breakthroughs in diseases of abnormal mineralization

OUR MISSION: Fulfill an unmet medical need with therapeutic breakthroughs in diseases of abnormal mineralization

December 2020

Legal Disclaimer

This presentation and any statements made orally during this presentation also contain estimates and other statistical data made by independent parties and by us relating to market size and other data about our industry. This data involves a number of assumptions and limitations, and you are cautioned not to give undue weight to such data and estimates. In addition, projections, assumptions and estimates of our future performance and the future performance of the markets in which we operate are necessarily subject to a high degree of uncertainty and risk. Neither Inozyme Pharma, Inc. nor its affiliates, advisors or representatives make any representations as to the accuracy or completeness of that data or undertakes to update such data after the date of this presentation.

Forward-Looking Statement Disclaimer

This presentation contains forward-looking statements that involve substantial risks and uncertainties. All statements, other than statements of historical facts, contained in this presentation, including statements regarding our strategy, future operations, future financial position, future revenue, projected costs, prospects, plans and objectives of management, are forward-looking statements. The words “anticipate,” “believe,” “continue,” “could,” “estimate,” “expect,” “intend,” “may,” “might,” “plan,” “potential,” “predict,” “project,” “should,” “target,” “will,” “would” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. We may not actually achieve the plans, intentions or expectations disclosed in these forward-looking statements, and you should not place undue reliance on these forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in these forward-looking statements. In addition, the forward-looking statements included in this presentation represent our views as of the date of this presentation. We anticipate that subsequent events and developments will cause our views to change. However, while we may elect to update these forward-looking statements in the future, we specifically disclaim any obligation to do so. These forward-looking statements should not be relied upon as representing our views as of any date subsequent to the date of this presentation.

2

Our mission is to fulfill an unmet medical need with therapeutic breakthroughs in diseases of abnormal mineralization.

Mission Statement

3

Our mission is to fulfill an unmet medical need with therapeutic breakthroughs in diseases of abnormal mineralization.

4

Highly experienced team with strong track record➢Deep understanding of rare disease research, clinical, regulatory and commercial strategy➢Upsized IPO in July 2020 raised $128.8 million in gross proceeds

Strong scientific rationale➢Novel biology in diseases with high unmet medical needs➢Genetic basis and biological pathway for disease pathophysiology well understood➢ Predictive animal models with strong POC data➢ Lead candidate (INZ-701) showed a good safety profile and an acceptable therapeutic index in animal studies

Efficient development approach➢ Enzyme replacement therapy is a generally established therapeutic modality➢ Lead candidate with opportunities for multiple rare genetic diseases➢ Regulatory strategy in place to initiate clinical development➢ Clinical development planned in near term with a clear path to generating clinical data

Untapped market opportunity➢Underserved market opportunity with high unmet medical need and limited competition➢ Received Orphan Drug Designation for INZ-701 for the treatment of ENPP1 deficiency in the US and the EU➢Worldwide, exclusive development and commercial rights to INZ-701; IP protected through 2036

CONFIDENTIAL

Key Investment Highlights

Steve BassoSenior Vice President of Finance

Steven JunglesSenior Vice President and Chief Technical Operations Officer

5

Pedro Huertas, M.D., Ph.D.Senior Vice President and Chief Medical Officer

B o a r d o f D i r e c t o r s

Henric BjarkeSenior Vice President and Chief Operating Officer

Axel Bolte Co-founder, President and Chief Executive Officer

Management Team and LeadershipBacked by Investors Committed to Progress in Life Sciences

Yves Sabbagh, Ph.D.Senior Vice President and Chief Scientific Officer

Sarah Bhagat Axel Bolte Reinaldo Diaz Martin Edwards

Rob Hopfner Ed Mathers Lynne Sullivan Doug Treco (Chair)

Kevin Johnson, Ph.D., MBASenior Vice President, Regulatory Affairs

6

INFANCY ADOLESCENCE ADULTHOOD

What do Diseases of Abnormal Mineralization Look Like?ENPP1 Deficiency Affects Patients of All Ages in Devastating Ways

For illustrative purposes only. Individual patient experiences may vary.

