Corporate Overview

November 2021

2

Intellia Therapeutics’ Legal Disclaimer

This presentation contains “forward-looking statements” of Intellia Therapeutics, Inc. (“Intellia”, “we” or “our”) within the meaning of the Private Securities Litigation Reform Actof 1995. These forward-looking statements include, but are not limited to, express or implied statements regarding Intellia’s beliefs and expectations regarding our: ability tocomplete clinical studies for NTLA-2001 for the treatment of transthyretin (“ATTR”) amyloidosis, successfully submit additional regulatory applications in other countries, andevaluate NTLA-2001 in a broader ATTR population; clinical data from the ongoing single- ascending dose portion of the Phase 1 study evaluating NTLA-2001; ability to initiatea clinical trial for NTLA-5001 for the treatment of acute myeloid leukemia (“AML”) by the end of 2021; ability to generate data to demonstrate NTLA-5001 as a potential best-in-class engineered T cell therapy designed to treat all genetic subtypes of AML; plans to evaluate in preclinical studies the potential use of NTLA-5001 to treat Wilms’ Tumor 1(“WT1”)-positive solid tumors; expectation to enroll a patient in a clinical study for NTLA-2002 for the treatment of hereditary angioedema (“HAE”) in 2021; expectations ofevaluating safety, tolerability and measures of activities of NTLA-2002 in patients with HAE; plans to nominate at least one additional development candidate in 2021; plans tonominate an allogeneic cell therapy candidate in 1H 2022; plans to advance and complete preclinical studies for our research programs; development of our modular platformto advance our complex genome editing capabilities; further development of our proprietary genome editing tools for research and therapeutic development, includingsequential editing and base editing; presentation of additional data at upcoming scientific conferences, and other preclinical data in 2021; advancement and expansion of ourCRISPR/Cas9 technology to develop human therapeutic products; ability to maintain and expand our related intellectual property portfolio, and avoid or acquire rights to validintellectual property of third parties; ability to demonstrate our platform’s modularity and replicate or apply results achieved in preclinical studies, including those in our ATTR,AML, and HAE programs, in any future studies, including human clinical trials; ability to develop other in vivo or ex vivo cell therapeutics of all types, and those targeting WT1 inAML in particular, using CRISPR/Cas9 technology; ability to optimize the impact of our collaborations on our development programs, including but not limited to ourcollaboration with Regeneron Pharmaceuticals, Inc. including our co-development programs for hemophilia A and hemophilia B; Regeneron’s ability to successfully co-developproducts in the hemophilia A and B programs, and the potential timing and receipt of future milestones and royalties, or profits, as applicable, based on our license,collaboration and, if applicable, co-development agreements with Regeneron and Novartis Institutes for BioMedical Research, Inc.; statements regarding the timing ofregulatory filings and clinical trial execution, including dosing of patients, regarding our development programs; potential commercial opportunities, including value and market,for our product candidates; our expectations regarding our use of capital and other financial results during 2021; and our ability to fund operations beyond the next 24 months.

Any forward-looking statements in this presentation are based on management’s current expectations and beliefs of future events, and are subject to a number of risks anduncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks anduncertainties include, but are not limited to: risks related to our ability to protect and maintain our intellectual property position; risks related to valid third party intellectualproperty; risks related to our relationship with third parties, including our licensors and licensees; risks related to the ability of our licensors to protect and maintain theirintellectual property position; uncertainties related to regulatory agencies’ evaluation of regulatory filings and other information related to our product candidates; uncertaintiesrelated to the authorization, initiation and conduct of studies and other development requirements for our product candidates; the risk that any one or more of our productcandidates, including those that are co-developed, will not be successfully developed and commercialized; the risk that the results of preclinical studies or clinical studies willnot be predictive of future results in connection with future studies; and the risk that our collaborations with Regeneron or our other ex vivo collaborations will not continue or willnot be successful. For a discussion of these and other risks and uncertainties, and other important factors, any of which could cause Intellia’s actual results to differ from thosecontained in the forward-looking statements, see the section entitled “Risk Factors” in Intellia’s most recent quarterly report on Form 10-Q as well as discussions of potentialrisks, uncertainties, and other important factors in Intellia’s other filings with the Securities and Exchange Commission (“SEC”). All information in this presentation is as of thedate of the release, and Intellia undertakes no duty to update this information unless required by law.

