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2

Sep 2012 License
•
TGFβ family protein modulators
•
Seven product candidates
Clinical Stage Programs
PINTA
745
Ph 2
STM
434
Ph 1
T-cell
EBV¹
Ph 2
T-cell
CMV²
Ph 2
T-cell
WT1³
Ph 1
¹ EBV = Epstein-Barr virus
² CMV = cytomegalovirus
³ WT1 = Wilms tumor 1
Sep 2014 Option
•
T-cell immunotherapies
•
Platform to develop additional product candidates
3

PINTA 745
4

Phase 2 Program with
Established Proof of
Concept (POC)
PINTA 745
•
Blocks myostatin, preventing it from inhibiting muscle production
•
Improved lean body mass, physical function, inflammation in CKD¹ model
•
Statistically significantly increased lean body mass and lower extremity muscle size in randomized, blinded Phase 1 study in prostate cancer; acceptable safety
Attractive Market
•
PEW – state of muscle wasting, inflammation, malnutrition in ESRD; no approved therapies
•
Decreased physical function, increased morbidity and mortality
•
~250K patients in US² and 800K worldwide
Upcoming Milestone
•
Randomized, blinded, placebo controlled Phase 2 trial (48 PEW patients)
•
Phase 2 data expected in 4Q:15
¹ CKD = chronic kidney disease
² Calculated utilizing 2011 data from USRDS extrapolated to December 31, 2013 as well as data from the recent study completed with DaVita Clinical Research
5

POC
8%
6%
4%
2%
0%
(2)%
(4)%
(6)%
Lean Body Mass Increase
N = 19 19 18 19
3.0 mg/kg PINTA 745 Placebo
• ~2% greater in lean body mass at EOS
• Difference in lean body mass compared to placebo continued to increase in 4 weeks after treatment (FUP)
PINTA 745
Lower Extremity Muscle Size Increase
18 19
4%
2%
0%
(2)%
(4)%
12%
10%
8%
6%
(6)%
N = 18
P=0.065
19
EOS
3.0 mg/kg PINTA 745
FUP
Placebo
P=0.007
• At EOS, muscle size increased by ~1.2% from baseline
• At FUP, the change from baseline increased to 2.7%
Source: Padhi et al., 2014. Pharmacological inhibition of myostatin and changes in lean body mass and lower extremity muscle size in patients receiving androgen deprivation therapy for prostate cancer. J Clin Endocrinol Metab 99(10):E1967
Note: The bottom and top of the boxes represent the first and third quartiles, and the horizontal band inside the box indicates the median value. The ends of the whiskers represent the minimum and maximum data in the range of observations
Note: EOS: end-of-study (at day 29); FUP: Follow-up Period (one month after day 29)
¹ ADT = androgen deprivation therapy
6

Survival Rates Based Upon Serum Albumin Levels
100%
80%
60%
40%
20%
Results at one year: ~11% of
PEW¹ patients died within one year compared to < 3% of non-
PEW patients
At three years: ~40% of PEW patients died in comparison with
~21% of non-PEW patients
0%
0 200 400 600 800 1000
Days from Entry into Database
Serum Albumin ≤ 3.8 g/dL Serum Albumin > 3.8 g/dL
1200
•
54% of dialysis patients suffer from PEW 1
•
Large unmet need; ~250,000 2 US; ~800,000 Worldwide
1
2
Based on a recent study we completed with DaVita Clinical Research, a division of DaVita Healthcare Partners Inc.
Calculated utilizing 2011 data from USRDS extrapolated to December 31, 2013 as well as data from the recent study completed with DaVita Clinical Research
PINTA 745
7

PINTA 745
Ctrl CKD
Received from William E. Mitch, Baylor College of Medicine, M.D.
Myostatin is Over-Expressed in CKD
60
56
52
* P<0.05
Mice…
*
160
150
140
130
120
110
…and PINTA 745/s Has a Demonstrated
Ability to Increase Body Weight…¹
* P<0.05
*
48
Placebo PINTA 745/s
Placebo PINTA 745/s
…Increase Protein Synthesis…¹ …Limit Protein Degradation…¹
¹ Based on a preclinical study conducted with Amgen (Zhang L & Mitch WE, FASEB J.
2011)
TNF -
α
.2
.175
.15
.125
.1
.075
.05
.025
0
P=0.033*
Placebo PINTA 745/s
IL - 6
P=0.036*
Placebo PINTA 745/s
4
2
8
6
0
14
12
10
…and Reduce Inflammation¹
8

PINTA 745
Phase 2 Data Expected 4Q:15
Phase 2 Trial in ESRD Patients with PEW
2014 2015 2016+
• Randomized, double-blind, placebo-controlled trial in 48 patients
• Primary endpoint – change in muscle mass
• Secondary endpoints – physical function, monitoring of inflammatory markers, effects on use of supportive care drugs, QOL¹ assessments
• Clinical Update
• No treatmentrelated serious adverse events, grade ≥ 3 adverse events
• Initial regimen safe and well tolerated
• Study enrollment ongoing
¹ QOL = Quality of Life
9

