INTRODUCTION METHODS OBJECTIVE RESULTS SUMMARY
Transcription
INTRODUCTION METHODS OBJECTIVE RESULTS SUMMARY
LBA4 Evaluation of Anaplastic Lymphoma Kinase (ALK) Inhibitor Brigatinib (AP26113) in Patients With ALK+ Non–Small Cell Lung Cancer (NSCLC) and Brain Metastases David Kerstein,1 Scott N Gettinger,2 Kathryn Gold,3 Corey J Langer,4 Alice T Shaw,5 Lyudmila A Bazhenova,6 Ravi Salgia,7 David J Dorer,1 Maureen G Conlan,1 D Ross Camidge8 1 ARIAD Pharmaceuticals, Inc., Cambridge, MA, USA; 2Yale Cancer Center, New Haven, CT, USA; 3The University of T exas MD Anderson Cancer Center, Houston, TX, USA; 4University of Pennsylvania Abramson Cancer Center, Philadelphia, PA, USA; 5 Massachusetts General Hospital, Boston, MA, USA; 6University of California San Diego Moores Cancer Center, La Jolla, CA, USA; 7The University of Chicago Medicine, Chicago, IL, USA; 8University of Colorado Cancer Center, Aurora, CO, USA INTRODUCTION Figure 1. Patient Stratification Figure 2. Time on Treatment Discontinued 100 90 80 79 ALK+ NSCLC patients a Patients (%) –– About half of patients have first disease progression in the central nervous system (CNS), suggesting inadequate CNS exposure5 Response Summary • Brigatinib demonstrated intracranial CNS antitumor activity with durable responses in ALK+ NSCLC patients with intracranial CNS metastases at baseline –– ORR in patients with §§ Measurable lesions: 53% §§ Nonmeasurable lesions: 30% –– Median duration of intracranial response: 18.9 months –– Median intracranial PFS: 22.3 months Figure 5. Duration of Intracranial Response Remain on study 137 total patients enrolled in the phase 1/2 trial • Crizotinib is active in ALK–rearranged (ALK+) NSCLC; however, most patients eventually develop disease progression3–5 SUMMARY Patients (n=49) • Anaplastic lymphoma kinase (ALK) gene rearrangements have been identified as driver mutations in non–small cell lung cancer (NSCLC) and other cancers1–2 RESULTS 70 60 50 40 30 20 –– Among patients with known brain metastases, the CNS was a site of development of new lesions or progression of nontarget lesions in 70% of crizotinib-treated patients with disease progression6 10 49 patients with intracranial CNS metastases identified on baseline MRI by central review • Brigatinib (AP26113) is an investigational oral tyrosine kinase inhibitor that has preclinical activity against rearranged ALK and clinically identified crizotinib-resistant mutants7 16 patients with measurable intracranial CNS metastases • A phase 1/2 study evaluated brigatinib in patients with advanced malignancies, including ALK+ NSCLC 0 25 50 75 100 125 150 0 175 0 6 12 24 30 Time (Months) Time on Treatment (Weeks) • Median time on study for ALK+ NSCLC patients with intracranial CNS metastases at baseline: 56.1 (0.1–150) weeks 33 patients with only nonmeasurable intracranial CNS metastases 18 Figure 3. Response in Brain • For patients with a response and a follow-up scan (n=16), median (Kaplan-Meier estimate) duration of intracranial response = 18.9 months Future Directions • A prospective evaluation of brigatinib in ALK+ NSCLC patients with intracranial CNS metastases is under way as part of a separate, pivotal, randomized, phase 2 trial in patients with ALK+ NSCLC resistant to crizotinib (ALTA: ALK in Lung Cancer Trial of AP26113) Figure 6. Intracranial PFS 100 OBJECTIVE METHODS Overall Trial • In this phase 1/2, single-arm, multicenter study (N=137; NCT01449461), patients with advanced malignancies received brigatinib at total daily doses of 30–300 mg • The primary efficacy endpoint of the phase 2 portion of the trial was objective response rate (ORR) by RECIST v1.18 • Secondary endpoints included safety, tolerability, best target lesion response, progression-free survival (PFS), and time to progression • Clinical data presented are as of 19 Jan 2015 Specific Methods for This Analysis • Contrast-enhanced brain magnetic resonance imaging (MRI) scans from ALK+ NSCLC patients with intracranial CNS metastases at baseline were analyzed by neuroradiologists in an independent central review. The reviewers were blinded to investigator assessment and systemic response • In this post hoc analysis, up to 5 measurable intracranial CNS metastases could be