J.P. Morgan 34thAnnual Healthcare Conference

J.P. Morgan 34thAnnual Healthcare Conference

J.P. Morgan 34thAnnual
Healthcare Conference
Ron Squarer
Chief Executive Officer
JANUARY 13, 2016
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.
2
Array’s Top Priority
3
Binimetinib & Encorafenib Development & Commercialization
SIGNIFICANT PROGRESS IN 2015
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)
…WITH IMPORTANT VALUE DRIVERS AHEAD IN 2016
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
NEMO
Meets Primary Endpoint
NRAS-Mutant Melanoma
JANUARY 13, 2016
Binimetinib Phase 3 Study
5
NEMO Meets Primary Endpoint
 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
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.
 PFS, overall survival (OS), overall response rate (ORR), safety
 Prespecified subgroup analyses including outcomes in patients who
received prior treatment with immunotherapy
JANUARY 13, 2016
Binimetinib + Ribociclib – 28-Day Regimen
6
Promising Preliminary Clinical Activity in NRAS-Mutant Melanoma
All 28-Day
Regimen Patients
n=22
All 21-Day
Regimen Patients
n=23
22
22
0
0
Partial Response Confirmed
5 (23)
3 (14)
PR Unconfirmed
4 (18)
1 (5)
Stable Disease (SD)
9 (41)
11 (50)
Progressive Disease
3 (14)
4 (18)
1 (5)
3 (14)
9 (41)
4 (18)
18 (82)
15 (68)
6.7
4
Response
n (%)
Evaluable Patients
Complete Response
Unknown
Overall Response Rate (ORR)a
Disease Control Rate
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)
aRate includes unconfirmed CR/PR
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
 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
JANUARY 13, 2016
LOGIC2/SECOMBIT
BRAF-Mutant Melanoma
JANUARY 13, 2016
LOGIC2 – Binimetinib + Encorafenib + Third Agent
8
BRAF-Mutant Melanoma Study Design
Patient Enrollment
on-going n=140
Part 1
n=89 as of 7/1/15
GROUP A
GROUP A
BRAF- and MEK-naïve patients
Binimetinib + Encorafenib
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
Part 2
n=20 as of 7/1/15
Binimetinib + Encorafenib + LEE011
(CDK 4/6 inhibitor)
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)
JANUARY 13, 2016
LOGIC2 – Binimetinib + Encorafenib Part 1
9
Encouraging Preliminary Clinical Activity
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)
Complete Response (CR)2
79%
(Note: 96% of patients continued to receive study treatment as of data cutoff)
3% (1)
Partial Response (PR)2
65% (26)
Stable Disease (SD)
28% (11)
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
– Once Daily; †BID – Twice Daily
Clinical trial number NCT02159066
*QD
JANUARY 13, 2016
LOGIC2 – Binimetinib + Encorafenib Part 1
10
Good Tolerability
Differentiated Safety: 12% pyrexia, 7% rash and no photosensitivity
Phase 2
(as of 7/1/15)
AE, n (%)
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
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, 2015.
*CPK – Creatine phosphokinase; †QD – Once Daily; ‡BID – Twice Daily
Clinical trial number NCT02159066
JANUARY 13, 2016
Published MEK/BRAF Data in BRAF-Mutant Melanoma
11
Safety Profile & Clinical Activity
Novartis – COMBI-D
Trametinib +
Novartis – COMBI-V
Trametinib +
Dabrafenib2
Roche – coBRIM
Cobimetinib + Vemurafenib3
n=209
n=350
n=247
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%
COMBI-D n=210
COMBI-V n=251
coBRIM4 n=247
69%
66%
70%
Select Adverse
Events of Interest
NR = Not Reported
ORR* (CR + PR)
Dabrafenib1
BRAFi-Naïve
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)
JANUARY 13, 2016
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
Patients with BRAFMutant Melanoma
Randomization
Ipilimumab + Nivolumab
Progression
Progression
Ipilimumab + Nivolumab
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)
JANUARY 13, 2016
Encorafenib
Metastatic Colorectal Cancer (mCRC)
JANUARY 13, 2016
Encorafenib Phase 2 BRAF-Mutant mCRC
14
Encouraging Clinical Activity
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
Evaluable Patientsa
Encorafenib + Alpelisib (BYL719, PI3K Inhibitor)
+ Cetuximab (EGFR Inhibitor)
n=49
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
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; bIncludes four unconfirmed PRs; cIncludes five unconfirmed PRs. CR and PR were confirmed by
repeat assessments performed ≥ four weeks after initial response
JANUARY 13, 2016
Encorafenib Phase 2 BRAF-Mutant Metastatic Colorectal Cancer
Good Tolerability
Across all treatment groups, most AEs were Grade 1 or 2
AE, n (%)
Encorafenib + Cetuximab
Encorafenib + Alpelisib + Cetuximab
n=42
n=49
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%)
10 (24%)
7 (17%)
4 ( 8%)
2 (4%)
Lipase Increased
Data cutoff date: May 22, 2015.
JANUARY 13, 2016
15
Published BRAF in BRAF-Mutant Metastatic Colorectal Cancer
Safety Profile & Clinical Activity
Triplet Therapy
Panitumumab + Dabrafenib
+ Trametiniba
Novartis – Phase 2
n=35
10%
26%
35%
Fatigue
45%
51%
94%
Nausea
40%
49%
83%
Diarrhea
45%
77%
89%
Rash
30%
37%
78%
Pyrexia
40%
46%
Not reported
ORR (CR + PR)*
Select
Adverse
Events of
Interest
Triplet Therapy
Cetuximab + Vemurafenib
+ Irinotecanb
Roche – Phase 1
n=18
Doublet Therapy
Panitumumab + Dabrafeniba
Novartis – Phase 2
n=20
No Doublet
Included
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)
JANUARY 13, 2016
16
Strategic Collaboration
with Pierre Fabre Oncology
JANUARY 13, 2016
Strategic Collaboration with Pierre Fabre Oncology
18
Selection Criteria & Summary of Deal Terms
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
JANUARY 13, 2016
Selumetinib
Neurofibromatosis Type 1/
Plexiform Neurofibromas
JANUARY 13, 2016
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.
3 Years
 NF affects more than cystic fibrosis, Duchenne muscular dystrophy and
Huntington’s disease combined
5 Years – PN Limits Mobility of Left Arm
JANUARY 13, 2016
Selumetinib & Other Agents Studied in Phase 2 PN
21
Selumetinib Is Only Agent With No Progression
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
JANUARY 13, 2016
Selumetinib in NF1 Pediatric Patients
22
PR Seen in 67% of Patients
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
JANUARY 13, 2016
Neurofibromatosis Type 1/Plexiform Neurofibromas
(NF1/PN) Pediatric Registration Study
Primary Objectives Achieved
Currently Enrolling Patients
Phase 1 Dose Escalation
Pediatric Registration Study
Children 3-18 y/o with NF1 and inoperable PN
n=24
Expansion
23
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: NCT01362803
JANUARY 13, 2016
Immuno-Oncology
Discovery Collaboration
JANUARY 13, 2016
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:
Axl
CSF1R
Axl
cancer cell
Adapted from Cancers 2015, 7(2), 736-762
25