10

Pathway to
Commercialization
Sponsored
Research
Ongoing and
Planned POC
Studies
• Allogeneic, cellular therapy platform technology developed by MSK
• Exclusive Option to license 3 clinical T-cell programs targeting some viral or cancer antigens
• Collaborate on further research to discover additional cellular therapies
• Leverage existing technology to target other antigens
• Develop additional cellular therapies and / or CAR-T cell programs
11

• “Off-the shelf” cellular therapeutic option for patients
• Manufacturing process designed to reduce risk of product-related GvHD¹
• MSK has developed libraries of EBV, CMV, and WT1 activated cell lines
MANUFACTURE 1
T-cells from
Donor Blood
2
Antigen exposure, expansion and characterization
EBV - CTLs
3
Targeted Tcell Banks
1
THERAPEUTIC
USE
1 GvHD = graft versus host disease
² HLA = human Leukocyte Antigen
Cancer or
Viral Infection
2
Blood Test:
HLA² Typing
3
Off-the-shelf
T-cell Doses
12

Current Treatment Approach
If Rituximab Failure
1 2
EBV - CTLs
3
EBV Reactivation:
Lymphoma
EBV-LPD Standard Rx: e.g., Rituximab
Rituximab (anti-CD20 Ab) is often used off-label as 1 st line therapy;
Historical survival in rituximab refractory patients median 16-56 days 1
Off-the-shelf EBV-Targeted
T-cell Doses
Time Course of a Complete Response Following Administration of EBV Targeted T-cell 2
¹ Prockop, S et al., Proc AACR (2015), Fox 2014, Ocheni 2008, Uhlin 2014
2 MSK Data on file
13

EBV - CTLs
•
•
rd
•
rd
•
•
•
14

Response Rate (RR): Primary vs. 3 rd party Donor
EBV - CTLs
2015 ASCO Presentation
Overall Survival: Rituximab Refractory
Patients Treated with 3 rd party EBV-CTL
EBV-CTL Source N
Prior
Rituximab RR
2 DCR 2 Study 11-130
Primary Donor 3 26 13 62% 69%
3 rd Party Donor 4 34 34 65% 70%
1 year OS = 71.8%
2 year OS = 63.8%
N = 22
• RR with primary HCT and 3rd party donor comparable
• RR in rituximab treated patients similar to overall RR
• Complete and partial responses were durable & led to the overall survival results observed
• Well tolerated, few serious related AEs; no cytokine release, 1 grade 1 GvHD resolved without systematic therapy
Study 95-024
1 year OS = 56.3%
2 year OS = 46.9%
N = 12
• Historical survival in rituximab refractory patients median
16-56 days
¹ Prockop, S et al., Proc AACR (2015), Prockop, S et al., Proc ASCO (2015), Based on results from two clinical trials of EBV-CTL conducted by MSK
2 RR = complete response + partial response; DCR = Disease control rate = complete response + partial response + stable disease
3 Prockop, S et al., Proc AACR (2015)
4 Prockop, S et al., Proc ASCO (2015), Includes 22 patients from Study 11-130 plus 11 patients from Study 95-024 plus one patient treated under a treatment IND
15

Response Rate (RR): EBV-LPD after SOT
EBV-CTL Source N
Prior
Rituximab
Prior
Chemo
3 rd Party Donor 13 13 11
RR 2
62%
Note: All patients had failed to respond or relapsed following rituximab treatment; 11 SOT recipients also progressed after 1-5 courses of rituximab and chemotherapy
OS in Rituximab Refractory EBV-LPD after SOT following treatment with 3rd party EBV-CTL
Results
• Response Rate (RR) for SOT of 62% is similar to RR for HCT
• 1 durable CR (>22mo) and 7 durable PRs (range: 6-114 mo) in heavily pre-treated patients
• 12 of the 13 patients had high risk disease 3 (Age ≥ 60 years; poor performance status; elevated LDH)
• Overall Survival (OS) of 58% at 2 years compares favorably with historical data
Historical Data 3
• Historical data show 33% OS at 2 years in patients with incomplete response to rituximab
• Historical data show 0% OS at 2 years in patients with high risk disease
¹ Prockop, S et al., Proc ASCO (2015), Based on results from two clinical trials of EBV-CTL conducted by MSK
2
3
RR = complete response + partial response
Choquet et al., 2007
16

