Isaac Ciechanover, MDFounder, President, & CEO

Jefferies Global Healthcare ConferenceJune 3, 2015

Proprietary Materials

Special Note Regarding Forward-Looking Statements

This presentation and the accompanying oral presentation contain forward-looking statements. All statements other than statements of historical facts contained in this presentation, including statements regarding our future results of operations and financial position, business strategy, product candidates, collaborations, regulatory approvals, the possible impact of accelerated approval and whether the receipt of breakthrough therapy designation will meaningfully impact review by the U.S. Food and Drug Administration or the likelihood that a product will be found to be safe and effective, our ability to sell, manufacture or otherwise commercialize our product candidates, research and development costs, the timing and likelihood of success, plans and objectives of management for future operations, any royalty payments, and our ability to obtain and maintain intellectual property protection for our product candidates, are forward-looking statements. These statements involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. These and other important risk factors are described more fully in documents filed by Atara with the Securities and Exchange Commission (SEC), including Atara’s annual report on Form 10-K for the year ended December 31, 2014. Because forward-looking statements are inherently subject to risks and uncertainties, some of which cannot be predicted or quantified and some of which are beyond our control, you should not rely on these forward-looking statements as predictions of future events. The events and circumstances reflected in our forward-looking statements may not be achieved or occur and actual results could differ materially from those projected in the forward-looking statements. Except as required by applicable law, we do not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information, future events, changed circumstances or otherwise.

Certain information contained in this presentation and statements made orally during this presentation relates to or is based on studies, publications, surveys and other data obtained from third-party sources and Atara's own internal estimates and research. While Atara believes these third-party studies, publications, surveys and other data to be reliable as of the date of this presentation, it has not independently verified, and makes no representation as to the adequacy, fairness, accuracy or completeness of, any information obtained from third-party sources. In addition, no independent source has evaluated the reasonableness or accuracy of Atara’s internal estimates or research and no reliance should be made on any information or statements made in this presentation relating to or based on such internal estimates and research.

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Foundation Built on World-Class Science

• T-cell immunotherapies• Platform to develop

additional product candidates

• TGF-β family protein modulators

• Seven product candidates

STM 434Ph 1

T-cell EBV¹Ph 2

T-cell CMV²Ph 2

T-cell WT1³Ph 1

PINTA 745Ph 2

Sep 2012 License Sep 2014 Option

3

Clinical Stage Programs

¹ EBV = Epstein-Barr virus² CMV = cytomegalovirus ³ WT1 = Wilms tumor 1

PINTA 745

Protein-Energy Wasting in End-Stage Renal Disease (ESRD)

PINTA 745

4

PINTA 745

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

PINTA 745: Potential First in Class Molecule for PEW

• 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

Phase 2 Program with Established Proof of

Concept (POC)

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

• Randomized, blinded, placebo controlled Phase 2 trial (48 PEW patients)

• Phase 2 data expected in 4Q:15Upcoming Milestone

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PINTA 745

Clinical POC in Patients with Prostate Cancer Receiving ADT¹

• ~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)

• At EOS, muscle size increased by ~1.2% from baseline

• At FUP, the change from baseline increased to 2.7%

Lean Body Mass Increase Lower Extremity Muscle Size Increase

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):E1967Note: 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 observationsNote: EOS: end-of-study (at day 29); FUP: Follow-up Period (one month after day 29)¹ ADT = androgen deprivation therapy

8%

6%

4%

2%

0%

(2)%

(4)%

(6)%

% o

f Bas

elin

e

N = 19 19 18 19

3.0 mg/kg PINTA 745 Placebo

12%

10%

8%

6%

4%

2%

0%

(2)%

(4)%

(6)%EOS FUP

% o

f Bas

elin

e

P=0.065 P=0.007

N = 18 19 18 19

3.0 mg/kg PINTA 745 Placebo

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PINTA 745

Increased Mortality in Patients with PEW

• 54% of dialysis patients suffer from PEW1

• Large unmet need; ~250,0002 US; ~800,000 Worldwide1 Based on a recent study we completed with DaVita Clinical Research, a division of DaVita Healthcare Partners Inc.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 7

