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(1)

J.P. Morgan 34

th

Annual

Healthcare Conference

Ron Squarer

(2)

Safe Harbor Statement

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 1995. 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)

3

Array’s Top Priority

Binimetinib & Encorafenib Development & Commercialization

…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)

SECOMBIT trial will address sequential use of MEK+RAF with

PD-1+CTLA4 in BRAF-mutant melanoma

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

(4)

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 0.47-0.80], p < 0.001

 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

Binimetinib Phase 3 Study

NEMO Meets Primary Endpoint

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

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)

aRate includes unconfirmed CR/PR

Response n (%) All 28-Day Regimen Patients n=22 All 21-Day Regimen Patients n=23 Evaluable Patients 22 22 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 6.7 4

Individual Patient Responses

 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

(7)

LOGIC2/SECOMBIT

(8)

8

LOGIC2 – Binimetinib + Encorafenib + Third Agent

BRAF-Mutant Melanoma Study Design

GROUP A

BRAF- and MEK-naïve patients

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 A

Binimetinib + Encorafenib

GROUP B Run-in Binimetinib + Encorafenib

GROUP C

Optional Binimetinib + Encorafenib Patient Enrollment

on-going n=140

Part 1 n=89 as of 7/1/15

After progressive disease, genetic assessment performed to

determine combination

Binimetinib + Encorafenib + LEE011 (CDK 4/6 inhibitor) Part 2 n=20 as of 7/1/15 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

(9)

9

Combination of binimetinib and encorafenib demonstrated encouraging preliminary clinical activity in

BRAFi/MEKi naïve patients

1ECC/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); 2Includes confirmed/unconfirmed responses; 3ORR=CR/PR, 4DCR=CR/PR or SD *QD – Once Daily; BID – Twice Daily

Clinical trial number NCT02159066

LOGIC2 – Binimetinib + Encorafenib Part 1

Encouraging Preliminary Clinical Activity

Phase 2 (as of 7/1/15)

Group A (MEKi + BRAFi Naïve)

Encorafenib 450mg QD* + Binimetinib 45mg BID† n=45

AE, n (%)

Binimetinib 45mg BID/Encorafenib 450mg QD 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)

(10)

10

Differentiated Safety: 12% pyrexia, 7% rash and no photosensitivity

Data cutoff date: July 1, 2015.

*CPK – Creatine phosphokinase; †QD – Once Daily; BID – Twice Daily

Clinical trial number NCT02159066

LOGIC2 – Binimetinib + Encorafenib Part 1

Good Tolerability

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

(11)

1Long et al ASCO Oral 2015; 2ESMO/ECC 2015; 3Product label; 4Larkin et. al. ASCO Oral 2015

*ORR = Overall Response Rate (Complete Response (CR) + Partial Response Rate (PR)

Published MEK/BRAF Data in BRAF-Mutant Melanoma

Safety Profile & Clinical Activity

11

Novartis – COMBI-D Trametinib + Dabrafenib1 n=209 Novartis – COMBI-V Trametinib + Dabrafenib2 n=350 Roche – coBRIM Cobimetinib + Vemurafenib3 n=247 Select Adverse Events of Interest Fever 52% 55% 28% Rash 24% 24% 16% 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 coBRIM4n=247

(12)

New Trial – SECOMBIT/Sequential Combo

Immuno and Target Therapy Study

12

Patients with BRAF-Mutant Melanoma

n=230

Ipilimumab + Nivolumab

Binimetinib + Encorafenib

Binimetinib + Encorafenib Progression

2 Cycles Progression Binimetinib + Encorafenib

Randomization

Ipilimumab + Nivolumab

Binimetinib + Encorafenib

Ipilimumab + Nivolumab

Primary Endpoint: Overall survival (OS)

Key Secondary Endpoint:Progression free survival (PFS)

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)

(13)

Encorafenib

(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.

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; bIncludes four unconfirmed PRs; cIncludes five unconfirmed PRs. CR and PR were confirmed by

repeat assessments performed ≥ four weeks after initial response

Encorafenib Phase 2 BRAF-Mutant mCRC

Encouraging Clinical Activity

14

Encorafenib + Cetuximab n=42

Encorafenib + Alpelisib (BYL719, PI3K Inhibitor) + Cetuximab (EGFR Inhibitor)

n=49

Evaluable Patientsa 38 43

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

(15)

15

Across all treatment groups, most AEs were Grade 1 or 2

Data cutoff date: May 22, 2015.