chosen as target lesions by the independent reviewers. Intracranial response (including PFS and duration of response) was defined using criteria based on RECIST8 –– Response in patients with at least 1 measurable intracranial CNS metastasis (≥10 mm) was defined as ≥30% decrease in sum of longest diameters of target lesions and nonprogression in nontarget lesions b 72/79 patients had baseline MRI scans available for central review at the time of this analysis Evaluable patients had at least 1 postbaseline MRI available for central review at the time of this analysis Baseline Table 1. Baseline Characteristics Characteristic Median age, y (range) • MRI scan dataset contains scans through 19 Jan 2015 ALK+ NSCLC With Intracranial CNS Metastases n=49 Total ALK+ NSCLC n=79 53 (30–73) 54 (29–83) Sex, n (%) Female 25 (51) 39 (49) Race, n (%) White 42 (86) 65 (82) Asian 5 (10) 10 (13) Other 2 (4) 4 (5) 0 20 (41) 30 (38) 1 28 (57) 48 (61) 2 1 (2) 1 (1) ECOG, n (%) a Prior crizotinib, n (%) Number of prior chemotherapy regimens, n (%) a 45 (92) 11 (22) 20 (25) 2 regimens 16 (33) 23 (29) ≥3 regimens 11 (22) 14 (18) 48 Weeks Figure 4. Activity in ALK+ NSCLC Patients With Measurable Intracranial CNS Metastases (n=15) Progressive disease Partial response Stable disease Complete response 40 rotocol amendment as of 30 November 2012 restricted enrollment to Eastern Cooperative Oncology Group (ECOG) performance P status 0 or 1 20 0 –40 50 40 ACKNOWLEDGMENTS 30 20 0 0 ALK+ NSCLC With Intracranial CNS Metastases n=49 Total ALK+ NSCLC n=79 Remain on study, n (%) 32 (65) 47 (59) Discontinued treatment, n (%) 17 (35) 32 (41) Documented progressive disease 8 (16) 16 (20) Adverse event 1 (2) 6 (8) Characteristic a Death 2 (4) 3 (4) Clinical progressive disease 2 (4) 2 (3) –60 2 (4) 2 (3) Withdrawal by subject 1 (2) 2 (3) Protocol violation 1 (2) 1 (1) Causes of death: 1 patient (180 mg qd) died from hypoxia considered possibly related to the study drug by the investigator (last dose, day 1) and 1 patient (240 mg qd) died from dyspnea considered not related by the investigator (last dose, day 397) b Causes of death: 2 patients listed in footnote a; 1 additional patient (90 mg qd) died from an unknown cause considered possibly related by the investigator (last dose, day 568) a 18 24 30 36 Systemic Efficacy • Brigatinib treatment achieved objective responses in 36/48 (75% [95% CI, 60%–86%]) patients with ALK+ NSCLC and intracranial CNS metastases –– Median duration of response = 11.2 months –– Median PFS = 12.9 months a One patient was not evaluable for response due to lack of follow-up scan ALK+ NSCLC Patients With Intracranial CNS Metastases n=49 –80 All Patients in Study N=137 5. Weickhardt AJ, Scheier B, Burke JM, et al. Local ablative therapy of oligoprogressive disease prolongs disease control by tyrosine kinase inhibitors in oncogene-addicted non–small-cell lung cancer. J Thorac Oncol. 2012;7:1807-1814. 6. Costa DB, Shaw AT, Ou SHI, et al. Clinical experience with crizotinib in patients with advanced ALK-rearranged non–small-cell lung cancer and brain metastases. J Clin Oncol. 2015 Jan 26. Epub ahead of print. 7. Squillace RM, Anjum R, Miller D, et al. AP26113 possesses pan-inhibitory activity versus crizotinib-resistant ALK mutants and oncogenic ROS1 fusions. Cancer Res. 2013; 73(8 suppl):5655. 8. Eisenhauer EA, Therasse P, Bogaerts J, et al. New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1). Eur J Cancer. 2009;45:228-247. 29 (59) 0 70 (51) 2 (1) DISCLOSURES Diarrhea 28 (57) 0 56 (41) 2 (1) Fatigue 24 (49) 2 (4) 55 (40) 5 (4) Cough 16 (33) 1 (2) 44 (32) 1 (<1) Headache 16 (33) 0 45 (33) 1 (<1) Increased lipase 15 (31) 7 (14) 24 (18) 12 (9) This study was sponsored by ARIAD Pharmaceuticals, Inc. DK: employment (ARIAD); SNG: nothing to disclose; KG: honoraria (Bristol-Myers Squibb), consulting or advisory role (Pfizer), research funding (Puma, ARIAD, Roche/Genentech, AstraZeneca, Bristol-Myers Squibb); CJL: research funding (ARIAD); ATS: honoraria (Pfizer, Novartis, Roche), consulting or advisory role (Pfizer, Novartis, Genentech, Roche, Ignyta), research funding (Pfizer, Novartis, Genentech, ARIAD); LAB: stock (Epic Sciences), honoraria (Novartis), consulting or advisory role (Clovis Pharmaceuticals, Boehringer Ingelheim, Seattle Genetics), speakers bureau (Genentech, Pfizer), research funding (ARIAD, Heat Bio, Mirati Pharmaceuticals, AstraZeneca, Boehringer Ingelheim, Roche, Merck, Astex Pharmaceuticals, Chugai Pharmaceuticals, Eisai, Eli Lilly, Johnson & Johnson, MedImmune, Novartis, NanoCarrier, Astellas); RS: nothing to disclose; DJD, MGC: employment (ARIAD); DRC: honoraria (ARIAD), research funding (ARIAD) Increased amylase 13 (27) 3 (6) 30 (22) 5 (4) CR, n (%) 1 (7) 9 (30) Increased AST 10 (20) 1 (2) 24 (18) 1 (<1) PR, n (%) 7 (47) NA SD or non-CR/ non-PD,b n (%) Back pain 10 (20) 1 (2) 22 (16) 2 (1) 5 (33) 17 (57) Constipation 10 (20) 0 27 (20) 0 PD, n (%) 2 (13) 4 (13) Dyspnea 10 (20) 3 (6) 31 (23) 9 (7) Hypertension 10 (20) 5 (10) 20 (15) 7 (5) Pyrexia 10 (20) 0 18 (13) 1 (<1) Presented at the 5th European Lung Cancer Conference, 15–18 April 2015, Geneva, Switzerland 4. Katayama R, Shaw AT, Khan TM, et al. Mechanisms of acquired crizotinib resistance in ALK-rearranged lung cancers. Sci Transl Med. 2012;4:120ra17. Nausea 9 (30) • Patients received 90 mg qd (n=9), 120 mg qd (n=1), 90 mg qd for 7 days followed by escalation to 180 mg qd (90Ò180 mg qd; n=17), 180 mg qd (n=14), 90 mg bid (n=1), and 240 mg qd (n=3) • Responses were observed at 90, 120, 90Ò180, 180, and 240 mg qd 3. Xalkori (crizotinib) prescribing information. New York, NY: Pfizer Inc; 2014. Grade ≥3 n (%) 8 (53) D for measurable brain metastases S Non-CR/non-PD for nonmeasurable brain metastases CR = complete response, NA = not applicable, PD = progressive disease, PR = partial response, SD = stable disease 2. Hallberg B, Palmer RH. Mechanistic insight into ALK receptor tyrosine kinase in human cancer biology. Nat Rev Cancer. 2013;13:685-700. Any Grade n (%) ORR, n (%) b 1. Pao W, Girard N. New driver mutations in non-small-cell lung cancer. Lancet Oncol. 2011;12:175-180. Grade ≥3 n (%) Patients With Only Nonmeasurable Intracranial CNS Metastases n=30 a REFERENCES Any Grade n (%) Patients With Measurable Intracranial CNS Metastases n=15 a Physician decision 12 Table 4. Treatment-Emergent Adverse Events, ≥20% in ALK+ NSCLC Patients With Intracranial CNS Metastases * Table 3. Intracranial Response in ALK+ NSCLC Patients With Intracranial CNS Metastases b 6 • For patients with a follow-up scan (n=45), median (Kaplan-Meier estimate) intracranial PFS = 22.3 months * Crizotinib-naive Dotted line at –30% indicates threshold for partial response Table 2. Patient Disposition and T reatment Exposure The authors would like to thank the patients, their families, and their caregivers; the phase 1/2 investigators and their team members at each study site; and colleagues from ARIAD Pharmaceuticals, Inc. Professional medical writing assistance was provided by Lela Creutz, PhD, of Peloton Advantage, LLC, Parsippany, New Jersey, USA, and funded by ARIAD Pharmaceuticals, Inc. Time (Months) a –20 * 60 10 • Patient with ALK+ NSCLC was previously treated with crizotinib and received brigatinib 180 mg qd • Partial response is ongoing as of 19 Jan 2015 71 (90) 1 regimen 8 Weeks Images courtesy of D R Camidge 70 –100 –– Response in patients with only nonmeasurable intracranial CNS metastases was defined as disappearance of all lesions • Limited data regarding local radiotherapy to the brain were collected and these data were not considered in this review 80 Best Change From Baseline in Target Brain Lesions (%) • To evaluate intracranial efficacy and safety of brigatinib in ALK+ NSCLC patients with intracranial CNS metastases at baseline in a phase 1/2 study a 90 30 patients evaluable for efficacyb Patients (%) 15 patients evaluable for efficacyb Safety Summary • The most common adverse events (nausea, diarrhea, fatigue, and cough) in patients with intracranial CNS metastases at baseline occurred at a similar incidence in the broader study population AST = aspartate aminotransferase • Treatment-emergent serious adverse events, ≥4%, for patients with intracranial CNS metastases included dyspnea (4 [8%]), hypoxia (3 [6%]), and pyrexia (2 [4%]) For an e-Print, scan this QR code or visit the web at: http://congressposters.ariad.com/item/75c483. 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