Pursuant to Section 13 or 15(d) of the Securities Exchange Act of 1934

Date of Report (Date of earliest event reported):  January 7, 2019


bluebird bio, Inc.

(Exact name of Registrant as Specified in Its Charter)






(State or Other Jurisdiction

of Incorporation)

(Commission File Number)

(IRS Employer

Identification No.)




60 Binney Street,

Cambridge, MA  



(Address of Principal Executive Offices)


(Zip Code)

Registrant’s Telephone Number, Including Area Code: (339) 499-9300

Not Applicable

(Former Name or Former Address, if Changed Since Last Report)



Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions (see General Instructions A.2. below):

Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Indicate by check mark whether the registrant is an emerging growth company as defined in as defined in Rule 405 of the Securities Act of 1933 (§ 230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§ 240.12b-2 of this chapter).

Emerging growth company 

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. 

Item 7.01Regulation FD Disclosure.


bluebird bio, Inc. (the “Company” or “bluebird”) will be conducting meetings with investors attending the 37th Annual J.P. Morgan Healthcare Conference in San Francisco, California beginning on January 7, 2019.  As part of these meetings, the Company will present the slides furnished to this Current Report as Exhibit 99.1, which is incorporated herein by reference.


The information in Item 7.01 of this Current Report on Form 8-K and Exhibit 99.1 attached hereto is intended to be furnished and shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934 (the “Exchange Act”) or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any filing under the Securities Act of 1933 or the Exchange Act, except as expressly set forth by specific reference in such filing.


Item 8.01Other Events.


On January 7, 2019, bluebird issued a press release announcing that bluebird entered into a license agreement with Inhibrx, Inc. for the research, development and commercialization of cell therapy products for the treatment of cancer.


The full text of bluebird’s press release regarding this announcement is filed as Exhibit 99.2 to this Current Report on Form 8-K and is incorporated herein by reference.

Item 9.01Financial Statements and Exhibits.

(d) Exhibits











Investor presentation provided by bluebird bio, Inc. on January 7, 2019.



Press release issued by bluebird bio, Inc. on January 7, 2019.




Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.







Date:  January 7, 2019

bluebird bio, Inc.





/s/ Jason F. Cole




Jason F. Cole




Chief Legal Officer






Slide 1

Making Hope A Reality – bluebird style January 2019 Exhibit 99.1

Slide 2

These slides and the accompanying oral presentation contain forward-looking statements and information. The use of words such as “may,” “might,” “will,” “should,” “expect,” “plan,” “anticipate,” “believe,” “estimate,” “project,” “intend,” “future,” “potential,” or “continue,” and other similar expressions are intended to identify forward-looking statements. For example, all statements we make regarding the initiation, timing, progress and results of our preclinical and clinical studies and our research and development programs, our ability to advance product candidates into, and successfully complete, clinical studies, and the timing or likelihood of regulatory filings and approvals are forward looking. All forward-looking statements are based on estimates and assumptions by our management that, although we believe to be reasonable, are inherently uncertain. All forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially from those that we expected. These statements are also subject to a number of material risks and uncertainties that are described in our most recent quarterly report on Form 10-Q, as well as our subsequent filings with the Securities and Exchange Commission. Any forward-looking statement speaks only as of the date on which it was made. We undertake no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future events or otherwise, except as required by law. Forward-Looking Statements

Slide 3

Potential 2019 Catalysts Lenti-D CALD Potential U.S./EU Filing LentiGlobin TDT EU Approval & First Launch Potential U.S. Filing 207 & 212 Data Update LentiGlobin SCD HGB-210 Study Start HGB-206 Group C Data Update bb2121 MM CRB-401 Data Update* KarMMa-1 Data Update* LentiGlobin TDT 207 & 212 Data Update LentiGlobin SCD HGB-206 Group C Data Update bb2121 MM KarMMa-2 & KarMMa-3 Study Start* Pipeline Analyst Day *Driven by Celgene/BMS bb21217 MM Data Update By End of Year By Mid Year Cash Position as of September 30, 2018: $2.0B CASH RUNWAY INTO 2022

Slide 4

RADICAL CARE We care in a way that’s intense and truly sets us apart. WE RECODE FOR LIFE THIS IS PERSONAL Gene therapy is about saving lives one person at a time. And we are, each of us, personally all in. PIONEERS WITH PURPOSE We’re exploring new frontiers for the sake of patients.

Slide 5

We LIVE By Our Non-negotiables

Slide 6

T H E G E N E T H E R A P Y P R O D U C T S C O M P A N Y LentiGlobin SCD 2022 Potential Filing/Approval LentiGlobin TDT 2019 EU Potential Approval 2020 U.S. Potential Approval Lenti-D CALD 2020 Potential Approval bb2121 Multiple Myeloma 2020 Potential Approval Products on the Market 4 INDs per year starting in 2020 1-2 Clinical Programs 5+ Patient Impact ∞ Our 2022 Vision -- Just Got BOLDER Products on the Market

Slide 7

SCD: Potential Global LAUNCH MM: Earlier Line APPROVALS & LAUNCHES 2023+ SCD: U.S. & EU FILING/APPROVALS MM: Earlier Line Studies 2022 TDT: Label EXPANSION CALD: Global EXPANSION MM: Global EXPANSION in Relapsed/Refractory Earlier Line Studies 2021 TDT: EU Country EXPANSION U.S. APPROVAL & LAUNCH Label EXPANSION CALD: U.S./EU APPROVAL MM: APPROVAL in Relapsed/Refractory 2020 TDT: EU APPROVAL & 1st LAUNCH 2019 UNPRECEDENTED OPPORTUNITY Anticipated research, development, regulatory and commercial milestones 1-2 INDs 1-2 INDs 1-2 INDs 1-2 Clinical Starts 5+ New Clinical Programs

