MDNA Q3 2020 September...Conc (pM) pSTAT5+ (%) Signaling in CD8+ T Cells rhIL-2 MDNA11 0.01 0.1 1 10 100 1000 10000 100000 0 20 40 60 80 100 Conc (pM) pSTAT5+ (%) MDNA11 MDNA11 rhIL-2

Nasdaq: MDNATSX: MDNA

©2020 Medicenna. All Rights Reserved.

Q3 2020

Forward-Looking Statements

Q3 2020 Medicenna Corporate Overview

Certain statements in this presentation are “forward-looking statements. Any statements that express or involve discussions with respect to predictions, expectations, beliefs, plans, projections, objectives, assumptions or future events or performance (often, but not always using words or phrases such as “expect”, “seek”, “endeavour”, “anticipate”, “plan”, “estimate”, “believe”, “intend”, or stating that certain actions, events or results may, could, would, might or will occur or be taken, or achieved) are not statements of historical fact and may be “forward-looking statements”.

Forward-looking statements are based on expectations, estimates and projections at the time the statements are made that involve a number of risks and uncertainties which would cause actual results or events to differ materially from those presently anticipated. Forward-looking statements are based on expectations, estimates and projections at the time the statements are made and involve significant known and unknown risks, uncertainties and assumptions. A number of factors could cause actual results, performance or achievements to be materially different from any future results, performance or achievements that may be expressed or implied by such forward-looking statements. These include, but are not limited to, the risk factors discussed in the public filings made by Medicenna with the applicable securities commissions, including the Annual Information Form dated May 14, 2020. Should one or more of these risks or uncertainties materialize, or should assumptions underlying the forward-looking statements prove incorrect, actual results, performance or achievements could vary materially from those expressed or implied by the forward-looking statements contained in this document. These factors should be considered carefully and prospective investors should not place undue reliance on these forward-looking statements.

Although the forward-looking statements contained in this document are based upon what Medicenna currently believes to be reasonable assumptions, Medicenna cannot assure prospective investors that actual results, performance or achievements will be consistent with these forward-looking statements. Except as required by law, Medicenna does not have any obligation to advise any person if it becomes aware of any inaccuracy in or omission from any forward-looking statement, nor does it intend, or assume any obligation, to update or revise these forward-looking statements to reflect new events or circumstances.

2

Company Overview

Nasdaq MDNA

TSX MDNA

Headquarters Toronto, CA

Cash CDN $40.6 million (as of June 30, 2020)

Debt $0

Preferred Shares 0

Cash Runway Funded through 2022

Issued and Outstanding 48,814,933

Fully Diluted 60,016,733

“

”

We’re focused on fine tuning cytokine signaling to better direct the immune response against a patient’s disease.

“

3Medicenna Corporate OverviewQ3 2020

Infinite Hope4

Visionary Medicines

Medicenna Corporate Overview

1. BioXcel Strategic Analysis Report, 2014.2. Globocan 2012: Estimated Cancer Incidence, Mortality and Prevalence Worldwide 2012.3. Decision Resources, Inc Glioblastoma Report, Sept 2013.

MDNA11: IL-2 SUPERKINE NEAR TERM MILESTONES CORPORATE SNAPSHOT

BEST IN CLASS IL-2 SUPER-AGONIST

EXCEPTIONAL CD122 SELECTIVITY

Boosts cancer killing immune cells without toxicity

EXCELLENT PHARMCOKINETIC

PROFILEVast improvement over Proleukin

COMPELLING CLINICAL EFFICACY

Positive Phase 2b clinical data in 44 glioblastoma (GBM) patients

ORPHAN/FAST TRACK

Orphan Drug (FDA, EMA) Fast Track (FDA)

$2 BILLIONPotential market of MDNA55 for

brain cancer ($US)1,3

SAFETY PORTION OF MDNA11 PHASE 1

MONOTHERAPY STUDYExpected completion in H2 2021

15 PATENT FAMILIESOffer strong protection for

proprietary technology platforms

WORLD CLASS EXPERTISE

Clinical and scientific advisors, collaborators and inventors

MDNA55: TARGETS IL4R

MDNA55 END OF PHASE 2 MEETING

To be held September 29, 2020

EXPERIENCED MANAGEMENT TEAM

C-suite has combined 6+ decades of experience in biotech/pharma

PRE-IND MEETING WITH FDA FOR MDNA11

In H2 2020

Q3 2020

Candidate Indication Discovery Preclinical Phase 1 Phase 2 Pivotal

MDNA55IL-4 Toxin

Fusion

Recurrent Glioblastoma (GBM)

