J.P. Morgan 34 th Annual Healthcare Conference

Transcription

1 J.P. Morgan 34 th Annual Healthcare Conference Ron Squarer Chief Executive Officer

2 Safe Harbor Statement 2 Forward-looking statements made in the course of this presentation are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of The audience is cautioned that such forward looking statements involve risks and uncertainties, including those described in our annual report filed on form 10-K for the year ended June 30, 2015, and other filings of the Company with the Securities and Exchange Commission, which may cause the Company's actual results and experience to differ materially from anticipated results and expectations expressed in these forward-looking statements.

3 Array s Top Priority Binimetinib & Encorafenib Development & Commercialization 3 SIGNIFICANT PROGRESS IN 2015 WITH IMPORTANT VALUE DRIVERS AHEAD IN 2016 Regained rights to binimetinib and acquired global rights to encorafenib along with $100 million+ payment from Novartis Completed Pierre Fabre collaboration including $30 million upfront, $425 million potential milestones and robust, tiered, double-digit royalties Array retains exclusive rights in key markets including U.S. & Japan Pierre Fabre has exclusive rights in other geographies, including Europe, Asia & Latin America NRAS-mutant melanoma Phase 3 (NEMO) trial achieved primary endpoint Published clinical results for BRAF-mutant colorectal cancer Phase 1/2 BRAF-mutant melanoma Phase 2 (LOGIC2) NRAS-mutant melanoma Phase 1/2 (CDK 4/6 combo) Phase 3/NRAS-mutant melanoma Present full results File for regulatory approval Phase 3 Part 1/BRAF-mutant melanoma Announce results Present full results File for regulatory approval Phase 3/LGS ovarian cancer Complete enrollment BRAF-mutant metastatic colorectal cancer Present update from Phase 2 expansion Initiate Phase 3 global registration trial SECOMBIT trial will address sequential use of MEK+RAF with PD-1+CTLA4 in BRAF-mutant melanoma January 13, 2016

4 NEMO Meets Primary Endpoint NRAS-Mutant Melanoma

5 Binimetinib Phase 3 Study NEMO Meets Primary Endpoint 5 NEMO is a pivotal Phase 3 trial comparing binimetinib to dacarbazine in patients with NRAS-mutated melanoma 20% of patients with metastatic melanoma have NRAS-mutations NRAS diagnostic being developed in collaboration with Qiagen NEMO study met its primary endpoint of improving progression free survival (PFS) compared with dacarbazine treatment Hazard ratio (HR) 0.62, [95% CI ], p < Median PFS on the binimetinib arm was 2.8 months versus 1.5 months on dacarbazine arm Binimetinib appeared to be generally well-tolerated Adverse events reported were consistent with results from previous, earlier phase binimetinib studies in NRAS-mutant melanoma patients No new safety signals were seen More data to be presented at medical conference in 2016 including PFS, overall survival (OS), overall response rate (ORR), safety Prespecified subgroup analyses including outcomes in patients who received prior treatment with immunotherapy Positive results from the NEMO trial further demonstrate the potential of binimetinib to provide an important new treatment option for patients with advanced/unresectable NRAS-mutant melanoma.

6 Binimetinib + Ribociclib 28-Day Regimen Promising Preliminary Clinical Activity in NRAS-Mutant Melanoma 6 Response n (%) All 28-Day Regimen Patients n=22 All 21-Day Regimen Patients n=23 Individual Patient Responses Evaluable Patients Complete Response 0 0 Partial Response Confirmed PR Unconfirmed 5 (23) 4 (18) 3 (14) 1 (5) Stable Disease (SD) 9 (41) 11 (50) Progressive Disease 3 (14) 4 (18) Unknown 1 (5) 3 (14) Overall Response Rate (ORR) a 9 (41) 4 (18) Disease Control Rate 18 (82) 15 (68) Median Progression Free Survival, Months ECC/ESMO 2015: A Phase 1b/2 study of ribociclib (LEE011; CDK4/6 inhibitor) in combination with binimetinib (MEK162; MEK inhibitor) in patients with NRAS-mutant melanoma naïve to BRAFi treatment (Abstract #3300) a Rate includes unconfirmed CR/PR Observed activity did not appear to be driven by higher doses of ribociclib as patients in lowest dose cohort of 200mg ribociclib + 45mg BID binimetinib achieved a 56% overall response rate (ORR) Safety: Binimetinib and ribociclib are combinable in NRAS-mutant melanoma patients The most common treatment-related adverse events included elevated creatine phosphokinase (CPK), skin and gastrointestinal events Potential for binimetinib beyond single agent in combinations *Patients with confirmed PR; Patients with prior immunotherapy treatment; BID Twice Daily Data cutoff date:, June 5, 2015