7

• When abnormalities or disruptions occur, effects of excess mineralization are seen in other systems, such as the vascular system

• Bone softening, clogged arteries, and blindness are all potentially caused by excess mineralization

• ENPP1 and ABCC6 deficiencies are examples of such mineralization diseases

• In addition to excess mineralization, ENPP1 and ABCC6 deficiencies can also cause tissue growth through neointimal proliferation

Mineralization is a Fundamental Process Within the Human BodyMineralization is How Bones are Calcified, and is Crucial to the Formation of the Skeleton

Abnormalities Have Potentially Fatal Systemic Impact

8

Diversity of Abnormal Mineralization Manifestation Allows Us to Pursue Multiple Therapeutic Opportunities

GENETIC DISEASES NON-GENETIC DISEASES

*Lead Indications

PREVALENCE

ENPP1 deficiency*

ABCC6 deficiency*

Calciphylaxis

Vascular disease with neointimal proliferation

Mineralization & Neointimal Proliferation

11,000 –12,000 (worldwide)

~1,800 (per year in the U.S.)

>67,000 (worldwide)

Indication dependent

Program Exploring Several Potential IndicationsInitial focus on Genetic Diseases followed by Expansion into Non-Genetic Diseases

9

PROGRAM ASSETSTAGE OF DEVELOPMENT NEXT

ANTICIPATED MILESTONEResearch

IND Enabling

Phase 1/2 Phase 2/3

GENETIC DISEASES

ENPP1 DeficiencyINZ-701 (ENPP1-Fc)

File IND* and CTA2H 2020

ABCC6 DeficiencyINZ-701 (ENPP1-Fc)

File CTA2H 2020

NON-GENETIC DISEASES

CalciphylaxisINZ-701 (ENPP1-Fc)

Generate pre-clinical proof of concept

Diseases of Neointimal Proliferation

INZ-701 (ENPP1-Fc)

Generate pre-clinical proof of concept

* Currently on clinical hold pending completion of ongoing GLP toxicology studies.

10

Understanding the Biology of ENPP1 and ABCC6

ABCC6 = Adenosine triphosphate binding cassette transporter protein subfamily C member 6; AMP=adenosine monophosphate; ARHR2 = Autosomal recessive hypophosphatemic rickets type 2; ATP=adenosine triphosphate; ENPP1 = ectonucleotide pyrophosphatase/phosphodiesterase 1; PPi = pyrophosphate

References: 1. Jansen RS, et al. Arterioscler Thromb Vasc Biol. 2014;34(9):1985-1989. 2. Nitschke Y, et al. Am J Hum Genet. 2012;90(1):25-39. 3. Nitschke Y, et al. Exp Mol Med. 2018;50(10):1-12.

How ENPP1 and ABCC6 Work The Biologic Pathway that Regulates Mineralization and Neointimal Proliferation

ATP

ATP

ABCC6 ENPP1 CD73

INTRACELLULAR

EXTRACELLULAR

Maintains Healthy Mineralization

• PPi inhibits growth and formation of hydroxyapatite – Maintains healthy bones and teeth– Inhibits pathological ectopic

mineralization (i.e., mineralization of arteries, organs, and joints)

Maintains Healthy Vessel Wall Thickness

• Adenosine inhibits neointimal proliferation

AdenosinePPi

Tunicaexterna

Arterylumen

Tunica media

Tunica intima

AMP

11

References: 1. Jansen RS, et al. Arterioscler Thromb Vasc Biol. 2014;34(9):1985-1989. 2. Nitschke Y, et al. Am J Hum Genet. 2012;90(1):25-39. 3. Nitschke Y, et al. Exp Mol Med. 2018;50(10):1-12. 4. Orriss IR, et al. Curr Opin Pharmacol. 2016;28:57-68. 5. Boyce AM, et al. Curr Osteoporos Rep. 2020;18(3):232-241.

ENPP1 DeficiencyLow Levels of PPi and Adenosine Lead to Pathological Mineralization and Neointimal Proliferation


ATP

ATP

ABCC6 ENPP1 CD73

INTRACELLULAR

EXTRACELLULAR

Pathological Mineralization Neointimal Proliferation

Ectopic mineralization(arteries, joints, and organs)

Under-mineralization of bones

Calcification of descendingaorta and arteries

Mineralization ofshoulder joint

Irregularities in the distal femoral metaphyses and rickets

Tunicaexterna

Arterylumen

Tunica media

NeointimalProliferation

Tunicaexterna

Arterylumen

Tunica media

AdenosinePPi

AMP

12


ABCC6 Deficiency Low Levels of PPi and ENPP1 Lead to Pathological Mineralization and Neointimal Proliferation

