Publications

Ponatinib

Cortes J, Kim D-W, Pinilla J, et al. (2011). Initial Findings from the PACE Trial: A Pivotal Phase 2 Study of Ponatinib in Patients with CML and Ph+ ALL Resistant or Intolerant to Dasatinib or Nilotinib, or with the T315I Mutation. Presented at the 53nd Annual Meeting of the American Society of Hematology (ASH) San Diego CA, 11 December 2011. Abstract 109.
Talpaz M, Shah N, Deininger M, et al. (2011). Ponatinib in Patients with Acute Myeloid Leukemia (AML): Preliminary Findings from a Phase 1 Study in Hematologic Malignancies. Poster at the 2011 American Society of Clinical Oncology (ASCO) Annual Meeting, Chicago, 03 June 2011. Abstract 6518.
Gozgit JM, Wong MJ, Wardwell SD, et al. (2011). Potent activity of ponatinib (AP24534) in models of FLT3-driven acute myeloid leukemia (AML) and other hematologic malignancies. Mol Cancer Ther. [In Print]
Zhou T, Commodore L, Huang WS, et al. (2011). Structural mechanism of the Pan-BCR-ABL inhibitor ponatinib (AP24534): lessons for overcoming kinase inhibitor resistance. Chem Biol Drug Des. 77(1):1-11.
Huang WS, Metcalf CA, Sundaramoorthi R, et al. (2010). Discovery of 3-[2-(imidazo[1,2-b]pyridazin-3-yl)ethynyl]-4-methyl-N-{4-[(4-methylpipera zin-1-yl)methyl]-3-(trifluoromethyl)phenyl}benzamide (AP24534), a potent, orally active pan-inhibitor of breakpoint cluster region-abelson (BCR-ABL) kinase including the T315I gatekeeper mutant. J Med Chem. 53(12):4701-4719.
O'Hare T, Shakespeare WC, Zhu X, et al. (2009). AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance. Cancer Cell 16(5):401-412.

Ponatinib Presentations

Gozgit J, Wong, M, Moran L, et al. (2011). Ponatinib (AP24534), a potent pan-FGFR inhibitor with activity in multiple FGFR-driven cancer models with distinct mechanisms of activation. Presented at the 102nd Annual Meeting of the American Association for Cancer Research (AACR) Orlando FL, 05 April 2011. Abstract 3560.
Cortes J, Talpaz M, Bixby D, et al. (2010). A phase 1 trial of oral ponatinib (AP24534) in patients with refractory chronic myelogenous leukemia (CML) and other hematologic malignancies: emerging safety and clinical response findings. Presented at the 52nd Annual Meeting of the American Society of Hematology (ASH) Orlando FL, 06 December 2010. Abstract 210.

Review Articles on BCR-ABL and CML

O'Hare T, Deininger MW, Eide CA, et al. (2011). Targeting the BCR-ABL signaling pathway in therapy-resistant Philadelphia chromosome-positive leukemia. Clin Cancer Res. 17(2):212-221.
Druker BJ. (2008). Translation of the Philadelphia chromosome into therapy for CML. Blood 112(13):4808-4817.

AP26113

Katayama R, Khan TM, Benes C, et al. (2011). Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK. Proc Natl Acad Sci USA. 108(18):7535-40.

AP26113 Presentations

Rivera VM, Anjum R, Wang F, et al. (2010). Efficacy and pharmacodynamic analysis of AP26113,a potent and selective orally active inhibitor of anaplastic lymphoma kinase (ALK). Presented at the 101st Annual Meeting of the American Association for Cancer Research (AACR) Washington DC, 20 April 2010. Abstract 3623.
Zhang S, Wang F, Keats J, et al. (2010). AP26113, a potent ALK inhibitor, overcomes mutations in EML4-ALK that confer resistance to PF 02341066. Presented at the 101st Annual Meeting of the American Association for Cancer Research (AACR) Washington DC, 20 April 2010. Abstract LB 298.

Review Articles on ALK

Shaw AT, Solomon B. (2011). Targeting anaplastic lymphoma kinase in lung cancer. Clin Cancer Res. 17(8):2081-2086.
Webb TR, Slavish J, George RE, et al. (2009). Anaplastic lymphoma kinase: role in cancer pathogenesis and small-molecule inhibitor development for therapy. Expert Rev Anticancer Ther. 9(3):331-356.

Ridaforolimus

Rivera VM, Squillace RM, Miller D, et al. (2011). Ridaforolimus (AP23573, MK-8669), a potent mTOR inhibitor, has broad antitumor activity and can be optimally administered using intermittent dosing regimens. Mol Cancer Ther. [In Print]
Sessa C, Tosi D, Vigano L, et al. (2010). Phase Ib study of weekly mammalian target of rapamycin inhibitor ridaforolimus (AP23573; MK-8669) with weekly paclitaxel. Ann Oncol. 21(6):1315-1322.
Perotti A, Locatelli A, Sessa C, et al. (2010). Phase IB study of the mTOR inhibitor ridaforolimus with capecitabine. J Clin Oncol. 28(30):4554-4561.
Hartford CM, Desai AA, Janisch L, et al. (2009). A phase I trial to determine the safety, tolerability, and maximum tolerated dose of deforolimus in patients with advanced malignancies. Clin Cancer Res. 15(4):1428-1434.
Rizzieri DA, Feldman E, Dipersio JF, et al. (2008). A phase 2 clinical trial of deforolimus (AP23573, MK-8669), a novel mammalian target of rapamycin inhibitor, in patients with relapsed or refractory hematologic malignancies. Clin Cancer Res. 14(9):2756-2762.
Mita MM, Mita AC, Chu QS, et al. (2008). Phase I trial of the novel mammalian target of rapamycin inhibitor deforolimus (AP23573; MK-8669) administered intravenously daily for 5 days every 2 weeks to patients with advanced malignancies. J Clin Oncol. 26(3):361-367.

Review Articles on ridaforolimus, mTOR and Sarcoma

Dancey J and Monzon, J (2011). Ridaforolimus: a promising drug in the treatment of soft-tissue sarcoma and other malignancies. Future Oncol. Jul;7(7):827-39
Vemulapalli S, Mita A, Alvarado Y, et al. (2011). The emerging role of mammalian target of rapamycin inhibitors in the treatment of sarcomas. Target Oncol. [In Print]
Blay JY. (2011). Updating progress in sarcoma therapy with mTOR inhibitors. Ann Oncol. 22(2):280-287.