MDNA11IL-2 Super

Agonist

Cancer Immunotherapies

MDNA413IL-4/13 Super

AntagonistSolid Tumors

MDNA132IL13Rα2 selective

IL-13Solid Tumors

Diverse Pipeline Anchored by MDNA11 and MDNA55

5Medicenna Corporate OverviewQ3 2020

Multiple Near-Term Value Inflection Milestones

6Medicenna Corporate Overview

End of Phase 2 Meeting with FDA

MDNA55

MDNA11 to be IND Ready

MDNA11

CORPORATE

H2 2020 H1 2021 H2 2021

End of Phase 2 meetingwith FDA

Pre-IND Meeting

Nasdaq Listing Strengthen Management and Advisory Team

Complete safety portion of Phase 1 monotherapy study

Q3 2020

Strengthen Management and Advisory Team

MDNA11IL-2 Super Agonist for Cancer Immunotherapy

8Q3 2020 Medicenna Corporate Overview

Targeting IL-2 Receptor Subunits in Cancer Therapy

Wild type IL-2 preferentially

stimulates CD25

IL-2 Receptor

IL-2

(CD25)

(CD122)

(CD132)

The IL-2 receptor (IL-2R) consists of three subunits

• CD25 (IL-2Rα)

• CD122 (IL-2Rβ)

• CD132 (IL-2Rγ)

Stimulation of CD122

• Key for the activation of cancer killing immune cell such as CD8+ T cells, naïve T cells, and NK cells.

Stimulation of CD25

• Leads to activation of immunosuppressive Tregs, which abrogate the anti-tumor response

• Causes extreme toxicity

Proleukin (recombinant human [rh] IL-2), which selectively stimulates CD25, is

approved for the treatment of metastatic melanoma and renal cell carcinoma

Medicenna has developed MDNA11 to overcome the shortcomings of Proleukin and competing IL-2 variants

9

Improved IL-2 Variants are Needed


Proleukin

Poor safety profile due to selective stimulation of CD25

• Patients are often unable to receive a full course of therapy

• Patients must be treated in the intensive care unit

Poor pharmacokinetic profile

• Half-life on the order of minutes

• Requires dosing every 8 hours for 9 days

Have low CD122 affinity• Limits efficacy

Often require complex manufacturing processes

• Increases cost of goods

Competing IL-2 variants

Q3 2020

MDNA109 Platform: Generating IL-2 Variants with 200-fold Higher Affinity for CD122 (IL-2Rβ)

10

Mutations in the core of IL-2 Improves affinity to CD122 on CD8+ T cells and NK cells

CD122 affinityKey for the activation of immune cells responsible for cancer killing (CD8+ T cells, naïve T cells, NK cells,…)

IL-2Rβ binding site

Helix C

Helix A

Helix B

Helix D

Levin, Bates, and Ring et. al, Nature, 2012

SPR data (nM) CD25 CD122

IL-2 6.6 280

MDNA109 6.6 1.4

Similar affinity to CD25

200X increase affinity to CD122


MDNA11 is Derived from the MDNA109 Platform

11Q3 2020 Medicenna Corporate Overview

MDNA 109

Enhance PKMDNA 109 - AlbMDNA 109 - Fc

Enhance Selectivity

MDNA11(MDNA109FEAA-Alb)

MDNA19(MDNA109FEAA-Fc)


MDNA11: Enhanced Affinity and Selectivity for CD122 Compared to rhIL-2

0 200 400 600 800 1000 1200

0.0

0.2

0.4

0.6

0.8

1.0

1.2

Time (sec)

CD

25 B

LI S

igna

l (nm

) 200 nM

100 nM

50 nM

25 nM

12.5 nM

6.25 nM

50 nM (No CD25 control)

KD = 24 ± 1 nM

rhIL

-2 –

CD

25 B

indi

ngrh

IL-2

–C

D12

2 B

indi

ng

MD

NA

11 –

CD

25 B

indi

ngM

DN

A11

–C

D12

2 B

indi

ng

Q3 2020 12


Competing IL-2 Variants NKTR-214 and THOR-707 are Weak CD122 Binders

IL2Rβ (CD122)

THOR-707: Reduced Binding to IL2Rβ (CD122) 1-PEG-IL2 (Most Active Form of NKTR-214)is a Weak IL2Rβ (CD122) Binder