Slide 8

RECODE THE SCIENCE: R&D with SOUL WHAT YOU SEE WHAT YOU DON’T SEE Internal Research Tools & Technology P13K Inhibition Enhanced Mftg TGF-B Flip CBL-B Edit DARIC Controls GAMMA DELTA Partners for Success T Cell megaTALs PRODUCT CANDIDATES PROGRAM AREA PRECLINICAL PHASE 1/2 PHASE 2/3 RIGHTS/PARTNER Severe Genetic Diseases Lenti-D™ Drug Product Worldwide LentiGlobin™ Drug Product Worldwide BCL11a shRNA (miR)* Worldwide Cancer bb2121 Celgene bb21217 Celgene Multiple Myeloma Third Line** Cerebral Adrenoleukodystrophy Transfusion-Dependent β-Thalassemia β0/β0 Multiple Myeloma Fourth Line Sickle Cell Disease Multiple Myeloma First Line** Multiple Myeloma Second Line** *Development is led by Dana-Farber/Boston Children's Cancer and Blood Disorders Center **Planned studies ** Multiple Myeloma Fourth Line Transfusion-Dependent β-Thalassemia Non-β0/β0 Sickle Cell Disease

Slide 9

Anti-Pure Play Principles - What Do We Mean? RECODING TRADITIONAL R&D 1:Many Target Strategy INTEGRATE ITERATE INTERNAL EXTERNAL Platform Tools & Technology R&D Enablers Clinical Insights MM - bb21217 SCD - BCL11a Liquid Tumor Programs Solid Tumor Programs SGD Programs TDT – LentiGlobin SCD – LentiGlobin MM – bb2121 CALD – Lenti-D

Slide 10

Our Philosophy Applied in a Tumor Microenvironment

Slide 11

Oncology Pipeline Enabled by Our Partners and Our Core Technologies Two Academic Clinical Trial Starts Planned in 2019 20+ 2+ 15+

Slide 12

Research Strategy Yielding Emerging Oncology Pipeline PRECLINICAL DEVELOPMENT EARLY CLINICAL LATE CLINICAL TARGET VALIDATION 2020 & BEYOND: 1-2 INDs PER YEAR bb21217 MM bb2121 MM LentiGlobin TDT LentiGlobin SCD Lenti-D CALD BCL11A SCD Dual-targeted CAR Liquid tumor Next gen + megaTAL edit Binders, Potency Internal Program Medigene Collaboration TCR target Solid tumors Next gen + Synbio Potency TCR target (viral antigen) Solid tumors Next gen + megaTAL edit Potency Fred Hutch Collaboration Clinic Ready 2019 CAR target Solid tumor Next gen + Synbio Target, Binders, Potency Regeneron Collaboration CAR target Solid tumors Next gen + Synbio Binders & Potency UNC Collaboration Clinic Ready 2019

Slide 13

RECODE THE SYSTEMS: ANYTHING BUT TRADITIONAL UNKNOWN IMPACT ONE-TIME POTENTIALLY CURATIVE OUR GOAL - MAKE IT SEAMLESS TO ALL STAKEHOLDERS Novel Science/Medicine Vector Production Bold & Balanced Access Model Supply Chain & Patient Management Drug Product Production

Slide 14

Virus Manufacturing Drug Product SCALABLE Clinical Data Real World Evidence to Support BLUE Style: Field Team Supply Chain Collecting Cells, Preparing, Shipping, Receiving Cells DELIVERY PLATFOM Platform Is Gearing Up for Launch TDT MAKE IT SEAMLESS

Slide 15

Preparing to Serve Patients in Europe in 2019 Apheresis Coordinator Apheresis Operator Cell Lab Operator Transplant Coordinator Transplant Nurse Transplant Physician Transplant Administrator bbb Manufacturing Logistics Apheresis Personnel Cell Lab Personnel Transplant Personnel (ATC) Manufacturer Launch Expectations: Optimal patient experience through a seamless delivery network Steady country by country launch with progressive build Get the model right for long term success Advance value-based payment over time reimbursement *Will support future launches in 2020+ 3 - Germany 4 - Italy 2 - UK 4 - France (in 2020)* 1 Drug Product Manufacturing Munich, Germany 9 Qualified Treatment Centers at 2019 Launch &

Slide 16

Value It: Time to Get It Right Value we can PROVE? Value we can MODEL? Price of the LAST LAUNCH? Value Demonstration Analogue Assessment Pricing Environment What the MARKET will BEAR? What we can GET AWAY WITH? Pulse Checking The value our products bring to patients should stand on its own for all stakeholders X X

Slide 17

Value It : Quick Answer is Value Based Payment Over Time “Free Up” system to recognize value over time “Buy time” to prove enduring value Fix cost density constraint Fix policy constraints (e.g., best price) Fix “portability of cure” concern Heighten awareness of true unmet need in terms of impact on life expectancy and cost Deliver credible and rigorous value platform arguments/data for value PAYMENT MODELS UNMET NEED VALUE EVIDENCE CONSTRAINTS & AMBITIONS BLUE “VALUE” PRINCIPLES Be focused on patient access to innovation  Be creative and disruptive (if needed) Be flexible and share risk  Be transparent and proactive with stakeholders Be proud Don’t do stupid short sighted stuff!

Slide 18

Our Quest to Constantly Innovate Continues COLLABORATORS

Slide 19

Transfusion Dependent β-Thalassemia

Slide 20

Transfusion-Dependent β-Thalassemia (TDT) Inherited blood disease that requires lifelong, frequent blood transfusions and iron reduction therapy PROGRAM OVERVIEW Filed MAA with European Medicines Agency General regulatory agreement with FDA for BLA filing Studies ongoing: Northstar-2 (HGB-207) Northstar-3 (HGB-212) HGB-205 Long-term follow-up: LTF-303

Slide 21

Transfusion-Dependent β-Thalassemia Basis of EU filing Original manufacturing process All genotypes Basis of EU and U.S. filings Refined manufacturing process Non-β0/β0 genotypes β0/β0 genotypes Refined manufacturing process HGB-204 HGB-207 HGB-212 Basis of EU filing (with Northstar) Original manufacturing process HGB-205

Slide 22

PRIME ADAPTIVE PATHWAYS EU Pursue CONDITIONAL APPROVAL in patients with non-β0/β0 genotypes on the basis of data from ongoing Northstar (HGB-204) & HGB-205 studies, as well as available data from Northstar-2 (HGB-207) study US Pursue approval in adults and adolescents with non-β0/β0 genotypes based on data from ongoing pivotal Northstar-2 (HGB-207) trial Pediatric population to be included as a cohort of HGB-207, rather than separate study Submission for approval in β0/β0 patients to be based on ongoing Northstar-3 (HGB-212) study BREAKTHROUGH THERAPY DESIGNATION ORPHAN DRUG DESIGNATION TDT Registration Strategy General agreement with EU & US regulators on the registration path for LentiGlobin for the treatment of transfusion-dependent β-thalassemia