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Intellia’s Investment Summary

Transforming lives of people with severe diseases

by developing curative genome editing treatments

Full-Spectrum

Strategy

Advancing therapies for

diseases with high unmet need

Leading Genome

Editing Platform

Building differentiated

modular solutions

Broad Portfolio

Opportunity

Driving pipeline expansion

with robust R&D engine

In Vivo

Ex Vivo

4

Building a Full-Spectrum Genome Editing Company

CRISPR creates

the therapy

CRISPR is

the therapy

Immuno-oncology

Autoimmune diseases

Genetic diseases

Modular Platform

LNP CELL

RNA

In Vivo Ex Vivo

LNP: Lipid Nanoparticle

CRISPR/Cas9

5

PROGRAM APPROACH ResearchCandidateSelection

IND-Enabling

Early-Stage Clinical

Late-Stage Clinical

PARTNER

In Vivo: CRISPR is the therapy

NTLA-2001: Transthyretin Amyloidosis Knockout

NTLA-2002: Hereditary Angioedema Knockout

NTLA-3001: AATD-Lung Disease Insertion

Hemophilia B Insertion

Hemophilia A Insertion

Research Programs Knockout, Insertion,Consecutive Edits

Research Programs Various

Ex Vivo: CRISPR creates the therapy

OTQ923 / HIX763: Sickle Cell Disease HSC

NTLA-5001: Acute Myeloid Leukemia WT1-TCR

Solid Tumors WT1-TCR

Allo Undisclosed Undisclosed

Other Novartis Programs CAR-T, HSC, OSC Undisclosed

Development Pipeline Fueled by Robust Research Engine

***

***

*

*

L E A D

L E A D

5* Lead development and commercial party ** Rights to certain in vivo targets *** Milestones & royalties only

AATD: Alpha-1 Antitrypsin Deficiency CAR-T: Chimeric Antigen Receptor T cells HSC: Hematopoietic Stem Cells OSC: Ocular Stem Cells TCR: T Cell Receptor

**

L E A D

*

6

NTLA-2001 for Transthyretin Amyloidosis (ATTR Amyloidosis):

o First-ever clinical data supporting safety and efficacy of in vivo CRISPR

genome editing in humans

o Report additional interim data from Phase 1 study Q1 2022

o Initiate Part 2, a single-dose expansion cohort, in Q1 2022

Executing Against Strategic Priorities and R&D Goals

Pipeline

Advancement

Platform

Innovation

NTLA-2002 for Hereditary Angioedema (HAE):

o Submitted first regulatory filing to initiate Phase 1 study

o Initiate enrollment in the first-in-human study by year-end

NTLA-5001 for Acute Myeloid Leukemia (AML):

o Submitted first regulatory filing to initiate Phase 1 study

o Initiate patient screening in the first-in-human study by year-end

Research Programs:

o Nominated NTLA-3001, a gene insertion development candidate, for alpha-1 antitrypsin deficiency (AATD)

o Nominated a Factor 9 gene insertion development candidate for hemophilia B in collaboration with Regeneron

o Nominate first allogeneic development candidate by 1H 2022

Clinical

Validation

o Demonstrated preclinical proof-of-concept for in vivo editing of bone marrow

o Presented first preclinical data on Intellia’s proprietary base editor

o Presented first preclinical data on Intellia’s allogeneic platform

✓

✓

✓

✓

✓

✓

✓

✓

7

LNP

RNA

CRISPR is the therapy

In Vivo

GENETIC DISEASES

Strategic Advantages:

Systemic non-viral delivery of CRISPR/Cas9 provides

transient expression

Potential curative therapy from single dose

Permanent gain of function with targeted gene insertion

Delivery to multiple tissue types enabling new therapeutic

applications

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Modular Approach to Unlocking Treatment of Genetic Diseases

PROPRIETARY LNP DELIVERY SYSTEM

Transient expression Large cargo capacity Redosing capability

ENABLES MULTIPLE EDITING STRATEGIES

Restore

Introduce functional DNA sequence

INSERT CONSECUTIVE EDITING

Any combination of knockout and insertion strategies

+AAV

Remove

Knockout toxic or compensatory genes

KNOCKOUT

Remove / Restore

++

9

NTLA-2001 for Transthyretin (ATTR) Amyloidosis

1 Ann Med. 2015; 47(8): 625–638. 2 Compiled from various sources ATTRv: Hereditary ATTR ATTRwt: Wild-Type ATTR

ATTR Amyloidosis

• Caused by accumulation of

misfolded transthyretin (TTR)

protein, which affects nerves,

heart, kidneys and eyes

• Chronic dosing is required

with current treatments

• 50,000ATTRv patients worldwide1

• ~200-500KATTRwt patients worldwide2

OUR APPROACH

• Potential to halt and

reverse disease

• Potential “one-and-done”

treatment

• Expect lifelong, stable TTR

reduction

Knock out TTR gene with a

single dose

• Reduce wild-type and

mutant TTR protein

• Aims to address

polyneuropathy and

cardiomyopathy

KEY ADVANTAGES

10

Control

Lead LNP:

3.0 mg/kg (n=3)

Lead LNP:

6.0 mg/kg (n=3)

Therapeutically

relevant serum TTR

knockdown

Single Dose

Sustained >95% Serum TTR Protein Reduction After a Single Dose in NHPs

11

NTLA-2001 Expanded Phase 1 Study

Two-part, open-label, multi-center study in adults with hereditary ATTR with

polyneuropathy (ATTRv-PN) or ATTR amyloidosis with cardiomyopathy (ATTR-CM)

SECONDARY OBJECTIVES

Evaluate efficacy on clinical measures of:

• Neurologic function in subjects with ATTRv-PN

• Cardiac disease in subjects with ATTR-CM

PRIMARY OBJECTIVES

Evaluate safety, tolerability, PK and PD

▪ Measure serum TTR levels

Single Dose

Expansion Cohort

Single Dose

Expansion Cohort

PART II

Single-Ascending

Dose Escalation

Cohorts

Single-Ascending

Dose Escalation

Cohorts

PART I Total Enrollment:

Up to 74 patients

Intervention:

Single dose

administered via an

intravenous (IV)

infusion

Potential to

advance toward

a pivotal trial for

NTLA-2001 based

on Phase 1 safety

and efficacy

data

Up to 38

ATTRv-PN

patients

Up to 36

ATTR-CM

patients

Administer selected dose

from Part I

Clinicaltrials.gov ID: NCT04601051

PK: Pharmacokinetics PD: Pharmacodynamics

12

SECONDARY OBJECTIVES

Evaluate efficacy on clinical measures of neurologic function

▪ Neuropathic impairment endpoints include NIS (Part 1 and 2) and

mNIS+7 (Part 2 only)

PRIMARY OBJECTIVES

Evaluate safety, tolerability, PK and PD

▪ Measure serum TTR levels

Total Enrollment:

Up to 38 patients,

age 18 to 80 years

PART II

Single Dose

Expansion Cohort

Intervention:

Single dose

administered via an

intravenous (IV)

infusion

Administer optimal dose

selected from Part IN = 8 subjects

Administer optimal dose

selected from Part I

*Minimum of 3 subjects per cohort Clinicaltrials.gov ID: NCT04601051

NIS: Neuropathy Impairment Score mNIS+7: modified NIS+7 PK: Pharmacokinetics PD: Pharmacodynamics

Hereditary transthyretin amyloidosis with polyneuropathy (ATTRv-PN)