At three years: ~40% of PEW patients died in comparison with ~21% of non-PEW patients

Results at one year: ~11% of PEW¹ patients died within one year compared to < 3% of non-PEW patients

0%

20%

40%

60%

80%

100%

0 200 400 600 800 1000 1200

Perc

enta

ge S

urvi

ving

Days from Entry into DatabaseSerum Albumin ≤ 3.8 g/dL Serum Albumin > 3.8 g/dL

Survival Rates Based Upon Serum Albumin Levels

PINTA 745

TNF - α IL - 6

…and Reduce Inflammation¹

Preclinical Proof of Concept in CKD Mice

CKDCtrl

Myostatin is Over-Expressed in CKD Mice…

…and PINTA 745/s Has a Demonstrated Ability to Increase Body Weight…¹

…Increase Protein Synthesis…¹ …Limit Protein Degradation…¹

Synt

hesi

s(n

mol

Phe

/g/h

r)

P<0.05*

*60

56

52

48Placebo PINTA 745/s

160

150

140

130

120

110Placebo

Degr

adat

ion

(nm

ol T

yr/g

/hr)

PINTA 745/s

P<0.05

*

*

pg/ m

l pg/ m

l

.2

.175

.15

.125

.1

.075

.05

.025

0Placebo PINTA 745/s

14

12

10

8

6

4

2

0Placebo PINTA 745/s

P=0.033*

P=0.036*

Received from William E. Mitch, Baylor College of Medicine, M.D.

¹ Based on a preclinical study conducted with Amgen (Zhang L & Mitch WE, FASEB J. 2011)8

PINTA 745

Ongoing Phase 2 Trial in ESRD Patients with PEW

Phase 2 Data Expected 4Q:15

• 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 treatment-related serious adverse events, grade ≥ 3 adverse events

• Initial regimen safe and well tolerated

• Study enrollment ongoing

2014 2015 2016+

Phase 2 Trial in ESRD Patients with PEW

9¹ QOL = Quality of Life

MSK – Collaboration

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• 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

Pathway toCommercialization

Ongoing and Planned POC

Studies

SponsoredResearch

Atara – MSK Collaboration Overview

MANUFACTURE

THERAPEUTIC USE

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Antigen exposure,

expansion and characterization

Targeted T-cell Banks

T-cells from Donor Blood

Cancer or Viral Infection

Blood Test:HLA² Typing

Off-the-shelf T-cell Doses

321

Platform Attributes• “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

1 GvHD = graft versus host disease² HLA = human Leukocyte Antigen

1 2 3

EBV - CTLs

Time Course of a Complete Response Following Administration of EBV Targeted T-cell 2

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Targeted T-Cell Therapy for EBV-LPD after HCT

Current Treatment Approach

EBV Reactivation:Lymphoma

EBV-LPD Standard Rx:e.g., Rituximab

Off-the-shelf EBV-Targeted T-cell Doses

If Rituximab Failure

1 2 3

Rituximab (anti-CD20 Ab) is often used off-label as 1st line therapy;

Historical survival in rituximab refractory patients median 16-56 days 1

¹ Prockop, S et al., Proc AACR (2015), Fox 2014, Ocheni 2008, Uhlin 20142 MSK Data on file

EBV - CTLs

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• Two separate clinical trials of EBV-CTL conducted by MSK• Study 95-024 – Primary HCT and 3rd party donor derived EBV-CTL• Study 11-130 – 3rd party donor derived EBV-CTL

• Includes EBV-LPD after HCT and solid organ transplant (SOT)

• Results in EBV-LPD after HCT presented in a Clinical Trials Plenary session at AACR 2015 (April 19, 2015)

• Results in EBV-LPD after SOT presented at ASCO 2015 (June 1, 2015)

Clinical Experience with EBV-CTL in EBV-LPD EBV - CTLs

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Clinical POC in EBV-LPD after HCT: Phase 2 Study Results¹