Slide 23

8/10 Patients with Non-β0/β0 Genotypes and 3/8 Patients with β0/β0 Genotypes are Free from Chronic RBC Transfusions 11.1 10.4 12.0 12.5 14.1 9.7 9.9 10.3 Time from treatment to last transfusion Time from last transfusion to last follow-up 9.1 10.3 10.9 Hb (g/dL) At last study visit Months Post Drug Product Infusion Data as of September 14, 2018 *Indicates male patients. Hb, hemoglobin; TI, transfusion independence (weighted average Hb ≥9 g/dL without any red blood cell transfusions for ≥12 months)

Slide 24

10/11 Patients Are Transfusion Free with Hemoglobin >11g/dL *Male patients; ‡Hb supported by transfusions; †Weighted average Hb ≥9 g/dL without any RBC transfusions for ≥12 months; Hb, hemoglobin; VCN, vector copy number (vector copies/diploid genome) Data as of September 14, 2018 Time free from chronic transfusions in patients with ≥3 months follow-up * * * * Safety profile post DP infusion remains consistent with myeloablative conditioning Patients 1 and 3 have achieved the protocol definition of transfusion independence† Hb (g/dL) Peripheral VCN At last study visit 13.3 3.2 11.3‡ 0.4 11.1 2.2 12.1 1.7 12.3 1.7 12.5 2.9 11.6 5.6 12.4 1.1 11.9 4.9 11.6 5.4 11.2 5.6 Initiation of phlebotomy Re-initiation of iron chelation

Slide 25

High Levels of Gene Therapy Derived HbAT87Q in 10/11 Patients *Male patients; ‡Patient is homozygous for IVS-I-5 β-globin mutation; ^Patient is heterozygous for IVS-I-5 β-globin mutation. Hb, hemoglobin. Transfused Data as of September 14, 2018 Transfused

Slide 26

Normal Total Hemoglobin in First Northstar-3 β0/β0 Patient Data as of September 14, 2018 unless otherwise noted *Includes investigator reported data as of November 19, 2018, not from programmed statistical outputs AEs, adverse events; DP, drug product; Hb, hemoglobin; VCN, vector copy number (vector copies/diploid genome) Safety profile post-drug product infusion remains consistent with myeloablative conditioning

Slide 27

Sickle Cell Disease

Slide 28

Sickle Cell Disease (SCD) Severe blood disorder that causes anemia, frequent pain crises and shortened lifespan Global annual birth incidence ~ 300,000 – 400,000 Mean age of death in the U.S. is 44 years1 PROGRAM OVERVIEW Plan to pursue accelerated development path based on hematological primary endpoint Phase 3 study to begin in 2019 HGB-206 amended and Group C expanded Source: Global Genes 1Paulukonis et al, California’s Sickle Cell Data Collection Cohort, 2005-2015* ASH 2017*

Slide 29

Increasing Momentum to #ConquerSCD “Unfortunately, some treated [SCD] patients will have no reduction of their symptoms and the disease will continue to progress,” says Ann T. Farrell, M.D., director of the FDA’s Division of Hematology Products, CDER. “Better therapies are desperately needed,” Farrell explains. “We will continue to work with sponsors as much as possible to help remove roadblocks to new product development. It’s important for the FDA to help as much as we can.” 2017 2018 March 2017, bluebird SCD case study published in NEJM July 2017, the FDA approved Endari (L-glutamine oral powder) to address acute complications of SCD February 2018, Admiral Brett Giroir, M.D., appointed as Assistant Secretary for Health, HHS, is shining a spotlight on the toll of SCD and the need for improved treatment options March 2018, NHLBI launched “Cure SCD Initiative” spearheaded by Dr. Francis Collins October 2018, FDA-ASH Sickle Cell Disease Clinical Endpoints Workshop

Slide 30

Ongoing Phase 1/2, single arm, multi-center, U.S. study N=41 (Group C) Primary Endpoint: HbAT87Q and Total Hb Key Secondary Endpoint: Reduction in severe VOEs ≥12 years of age - ≤50 years of age Phase 1/2, single-center in France N=7 (4 β-thalassemia) HGB-205 (Transfusion-dependent b-thalassemia & severe sickle cell disease) All thalassemia subjects dosed as of Sep 2015 2 year study duration; last β-thalassemia subject visit ≈Sep 2017 Phase 3, single arm, multi-center, global study HGB-210 (Sickle Cell Disease, history of VOEs over 24 months) Primary Endpoint: HbAT87Q and Total Hb Key Secondary Endpoint: Reduction in severe VOEs HGB-206 Group C (Sickle Cell Disease, history of VOEs over 24 months) Accelerated Development Plan Using Novel Composite Primary Endpoint Based on Hemoglobin NEW Planned for 2019 EXPANDED Updated Primary Endpoint Up to add’l 21 patients Expanded age range Additional Clinical Investigation in Other Patient Types and Ages Planned Plans Based on Ongoing Engagement with Regulators

Slide 31

HGB-206: Evolution of LentiGlobin in SCD Bone Marrow Original Protocol and Manufacturing Process Bone Marrow Modified Protocol and Mixed Manufacturing Process Peripheral Blood Modified Protocol and Refined Manufacturing Process Medium Low Low Group A High Medium High Group C High High High Yes Group B Transfusions (Pre-Treatment) Conditioning Total Cell Dose Transduction (VCN & % Transduced) Planned Cell Source Shift Cell Source: Apheresis Cell Source: Bone Marrow High CD34 Phenotype (% CD34 Bright) Medium Medium No Yes

Slide 32

Group C: Patient Characteristics N=14 Patients Who Started Cell Collection Parameter Group C N=14 Age at consent median (min – max), years 25.5 (18 – 36) Gender 6 F 8 M Genotype βS/βS 14 Prior SCD History Hydroxyurea use, n 8 Recurrent VOCs*, n Annualized no. of events, median (min – max) 9 6.5 (3.5 – 14.0) ACS†, n Annualized no. of events, median (min – max) 2 1 (1 – 1) Any history of stroke, n 3 TRJV >2.5 m/s, n 0 * ≥2 events/year in preceding 2 years; † ≥2 episodes in preceding 2 years, with at least one episode in the past year or in the year prior to the initiation of a regular transfusion program Data as of September 14, 2018 ACS, acute chest syndrome; F, female; M, male; VOC, vaso-occlusive crisis; pRBC, packed red blood cell; TRJV, tricuspid regurgitant jet velocity