7 LOGIC2/SECOMBIT BRAF-Mutant Melanoma

8 LOGIC2 Binimetinib + Encorafenib + Third Agent BRAF-Mutant Melanoma Study Design 8 Patient Enrollment on-going n=140 Part 1 n=89 as of 7/1/15 Part 2 n=20 as of 7/1/15 GROUP A BRAF- and MEK-naïve patients GROUP A Binimetinib + Encorafenib Binimetinib + Encorafenib + LEE011 (CDK 4/6 inhibitor) GROUP B Patients with any BRAF/MEK combo or single agents (non-naïve) GROUP C Patients previously in COLUMBUS, LOGIC1, CMEK162X2110, or Group A (non-naïve) GROUP B Run-in Binimetinib + Encorafenib GROUP C Optional Binimetinib + Encorafenib After progressive disease, genetic assessment performed to determine combination Binimetinib + Encorafenib + BGJ398 (pan FGFR inhibitor) Binimetinib + Encorafenib + BKM120 (pan PI3K inhibitor) Binimetinib + Encorafenib + INC280 (c-met inhibitor) Primary Endpoint: Overall response rate (ORR) (Part 2) Secondary Endpoint: Safety After Progressive Disease in Part 1: Tumor biopsy genetic assessment performed to determine combination treatment in Part 2 Part 2 Third Agent: LEE011 (CDK 4/6 inhibitor), BGJ398 (pan FGFR inhibitor), BKM120 (pan PI3K inhibitor) or INC280 (c-met inhibitor)

9 LOGIC2 Binimetinib + Encorafenib Part 1 Encouraging Preliminary Clinical Activity 9 Combination of binimetinib and encorafenib demonstrated encouraging preliminary clinical activity in BRAFi/MEKi naïve patients Phase 2 (as of 7/1/15) Group A (MEKi + BRAFi Naïve) Encorafenib 450mg QD* + Binimetinib 45mg BID n=45 Binimetinib 45mg BID/Encorafenib 450mg QD AE, n (%) BRAFi/MEKi Naïve Patients n=40 Overall Response Rate (ORR) 2,3 68% Disease Control Rate (DCR) 2,4 95% 6-Month Median Progression Free Survival (PFS) 79% (Note: 96% of patients continued to receive study treatment as of data cutoff) Complete Response (CR) 2 3% (1) Partial Response (PR) 2 65% (26) Stable Disease (SD) 28% (11) 1 ECC/ESMO 2015: LOGIC2: Phase 2, multi-center, open-label study of sequential encorafenib/binimetinib combination followed by a rational combination with targeted agents after progression, to overcome resistance in adult patients with locally-advanced or metastatic BRAF V600 melanoma (Abstract #3310); 2 Includes confirmed/unconfirmed responses; 3 ORR=CR/PR, 4 DCR=CR/PR or SD * QD Once Daily; BID Twice Daily Clinical trial number NCT

10 LOGIC2 Binimetinib + Encorafenib Part 1 Good Tolerability 10 Differentiated Safety: 12% pyrexia, 7% rash and no photosensitivity Phase 2 (as of 7/1/15) Group A (MEKi + BRAFi Naïve) Encorafenib 450mg QD + Binimetinib 45mg BID n=45 Group B (Prior BRAFi and/or MEKi) Encorafenib 450mg QD + Binimetinib 45mg BID n=43 All Patients n=89 AE, n (%) All Grades n (%) Grade 3/4 n (%) All Grades n (%) Grade 3/4 n (%) All Grades n (%) Grade 3/4 n (%) Total 42 (93) 16 (36) 39 (91) 21 (49) 82 (92) 37 (42) Nausea 12 (27) 3 (7) 12 (28) 2 (5) 24 (27) 5 (6) Diarrhea 14 (31) 0 8 (19) 0 23 (26) 0 Fatigue 9 (20) 1 (2) 12 (28) 2 (5) 22 (25) 3 (3) Retinopathy 14 (31) 0 7 (16) 0 21 (24) 0 Vomiting 7 (16) 1 (2) 7 (16) 0 15 (17) 1 (1) Blood CPK increased 11 (24) 1 (2) 3 (7) 0 14 (16) 1 (1) Pyrexia 5 (11) 1 (2) 6 (14) 0 11 (12) 1 (1) Abdominal Pain 7 (16) 0 3 (7) 0 10 (11) 0 Anemia 4 (9) 1 (2) 6 (14) 3 (7) 10 (11) 4 (5) Vision blurred 5 (11) 0 4 (9) 0 9 (10) 0 Data cutoff date: July 1, *CPK Creatine phosphokinase; QD Once Daily; BID Twice Daily Clinical trial number NCT

