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

Ponatinib - Clinical - Translational

  • Cortes J, et al. Ponatinib efficacy and safety in heavily pretreated leukemia patients: 3-year results of the PACE trial [abstract P234]. Haematologica 2015;100(suppl 1):64.
  • Müller M, et al. Responses at early landmark time points are associated with outcomes in heavily pretreated CP-CML patients (pts) treated with ponatinib [abstract P235]. Haematologica 2015;100(suppl 1):65.
  • Baccarani M, et al. Long-term follow-up of ponatinib efficacy and safety in patients (pts) with the T315I mutation in the phase 1 and phase 2 (PACE) trials [abstract P236]. Haematologica. 2015;100(suppl 1):65.
  • Nicolini FE, et al. Ponatinib efficacy and safety in patients with a history of stem cell transplantation (SCT) in the PACE trial [abstract E1104]. Haematologica. 2015;100(suppl 1):440.
  • Pritchard J, et al. Analysis of the relationship between dose and BCR-ABL halving time in CP-CML patients treated with ponatinib or imatinib [abstract E1122]. Haematologica. 2015;100(suppl 1):448-449.
  • Talpaz M, et al. Four-year minimum follow-up of ongoing patients (pts) with chronic-phase chronic myeloid leukemia (CP-CML) in a phase 1 trial of ponatinib (PON) [abstract 7047]. J Clin Oncol 2015;33(15 suppl).
  • Khoury HJ, et al. Elevated blood pressure (BP) and adverse events (AEs) of hypertension (HTN) in ponatinib (PON) leukemia trials [abstract 7049]. J Clin Oncol 2015;33(15 suppl).
  • Heinrich MC, et al. Ponatinib efficacy and safety in patients (pts) with advanced gastrointestinal stromal tumors (GIST) after tyrosine kinase inhibitor (TKI) failure: results from a phase 2 study [abstract 10535]. J Clin Oncol 2015;33(15 suppl).
  • Lipton JH, et al. EPIC: a phase 3 trial of ponatinib compared with imatinib in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CP-CML) [abstract 519]. Blood 2014;124.
  • Knickerbocker R, et al. Impact of dose intensity of ponatinib on selected adverse events: multivariate analyses from a pooled population of clinical trial patients [abstract 4546]. Blood 2014;124.
  • Tojo A, et al. Update of a phase 1/2 study of ponatinib in Japanese patients with Philadelphia positive leukemias [abstract OS-2-130]. Proceedings of the 76th Annual Meeting of the Japanese Society of Hematology October 31 to November 2, 2014; Osaka, Japan.
  • Talpaz M, Cortes JE, Kantarjian HM, et al. Longer-term follow up of a phase 1 study of ponatinib in patients (pts) with Philadelphia chromosome-positive (Ph+) leukemias. J Clin Oncol 32:5s, 2014 (suppl; abstr 7078).
  • Kantarjian HM, Kim DW, Pinilla-Ibarz J, et al. Ponatinib (PON) in patients (pts) with Philadelphia chromosome-positive (Ph+) leukemias resistant or intolerant to dasatinib or nilotinib, or with the T315I mutation: Longer-term follow up of the PACE trial. J Clin Oncol 32:5s, 2014 (suppl; abstr 7081).
  • Hochhaus A, et al. Clinical impact of dose modification and dose intensity on response to ponatinib (PON) in patients (pts) with Philadelphia chromosome-positive (Ph+) leukemias [abstract 7084]. J Clin Oncol. 2014;32(15 suppl).
  • Lipton JH, Chuah C, Guerci-Bresler A, et al. EPIC: A phase III trial of ponatinib (PON) versus imatinib (IM) in patients (pts) with newly diagnosed CP-CML. J Clin Oncol 32:5s, 2014 (suppl; abstr 7023).
  • Heinrich MC, vonMehren M, Demetri GD, et al. A phase 2 study of ponatinib in patients (pts) with advanced gastrointestinal stromal tumors (GIST) after failure of tyrosine kinase inhibitor (TKI) therapy: Initial report. J Clin Oncol 32:5s, 2014 (suppl; abstr 10506).
  • 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 [abstract 651]. Blood. 2013;122.
  • 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) [abstract 1496]. Blood. 2013;122.
  • Hochhaus A, et al. Efficacy and safety of ponatinib following failure of dasatinib in patients (pts) with chronic phase chronic myeloid leukemia (CP-CML) in the PACE trial [abstract 1498]. Blood. 2013;122.
  • 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 [abstract 2738]. Blood. 2013;122.
  • 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. Comparative efficacy among chronic phase-chronic myeloid leukemia (CP-CML) patients after failure of 2nd generation tyrosine kinase inhibitors (2G TKIs) [abstract 4010]. Blood. 2013;122.
  • 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 M, 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) [abstract 652]. Blood. 2013;122.
  • 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, et al. A phase 2 trial of ponatinib in Philadelphia chromosome–positive leukemias. N Engl J Med. 2013;369:1783-1796.
  • Cortes JE, et al. Ponatinib in refractory Philadelphia chromosome–positive leukemias. N Engl J Med. 2012;367:2075-2088.
  • 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. Comparative analysis of BCR-ABL and VEGFR2 inhibitory activities of ponatinib, axitinib, and PF-114 [abstract E1075]. Haematologica. 2015;100(suppl 1):427.
  • Gozgit JM, et al. Ponatinib demonstrates anti-tumor activity in RET- and FGFR-driven patient-derived xenografts [abstract 783]. Cancer Res. 2015;75(15 suppl).
  • Rivera VM, et al. Comparative TKI profiling analyses to explore potential mechanisms of ponatinib-associated arterial thrombotic events [abstract 1783]. Blood 2014;124.
  • 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 [abstract 3992]. Blood 2013;122.
  • Schrock AB, et al. Ponatinib potently inhibits the activity of mutant variants of FGFR commonly found in endometrial, lung and other cancers [abstract 2083]. Cancer Res. 2013;73(8 suppl).
  • Garner AP, et al. Ponatinib inhibits polyclonal drug-resistant KIT oncoproteins and shows therapeutic potential in heavily pretreated gastrointestinal stromal tumor (GIST) patients. Clin Cancer Res. 2014:20:5745-5755.
  • 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, et al. 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;71:1315-1323.
  • 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, et al. Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD. Blood 2013;121:3165-3171.
  • Gozgit JM, et al. Ponatinib, a potent pan-BCR-ABL inhibitor, retains activity against gatekeeper mutants of FLT3, RET, KIT, PDGFRα/β and FGFR1 [abstract 853]. Cancer Res. 2012;72(8 suppl).
  • 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, 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, 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, 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, et al. Discovery of 3-[2-(imidazo[1,2-b]pyridazin-3-yl)ethynyl]-4-methyl-N-{4-[(4-methylpiperazin-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. 2010;53:4701-4719.
  • O'Hare T, 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.

