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Summarized below are key publications and presentations on ARIAD’s products/product candidates.

Ponatinib - Clinical

  • Cortes JE, et al. Ponatinib In Patients (pts) With Chronic Myeloid Leukemia (CML) and Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph+ ALL) Resistant Or Intolerant To Dasatinib Or Nilotinib, Or With The T315I BCR-ABL Mutation: 2-Year Follow-Up Of The PACE Trial. Blood 2013; 122:Abstract 650.
  • Parker WT, et al. Additional BCR-ABL1 Mutations Identified By Sensitive Mass Spectrometry In Chronic Phase CML Patients With T315I Treated With Ponatinib Are Associated With Relatively Inferior Responses and Outcome. Blood 2013; 122:Abstract 651.
  • Deininger MW, et al. Impact Of Baseline (BL) Mutations, Including Low-Level and Compound Mutations, On Ponatinib Response and End Of Treatment (EOT) Mutation Analysis In Patients (Pts) With Chronic Phase Chronic Myeloid Leukemia (CP-CML). Blood 2013; 122:Abstract 652.
  • le Coutre PD, et al. Ponatinib In Heavily Pretreated Patients With Chronic Phase Chronic Myeloid Leukemia (CP-CML): Management Of Adverse Events (AEs). Blood 2013; 122:Abstract 1496.
  • Hochhaus A, et al. Efficacy and Safety Of Ponatinib Following Failure Of Dasatinib In Patients With Chronic Phase Chronic Myeloid Leukemia (CP-CML) In The PACE Trial. Blood 2013;122:Abstract 1498.
  • Kantarjian HM, et al. Efficacy and Safety Of Ponatinib Following Failure Of Nilotinib In Patients With Chronic Phase Chronic Myeloid Leukemia (CP-CML) In The PACE Trial. Blood 2013;122:Abstract 2738.
  • Pinilla-Ibarz J, et al. Clinical Impact Of Dose Modification On Response To Ponatinib In Patients With Chronic Phase Chronic Myeloid Leukemia (CP-CML). Blood 2013; 122:Abstract 4007.
  • Lipton JH, et al. Comparitive Efficacy Among Chronic Phase-Chronic Myeloid Leukemia (CP-CML) Patients After Failure of 2nd Generation Tyrosine Kinase Inhibitors (2G TKIs). Blood 2013; 122:Abstract 4010.
  • Mauro MJ, Cortes JE, Kantarjian H, et al. Safety and durability of ponatinib in patients with Philadelphia chromosome-positive (Ph+) leukemia: Long-term follow-up of an ongoing phase I study. J Clin Oncol 2013;31(Suppl):Abstract 7063.
  • Khoury HJ, Cortes JE, Kim DW, et al. Analysis of the cardiovascular risk profile of Ph+ leukemia patients treated with ponatinib. J Clin Oncol 2013;31(Suppl):Abstract 7048.
  • Deininger MW, Cortes JE, Kim DW, et al. Impact of baseline mutations on response to ponatinib and end of treatment mutation analysis in patients with chronic myeloid leukemia. J Clin Oncol 2013;31(Suppl):Abstract 7001.
  • Cortes JE, Kantarjian H, Shah NP, et al. Ponatinib in refractory Philadelphia chromosome-positive leukemias. N Engl J Med 2012;367:2075-88.
  • Deininger MW, Cortes JE, Kantarjian HM, et al. Long-term anti-leukemic activity of ponatinib in patients with Philadelphia chromosome-positive leukemia: updated results from an ongoing phase 1 study. Blood 2012;120:Abstract 3743.
  • Cortes JE, Kim DW, Pinilla-Ibarz J, et al. A pivotal phase 2 trial of ponatinib in patients with chronic myeloid leukemia (CML) and philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL) resistant or intolerant to dasatinib or nilotinib, or with the T315I BCR-ABL mutation: 12-month follow-up of the PACE trial. Blood 2012;120:Abstract 163.
  • Kantarjian HM, Kim DW, Pinilla-Ibarz J, et al. Efficacy and safety of ponatinib in patients with accelerated phase or blast phase chronic myeloid leukemia (AP-CML or BP-CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL): 12-month follow-up of the PACE trial. Blood 2012;120:Abstract 915.
  • Hochhaus A, Kim DW, Pinilla-Ibarz J, et al. Molecular responses with ponatinib in patients with Philadelphia chromosome positive (Ph+) leukemia: results from the PACE trial. Blood 2012;120:Abstract 3763.
  • Mauro MJ, Cortes JE, Kim DW, et al. Multivariate analyses of the clinical and molecular parameters associated with efficacy and safety in patients with chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) treated with ponatinib in the PACE trial. Blood 2012;120:Abstract 3747.
  • Kim DW, Cortes JE, Pinilla-Ibarz J, et al. Efficacy and safety of ponatinib according to prior approved tyrosine kinase inhibitor (TKI) therapy in patients with chronic myeloid leukemia in chronic phase (CP-CML): results from the PACE trial. Blood 2012;120:Abstract 3749.