Current Treatment Approach
If Treatment Failure or Intolerance
1 2 3
CMV - CTLs
CMV Reactivation:
Viremia or Disease
CMV Standard Rx: e.g., Ganciclovir or Foscarnet
Off-the-shelf CMV-Targeted
T-cell Doses
Responses Following Administration of CMV Targeted T-cells
25
Evaluable
Patients
Viremia Only 2
9
Complete Responses
7
Partial Responses
Response Rate = 64%
9
Evaluable
Patients
CMV Disease 3
5
Complete Responses
1
Partial Responses
Response Rate = 67%
Interim data presented at ASH 2014; No de novo GvHD or flare of pre-existing GvHD was noted
¹ Prockop, S et al., Proc ASH (2014), MSK (data on file)
2 Responses in patients treated for viremia alone were considered complete if the viremia resolved completely and partial if it fell by more than 100-fold
3 Responses in disease were considered complete if all detectable CMV viremia and disease resolved and partial if patients became asymptomatic
17

STM 434
18

Phase 1 Program with
Pre-clinical POC
STM 434
•
Inhibits Activin A, which is involved in proliferation of OC and other solid tumor
•
Reduced tumor size as single agent and with chemotherapy preclinically
•
Demonstrated efficacy in granulosa / clear cell preclinical models of
OC
•
Gene mutations in FOXL2 and ARID1A link Activin to granulosa and clear cell OC, respectively
Attractive Market
•
Opportunity for rapid development in difficult-to-treat clear and granulosa cell OC
•
Expansion opportunities in serous OC and other solid tumors
•
~22K new OC cases in 2013 in the US 1
Upcoming Milestone
¹ National Cancer Institute estimate
•
3 part Phase 1 ongoing including dose escalation, dose expansion, chemo combo
•
Initial Phase 1 data expected 1H:16
19

Improvement in Survival 1
STM 434
Right
Suppressed Tumor Growth
Ovarian Tumor Size
Normal Control
Treated with
Placebo
Inhibin Knockout
Treated with
Placebo
Inhibin Knockout
Treated with
STM 434/s
Left
• FOXL2 – granulosa cell tumor gene linkage 2
• In normal cells, FOXL2 protein turns on follistatin when activin signal received; shuts off activin signal
• In granulosa cell OC, mutant FOXL2 is not able to turn on follistatin; activin signals unchecked
• Mutation was present in 97% of granulosa cell tumors
¹ Zhou X, et al. Cell . 2010; 142(4):531-43
2 Shah S. P., et al. NEJM. 2009; 360: 2719-29
20

Significant Reduction in Tumor Volume¹ Enhanced Body Weight¹
STM 434
• ARID1A – clear cell tumor gene linkage 2
• ARID1A mutations drive upregulation in signaling cascade triggered by ActR2B receptor
• Mutations present in 46%-55% of ovarian clear cell tumors
• Increased activin levels, like ARID1A mutations, may contribute to clear cell tumor proliferation
¹ Lu J, Haqq C, & Han HQ. ASCO Annual Meeting (2013)
2 Wiegard., et al. NEJM. 2010; 363: 1532-43
21

First Patient Dosed 10/14; Initial Data Readout Expected 1H:16
Dose Escalation – in Solid Tumors
Monotherapy Dose Expansion – in OC
STM 434
Combo Chemotherapy – in OC
2014 2015 2016+
• Three part open-label Phase 1 study in up to 66 patients
• Objectives include:
• Evaluate whether STM 434 is safe and well tolerated
• Obtain preliminary efficacy data in ovarian cancer and other solid tumors
• Explore biomarkers predictive of response to treatment
• Define recommended Phase 2 dose
22

Validated Clinical
Programs
Attractive Markets
•
PINTA 745: Myostatin inhibitor for protein-energy wasting (PEW)
•
MSK T-Cell Programs: Option to license T-cell platform technology with 3 clinical stage, “off-the-shelf”, immune therapies; Breakthrough
Therapy Designation granted in February 2015 for EBV-CTL in patients with EBV-LPD
•
STM 434: Activin inhibitor for ovarian cancer and solid tumors
•
PEW: Increased morbidity / mortality; ~250K patients in the US¹ and
800K worldwide; no approved therapeutics
•
EBV-LPD (~1200 patients in US + EU³) and anti-viral drug resistant
CMV viremia or disease (~1100 patients in US + EU 4 ); potentially rapid path to approval
•
Ovarian Cancer (OC): One of the deadliest cancers in women in the
US; ~22K new cases in 2013 in the US 2 ; expansion opportunities in other solid tumors
Upcoming Milestones
•
PINTA 745: Phase 2 data in 4Q:15
•
EBV-CTL: Data presented at AACR Clinical Trials Plenary April 19, 2015
Oral presentation at ASCO June 1, 2015
•
MSK T-cell Programs: Data submitted to multiple conferences in 2015
•
STM 434: Phase 1 data in 1H:16
¹ Calculated utilizing 2011 data from USRDS extrapolated to December 31, 2013 as well as data from the recent study completed with DaVita Clinical Research
² National Cancer Institute estimate
4
³ Atara estimate based on the CIBMTR reports of number of HCT in the US in 2011 and a report in the journal Haematologica (2013)
Atara estimate based on investigator experience
23

June 2015