Brigatinib – Clinical

  • Camidge DR, et al. Safety and efficacy of brigatinib (AP26113) in advanced malignancies, including ALK+ non–small cell lung cancer (NSCLC) [abstract 8062]. J Clin Oncol. 2015;33(15 suppl).
  • Rosell R, et al. Phase 1/2 study of AP26113 in patients (pts) with advanced malignancies, including anaplastic lymphoma kinase (ALK)–positive non-small cell lung cancer (NSCLC): analysis of safety and efficacy at selected phase 2 doses [abstract 99O]. Ann Oncol. 2015;26(suppl 1):i30.
  • Kerstein D, et al. Evaluation of anaplastic lymphoma kinase (ALK) inhibitor brigatinib [AP26113] in patients (pts) with ALK+ non–small cell lung cancer (NSCLC) and brain metastases [abstract LBA4]. J Clin Oncol 2015;26(suppl 1):i60-i61.
  • Gettinger SN, Bazhenova L, Salgia R, et al. Updated efficacy and safety of the ALK inhibitor AP26113 in patients (pts) with advanced malignancies, including ALK+ non-small cell lung cancer (NSCLC). Ann Oncol. 32:5s, 2014 (suppl; abstr 8047).
  • 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.

Brigatinib - Preclinical

  • Zhang S, et al. The potent ALK inhibitor AP26113 can overcome mechanisms of resistance to first- and second-generation ALK TKIs in preclinical models [abstract 781]. Cancer Res. 2015;75(15 suppl).
  • Huang WS, et al. Discovery of AP26113, a potent, orally active inhibitor of anaplastic lymphoma kinase and clinically relevant mutants [abstract 2827]. Cancer Res. 2015;75(15 suppl).
  • Squillace RM, et al. AP26113 possesses pan-inhibitory activity versus crizotinib-resistant ALK mutants and oncogenic ROS1 fusions [abstract 5655]. Cancer Res. 2013;73(8 suppl).
  • 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, et al. Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK. Proc Natl Acad Sci USA. 2011:108:7535-7540.
  • Zhang S, et al. AP26113, a potent ALK inhibitor, overcomes mutations in EML4-ALK that confer resistance to PF-02341066 (PF1066) [abstract LB-298].Cancer Res. 2010;70(8 suppl).
  • Rivera VM, et al. Efficacy and pharmacodynamic analysis of AP26113, a potent and selective orally active inhibitor of Anaplastic Lymphoma Kinase (ALK) [abstract 3623]. Cancer Res. 2010;70(8 suppl).
  • Shakespeare W, et al. Discovery of potent and selective orally active inhibitors of anaplastic lymphoma kinase [abstract 3738]. Cancer Res. 2009;69(9 suppl).

 

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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