Slide 33

Group C: Safety Profile Generally Consistent with Myeloablative Busulfan Conditioning Data as of September 14, 2018 Non-hematologic* grade ≥ 3 AEs Post-DP infusion in ≥2 patient n (%) N=9 Febrile neutropenia 6 (67) Stomatitis 6 (67) Serious AEs* Post-DP infusion in ≥1 patient n (%) N=9 Abdominal pain 1 (11) Depression 1 (11) Drug withdrawal syndrome 1 (11) Hallucination 1 (11) Mucosal inflammation 1 (11) Nausea 1 (11) Non-cardiac chest pain 1 (11) Splenic hematoma 1 (11) Vomiting 1 (11) AE, adverse event; DP, drug product; RCL, replication competent lentivirus; SAE, serious adverse event; VOD, veno occlusive liver disease; VOE, vaso-occlusive event; LVV, lentiviral vector *Hematologic AEs commonly observed post-transplant have been excluded No VOEs post-DP infusion in 9 patients SAEs were reported in 4 patients No AE considered related to DP No cases of VOD observed to date No vector-mediated RCL detected to date Integration site (IS) analysis data available for two patients at 6 month visit Total IS: Showed consistent polyclonality One patient in Group A: MDS diagnosed 36 months post-DP infusion: no evidence of LVV integration in dysplastic cells; monosomy 7 mutation identified (associated with sporadic and chemotherapy-related MDS)

Slide 34

Critical Elements of LentiGlobin Success in SCD Fundamentally Improving Red Blood Cell Physiology 4 out of 4 patients with ≥47% anti-sickling Hb (range: 47% - 62%) at 6 months Sustained expression of HbAT87Q levels through 9 months follow-up High & Stable Levels of HbAT87Q Derived Hemoglobin & Total Hemoglobin Correction of Hemolysis Pancellular Expression of HbAT87Q Resulting in Reduction of Sickling Normalization of reticulocyte counts, lactate dehydrogenase and bilirubin levels Pancellular expression shown in two independent assays of patient cells Reduction of sickling of patient RBCs at levels consistent with sickle trait cells Increased total hemoglobin and robust HbAT87Q production No VOEs in early clinical follow up Improvement of Clinical Outcomes GOAL GROUP C RESULTS

Slide 35

Group C: Stable Peripheral Blood VCN, HbAT87Q Trajectory Robust and Consistent Data as of September 14, 2018 For Group A patients, medians (Q1, Q3) depicted; Group A patients with month 36 study visit (N=2)

Slide 36

Group C Patients Achieving Sickle Trait-like Hemoglobin Distribution Data as of September 14, 2018 βS-globin decreasing with increasing HbAT87Q (average concentration of hemoglobin per cell has not changed post-treatment) Increase in βA-T87Q Results in Decrease in βS βS βA -T87Q βS Pre-Infusion Post-Infusion 34% 51% 38% 46% 53% 43% βS VCN = βA-T87Q

Slide 37

Impact on Clinical Outcomes of SCD in Group C Normalization of Key Biomarkers of Hemolysis Over Time Reticulocyte Counts Lactate Dehydrogenase Median (Q1, Q3) depicted Dot-dash lines denote lower and upper limits of normal values Data as of September 14, 2018 Total Bilirubin

Slide 38

Healthy Donor [AA] (n = 4) Sickle Trait [AS] (n = 12) Sickle Cell [SS] (n = 6) Hereditary Persistence of Fetal Hemoglobin with SS (n = 4)* *HbF levels in HPFH donors ranged from 28.1 to 42.3% Subject 206-114-1315 PB at 9 months post-infusion LentiGlobin has Anti-Sickling Activity Comparable to Sickle Trait Reduction in % Sickled and Time to Sickling in Patient RBCs Post-Treatment

Slide 39

Two Independent Assays Reveal Near Pancellular βA-T87Q Distribution Majority of Patient RBCs are Positive for Anti-Sickling Globin 8.6% 91.4% Subject 1315 M9 Single Cell Western Subject 1315 M9 Flow Cytometry βS Healthy Donor (A/A) βS Sickle Cell Disease (S/S) βS βA or βA-T87Q 100% 100% A/S 100% Sickle Trait (A/S) βA or βA-T87Q βA or βA-T87Q βS Fluorescence Intensity Count S/S A/S A/A 1315 85.5%

Slide 40

Impact on Clinical Outcomes of SCD Resolution of Anemia (and Robust HbAT87Q Levels) in All Patients by 6 Months; No VOEs Since DP Infusion Data as of September 14, 2018 * Denotes female patients; ╪ Patient current receiving phlebotomy Group C: All patients free of VOEs as of data cut-off

Slide 41

A Case of Myelodysplastic Syndrome with Excess Blasts

Slide 42

Multiple Myeloma

Slide 43

Multiple Myeloma A lethal blood cancer that often infiltrates the bone marrow causing anemia, kidney failure, immune problems and bone fractures BCMA PROGRAM OVERVIEW bb2121: Enrollment in KarMMa registration-enabling study complete (N=140) Additional studies advancing: KarMMa-2 in 2nd line Phase 2 study enrolling soon KarMMa-3 in 3rd line+ Phase 3 study enrolling soon Opportunities for bb2121 in newly diagnosed MM including high risk, transplant ineligible and transplant eligible vs. transplant under evaluation

Slide 44

CRB-401 Data at ASCO 2018 - Baseline Demographics and Clinical Characteristics Parameter Escalation (N=21) Expansion (N=22) Median (min, max) follow-up, d 345 (46, 638) 87 (29, 184) Median (min, max) age, y 58 (37, 74) 65 (44, 75) Male, n (%) 13 (62) 16 (73) Median (min, max) time since diagnosis, y 4 (1, 16) 6 (1, 36) ECOG PS,1 n (%) 0 1 10 (48) 11 (52) 6 (27) 16 (72) High-risk cytogenetics, n (%) del(17p), t(4;14), t(14;16) 8 (38) 9 (41) ECOG, Eastern Cooperative Oncology Groups performance status; ISS, international staging system; NA, not available. 1Data at screening presented. Data cutoff: March 29, 2019