Encorafenib Phase 2 BRAF-Mutant Metastatic Colorectal Cancer

Good Tolerability

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%)

(16)

aESMO GI 2015; bASCO 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)

Published BRAF in BRAF-Mutant Metastatic Colorectal Cancer

Safety Profile & Clinical Activity

16

Doublet Therapy Panitumumab + Dabrafeniba Novartis – Phase 2 n=20 Triplet Therapy Panitumumab + Dabrafenib + Trametiniba Novartis – Phase 2 n=35 No Doublet Included Triplet Therapy Cetuximab + Vemurafenib + Irinotecanb Roche – Phase 1 n=18 ORR (CR + PR)* 10% 26% 35% Select Adverse Events of Interest Fatigue 45% 51% 94% Nausea 40% 49% 83% Diarrhea 45% 77% 89% Rash 30% 37% 78%

(17)

Strategic Collaboration

(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

Strategic Collaboration with Pierre Fabre Oncology

Selection Criteria & Summary of Deal Terms

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)

 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

20

No Standard Medical Therapies for Patients

with NF1/PN

3 Years

(21)

21

Selumetinib offers a promising future for the development of effective medical therapies for

neurofibromatosis type 1 (NF1) related plexiform neurofibromas (PNs)

Selumetinib & Other Agents Studied in Phase 2 PN

Selumetinib Is Only Agent With No Progression

Presented June 2015

(22)

22

All neurofibromatosis type 1 (NF1) patients remained on treatment

Selumetinib in NF1 Pediatric Patients

PR Seen in 67% of Patients

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 functionReduction in PN related pain and disfigurement *PR and PD – Defined by NCI investigators as a PN volumetric decrease of ≥20% using MRI

(23)

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

23

Neurofibromatosis Type 1/Plexiform Neurofibromas

(NF1/PN) Pediatric Registration Study

Primary Objectives Achieved

Currently Enrolling Patient

s

Phase 1 Dose Escalation

Children 3-18 y/o with NF1 and inoperable PN n=24

Pediatric Registration Study

Children 2-18 y/o with NF1 and inoperable PN Selumetinib

(25mg/m2/dose BID) n=50

Expansion

(24)

Immuno-Oncology

(25)

25

Immunotherapy – Small Molecule Opportunity

 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

 Collaborating with world-class scientific advisory board (SAB) and leading academic partners to pursue

immuno-oncology programs

 SAB includes:

 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) Axl

Axl

cancer cell

Adapted from Cancers 2015, 7(2), 736-762

(26)

Multi-program immuno-oncology collaboration

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

26

New Immuno-Oncology Preclinical Collaboration

Enabling Novel Drug Target Prosecution in Immuno-Oncology

(27)

ARRY-797

P38 Inhibitor for LMNA-Related Dilated

Cardiomyopathy (DCM)

(28)

LMNA-Related Dilated Cardiomyopathy (DCM)

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

28

Dilated Cardiomyopathy (DCM) ~250,000 patients Idiopathic DCM 120-150,000 patients Diagnosed <1,000

U.S. Prevalence Estimate

LMNA-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

29

Rationale for ARRY-797 in Treatment of LMNA-Related Dilated

DCM

Cytoplasm Extracellular

Stress

Apoptotic/Survival Pathways and

RAC1 CDC42 MLK1 p38 MAPK MKK3, 6 ARRY-797: p38 Inhibitor LMNA Genetic Mutation Stress Nuclear Envelope DNA Transcription/Translation p38 MAPK RNA binding proteins p53 MAPKAP-K2 and K3 ATF2 Fax MEF2 Bax Transcription factors

(30)

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

30

ARRY-797 Proof-of-Concept Trial

LMNA-Related Dilated Cardiomyopathy (DCM)

Crossover from lower to higher dose allowed for inadequate response

LMNA-Related DCM Patients n=12 ARRY-797 (Dose 1) ARRY-797 (Dose 2)

(31)

31

ARRY-797 secondary endpoint measures also suggest encouraging activity (NT-proBNP, patient reported

outcomes)

Patient experience out to 48 weeks continues to be encouraging

Compared with Historical Benchmarks, Encouraging Data

Emerging from Ongoing Phase 2 Trial

Product Company Indication ApprovedFDA

ARRY-797 Array LMNA-DCM No

Bosentan Actelion PAH Yes

Idursulfase Shire MPS II Yes

Riociguat Bayer CTEPH & PAH Yes

Elosulfase Alfa BioMarin MPS IVA Yes

Ambrisentan Gilead PAH Yes

Laronidase Genzyme MPS I Yes

0 10 20 30 40 50 Meters

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

(32)
(33)

Indication(s) Status 1H 2016 2H 2016 Binimetinib & Encorafenib BRAF Melanoma (COLUMBUS) (binimetinib+encorafenib)

Phase 3 COLUMBUS Part 1 Results

Regulatory Submission

NRAS Melanoma (NEMO)

(binimetinib)

Phase 3 Regulatory Submission

NEMO Publication

LGS Ovarian (MILO)

(binimetinib)

Phase 3 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)

Phase 3 Registration trial

SELECT-1 Top-Line Results

Thyroid Cancer

(ASTRA) Enrollment Ongoing

NF1 Enrollment Ongoing

ARRY-797 LMNA-related DCM Phase 2 Trial Ongoing

33

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

Array Product Portfolio

(34)

References

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