Q3 2020 13


THOR-707

MDNA11

MDNA11: Enhanced Selectivity and Potency Toward Immune Effector Cells

14

Naï

ve C

D8+

T-ce

lls

0.01 0.1 1 10 100 1000 10000 1000000

20

40

60

80

100

Conc (pM)

pSTA

T5+

(%)

Signaling in CD8+ T Cells

rhIL-2MDNA11

0.01 0.1 1 10 100 1000 10000 1000000

20

40

60

80

100

Conc (pM)

pSTA

T5+

(%)

MDNA11

MDNA11rhIL-2

EC50 pM

rhIL-2 3390

MDNA11 460

EC50 pM

rhIL-2 5.6

MDNA11 160

Compared to WT IL-2 (proleukin) MDNA11 has:

Enhanced potency toward anti-tumor CD8+ T-cells

Reduced potency toward pro-tumor Treg cells

Compared to WT IL-2 (proleukin) THOR-707 has:

Reduced potency toward anti-tumor CD8+ T-cells

Reduced potency toward pro-tumor Treg cells

Naï

ve C

D8+

T-ce

lls

Treg

sTr

egs

Q3 2020

Comparison of MDNA11 with NKTR-214 in Combination with Anti-CTLA4 in CT26 Tumor Model

15

Charych, D. et al, Clin Cancer Res, 2016

MDNA11 (5 mg/kg, IP, 1x/wk for 2 wks)Anti-CTLA4 (4F10, 100 µg, 2x/wk for 2 wks)

Average tumor size at initiation of dosing ~ 90 mm3

NKTR-214 (0.8 mg/kg, IP, 1x/9 days for 3 doses)Anti-CTLA4 (4F10, 100 µg, 2x/wk through day 18)

Average tumor size at initiation of dosing ~ 100 mm3

Treatment duration

0 5 10 15 20 25 30 35

0

500

1000

1500

2000

2500

3000

Days Post Implant

Tum

or V

olum

e (m

m3 )

Vehicle

Anti-CTLA4

MDNA11 + Isotype

MDNA11 + Anti-CTLA

Vehicle + IsotypeAnti-CTLA4

MDNA11 + Anti-CTLA4MDNA11

Days0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75

0

500

1000

1500

2000

2500

3000

Tum

or V

olum

e (m

m3 )


MDNA11 + Anti-CTLA4 (n=10/group) NKTR-214 + anti-CTLA4 (n=12/group)

Days

Q3 2020

MDNA11 Inhibits Tumor Growth and Induces a Strong Memory Response

16

Vehicle + Isotype

0 25 50 75 100 125 150 175 2000

500

1000

1500

2000

2500

3000

3500

Days Post Implant

Tum

or v

olum

e (m

m3 )

N = 5

0 25 50 75 100 125 150 175 2000

500

1000

1500

2000

2500

3000

3500

Days Post Implant

Tum

or v

olum

e (m

m3 )

Vehicle

4/8 CR

Anti-CTLA4

0 25 50 75 100 125 150 175 2000

500

1000

1500

2000

2500

3000

3500

Days Post Implant

Tum

or v

olum

e (m

m3 )

⍺CTLA4

5/8 CR

MDNA11 + Isotype

0 25 50 75 100 125 150 175 2000

500

1000

1500

2000

2500

3000

3500

Days Post Implant

Tum

or v

olum

e (m

m3 )

MDNA11

8/8 CR

MDNA11 + Anti-CTLA4

0 25 50 75 100 125 150 175 2000

500

1000

1500

2000

2500

3000

3500

Days Post Implant

Tum

or v

olum

e (m

m3 )

MDNA11 + ⍺CTLA4

CT26 tumor (~60 mm3) bearing Balb/c mice were treated with MDNA11 (5 mg/kg 1x/week, 2 weeks) or Anti-CTLA4 (200 µg 2x/week, 2 weeks) by IP injection.

Re-challenge experiment performed by implanting 2 x 106 CT26 cells in opposite flank (Day 49, Day 116 and Day 165), without further treatment.

0 25 50 75 100 125 150 175 2000

500

1000

1500

2000

2500

3000

3500

Days Post Implant

Tum

or v

olum

e (m

m3 )

Re-challenge

N = 4

Re-challenge#1

Re-challenge#2

Re-challenge#3

0 25 50 75 100 125 150 175 2000

500

1000

1500

2000

2500

3000

3500

Days Post Implant

Tum

or v

olum

e (m

m3 )

Re-challenge

N = 5

Re-challenge#1

Re-challenge#2

Re-challenge#3

0 25 50 75 100 125 150 175 2000

500

1000

1500

2000

2500

3000

3500

Days Post Implant

Tum

or v

olum

e (m

m3 )

Re-challenge

N = 8

Re-challenge#1

Re-challenge#2

Re-challenge#3


Prim

ary

Tum

orR

e-ch

alle

nge

Q3 2020

PilotNon-human Primate (Cynomolgus Monkey) Study

18

Adult cynomolgus monkeys (age: 8-12 years) received 2 doses of MDNA11 by slow IV bolus 14-days apart and monitored for total of 28 days.