ATP

ATP

ABCC6 ENPP1 CD73

INTRACELLULAR

EXTRACELLULAR

AdenosinePPi

AMP

Pathological Mineralization

CT Scan of Calcification Histology of Vascular Calcification Skin Histology of Skin Alterations

13

1Hypophosphatasia Reported in Whyte et al. JCI Insight. 2016;1(9):e859712Nitschke et al., 20183Kauffenstein et al., 20184O'Neill et al, 2010

14

Normalization of PPi is an Objective in Several Disease Conditions

ENPP1 Deficiency / GACI/ARHR22

ABCC6 Deficiency / Pseudoxanthoma Elasticum (PXE)3

HPP1

No

rmal

Pla

sma

PPi (

nM

)

Chronic Kidney Disease4

Inozyme Therapeutic Objective:Normalization of PPi-Levels

Strensiq

Extracellular domain

Fcfragment

INZ-701

INZ-701: Inozyme’s Drug CandidateDrug Candidate Designed to Replace Lost Enzymatic Function of ENPP1 and ABCC6

15

• Protein: Recombinant human ENPP1 (Ectonucleotide pyrophosphatase/phosphodiesterase 1)

• Construct: Recombinant Fc fusion protein with soluble extracellular domain of ENPP1

• Dosing: s.c. / Potentially as long as weekly

• Enzymatic Properties: High catalytic efficiency (Kcat/Km)

INTR

AC

ELLU

LAR

EXTRACELLULAR

ENPP1

I NZ-701

+

16


*Lead Indications

PREVALENCE

Calciphylaxis


~1,800 (per year in U.S.)

>67,000 (worldwide)


11,000 –12,000 (worldwide)ENPP1 deficiency*

ABCC6 deficiency*


Biochemical Consequences of Calcification Results of Tx Restoring Growth Increased Survival

100% survival of treated asj/asj-mice; normalized PPi levels

Dosing: 10mg/kg ENPP1-Fc, QD, s.c.

0

50

100

0 20 40 60

Per

cen

t Su

rviv

al

Days Elapsed

Treated

Untreated

0

5

10

15

WT Treated Untreated

uM

PP

i

Plasma PPi (uM)

5

10

15

20

10 20 30 40 50

Wei

ght

(g)

Age (days)

0

20

40

60

80

100

WT+ Veh

HOM,2 wkold

Veh ENPP11250

ENPP12500

ENPP15000

Ao

rta

Cal

ciu

m C

on

ten

t(n

mo

l/m

g ti

ssu

e)

Aorta Calcification

HOM

80%

**95%

**

17

Sources: 1, 3, 4: Albright RA, et al., 2015; 2: Khan T, Dis Model Mech, 2018 Oct 8; 11 (10)

WT

Treated

Untreated

Treatment with ENPP1-Fc prevented early mortality of asj mice

ENPP1-Fc Replacement Prevented Vascular Calcification and Mortality in a Mouse Model

Treatment with ENPP1-Fc normalized plasma PPi levels in asj mice

Reduced arterial calcification Restored weight

1 2 3 4

INZ-701 Restored PPi-Levels in a Predictive Murine Model

18

WT, V

ehic

le

asj,

Vehic

le

asj,

0.2m

g/kg

asj,

1mg/k

g

asj,

5 m

g/kg

0

500

1000

1500

ENPP1 Activity

EN

PP

1 a

cti

vit

y (

mO

D/m

in)

WT, V

ehic

le

asj,

Vehic

le

asj,

0.2m

g/kg

asj,

1mg/k

g

asj,

5 m

g/kg

-1

0

1

2

3

4

5

PPi

Pla

sm

a P

Pi (

M)

Asj-Mouse Model:

• Failure to thrive and gain weight

• Extensive vascular calcification

• Premature mortality• Mimics human disease

Therapy start at age of 2 weeks (D1)and end at 10 weeks (D56)

Sources: Internal, Unpublished Data

INZ-701 Prevented Cardiovascular Calcification

19CONFIDENTIAL

INZ-701 Prevented Calcification in the Kidney, Spleen, Lung and Liverof asj Mice

Mice on the acceleration diet, starting at week two, with both INZ-701 and vehicle control every other day for eight weeks.