11 Published MEK/BRAF Data in BRAF-Mutant Melanoma Safety Profile & Clinical Activity 11 Novartis COMBI-D Trametinib + Dabrafenib 1 n=209 Novartis COMBI-V Trametinib + Dabrafenib 2 n=350 Roche cobrim Cobimetinib + Vemurafenib 3 n=247 Fever 52% 55% 28% Rash 24% 24% 16% Select Adverse Events of Interest Diarrhea 18% 34% 60% Chills 28% 33% 10% Hypertension 10% 29% 15% Photosensitivity NR (<10%) 4% 46% NR = Not Reported COMBI-D n=210 COMBI-V n=251 cobrim 4 n=247 ORR* (CR + PR) BRAFi-Naïve 69% 66% 70% 1 Long et al ASCO Oral 2015; 2 ESMO/ECC 2015; 3 Product label; 4 Larkin et. al. ASCO Oral 2015 *ORR = Overall Response Rate (Complete Response (CR) + Partial Response Rate (PR)

12 New Trial SECOMBIT/Sequential Combo Immuno and Target Therapy Study 12 One of the most comprehensive studies assessing sequencing strategies for targeted and immunotherapies in BRAF-mutant melanoma Evaluate best sequencing approach with combination of target agents (encorafenib + binimetinib) and the combination of immunomodulatory antibodies (ipilimumab + nivolumab) in patients with BRAF-mutant melanoma Multicenter, international cooperative group trial: Clinical Research Technology and Fondazione Melanoma Onlus; supported jointly by Bristol-Myers Squibb and Array (via Novartis) Binimetinib + Encorafenib Progression Ipilimumab + Nivolumab Patients with BRAF- Mutant Melanoma Randomization Ipilimumab + Nivolumab Progression Binimetinib + Encorafenib n=230 Binimetinib + Encorafenib 2 Cycles Ipilimumab + Nivolumab Progression Binimetinib + Encorafenib Primary Endpoint: Overall survival (OS) Key Secondary Endpoint: Progression free survival (PFS)

13 Encorafenib Metastatic Colorectal Cancer (mcrc)

14 Encorafenib Phase 2 BRAF-Mutant mcrc Encouraging Clinical Activity 14 Historically, response rates are very low for either single-agent EGFR or RAF inhibitor therapy in patients with BRAF-mutant metastatic colorectal cancer (mcrc). Data in this study suggest a synergistic effect for the combination of encorafenib and cetuximab in this population. Encorafenib + Cetuximab n=42 Encorafenib + Alpelisib (BYL719, PI3K Inhibitor) + Cetuximab (EGFR Inhibitor) n=49 Evaluable Patients a Partial Response Rate (PR) 11 (29%) b 15 (35%) c Stable Disease (SD) 20 (53%) 19 (44%) Progressive Disease (PD) 1 (3%) 3 (7%) Unknown 6 (16%) 6 (14%) Overall Response Rate (ORR) 11 (29%) b 15 (35%) c Disease Control Rate (DCR) 31 (82%) 34 (79%) Data cutoff date: May 22, 2015 * Evaluable patients had a tumor assessment at 12 week visit or later and/or started treatment 13 weeks prior to data cutoff; b Includes four unconfirmed PRs; c Includes five unconfirmed PRs. CR and PR were confirmed by repeat assessments performed four weeks after initial response