Slide 45

Parameter Escalation (N=21) Expansion (N=22) Exposed Refractory Exposed Refractory Prior therapies, n (%) Bortezomib 21 (100) 14 (67) 22 (100) 16 (73) Carfilzomib 19 (91) 12 (57) 21 (96) 14 (64) Lenalidomide 21 (100) 19 (91) 22 (100) 18 (82) Pomalidomide 19 (91) 15 (71) 22 (100) 21 (96) Daratumumab 15 (71) 10 (48) 22 (100) 19 (86) Cumulative exposure, n (%) Bort/Len 21 (100) 14 (67) 22 (100) 14 (64) Bort/Len/Car/Pom/Dara 15 (71) 6 (29) 21 (96) 7 (32) Parameter Escalation (N=21) Expansion (N=22) Median (min, max) prior regimens 7 (3, 14) 8 (3, 23) Prior autologous SCT, n (%) 21 (100) 19 (86) 0 0 3 (14) 1 15 (71) 14 (64) >1 6 (29) 5 (23) SCT, stem cell transplant. Data cut-off: March 29, 2018. CRB-401 Data at ASCO 2018 - Heavily Pretreated Patient Population

Slide 46

CR, complete response; mDOR, median duration of response; ORR, objective response rate; PD, progressive disease; PR, partial response; sCR, stringent CR; VGPR, very good partial response. Data cut-off: March 29, 2018. 1Patients with ≥2 months of response data or PD/death within <2 months. ORR is defined as attaining sCR, CR, VGPR, or PR, including confirmed and unconfirmed responses. Low BCMA is <50% bone marrow plasma cells expression of BCMA; high BCMA is defined as ≥50%. Tumor Response By Dose1 Tumor Response By BCMA Expression1 ORR=33.3% mDOR=1.9 mo ORR=57.1% mDOR=NE 150 x 106 (n=14) >150 x 106 (n=22) 50 x 106 (n=3) ORR=95.5% mDOR=10.8 mo 450 x 106 High BCMA (n=11) Median follow-up (min, max), d 87 (36, 638) 84 (59, 94) 194 (46, 556) Median follow-up (min, max), d 450 x 106 Low BCMA (n=8) 311 (46, 556) ORR=100% ORR=91% 168 (121, 184) CRB-401 Data at ASCO 2018 - Tumor Response: Dose-related and Independent of Myeloma BCMA Expression Levels 80.6% ORR across active dose cohorts (150-800 x 106)

Slide 47

Data cut-off: March 29, 2018. Median and 95% CI from Kaplan-Meier estimate. NE, not estimable. 1PFS in dose escalation cohort. mPFS of 11.8 months at active doses (≥150 x 106 CAR+ T cells) in 18 subjects in dose escalation mPFS of 17.7 months in 16 responding subjects from all study cohorts who are MRD-negative PFS at Inactive (50 x 106) and Active (150–800 x 106) Dose Levels1 PFS in MRD-Negative Responders Escalation and Expansion Cohorts 50 x 106 (n=3) 150–800 x 106 (n=18) Events 3 10 mPFS (95% CI), mo 2.7 (1.0, 2.9) 11.8 (8.8, NE) ≥ mPFS = 11.8 mo mPFS = 2.7 mo CRB-401 Data at ASCO 2018 - Hitting the Mark for Progression Free Survival PFS progression-free survival; MRD, minimal residual disease. Includes patients treated with <50 x 106 CAR T cells who were MRD-negative at >1 postbaseline time point 150–800 × 106 (n=16) mPFS (95% CI), mo 17.7 (5.8, NE) mPFS = 17.7 mo

Slide 48

TEAE, n (%) Overall Grade ≥3 Cytokine release syndrome1 27 (63) 2 (5) Neurotoxicity2 14 (33) 1 (2) Neutropenia 35 (81) 34 (79) Thrombocytopenia 26 (61) 22 (51) Anemia 24 (56) 19 (44) Infection3 Overall First Month 26 (61) 10 (23) 9 (21) 2 (5) CAR T Treatment-Emergent Adverse Events All Infused Patients (N=43) Data cut-off: March 29, 2018. NE, not estimable.1CRS uniformly graded per Lee et al., Blood 2014;124:188-195. 2Events occurring in first 28 d and including dizziness, bradyphrenia, somnolence, confusional state, nystagnmus, insomnia, memory impairment, depressed level of consciousness, neurotoxicity, lethargy, tremor and hallucination. 3Includes the SOC Infections and Infestations. Events observed in >10% include upper respiratory tract infection and pneumonia. 4Includes patients treated with active doses (150–800 × 106 CAR+ T cells; N=40). Median and 95% CI from Kaplan-Meier estimate. 5Time from first bb2121 infusion to the first grade ≤2 event after day 32. No grade 4 CRS events No fatal CRS or neurotoxicity events Cytokine Release Syndrome By Dose Level Dose Level2 39% 82% >150 x 106 (n=22) 150 x 106 (n=18) Maximum Toxicity Grade1 Patients with a CRS event, 63% CRB-401 Data at ASCO 2018 - bb2121 Continues to be Generally Well-Tolerated; No New Safety Signals

Slide 49

Response to Current Standard of Care in Late Line RRMM Chari, A. Blood 2017 43

Slide 50

bb2121 Patient Case: 21 Months in sCR General Information Age & Gender 52 year old Male Dose group 150x10^6 Tumor Burden High High Risk Cytogenetics (based on FISH) No Number of prior regimens 6 Initial diagnosis May, 2010 BCMA% (prescreen, baseline) 60, 75 VRD, Doxo VRD, M, ASCT K Pom bb2121 Duration/ Best Rx 30M PR 2M SD 3M N/A 5M PD 2M N/A 19M CR VRD Dara Treatment history 21M sCR KEY minimal residual disease (MRD)-negative PR VGPR VGPR VGPR VGPR sCR VGPR VGPR sCR sCR ASCT: autologous stem cell transplant, R: Revlimid, M: melphalan, d: dexamethasone, V: Velcade, K: Kyprolis, P/Pom: Pomalyst, Vor: vorinostat, Dara: daratumumab, Doxo:Doxorubicin

Slide 51

Advancing bb2121 into Earlier Lines of Multiple Myeloma Multiple Myeloma Trials planned in 2019 KarMMa 3 (MM-003) KarMMa 2 (MM-002) KarMMa (MM-001) Phase 3 Phase 2 Phase 1 Registration-enabling trial in late line enrollment complete Front line setting Phase 2 studies planned in 2019 3rd line+ Phase 3 study enrolling soon 2nd line Phase 2 study enrolling soon ✓ Lines of therapy Anticipated Approval in 2020 ✓ ✓

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Key Takeaways from CRB-401 Presented at ASCO Efficacy? Durability? BCMA? MRD? Safety? Path forward? 95.5% ORR in doses above 150M cells. 50% CR rate at doses above 150M cells. 11.8 months median PFS in dose-escalation active doses. 17.7 months median PFS in MRD(-) patients with response (escalation and expansion). Consistent responses across BCMA expression levels. 16/16 responding, MRD-evaluable patients were MRD negative. No new safety signals (G3/G4 CRS or Neurotox). KarMMa amendment raised high end of dose range to 450 based on observed dose-response and acceptable safety profile. Potential approval on track for 2020. Earlier line development plan advancing.