Ponatinib - Preclinical

  • Gozgit JM, et al. Comprehensive Analysis Of The In Vitro Potency Of Ponatinib, and All Other Approved BCR-ABL Tyrosine Kinase Inhibitors (TKIs), Against a Panel Of Single and Compound BCR-ABL Mutants. Blood 2013;122:Abstract 3992.
  • Alexa B. Schrock, Joseph M. Gozgit, Tim Clackson, Victor M. Rivera. Ponatinib potently inhibits the activity of mutant variants of FGFR commonly found in endometrial, lung and other cancers. Proceedings of the 104th Annual Meeting of the American Association for Cancer Research 2013 Apr 6-10; Washington, DC. Abstract nr 2083.
  • Andrew P. Garner, Rana Anjum, Sadanand Vodala, Alexa Schrock, Tianjun Zhou, Tim Clackson, Joseph M. Gozgit, Victor M. Rivera. Ponatinib, a pan-BCR-ABL inhibitor, potently inhibits key activating and drug-resistant KIT mutants found in GIST. Proceedings of the 104th Annual Meeting of the American Association for Cancer Research 2013 Apr 6-10; Washington, DC. Abstract nr 3394.
  • De Falco V, Buonocore P, Muthu M, Torregrossa L, Basolo F, Billaud M, Gozgit JM, Carlomagno F, Santoro M. Ponatinib (AP24534) Is a Novel Potent Inhibitor of Oncogenic RET Mutants Associated With Thyroid Cancer. J Clin Endocrinol Metab. 2013 May;98(5):E811-9. Epub 2013 Mar 22.
  • Gozgit JM, Squillace RM, Wongchenko MJ, Miller D, Wardwell S, Mohemmad Q, Narasimhan NI, Wang F, Clackson T, Rivera VM. Combined targeting of FGFR2 and mTOR by ponatinib and ridaforolimus results in synergistic antitumor activity in FGFR2 mutant endometrial cancer models. Cancer Chemother Pharmacol. 2013 May;71(5):1315-23. Epub 2013 Mar 7.
  • Ren M, Qin H, Ren R, et al. Ponatinib suppresses the development of myeloid and lymphoid malignancies associated with FGFR1 abnormalities. Leukemia 2013;27:32-40.
  • Smith CC, Lasater EA, Zhu X, et al. Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD. Blood; 2013:Feb 21 Epub.
  • Gozgit JM, Wong MJ, Zhu X, et al. Ponatinib, a potent pan-BCR-ABL inhibitor, retains activity against gatekeeper mutants of FLT3, RET, KIT, PDGFRα/β and FGFR1. Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, Illinois. Abstract 853.
  • Gozgit JM, Chen T-H, Schrock AB, et al. A broad tumor cell line panel screen of ponatinib, a pan-BCR-ABL and multitargeted kinase inhibitor. Proceedings of the 24th EORTC-NCI-AACR Symposium on ‘Molecular Targets and Cancer Therapeutics’; 2012 Nov 6-9; Dublin, Ireland. Abstract 407.
  • Gozgit JM, Wong MJ, Moran L, et al. Ponatinib (AP24534), a multitargeted pan-FGFR inhibitor with activity in multiple FGFR-amplified or mutated cancer models. Mol Cancer Ther 2012;11:690-699.
  • Zhou T, Commodore L, Huang WS, et al. Structural mechanism of the Pan-BCR-ABL inhibitor ponatinib (AP24534): Lessons for overcoming kinase inhibitor resistance. Chem Biol Drug Des 2011;77:1-11.
  • Gozgit JM, Wong MJ, Wardwell S, et al. Potent activity of ponatinib (AP24534) in models of FLT3-driven acute myeloid leukemia and other hematologic malignancies. Mol Cancer Ther 2011;10:1028-1035.
  • Huang WS, Metcalf CA, Sundaramoorthi R, et al. Discovery of 3-[2-(imidazo[1,2-b]pyridazin-3-yl)ethynyl]-4-methyl-N-{4-[(4-methylpiperazin-1-y l)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 2010;53:4701-4719.
  • O'Hare T, Shakespeare WC, Zhu X, et al. AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance. Cancer Cell 2009;16:401-412.

AP26113 – Clinical

  • Camidge DR, Bazhenova L, Salgia R, et al. First-in-human dose-finding study of the ALK/EGFR inhibitor AP26113 in patients with advanced malignancies: Updated results. J Clin Oncol. 2013;31(Suppl):Abstract 8031.
  • Gettinger S, Weiss GJ, Salgia R, et al. A first in-human dose finding study of the ALK/EGFR inhibitor AP26113 in patients with advanced malignancies. Proceedings of the European Society of Medical Oncology, September 28, 2012, Vienna, Austria:Abstract 439O.

AP26113 - Preclinical

  • Camidge DR, Bazhenova L, Salgia R, et al. First-in-human dose-finding study of the ALK/EGFR inhibitor AP26113 in patients with advanced malignancies: Updated results. J Clin Oncol. 2013;31(Suppl):Abstract 8031.
  • Ceccon M, Mologni L, Bisson W, Scapozza L, Gambacorti-Passerini C. Crizotinib-resistant NPM-ALK mutants confer differential sensitivity to unrelated Alk inhibitors. Mol Cancer Res 2013;11:122-32.
  • Katayama R, Khan TM, Benes C, et al. Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK. Proc Natl Acad Sci U S A 2011;108:7535-40.

 

For more information, please contact ARIAD at 1-855-55-ARIAD (1-855-552-7423) or outside the U.S. please +800 00027423. Please note, per country requirements, you may be required to dial (+), (0), or (00) before the EU phone number.

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