NTLA-2001 Phase 1 Study: Polyneuropathy Arm

PART I

Single-Ascending Dose

N = Up to 30 subjects*

Up to 4 dose-escalation

cohorts

13*Minimum of 3 subjects per cohort Clinicaltrials.gov ID: NCT04601051

NYHA: New York Heart Association PK: Pharmacokinetics PD: Pharmacodynamics 6MWT: 6 Minute Walk Test

PART II

Single Dose

Expansion Cohort

Administer optimal dose

selected from Part IN = 12 subjects

Administer selected

dose from Part I

Hereditary transthyretin amyloidosis with cardiomyopathy (ATTRv-CM)

or wild-type cardiomyopathy (ATTRwt-CM), NYHA Class I - III

NTLA-2001 Phase 1 Study: Cardiomyopathy Arm

PART I

Single-Ascending Dose

N = Up to 24 subjects*

Up to 2 dose-escalation

cohorts

Total Enrollment:

Up to 36 patients,

age 18 to 90 years

Intervention:

Single dose

administered via an

intravenous (IV)

infusion

SECONDARY OBJECTIVES

Evaluate efficacy on clinical measures of cardiac disease

▪ Cardiac imaging, biomarkers, cardiopulmonary exercise test, 6MWT

PRIMARY OBJECTIVES

Evaluate safety, tolerability, PK and PD

▪ Measure serum TTR levels

14

NTLA-2001 Generally Well Tolerated in Acute Phase (N=6) by Day 28: All AEs Grade 1 with No Serious AEs

Preferred Term0.1 mg/kg

(n = 3)

0.3 mg/kg(n = 3)

Subjects with at least one TEAE 2 1

Headache 2

Diarrhea 1

Nausea 1

Infusion-related reaction 1

Skin abrasion 1

Vertigo positional 1

Foreign body sensation in eyes 1

Catheter site swelling 1

Acute sinusitis 1

Thyroxine decreased 1

Rhinorrhea 1

Pruritis 1

Rash 1

Data disclosed on June 26, 2021 at 2021 Peripheral Nerve Society (PNS) Annual Meeting

AE, adverse event; TEAE, treatment-emergent adverse event

No liver findings or

coagulopathy based

on laboratory testing

15

Landmark Clinical Data Show Deep, Dose-Dependent Serum TTR Reduction After Single Dose of NTLA-2001

–100

–80

–60

–40

–20

Ch

an

ge

inse

rum

TT

R

from

ba

selin

e(%

)

B

0

0 7 14

Day

21 28

Change in serum TTR in individual patients

52%47%

56%

–100

–80

–60

–40

–20

B

0

0 7 14

Day

21 28

Change in serum TTR in individual patients

84%80%

96%

Data disclosed on June 26, 2021 at 2021 PNS Annual Meeting

at 0.1 mg/kg (n = 3) at 0.3 mg/kg (n = 3)

16

✓ First-ever clinical data supporting safety and efficacy

of in vivo CRISPR genome editing in humans

✓ Reported positive interim clinical data from ongoing

Phase 1 study

Report additional interim data from Phase 1 study in

Q1 2022

Initiate Part 2, a single-dose expansion cohort,

in Q1 2022

Achievements

and Next Steps

NTLA-2001 Holds Promise to Transform the Lives of People with ATTR

17

NTLA-2002 for Hereditary Angioedema (HAE)

1 Zuraw BL. Hereditary angioedema. N Engl J Med. 2008;359:1027-1036

OUR APPROACH

• Potential “one-and-done”

treatment

• Extensive and continuous

reduction in kallikrein

activity

‒ Minimizes the risk of

breakthrough attacks

• Potential to eliminate

significant treatment burden

Knock out KLKB1 gene with

a single dose

• Reduce kallikrein activity

to prevent attacks

KEY ADVANTAGESHAE

• Genetic disease

characterized by recurring,

severe and unpredictable

swelling in various parts of

the body

• Chronic dosing is required

with current treatments

• Attacks can occur every

7-14 days on average for

untreated patients1

• 1 in 50,000HAE patients worldwide1

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LNP Delivery System:

gRNA Reprograms Genetic Target

Cas9

mRNA

AAAA

AA

AA

KLKB1

gRNA

AA

AA

Target-

specific

gRNA

TTR

gRNA

Modular Delivery Solution Enables Rapid and Reproducible Path to Clinical Development