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Hypothesis: Increasing long-lived, memory-like T Cell subsets in the drug product may result in enhanced persistence of functional anti-BCMA CAR T cells in vivo TN Cell TSCM Cell TCM Cell TEM Cell TEFF Cell T Cell Plasticity Self Renewal Long-lived Terminally Differentiated No Self Renewal Short-lived bb21217: PI3K Inhibition During Manufacturing Drives Increase in Long-lived, Memory-like T Cells CD27+ CD62L+

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Preclinical Models: bb21217 is Enriched for Memory-like T Cells Exhibits; Enhanced Persistence of Anti-tumor Effect CD62L and CD27 are markers of memory-like T cells bb21217 is significantly enriched for T cells with this memory-like phenotype bb007 enhances anti-tumor effect in mouse models ONLY CAR T cells cultured with PI3K inhibitor bb007 (i.e. bb21217) clear a second tumor challenge Data are consistent with improved persistence of functional CAR T cells leading to sustained anti-tumor effect Re-challenge With Tumor (opposite flank) 1o tumor 2o tumor CAR T only CAR T+bb007

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CRB-402 Phase 1 Study Design and Status 3 + 3 dose escalationa 300 × 106 450 × 106 800 × 106 150 × 106 Collected N=13 Dosed N=12 (150 × 106 dose) HTBb n=6LTBb n=6 Study Status as of Oct 18, 2018 Median (min, max) follow-up 26 wk (4, 51) Primary endpoints: AEs, DLTs Other endpoints: Responsec, PFS, OS, MRD, CAR+ T cell expansion and persistence N ≈ 50 R/R MM ≥3 prior regimens IMiDs and Proteasome inhibitors Or double-refractory ≥50% BCMA expression (dose escalation only) NCT03274219 AE, adverse events; BCMA, B-cell maturation antigen; DLT, dose-limiting toxicity; HTB, high tumor burden; IMiD, immunomodulatory imide drugs; LTB, low tumor burden; MRD, minimal residual disease; OS, overall survival; PFS, progression-free survival; R/R MM, relapsed/refractory multiple myeloma. aAll patients to date received 150 × 106 CAR+ T cells; an intermediate dose of 300 × 106 CAR+ T cells will be the next dose level. bHTB defined as ≥50% bone marrow plasma cells pre-infusion; LTB <50%. cPer International Myeloma Working Group criteria. CAR+ T cell dose

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CRS occurred in 67% of patients Mostly grade 1/2, 1 grade 3, no grade 4 Median time to onset of CRS 4.5 days (2,11) Manageable with or without tocilizumab 1 patient experienced DLT (grade 4 encephalopathy and grade 3 CRS) Patient had high tumor burden and rapidly accelerating disease at baseline No other DLTs occurred 1 grade 3 catheter-related infection; no other severe infections reported to date 4 patients experienced 1 or more SAEs No deaths on study to date Data as of October 18, 2018 AE, adverse event; DLT, dose-limiting toxicity; SAE, serious adverse event. aAEs occurring between bb21217 infusion and disease progression. bCytokine release syndrome (CRS) uniformly graded according to Lee et al., Blood 2014;124:188-195. cEvents selected as CAR T neurotoxicity on the case report form occurring within 90 days after bb21217 infusion. Grade ≥3 AEs in >1 Patienta AEs of Special Interesta Grade, n (%) 1 2 3 4 CRSb 4 (33) 3 (25) 1 (8) – Neurotoxicityc 1 (8) 1 (8) – 1 (8) Early Clinical Safety and Tolerability Consistent with CAR T Experience

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Clinical Data is Early But Consistent with Goal of Enhanced Persistence Robust and reliable bb21217 CAR T cell expansion post-infusion observed at first dose Early bb21217 clinical data is consistent with robust functional CAR T cell persistence Enrichment for memory-like CAR T cells observed in preclinical studies, and in patients post-infusion Vector detectable up to 9 months post-infusion, and in 3/3 patients at 6-month time point Sustained sBCMA suppression observed, reflecting ongoing plasma cell aplasia Data as of October 18, 2018 Month 1 Month 3 Month 6 Month 9 At risk, n 9 7 3 1 With detectable vector, n (%) 9 (100) 6 (86)a 3 (100) 1 (100) Vector Copy Number Over Time by Baseline Tumor Burden (n=5) (n=6) HTB, high tumor burden; LLOQ, lower limit of quantitation; LTB, low tumor burden. aOne patient with undetectable vector received cyclophosphamide on day 15 for grade 4 encephalopathy.

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Clinical Responses Observed in 10/12 Patients (83%) at First Dose Level Tested (150 x 106 CAR+ T cells) Data as of October 18, 2018 b b a Clinical Responses Over Time CR, complete response; MRD, minimal residual disease; PR, partial response; VGPR, very good partial response. *Patients with high tumor burden. aProgression based exclusively on appearance of new bone lesions. bMRD status not available. 10/12 patients (83%) achieved an objective response at the first tested dose (150 × 106 CAR+ T cells) Deepening responses over time; CR achieved as late as month 10 100% MRD negativity in 4/4 responders evaluable for MRD status Responses are ongoing in all but 1 responder; the first patient dosed continues response >1 year after treatment