WT, V

ehic

le

asj m

ice,

veh

icle

asj m

ice,

0.2

mg/k

g

asj m

ice,

1m

g/kg

asj m

ice,

5m

g/kg

0

50

100

150

200

250

Kidney

Calc

ium

co

nte

nt

(nm

ol/m

g o

f ti

ssu

e)

******

****

(P=0.006)

(P<0.0001)

(P<0.0001)

WT, V

ehic

le

asj m

ice,

veh

icle

asj m

ice,

0.2

mg/k

g

asj m

ice,

1m

g/kg

asj m

ice,

5m

g/kg

0

10

20

30

40

50

Spleen

Calc

ium

co

nte

nt

(nm

ol/m

g o

f ti

ssu

e)

********

ns (P=0.3472)

(P<0.0001)

(P<0.0001)

WT, v

ehic

le

asj m

ice,

veh

icle

asj m

ice,

0.2

mg/k

g

asj m

ice,

1m

g/kg

asj m

ice,

5m

g/kg

0

1

2

3

4

5

Lung

Calc

ium

co

nte

nt

(nm

ol/m

g o

f ti

ssu

e)

******

ns (P=0.1966)

(P=0.0003)

(P=0.0001)

WT, v

ehic

le

asj m

ice,

veh

icle

asj m

ice,

0.2

mg/k

g

asj m

ice,

1m

g/kg

asj m

ice,

5m

g/kg

0

1

2

3

Liver

Calc

ium

co

nte

nt

(nm

ol/m

g o

f ti

ssu

e)

*******

** (P=0.0032)

(P=0.0005)

(P<0.0001)

20Sources: Internal, Unpublished Data

INZ-701 Prevented Bone Loss and Restored Growth in asj Mice

21

Corrected bone defects1

Rescued growth defect2

Restores Trabecular Number

RestoresCorticalThickness

WT Untreated Treated

ENPP1 Deficient


Average Trabecular Number (1/mm)

Average Cortical Thickness (mm)

2.601

0.174

1.407

0.113

2.213

0.148

0 20 40 60

5

10

15

20

25

Days

Bo

dy

We

igh

t (g

ram

)

WT

Untreated

Treated

ENPP1Deficient

INZ-701 Prevented Neointimal Proliferation in ENPP1-DeficientMurine Model

22

Histology1

Intimal Area2

ttw/tt

w v

ehic

le

ttw/tt

w E

NPP1

0.0

0.1

0.2

0.3

0.4

0.5

0.6

0.7 ***

inti

mal

are

a [

mm

2]

Untreated Treated

ENPP1 Deficient

p<0.001

Histological Analysis of Preventive Treatment in Mice Ligated for 14 Days


23


*Lead Indications

PREVALENCE

Calciphylaxis



>67,000 (worldwide)



ABCC6 deficiency*


INZ-701 normalized PPi and reduced Tissue Calcification in Abcc6 -/- miceSupports Clinical Development of INZ-701 in PXE

24

• Dose: 2 and 10mg/kg, q.o.d.• Duration: ~4wk of age to ~6 wk of age • All animals are given GK1.5• All animals on normal diet

WT*

Veh

icle

2mg/k

g

10m

g/kg

0

100

200

300

Ca

(

g/g

ram

tis

su

e)

Vibrissae Calcification

Abcc6-/-

********

• Dose: 2 and 10mg/kg, q.o.d.• Duration: ~4wk of age to ~12 wk of age • All animals are given GK1.5• All animals on normal diet

WT*: age-matched WT mice

WT

vehic

le

2mg/k

g

10m

g/kg

0

1

2

3

4

5

Plasma PPi

PP

i (

M)

Abcc6-/-

Sources: Internal, Unpublished Data**** P ≤ 0.0001

25


*Lead Indications

PREVALENCE

Calciphylaxis



>67,000 (worldwide)



ABCC6 deficiency*


26

Histology1

Intimal Area2

Histological Analysis of Preventive Treatment in Mice Ligated for 14 Days

WT vehicle WT ENPP10.0

0.1

0.2

0.3 ***

inti

mal

are

a [

mm

2]

Future Expansion Possibility in Non-Genetic Diseases INZ-701 Treatment Prevented Neointimal Proliferation in Normal Mice

Sources: Internal, Unpublished Data*** P ≤ 0.001

27

Our Approach to Establish Preclinical Proof of Concept for INZ-701 for Multiple Indications


*Lead Indications

PREVALENCE

ENPP1 deficiency*

ABCC6 deficiency*

Calciphylaxis



11,000 –12,000 (worldwide)