NTLA-2002 for HAE:

Builds on ATTR program’s infrastructure,

including modular LNP delivery system

Applies insights gained from ATTR and other

research programs to liver knockout target

Platform advances expedite progression to

NHP proof-of-concept and clinical development

gRNA: Guide RNA

AAAA

19

Achieved Sustained Therapeutically Relevant Kallikrein Activity Reduction

After a Single Dose in NHPs

*Banerji et al., NEJM, 2017

Kallikrein Activity Reduction

Single Dose

Control

Dose Level #1 (n=3)

Dose Level #2 (n=3)

Dose Level #3 (n=3)

Therapeutically

relevant impact

on attack rate*

0 4 8 12 16 20 24 28 32 36 40 44 48 52

0

20

40

60

80

100

120

140

160

180

Time (Weeks)

Pla

sm

a K

allik

rein

Acti

vit

y (

% o

f B

asal)

20

PK: Pharmacokinetics PD: Pharmacodynamics

* 3 to 6 subjects per cohort; up to 2 additional cohorts, if necessary

** Optional cohort

NTLA-2002 Phase 1/2 Trial Design

Intervention: Single dose

administered via

an intravenous

(IV) infusion

International, multi-center study to assess safety, tolerability, PK, PD and

effect of NTLA-2002 on attacks in adults with Type I or Type II HAE

KEY ENDPOINTS

Random

ized Dose 1 (N=10)

Dose 2** (N=10)

Placebo Arm (N=5)

PHASE 1

Open-label,

Single-ascending Dose

PHASE 2

Expansion study to

confirm recommended doseTotal

Enrollment:

Up to 55 patients,

age 18 and older

• Evaluate safety and tolerability

• Change in plasma kallikrein protein and activity levels

• Change in attack rates (Phase 2)

3 dose-escalation cohorts*

21

✓ Achieved year-long therapeutically relevant kallikrein

activity reduction after a single dose in NHPs

✓ Submitted first regulatory filing to initiate a Phase 1 study

Initiate enrollment in the first-in-human study by year-end

NTLA-2002 for HAE: Advancing Toward the Clinic

Achievements

and Next Steps

22

GOI

GOI

Promoter

Precisely Create

Insertion Site

LNP AAV

Deliver Insertion

Template

Targeted, Stable Gene Insertion

Beyond Knockout: Insertion Technology Enables Production of High Levels of

Therapeutic Protein

Potential best-in-class modality

for a gain of function

1 Stoller & Aboussouan The Lancet, 2005

Normal range of circulating human A1AT protein levels(~1000-2700 µg/mL, or 20-53 µM)1

Insertion (n=3)

Buffer Control (n=3)

Therapeutically relevant1

(571 µg/mL, or 11 µM)

2000

1500

1000

500

0

0 4 8 12 16 20 24 28 32 36 40 44 48 52

Cir

cu

lati

ng

hA

1A

T (µ

g/m

L)

Time (weeks post insertion)

Normal

range1

1 Stoller & Aboussouan The Lancet, 2005

Alpha-1 Antitrypsin Deficiency (AATD)

Achieved Normal hA1AT Protein Levels in NHPs

23

Clinical Validation of LNP Delivery Platform Supports In Vivo Pipeline Acceleration

Genetic Diseases

Targets Across

Multiple Tissues

Unlock

Full Potential

First Wave of Products

Unlock Liver Targets

Address diseases with genetically

defined targets in the liver

❑ Remove a toxic protein via knockout

❑ Restore a functional protein via insertion

Enable access to treat

diseases across multiple

tissue types

ATTR, HAE, AATD, Hem B

Hem A, PH, Undisclosed Indications

Bone Marrow, CNS,

Other Tissues

CNS: Central Nervous System Hem A and B: Hemophilia A and B PH: Primary Hyperoxaluria`