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High Clinical Response Rate Observed at First Dose Level (150 x 106 CAR+ T cells) Clinical Response bb21217-Treated (N=12) ORR,a n (%) [95% CI] 10 (83.3) [51.6, 97.9] sCR/CR 3 (25) ≥VGPR 6 (50) MRD status in bone marrow, n MRD-evaluable respondersb 4 MRD-neg 4c Median time to first response (min, max), a,d mo 1 (1, 2) Median time to best response (min, max), a,d mo 1 (1, 10) Median follow-up duration (min, max), mo 5.9 (1.0, 11.8) CR, complete response; MRD, minimal residual disease; ORR, objective response rate; PR, partial response; VGPR, very good partial response. *Patients with high tumor burden. aIncludes unconfirmed responses. bPatients with ≥PR and valid MRD assessments. cTwo MRD-neg. responses at 10-6 and 2 at 10-5 sensitivity level by Adaptive next-generation sequencing. dAmong 10 responders with ≥PR. Data as of October 18, 2018

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Promising Early Data with Next-Generation Anti-BCMA CAR T bb21217 demonstrated promising early clinical activity in heavily pretreated patients with relapsed/refractory multiple myeloma at first dose level tested 83% ORR with 90% of responses ongoing Elimination of MRD in the bone marrow of all 4 evaluable responders Early indications of increased persistence using enriched CAR T cells Safety profile appears consistent with known toxicities of CAR T cell therapies Dose escalation is ongoing

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Cerebral Adrenoleukodystrophy Severe, often fatal neurological disease in boys UNMET NEED Treatment limited to allo-HSCT Sometimes severe treatment-related risks and complications, especially when donor is not a matched sibling EPIDEMIOLOGY Global incidence of ALD: 1 in ~21,000 newborns Cerebral form develops in ~40% of affected boys 1Salzman, R., Kemp, S. (2017, December 06) Newborn Screening. Retrieved from Ethan’s family spent nearly two years trying different medications and meeting with specialists to try and resolve his symptoms. Tragically, during this period, the ravaging effects of ALD were continuing to damage Ethan’s brain and adrenal glands. Ethan Zakes 2000 - 2011 Source: Ethan Zakes Foundation

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Lenti-D Treatment Halts CALD Disease Progression 15/17 patients (88%) alive and MFD-free at 24 months follow-up; all patients continue to be MFD-free as of April 25, 2018 Exceeds pre-determined efficacy benchmark for the study MFD-free survival in 13/15 (76%) 12 additional patients treated in Starbeam study No MFDs reported as of April 25, 2018; median follow-up for this additional cohort of patients is 4.2 months (0.4 – 11.7 months) Safety profile consistent with autologous transplantation No GvHD, no graft rejection Two patients did not meet primary endpoint: Patient 2016: Withdrew Patient 2018: Rapid disease progression early in the study October 4, 2017 N Engl J Med 2017; 377:1630-1638 Data as of April 25, 2018

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Recent Collaborations

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Science-Driven and Highly Complementary Partnership BLUE remains BLUE: Clear value proposition through product rights, shared funding and capabilities Science: best-in-class technology platforms joining forces to crush cancer Culture: science- and patient-focused companies with a willingness to push boundaries of novel technologies Investment: All-in mindset driving shared and enhanced funding for R&D efforts Structure: Aligned and streamlined operating model to enable flexible research and decision making

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Engaging the Right Target with the Optimal Target Binder Pick Great Targets Fully Human CARs Identify Human TCRs Better Models …rapid generation of genetically engineered mice ...fully human antibodies through immunization …rapid identification & preclinical testing of target specific antibodies …fully human T cell receptors from an engineered mouse …immunodeficient mouse platform - study of human cells & tumors …target validation at unprecedented pace and precision

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Partnership Highlights Share costs equally through pre-IND research and into Phase 1/2 development For 50/50 collaboration products, development and commercialization costs (by region) are shared equally bluebird funds development and commercialization of its wholly-owned products $100 million equity investment by Regeneron in BLUE - 420,000 shares at $238.10 per share or a 59% premium* Research bluebird leads R&D managed by a Joint Steering Committee bluebird retains significant product rights; Regeneron receives milestone payments and royalties Regeneron can opt-in to multiple products to become 50/50 partners Joint late-stage development and commercialization allocated between bluebird and Regeneron or future partners on a regional basis Five-year research collaboration Refreshable list of six targets Access to Regeneron VelociSuite® Platform technologies Leveraging bluebird expertise in cell biology and vector technology Brings together two science driven organizations with synergistic technology and expertise Development Funding *Premium of approximately $37 million will be used to cover part of Regeneron’s share of research costs; bluebird intends to use the balance of the proceeds to support its research activities in the collaboration.

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Gritstone complements bluebird’s approach to generating novel therapeutics for oncology Patient biopsy Tumor targets TCR Cell therapy Patient therapy gritstone Routine clinical biopsy gritstone Mass spec validation of expressed tumor targets in patients and sequencing of tumor transcriptome Select patients with target Validate 10 targets Medigene , Regeneron, gritstone Identify TCR sequences which bind to validated tumor targets bluebird Generate TCR cell therapy targeting validated tumor antigens using patient’s white blood cells bluebird Genetically engineered patient cells infused back into patient

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Early Pipeline

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Good Is Never Good Enough For Patients: BLUE Toolbox Strategy Product Engine Novel areas; autoimmune In vivo gene editing Optimized severe genetic disease products New & enhanced oncology products Transduction Durability BCMA (bb2121) LentiGlobin BCMA & PI3Ki (bb21217) LentiGlobin & Enhancers v1.0 v2.0 vFuture BCMA & Solid Tumors LentiGlobin MegaTAL Gene Editing LNPs Lentivirus mRNA

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Initial Proof of Concept: LVV Approach to Suppression of BCL11a in SCD As of July 28, 2018, one patient had received treatment with HSCs transduced with an LVV encoding the BCL11a shRNAmiR As of day 76: Sustained Hb of >10 g/dL 59.7% total HbF cells; 30% HbF as a fraction of all β-like globin Notable absence of irreversibly sickled cells on peripheral smear Low absolute reticulocyte count consistent with markedly reduced hemolysis Hb Safety profile consistent with myeloablative conditioning

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CBLB Knock-out Enhances CAR-T Cell Anti-tumor Activity Novel Technology for Improving T Cell Function in Liquid and Solid Tumors 2 3 1 CBLB megaTAL induces a high rate of gene editing and corresponding knockdown of CBLB protein levels CBLB megaTAL treatment enhances production of cytokines in vitro by CAR-T cells Genetic deletion of CBLB enhances anti-tumor activity of CAR-T cells in a mouse solid tumor xenograft model