15 Encorafenib Phase 2 BRAF-Mutant Metastatic Colorectal Cancer Good Tolerability 15 Across all treatment groups, most AEs were Grade 1 or 2 Encorafenib + Cetuximab n=42 Encorafenib + Alpelisib + Cetuximab n=49 AE, n (%) All Grades Grade 3/4 All Grades Grade 3/4 Total 37 (88%) 12 (29%) 46 (94%) 24 (49%) Diarrhea 9 (21%) 1 (2%) 19 (39%) 4 (8%) Nausea 13 (31%) 0 18 (37%) 3 (6%) Fatigue 15 (36%) 0 16 (33%) 3 (6%) Hyperglycemia 1 (2%) 0 15 (31%) 7 (14%) Rash 7 (17%) 0 13 (27%) 0 Stomatitis 4 (10%) 0 13 (27%) 2 (4%) Decreased Appetite 9 (21%) 0 11 (22%) 1 (2%) Pruritus 7 (17%) 0 11 (22%) 0 Dry Skin 5 (12%) 0 10 (20%) 0 Maculopapular Rash 1 ( 2%) 0 10 (20%) 2 (4%) Lipase Increased 10 (24%) 7 (17%) 4 ( 8%) 2 (4%) Data cutoff date: May 22, 2015.

16 Published BRAF in BRAF-Mutant Metastatic Colorectal Cancer Safety Profile & Clinical Activity 16 Doublet Therapy Panitumumab + Dabrafenib a Novartis Phase 2 n=20 Triplet Therapy Panitumumab + Dabrafenib + Trametinib a Novartis Phase 2 n=35 No Doublet Included Triplet Therapy Cetuximab + Vemurafenib + Irinotecan b Roche Phase 1 n=18 ORR (CR + PR)* 10% 26% 35% Fatigue 45% 51% 94% Select Adverse Events of Interest Nausea 40% 49% 83% Diarrhea 45% 77% 89% Rash 30% 37% 78% Pyrexia 40% 46% Not reported a ESMO GI 2015; b ASCO 2015; Panitumumab: EGFR inhibitor, dabrafenib: RAF inhibitor, trametinib: MEK inhibitor Cetuximab: EGFR inhibitor, vemurafenib: RAF inhibitor, irinotecan: Cytotoxic *ORR (CR + PR) Overall response rate (complete response rate + partial response rate)

17 Strategic Collaboration with Pierre Fabre Oncology

18 Strategic Collaboration with Pierre Fabre Oncology Selection Criteria & Summary of Deal Terms 18 Array s Selection Criteria for Strong European Commercial Partner was Met by Pierre Fabre Company with Europe as leading geographic priority with robust emerging market capability to provide scale to collaboration Company with significant footprint in Oncology Development, Sales & Marketing Company willing to commit significant resources to ensure binimetinib and encorafenib success Company providing robust downstream economics (royalties) for ready-to-file products The agreement was reviewed and approved by the European Commission on Competition in December 2015 Benefits to Array $30 million upfront 40% funding for certain future clinical development Up to $425 million in potential development and commercialization milestones Robust, tiered double-digit royalties Commercialization Rights Array retains exclusive rights in: United States Canada Japan Korea Israel Pierre Fabre will have exclusive rights in all other geographies, including Europe, Asia and Latin America

19 Selumetinib Neurofibromatosis Type 1/ Plexiform Neurofibromas

20 No Standard Medical Therapies for Patients with NF1/PN 20 Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder that can cause tumors to grow on nerves throughout the body Most tumors are inoperable NF1 may lead to blindness, bone abnormalities, cancer, deafness, disfigurement, learning disabilities and excruciating and disabling pain Plexiform neurofibromas (PN) exhibit the most rapid growth in young children Early intervention in children with growing PNs may result in the greatest clinical benefit NF affects one in every 3,000 individuals; 100,000 in the U.S. NF affects more than cystic fibrosis, Duchenne muscular dystrophy and Huntington s disease combined 3 Years 5 Years PN Limits Mobility of Left Arm

21 Selumetinib & Other Agents Studied in Phase 2 PN Selumetinib Is Only Agent With No Progression 21 Selumetinib offers a promising future for the development of effective medical therapies for neurofibromatosis type 1 (NF1) related plexiform neurofibromas (PNs) Presented June 2015 Median Time to Progression