✓

24

CRISPR creates the therapy

Ex Vivo

IMMUNO-ONCOLOGY / AUTOIMMUNE DISEASES

Strategic Advantages:

Utilizing proprietary CRISPR engineering platform to create

differentiated cell therapies for IO and AI diseases

Targeting modalities, such as TCR, with broad potential

in multiple indications

Focused on reproducing natural cell physiology for improved

safety and efficacy

CELL

25

Proprietary Engineering Platform to Power Next-Generation Engineered Cell Therapies

LNP-BASED CELL ENGINEERING PLATFORM

Highly efficient sequential editing Optimal cell performance Scalable manufacturing process

ENABLES VERSATILE SOLUTIONS BY “MIXING AND MATCHING”

Targeting Modality

TCRs

Cell Type Rewiring Instructions

HSCs, T cells

NK: Natural Killer TCR: T Cell Receptor

Immune-enhancing edits

26

Enhanced T cell

expansion

Improved Safety Profile vs.

Traditional Multiplex Editing

Unt

reat

ed

Sta

ndar

d Pro

cess

Inte

llia P

roce

ss

0

5

10

15

Cum

ula

tive T

ranslo

cation

Events

per

200 C

ells

Complex Translocations

Reciprocal Translocations

Translocations to other chromosomes

LNP-Based Cell Engineering Technology Optimizes Cell Health and Function

Platform capability can be applied broadly to various cell types and targeting receptors

Standard Process: Cas9/sgRNA RNP electroporation based on manufacturer’s instructions

Enhanced T cell

Expansion

Unt

reat

ed

Stand

ard

Pro

cess

Inte

llia P

roce

ss

0

50

100

Fold

Expansio

n

27

NTLA-5001 for Acute Myeloid Leukemia (AML)

1 NIH SEER Cancer Stat Facts: Leukemia – Acute Myeloid Leukemia (AML)2 GlobalData EpiCast Report: Acute Myeloid Leukemia July 2020, 7MM: Seven Major Markets (includes U.S.)

OUR APPROACH

• Potential to address all

mutational subtypes of AML

• Low WT1 expression in

normal tissues for improved

safety

• TCR sourced from healthy

donor T cells minimizes

immune toxicity

KEY ADVANTAGESAML

• Most common acute leukemia

in adults1

• ~20KNew cases in the U.S. in 20201

• > 40KNew cases in the 7 Major

Markets in 20192

• < 30%5-year overall survival1

Engineer Wilms’ Tumor

Type 1 (WT1)-directed

TCR-T cells capable of

specifically killing

AML blasts

28

NTLA-5001: Potential Best-in-Class Engineered T Cell Therapy For AML

WT1-specific TCR Inserts a natural, high-avidity TCR to replace

native TCR for upgraded safety profile

‒ Activates both cytotoxic and helper T cells

Specifically targets Wilms’ Tumor 1 (WT1),

an antigen overexpressed in >90% of AML blasts1

‒ Recognizes an epitope (VLD2) presented broadly

by AML blasts with the HLA-A*02:01 allele3

Modified by proprietary cell engineering

technology for optimized cell health and function

1Cilloni et al., J Clin Oncol, 20092VLD is the WT1(37-45) epitope VLDFAPPGA3 Refer to http://www.allelefrequencies.net for HLA frequency data

In collaboration with IRCCS Ospedale San Raffaele

29

NTLA-5001: Robust Anti-Tumor Efficacy Observed Against Patient-Derived AML Blasts in Mouse Model

0 5 10 15 200

50

100

150

200

25 30 35 40 45 50 55

500

1000

1500

2000

2500

Days post AML Infusion

pA

ML C

ells

/μL o

f B

lood

T cell infusions

****

*****

MART1-TCR (Control, Electroporation Process)