• 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

• Historical survival in rituximab refractory patients median 16-56 days

EBV-CTL Source N Prior Rituximab RR 2 DCR 2

Primary Donor3 26 13 62% 69%

3rd Party Donor 4 34 34 65% 70%

Response Rate (RR): Primary vs. 3rd party Donor

2015 ASCO Presentation Overall Survival: Rituximab Refractory

Patients Treated with 3rd party EBV-CTL

EBV - CTLs

1 year OS = 71.8%2 year OS = 63.8%N = 22

1 year OS = 56.3%2 year OS = 46.9%N = 12

Study 11-130

Study 95-024

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 MSK2 RR = complete response + partial response; DCR = Disease control rate = complete response + partial response + stable disease3 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

EBV-CTL: EBV-LPD after SOT – 2nd Indication¹

EBV-CTL Source N Prior Rituximab

Prior Chemo RR 2

3rd Party Donor 13 13 11 62%

Response Rate (RR): EBV-LPD after SOT

• 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

OS in Rituximab Refractory EBV-LPD after SOT following treatment with 3rd party EBV-CTL

Results

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

¹ Prockop, S et al., Proc ASCO (2015), Based on results from two clinical trials of EBV-CTL conducted by MSK2 RR = complete response + partial response3 Choquet et al., 2007

Historical Data3

• 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

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Current Treatment Approach

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CMV Reactivation:Viremia or Disease

CMV Standard Rx:e.g., Ganciclovir or Foscarnet

Off-the-shelf CMV-Targeted T-cell Doses

Viremia Only2 CMV Disease3

25Evaluable Patients

9 Complete Responses

7 Partial Responses

Response Rate = 64%

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-fold3 Responses in disease were considered complete if all detectable CMV viremia and disease resolved and partial if patients became asymptomatic

9Evaluable Patients

5Complete Responses

1 Partial Responses

Response Rate = 67%

If Treatment Failureor Intolerance

Phase 2 Clinical POC in antiviral resistant CMV after HCT¹

Interim data presented at ASH 2014; No de novo GvHD or flare of pre-existing GvHD was noted

1 2 3

Responses Following Administration of CMV Targeted T-cells

CMV - CTLs

STM 434

STM 434Ovarian Cancer and Other Solid Tumors

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STM 434

¹ National Cancer Institute estimate

STM 434: Potential First in Class Molecule for Ovarian Cancer and Other Solid Tumors

• 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

Phase 1 Program with Pre-clinical POC

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 US1

• 3 part Phase 1 ongoing including dose escalation, dose expansion, chemo combo

• Initial Phase 1 data expected 1H:16Upcoming Milestone

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STM 434

Suppressed Tumor Growth Improvement in Survival1

Ovarian Tumor SizeNormal Control

Treated withPlacebo

Inhibin KnockoutTreated withSTM 434/s

Inhibin KnockoutTreated with

Placebo

Right

Left

• FOXL2 – granulosa cell tumor gene linkage2

• 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

20¹ Zhou X, et al. Cell. 2010; 142(4):531-432 Shah S. P., et al. NEJM. 2009; 360: 2719-29

Pre-clinical POC in Granulosa Cell Ovarian Tumors

STM 434

Significant Reduction in Tumor Volume¹ Enhanced Body Weight¹

• ARID1A – clear cell tumor gene linkage2

• 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

Pre-clinical POC in Clear Cell Ovarian Tumors

STM 434

Ongoing First-in-Human (Phase 1) Study

• 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

First Patient Dosed 10/14; Initial Data Readout Expected 1H:16

2014 2015 2016+

Dose Escalation – in Solid Tumors

Monotherapy Dose Expansion – in OC

Combo Chemotherapy – in OC

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¹ Calculated utilizing 2011 data from USRDS extrapolated to December 31, 2013 as well as data from the recent study completed with DaVita Clinical Research² National Cancer Institute estimate³ Atara estimate based on the CIBMTR reports of number of HCT in the US in 2011 and a report in the journal Haematologica (2013)4 Atara estimate based on investigator experience

Multiple Opportunities for Value Creation• 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

Validated Clinical Programs

Attractive Markets

• 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 + EU4); 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 US2; expansion opportunities in other solid tumors

• 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

Upcoming Milestones

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June 2015