. It has heretofore been thought that CD22 was exclusively expressed on B-cells. The observation that CD22 is expressed on NSCLC and prostate cancers identifies an unexplored mechanism of tumorigenesis and moreover provides a method for CD22 antigen-targeted therapy for lung cancer and prostate cancer where there are few if any tumor-specific targets.
The present invention provides methods of preventing, reducing, delaying or inhibiting the proliferation and/or growth of a lung cancer cell and a prostate cancer cell. In some embodiments, the methods comprise contacting the lung cancer cell or prostate with an antigen binding molecule that binds to CD22 expressed on the surface of the lung cancer cell. The invention also provides methods of preventing, reducing, delaying or inhibiting the proliferation and/or growth and/or metastasis of a lung cancer or a prostate cancer in a subject in need thereof.
Patent Status:
- Priority date: June 8th, 2011
- Filing date: June 8th, 2012
- Publication date: September 4th, 2014
Publications:
1. CD22 antigen is broadly expressed on lung cancer cells and is a target for antibody-based therapy. Tuscano JM, Kato J, Pearson D, Xiong C, Newell L, Ma Y, Gandara DR, O'Donnell RT. Cancer Res. 2012 Nov 1;72(21):5556-65. doi: 10.1158/0008-5472.CAN-12-0173. Epub 2012 Sep 17.
2. Phosphatase inhibition augments anti-CD22-mediated signaling and cytotoxicity in non-hodgkin's lymphoma cells. O'Donnell RT, Pearson D, McKnight HC, Ma YP, Tuscano JM. Leuk Res. 2009 Jul;33(7):964-9. doi: 10.1016/j.leukres.2009.01.026. Epub 2009 Feb 23.
3. The HB22.7 Anti-CD22 monoclonal antibody enhances bortezomib-mediated lymphomacidal activity in a sequence dependent manner. Martin SM, Churchill E, McKnight H, Mahaffey CM, Ma Y, O'Donnell RT, Tuscano JM. J Hematol Oncol. 2011 Dec 1;4:49. doi: 10.1186/1756-8722-4-49.
4. Dose, timing, schedule, and the choice of targeted epitope alter the efficacy of anti-CD22 immunotherapy in mice bearing human lymphoma xenografts. O'Donnell RT, Ma Y, McKnight HC, Pearson D, Tuscano JM. Cancer Immunol Immunother. 2009 Dec;58(12):2051-8. doi: 10.1007/s00262-009-0713-8. Epub 2009 May 13.
Inventor Bio: Joseph M. Tuscano and Robert T. O'Donnell
http://www.ucdmc.ucdavis.edu/publish/providerbio/internalmedicine/76
http://www.ucdmc.ucdavis.edu/publish/providerbio/search/201