>67,000 (worldwide)


Our Indications, Clinical Development Plans, Regulatory Status and CMC

28

ENPP1 Deficiency: A Disease With High Morbidity and Mortality

29

Calcification Skeletal Defects

Generalized Arterial Calcification of Infancy (GACI) Autosomal Recessive Hypophosphatemic Rickets Type 2 (ARHR2)Historical Definition

ENPP1 DeficiencyNew Definition

0 – 3 Years 18+ Years3 – 18 Years

Organ Calcification & Neointimal Proliferation

Organ and arterial calcification

Obstructive neointimal proliferation

ENPP1 Deficiency Natural History Study Informs Clinical Development

30

Calcification and Organ Dysfunction Occur Sequentially and Progressively

in ENPP1 Deficiency

3Calcification, Skeletal Abnormalities, and Rickets

Occur Simultaneously From Birthin ENPP1 Deficiency

2Natural History Study Includes Data From 2 Sites:

NIH and Universität Münster (n=127)

1

0 5 3025201510

Age (Year)

0 5 3025201510

Age (Year)

Tim

e to

Eve

nt

Tim

e to

Eve

nt

Tim

e to

Eve

nt

• 25% quartile estimate: 0.1 years (95% CI: 0.04 to 0.17)• Median survival estimate: 14.9 years (95% CI: 0.41 to NR)

Over 40% mortality in first 12 months of life with a diagnosis of ENPP1 Deficiency

Postnatal Rickets

P s e u d o x a n t h o m a e l a s t i c u m ( P X E )

31

ABCC6 Deficiency (PXE) is Also a Serious Disease Involving Pathological Mineralization and Neointimal ProliferationFocus on Patients with Severe Manifestation Leading to High Unmet Medical Need

Pseudoxanthoma elasticum (PXE)Historical Definition

ABCC6 DeficiencyNew Definition

Onset in 20s-30s | Progressively Effects Adult Population

Skin Cardiovascular

z z

Retina Calcification

Two Planned First-in-Human Phase 1/2 Trials (In Patients)

32

ENPP1 Deficiency

ABCC6 Deficiency

Post Regulatory submissions (US ENPP1 Deficiency*)

Open label

Dose escalation

Age >18 years

Sample size n=9

Safety and tolerability

PK/PD

Plasma PPi levels

Biochemical and physiological parameters

7-week duration

Trial1

Trial2

* Currently on clinical hold pending completion of ongoing GLP toxicology studies.

Endpoint Measurement

PPi Blood Biochemistry

Calcification High resolution radiography

Survival Alive After 6 Months

Illustrative Goals of our Planned Trials



BMDHigh resolution radiography

Rickets, Growth, Organ Function

MRI, RGI-C, RSS, Dexa



Bone Pain Pain Scores

Osteomalacia MRI, Bone biopsies

ENPP1 Deficiency: Clinical Strategy for INZ-701 is to Link Restoration of Plasma PPi to Measures of Physiological and Clinical Efficacy

0 – 3 Years 18+ Years3 – 18 Years

33

18+ Years

ABCC6 Deficiency (PXE)



CalcificationHigh resolution radiography

Cardiac Function/Pain

Doppler, EGG, CT scan, Pain scores

ABCC6 Deficiency: Clinical Strategy for INZ-701 is to Link Restoration of Plasma PPi to Measures of Physiological and Clinical Efficacy

Illustrative Goals of our Planned Trial

34

Regulatory Status and Strategy for Phase 1 / 2 Trials in ENPP1 Deficiency

Status

➢ Orphan drug designation obtained in US and EU➢ IND filed with the FDA July 2020➢ Pre CTA meetings held with European Authorities➢ CTA filed with MHRA October 2020➢ Scientific advice meetings held with EMA

Next Steps➢ Address FDA clinical hold with additional data and File CTA➢ Engage with regulatory authorities at End of Phase 1/2 meeting to discuss registration endpoints

35

2018 2019 2020

June 2018

Orphan designation received

April 2019Pre-IND Meeting, face-to-face

Mar 2020

2nd Pre-IND Meeting

2018 2019 2020

July 2018

Orphan designation received

July 2019Scientific Advice Meeting, face-to-face

May 2020

Pre CTA meetings

July 2020

Filed IND

Robust CMC Process Designed for Stability and Scalability

Formulation DevGMP Mfg

GMP Mfg

GMP Mfg

Virus Removal Validation

Ongoing Stability

QC Assay Dev

36

✓ Recombinant Fc-fusion protein with the soluble extracellular domain of ENPP1 produced in CHO cells, titers ranging from 800 to 900 mg/L