WT1-TCR (Electroporation Process)

WT1-TCR (LNP Process)

pAML Alone

NTLA-5001’s

lead TCR-T cells

30

NTLA-5001: Uniform Expression of Therapeutic TCR for Potent Tumor Targeting

Apheresis & T Cell

CryopreservationThaw and

Re-infusion

Rapid Cell Engineering: 10 Days

THAWT cells

ACTIVATET cells

REMOVE endogenous TCR

EXPANDrapidly

HARVEST

and FREEZE

INSERT WT1 TCR in locus

Estimated

vein-to-vein

time of

~3 weeks

Sequential KO of TRAC and TRBC

Insert

tgTCR

31

CRISPR Engineering Overcomes Key Challenges of Traditional TCR Approaches

Traditional tgTCR Addition

CRISPR/Cas9 tgTCR Replacement

Mixed TCRs

tgTCRs only

Heterogenous

Cell Product

Homogenous

Cell Product

tgTCR: transgenic therapeutic TCR

Removal of Endogenous TCR

Prevents Mispairing60

40

20

0

% C

ell

s w

ith

Mis

pa

ired

TC

Rs

TCR A TCR B TCR C TCR D

TRAC KO Only + Insertion

Intellia’s Approach (TRAC and TRBC KO + Insertion)

32

NTLA-5001 Phase 1/2a Trial Design

*3-6 subjects per cohort Clinicaltrials.gov ID: NCT05066165

Lower disease burden: Patients with less than 5% AML blasts in bone marrow

Higher disease burden: Patients with relapsed/refractory disease with greater than or equal to 5% AML blasts in bone marrow

KEY

ENDPOINTS

• Evaluate safety and tolerability

• Characterize cell kinetics of NTLA-5001

• Determine anti-tumor activity

Dose 1 (N=9)

Dose 2 (N=9)

PHASE 1

Dose Escalation

Two-ascending arms: Up to 3 cohorts*

PHASE 2

Expansion CohortsTo confirm recommended

dose from each arm of Phase 1

Total Enrollment:

Up to 54 patients,

age ≥18 years

Key Inclusion Criteria:

• Relapsed/refractory AML

after one or more therapies

• Post transplant patients

are eligible

• HLA-A*02:01 positive

Open-label, multi-center study of NTLA-5001, a WT1-directed TCR immunotherapy, in adults with AML

ARM 2: Higher Disease Burden

ARM 1: Lower Disease BurdenIntervention:

Single dose

administered via

intravenous (IV)

infusion

33

✓ Demonstrated high anti-tumor activity in preclinical proof-

of-concept models

✓ Submitted first regulatory filing to initiate Phase 1 study

Initiate patient screening in the first-in-human study by

year-end

NTLA-5001 for AML: Advancing Toward the Clinic

Achievements

and Next Steps

34

Ex Vivo Pipeline Expansion Strategy

Unlock

Full Potential

First Wave of Products

Address a variety of cancers

• Target new antigens with TCR

identification and cell engineering platform

• Allogeneic solution

Advance cell therapy for

cancer and autoimmune

diseases

• Novel immune-enhancing edits

AML, Undisclosed IndicationsPrioritize diseases with

significant unmet need

Immuno-oncology

Novel Cell Rewiring

for Cancers and

Autoimmune DiseasesHematological and Solid Tumors

35

Upcoming 2021 and Beyond Milestones

ATTR

AMLInitiate patient screening in the first-in-human study by year-end

Initiate enrollment in the first-in-human study by year-end

In Vivo

In Vivo

Ex Vivo

NTLA-2001

NTLA-5001

R&D

Advancements

HAE

NTLA-2002

Initiate Part 2, a single-dose expansion cohort, in Q1 2022

Report additional interim data from Phase 1 study in Q1 2022

Nominate first allogeneic development candidate by 1H 2022

36

Unlocking the Full Potential of CRISPRSolving in vivo delivery supports rapid expansion of pipeline to broad patient population