22 Selumetinib in NF1 Pediatric Patients PR Seen in 67% of Patients 22 All neurofibromatosis type 1 (NF1) patients remained on treatment Partial Response (PR)* 67% (16 out of 24) Progressive Disease (PD)* 0% Common Adverse Events (AEs) Acneiform rash, asymptomatic CK elevation, GI; all toxicities reversible Median Cycle (1 Cycle = 28 Days) 18 (6-43) Other Observations Improvement in function Reduction in PN related pain and disfigurement *PR and PD Defined by NCI investigators as a PN volumetric decrease of 20% using MRI

23 Neurofibromatosis Type 1/Plexiform Neurofibromas (NF1/PN) Pediatric Registration Study 23 Primary Objectives Achieved Phase 1 Dose Escalation Children 3-18 y/o with NF1 and inoperable PN n=24 Expansion Currently Enrolling Patients Pediatric Registration Study Children 2-18 y/o with NF1 and inoperable PN Selumetinib (25mg/m 2 /dose BID) n=50 Primary Endpoint: Confirmed response rate by volumetric MRI Secondary Endpoint: PRO: Pain, Quality of Life (QOL), function (all patients) Disfigurement: Photography (patients with visible PN) Function: All patients based on PN location Orbit, airway, motor, bladder, other PK, PD: Blood cytokines, BM cells All patients pre-selumetinib and on treatment Long term safety, bone mineral density, optic glioma ClinicalTrials.gov identifier: NCT

24 Immuno-Oncology Discovery Collaboration

25 Immunotherapy Small Molecule Opportunity 25 Axl Many targets from multiple target classes are implicated in the immunosuppressive state of the tumor microenvironment. Many targets are uniquely suited to small molecule approaches and not modulation by biotherapeutics Small molecule target modulation is underexplored in Immuno-Oncology CSF1R Collaborating with world-class scientific advisory board (SAB) and leading academic partners to pursue immuno-oncology programs SAB includes: Adapted from Cancers 2015, 7(2), Axl cancer cell Keith Flaherty (MGH) Ben Cravatt (TSRI) David McDermott (BIDMC) Doug Lauffenburger (MIT) Kwok- Kin Wong (DFCI/HMS) Kris Vaddi (Ex-InCyte) Jedd Wolchok (MSKCC) Forest White (MIT/Koch) Trevor Bivona (UCSF) Peter Hammerman (DFCI/HMS) Gregory Beatty (UPenn)

26 New Immuno-Oncology Preclinical Collaboration Enabling Novel Drug Target Prosecution in Immuno-Oncology 26 Multi-program immuno-oncology collaboration Partners Leveraging Array s capabilities and track record in small molecule drug discovery Medicinal Chemistry and Structure Enabled Drug Design Pharmacology, Pharmaceutics and Pharmacokinetics Target identification through chemical biology Leveraging Belfer s immuno-oncology expertise and connectivity to Dana-Farber Cancer Institute (DFCI) investigators, knowledge base and capabilities for Target identification and validation Novel preclinical models for immunotherapeutic drug assessment Tumor immune infiltrate profiling in clinical samples for mechanistic assessment and patient selection Array and DFCI scientists discovering innovative immunotherapies

27 ARRY-797 P38 Inhibitor for LMNA-Related Dilated Cardiomyopathy (DCM)

28 LMNA-Related Dilated Cardiomyopathy (DCM) 28 LMNA-related DCM is a rare, degenerative cardiovascular disease characterized by DCM diagnosis (ejection fraction <40%, dilated ventricle) Presence of mutations in lamin A/C gene Poor prognosis, ~70% of patients have death, major cardiac event or transplant by age 45 Events defined as cardio vascular (CV) death, heart transplant or major cardiac event LMNA-related DCM under-diagnosed due to infrequent genetic testing Presence of LMNA mutation does not currently change treatment practice Early/mid-stage patients: ACE inhibitors, beta blockers and diuretics Advanced patients: Pacemaker/defibrillator, heart transplant U.S. Prevalence Estimate Dilated Cardiomyopathy (DCM) ~250,000 patients Idiopathic DCM ,000 patients LMNA-DCM 6-8,000 patients Diagnosed <1,000