✓ Fully tested master cell bank stored in multiple locations for redundancy

✓ Large scale production confirmed (GMP run at 1000L scale)

✓ Protein purified using a well-defined process suitable for cGMP manufacturing, Protein A purification with multiple virus removal and virus inactivation steps

✓ Final product concentrated to 50 mg/mL for SQ injections (Once weekly)

✓ Consistent process performance through scale-up—process easily scalable, supply chain established

37

Commercial Opportunity

38

Abnormal Mineralization is the Underlying Cause of Several Debilitating Diseases Allowing Us to Pursue Multiple Therapeutic Opportunities

P R E VA L E N C E O F L E A D I N D I C AT I O N S

ENPP1 Deficiency

ABCC6 Deficiency


11,000 –12,000 (worldwide)

>67,000 (worldwide)

39

SCREENING SURVEY COMPLETES:

# of Physicians US Canada UK France Germany Italy Spain

Geneticists 42 5 10 7 4 19 11

Endocrinologists 160 25 63 54 35 97 72

Ped Endos 33 3 10 9 6 13 16

Ped Cardiologists 24 -- 1 4 7 3 5

Orthopedists 174 8 56 33 78 33 24

Neonatologists 75 8 34 22 35 18 31

TOTAL 508 49 174 129 165 183 159

Source: Global online survey, conducted in local language, March 22 to April 15, 2019.

1,367 Target Physicians in 7 Key Markets Responded to Survey

37% 26%Confirmed Patients (N=506 Physicians)

Managing Patients(N=355 Physicians)

2,976 Confirmed Patients 1,682 Managed Patients

1,001 Patient Profiles Collected

Over 600 Patients Alive

International Physician Survey Identified Significant Numbers of Treatable ENPP1 Deficiency Patients

1,367 Physician Responses

40

Advocating

Presenting

Discussing

Educating

Ongoing Physician Identification and Educational ActivitiesBuilding KOL Relationships and Educating the Scientific and Patient Community

41

Finance

Financial Overview and Upcoming Anticipated Milestones

42

ENPP1 Deficiency ABCC6 Deficiency New Indications and Pipeline

Clearance of IND and CTAsEarly 2021

Initiation of Phase 1/2 clinical trialH1 2021

Initiation of prospective natural history studyH1 2021

Preliminary safety and biomarker data from Phase 1/2 clinical trialH2 2021

Neointimal proliferationpre-clinical POC

Calciphylaxispre-clinical POC

Gene Therapy Programselect development candidate

FundingHistory

Pre IPO • $116 M in Private Financings : $49 M January 2017, $67 M March 2019

IPO • July 2020 – Net proceeds of approximately $116.5 M

Cash Position • Cash of $171.7 million as of September 30, 2020

Clearance of CTAsEarly 2021

Initiation of Phase 1/2 clinical trialH1 2021

Preliminary safety and biomarker data from Phase 1/2 clinical trialH2 2021

43

Highly experienced team with strong track record➢Deep understanding of rare disease research, clinical, regulatory and commercial strategy➢Upsized IPO in July 2020 raised $128.8 million in gross proceeds

Strong scientific rationale➢Novel biology in diseases with high unmet medical needs➢Genetic basis and biological pathway for disease pathophysiology well understood➢ Predictive animal models with strong POC data➢ Lead candidate (INZ-701) showed a good safety profile and an acceptable therapeutic index in animal studies

Efficient development approach➢ Enzyme replacement therapy is a generally established therapeutic modality➢ Lead candidate with opportunities for multiple rare genetic diseases➢ Regulatory strategy in place to initiate clinical development➢ Clinical development planned in near term with a clear path to generating clinical data

Untapped market opportunity➢Underserved market opportunity with high unmet medical need and limited competition➢ Received Orphan Drug Designation for INZ-701 for the treatment of ENPP1 deficiency in the US and the EU➢Worldwide, exclusive development and commercial rights to INZ-701; IP protected through 2036

Key Investment Highlights

44

Thank You!

Inozyme Pharma, Inc.321 Summer Street, Suite 400Boston, MA 02210

breakthroughs in diseases of abnormal mineralization

Documents