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ASH Highlights: Next Generation Programs / Platforms First clinical demonstration of the potential to genetically manipulate HbF levels through BCL11a Novel LVV expressing a shRNAmiR to knock down BCL11a at the level exclusively in erythroid cells Robust knock down of BCL11a observed in patient cells At ≥4 months post-gene therapy, ~70% F cells were observed and HbF contributed ~25-30% of total Hb Example of bbb’s T cell enhancement technologies aimed at delivering transformative outcomes for solid tumors bbb megaTAL technology used to efficiently and specifically knockout CBL-B in CAR T cells via gene editing Increases cytokine production in response to tumor cells in vitro Enhances anti-tumor activity of CAR T cells in a mouse xenograft model Flipping the Switch: Initial Results of Genetic Targeting of the Fetal to Adult Globin Switch in Sickle Cell Patients Esrick et al. (Abstract #801) Knockout of CBL-B Greatly Enhances Anti-Tumor Activity of CAR T Cells Hooper et al. (Abstract #338)

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Go TRUE BLUE We Must Make Hope a Reality


Exhibit 99.2


bluebird bio and Inhibrx Announce Collaboration to Research, Develop and Commercialize CAR T Cell Immunotherapies  


CAMBRIDGE, Mass and SAN DIEGO, Calif. January 7, 2019bluebird bio, Inc. (Nasdaq: BLUE) and Inhibrx, Inc. (Inhibrx) today announced that they have entered into an exclusive license agreement to research, develop and commercialize chimeric antigen receptor (CAR) T cell therapies using Inhibrx’s proprietary single domain antibody (sdAb) platform to multiple cancer targets. The small size of sdAbs may enable the generation of more complex CAR T cell products such as those designed to combine additional functions into a single CAR molecule or recognize multiple tumor antigens simultaneously.


“Access to the Inhibrx sdAb binder technology will allow us to combine the advancements we’ve made with our T cell therapy platform with their sdAb binder technology to generate novel cellular therapies with the potential to help patients in their fight against cancer,” said Philip Gregory, D. Phil., chief scientific officer, bluebird bio. “The technology from Inhibrx adds to our growing portfolio of tools and technologies that we can combine with our internal lentiviral vector, CAR and T cell expertise to discover potential new product candidates designed to recognize tumor-specific proteins expressed by cancer cells and kill them upon engagement.”


“We are pleased to have formalized our relationship with bluebird bio, allowing us to couple our proprietary sdAb platform with a leading cell therapy platform,” said Brendan Eckelman, Chief Scientific Officer and Executive Vice President of Corporate Strategy of Inhibrx. “Together with bluebird bio, we have generated compelling proof of concept preclinical data on the utility of incorporating our sdAbs into bluebird bio’s constructs for CAR-T cell generation.”


Under the terms of the license agreement, Inhibrx will provide bluebird bio the exclusive worldwide rights to develop, manufacture and commercialize certain cell therapy products containing sdAbs directed to various cancer targets. bluebird bio will be responsible for the clinical development and commercialization of the cancer-targeting CAR-T products. Inhibrx received a $7.0 million upfront payment and is also entitled to receive specified developmental milestone payments as well as percentage tiered royalties on future product sales.


About Inhibrx, Inc.

Inhibrx is a clinical-stage biotechnology company focused on developing a broad pipeline of novel biologic therapeutic candidates. Inhibrx utilizes diverse methods of protein engineering to address the specific requirements of complex target and disease biology, including its proprietary sdAb platform. The Inhibrx pipeline is focused on oncology, orphan diseases and infectious diseases. Inhibrx has a collaboration with Celgene and has received awards from several granting agencies, including NIH, NIAID and CARB-X. For more information, please visit


About bluebird bio, Inc.
With its lentiviral-based gene therapies, T cell immunotherapy expertise and gene editing

capabilities, bluebird bio has built a pipeline with broad potential application in severe genetic diseases and cancer.


bluebird bio's gene therapy clinical programs include investigational treatments for cerebral adrenoleukodystrophy, transfusion-dependent β-thalassemia and sickle cell disease.


bluebird bio's oncology pipeline is built upon the company's lentiviral gene delivery and T cell engineering, with a focus on developing novel T cell-based immunotherapies, including chimeric antigen receptor (CAR T) and T cell receptor (TCR) therapies. The company’s lead oncology programs are anti-BCMA CAR T programs partnered with Celgene.


bluebird bio’s discovery research programs include utilizing megaTAL/homing endonuclease gene editing technologies with the potential for use across the company's pipeline.


bluebird bio has operations in Cambridge, Massachusetts; Seattle, Washington; Durham, North Carolina and Zug, Switzerland. For more information, visit


Follow bluebird bio on social media: @bluebirdbio, LinkedIn, Instagram, YouTube.


bluebird bio Forward-Looking Statements

This release contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, including statements regarding the research, development and advancement of bluebird bio’s potential product candidates and research program, and the benefits of each company’s strategic plans and focus. Any forward-looking statements are based on management’s current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to, the risk that the research programs for these targets or using the technology licensed from Inhibrx will be unsuccessful and not result in any viable product candidates, the risk that our collaboration with Inhibrx will not continue or will not be successful, the risk of cessation or delay of any planned clinical studies and/or our development of our product candidates, and the risk that any one or more of our product candidates will not be successfully developed and commercialized. For a discussion of other risks and uncertainties, and other important factors, any of which could cause our actual results to differ from those contained in the forward-looking statements, see the section entitled “Risk Factors” in our most recent quarterly report on Form 10-Q, as well as discussions of potential risks, uncertainties, and other important factors in our subsequent filings with the Securities and Exchange Commission. All information in this press release is as of the date of the release, and bluebird bio undertakes no duty to update this information unless required by law.

Inhibrx Forward-Looking Statements

Certain statements in this press release are forward looking statements that involve a number of risks and uncertainties. These statements include statements about Inhibrx’s strategy, therapeutic candidates, including its sdAb platform. These statements represent Inhibrx’s judgements and expectations as of the date of this release. Actual results may differ due to a number of factors, including, but not limited to, the potential success and efficacy of Inhibrx’s

therapeutic candidates. Inhibrx disclaims any intent or obligation to update these forward looking statements, other than as may be required by applicable law.




For bluebird bio:
Elizabeth Pingpank, 617-914-8736

Jenn Snyder, 617-448-0281


For Inhibrx:

Amy Conrad

Juniper Point