29 Rationale for ARRY-797 in Treatment of LMNA-Related Dilated DCM 29 Mechanical stress-induced apoptosis has been proposed as the mechanism underpinning DCM in lamin A/C deficient hearts p38 MAPK signaling regulates myocyte growth and survival in response to mechanical stress and has been implicated in cardiac dysfunction in laminopathies ARRY-797 is a potent inhibitor of p38 MAPK ARRY-797 normalizes left ventricular morphology and improves function in a LMNAN195K model of DCM Physician-sponsored single-patient IND indicated ARRY-797 treatment has been associated with cardiac function improvements and was well tolerated Nuclear Envelope RAC1 ARRY-797: p38 Inhibitor p53 MAPKAP-K2 and K3 Transcription factors Stress MLK1 MKK3, 6 p38 MAPK p38 MAPK CDC42 RNA binding proteins DNA Transcription/Translation ATF2 Fax Extracellular Cytoplasm LMNA Genetic Mutation MEF2 Bax Stress Apoptotic/Survival Pathways and Cardiomyocyte Remodeling Factors

30 ARRY-797 Proof-of-Concept Trial LMNA-Related Dilated Cardiomyopathy (DCM) 30 LMNA-Related DCM Patients n=12 ARRY-797 (Dose 1) ARRY-797 (Dose 2) Crossover from lower to higher dose allowed for inadequate response Primary Endpoints: Change from baseline in 6-minute walk test (12 weeks) Secondary Endpoints Measures of left and right ventricular function Ejection fraction (Imaging study directly measures cardiac function); fractional area shortening Circulating biomarkers of cardiac function N-Terminal pro-brain Derived Natriuretic Peptide: Blood test that indirectly measures cardiac wall stress and severity and prognosis in cardiac failure Disease specific patient reported outcomes: Measures patient perception of improvement in functional status Others Trial Sites: Brigham and Women s Hospital/Harvard, Johns Hopkins University, Meriter Wisconsin Heart, University of Colorado, Ohio State University, Stanford University *6MWT: Integrated assessment of cardiac, respiratory, circulatory, and muscular capacity that has served as a basis for regulatory approvals of a number of drugs across therapeutic areas including cardiovascular diseases

31 Compared with Historical Benchmarks, Encouraging Data Emerging from Ongoing Phase 2 Trial 31 Product Company Indication FDA Approved 6MWT: Mean Change vs. Baseline (Absolute Meters) ARRY-797 Array LMNA-DCM No Bosentan Actelion PAH Yes Idursulfase Shire MPS II Yes ARRY-797 absolute mean improvement in 6MWT at 12 weeks is encouraging and suggests a path forward when benchmarked against drugs approved based on 6MWT Riociguat Bayer CTEPH & PAH Yes Elosulfase Alfa BioMarin MPS IVA Yes Ambrisentan Gilead PAH Yes Laronidase Genzyme MPS I Yes ARRY-797 secondary endpoint measures also suggest encouraging activity (NT-proBNP, patient reported outcomes) Patient experience out to 48 weeks continues to be encouraging Meters

32 Value Drivers

33 Array Product Portfolio 2016 Value Drivers 33 Indication(s) Status 1H H 2016 BRAF Melanoma (COLUMBUS) (binimetinib+encorafenib) Phase 3 COLUMBUS Part 1 Results Regulatory Submission Binimetinib & Encorafenib NRAS Melanoma (NEMO) (binimetinib) LGS Ovarian (MILO) (binimetinib) Phase 3 Phase 3 Regulatory Submission NEMO Publication Complete Enrollment BRAF Colorectal Cancer (CRC) (Encorafenib+other agent(s) Phase 2/3 Phase 2 BRAF CRC Update Phase 3 global registration trial (start date TBA) Selumetinib NSCLC (SELECT-1) Thyroid Cancer (ASTRA) NF1 Phase 3 Registration trial SELECT-1 Top-Line Results Enrollment Ongoing Enrollment Ongoing ARRY-797 LMNA-related DCM Phase 2 Trial Ongoing MILO: MEK Inhibitor in Low Grade Serous Ovarian Cancer; NEMO: NRAS melanoma and MEK inhibitor; COLUMBUS: Combination of LGX818 used with MEK162 in BRAF mutant unresectable skin cancer; ASTRA: Pivotal trial in differentiated thyroid cancer; SELECT-1: selumetinib + docetaxel in patients with KRAS NCSLC

34 Thank You arraybiopharma.com