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)
JANUARY 13, 2016
New Immuno-Oncology Preclinical Collaboration
26
Enabling Novel Drug Target Prosecution in Immuno-Oncology
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
JANUARY 13, 2016
ARRY-797
P38 Inhibitor for LMNA-Related Dilated
Cardiomyopathy (DCM)
JANUARY 13, 2016
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
28
U.S. Prevalence Estimate
Dilated Cardiomyopathy (DCM)
~250,000 patients
Idiopathic DCM
120-150,000 patients
LMNA-DCM
6-8,000 patients
Diagnosed
<1,000
 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
JANUARY 13, 2016
Rationale for ARRY-797 in Treatment of LMNA-Related Dilated
DCM
Stress
 Mechanical stress-induced apoptosis
has been proposed as the
mechanism underpinning DCM in
lamin A/C–deficient hearts
Cytoplasm
RAC1
 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
CDC42
MLK1
 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
Extracellular
MKK3, 6
p38 MAPK
ARRY-797:
p38 Inhibitor
LMNA
Genetic
Mutation
Stress
p38 MAPK
Nuclear Envelope
Transcription
factors
RNA binding
proteins
DNA Transcription/Translation
p53
ATF2
MEF2
MAPKAP-K2
and K3
Fax
Bax
Apoptotic/Survival Pathways and
Cardiomyocyte Remodeling Factors
JANUARY 13, 2016
29
ARRY-797 Proof-of-Concept Trial
30
LMNA-Related Dilated Cardiomyopathy (DCM)
ARRY-797
(Dose 1)
LMNA-Related
DCM Patients
n=12
Crossover from lower to higher dose
allowed for inadequate response
ARRY-797
(Dose 2)
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
JANUARY 13, 2016
Compared with Historical Benchmarks, Encouraging Data
Emerging from Ongoing Phase 2 Trial
Product
Company
Indication
FDA
Approved
LMNA-DCM
No
PAH
Yes
ARRY-797
Array
Bosentan
Actelion
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
6MWT: Mean Change vs. Baseline (Absolute 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
0
10
20
30
40
50
Meters
ARRY-797 secondary endpoint measures also suggest encouraging activity (NT-proBNP, patient reported
outcomes)
Patient experience out to 48 weeks continues to be encouraging
JANUARY 13, 2016
31
Value Drivers
JANUARY 13, 2016
Array Product Portfolio
33
2016 Value Drivers
Indication(s)
BRAF Melanoma
(COLUMBUS)
Status
1H 2016
2H 2016
COLUMBUS Part 1 Results
Phase 3
Regulatory Submission
(binimetinib+encorafenib)
Binimetinib &
Encorafenib
NRAS Melanoma
(NEMO)
Regulatory Submission
Phase 3
(binimetinib)
LGS Ovarian
(MILO)
Phase 3
NEMO Publication
Complete Enrollment
(binimetinib)
BRAF Colorectal Cancer
(CRC)
Phase 2 BRAF CRC Update
Phase 2/3
(Encorafenib+other agent(s)
NSCLC
(SELECT-1)
Selumetinib
Thyroid Cancer
(ASTRA)
NF1
ARRY-797
LMNA-related DCM
Phase 3 global registration trial (start date TBA)
SELECT-1 Top-Line Results
Phase 3
Enrollment Ongoing
Registration trial
Enrollment Ongoing
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
JANUARY 13, 2016
Thank You
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