• Dose: 10, 30, 100, 300, and 600 mcg/kg

• One male monkey per group

• One monkey also received single dose of 300 mcg/kg MDNA11 and total of 21 days monitoring

Study measurements included

(1) Clinical observations

(2) Clinical chemistry

(3) Hematology

(4) Immune-profiling with Ki67 analysis of peripheral blood

(5) organ weights and macroscopic pathology

Sample collection also for (1) PK , (2) ADA and (3) cytokines/chemokines.

Study Design to Evaluate Safety, PK and PD Profile

Medicenna Corporate OverviewQ3 2020

19

Dose Dose

MDNA11 Induces Durable & Dose Dependent Ki67 Expression and Expansion of CD8+ T-Cells

-4 -2 0 2 4 6 8 10 12 14 16 18 20 22 24 26 280

20

40

60

80

100

Day

Ki6

7+ (%

of C

D8)

CD8 Ki67% - MDNA11

CTL

MDNA11-0.01

MDNA11-0.03

MDNA11-0.1

MDNA11-0.3MDNA11 - 0.6

-2 0 2 4 6 8 10 12 14 16 18 20 22 24 26 280

2

4

6

8

10

Day

CD8

T Ce

ll Fo

ld-C

hang

e

CD8 Normalzied to Pre-D - MDNA11

CTLMDNA11-0.01

MDNA11-0.03

MDNA11-0.1

MDNA11-0.3

MDNA11 - 0.6

DoseDose

Ki67 is a marker of anti-tumor CD8+ T-cell proliferation

Target Ki67 expression of greater than 50% was clearly demonstrated with MDNA11 treatment

Vehicle

0.1 mg/kg0.3 mg/kg

0.6 mg/kg

0.01 mg/kg0.03 mg/kg

-2 0 2 4 6 8 10 12 14 16 18 20 22 24 26 280

2

4

6

8

10

Day

CD

8 T

Cel

l Fo

ld-C

han

ge

CD8 Normalzied to Pre-D - MDNA11

CTLMDNA11-0.01

MDNA11-0.03

MDNA11-0.1

MDNA11-0.3

MDNA11 - 0.6


MDNA11 Induces Proliferation & Expansion of CD4+ T, CD8+ T, and NK Cells, But Not Tregs in Non-human Primates

20

-4 -2 0 2 4 6 8 10 12 14 16 18 20 22 24 26 280

1000

2000

3000

4000

5000

Day

Cell/

uL

of

blo

od

MDNA110.3 mg/kg

MDNA11 - 0.6

MDNA11 - 0.6

MDNA11 - 0.6

MDNA11 - 0.6

Tregs CD4+ T Cell CD8+ T Cell NK Cell

0

2

4

6

8

10

12

Control 0.01 0.03 0.1 0.3 0.6

MDNA11 (mg/kg)

% K

i67+

Fold

-cha

nge

to P

re-d

ose

0.6 mg/kg 0.6 mg/kg


21

MDNA11 Induces Expansion of Lymphocytes, But Not Eosinophils

• Increase in lymphocytes numbers following treatment.

• No expansion of eosinophils, which are responsible for vascular leak syndrome and the induction of cytokine storms.

Lymphocytes Eosinophils

N = 1 per dose

0

5

10

15

20

Pre-treatment

Post 1st

DosePost 2nd

Dose

Cel

l cou

nts

x 10

3 /µL

Cel

l cou

nts

x 10

3 /µL

2.7x

4.4x

MDNA11(100 µg/kg; IV bolus)

Cell

coun

ts x

103

/µL

0

5

10

15

20

Pre-treatment

Post 1st

DosePost 2nd

Dose

3.3x2.3x

0

5

10

15

20

9x

5.6x

Pre-treatment

Post 1stDose

Post 2ndDose




22

IL-2 Superkine Program: Next Steps


Pre-IND meeting with the FDA(H2 2020)

Initiate Phase 1 clinical trial (Mid 2021)

Complete safety portion of Phase 1 monotherapy study(H2 2021)

MDNA109

Platform

Arming Oncolytic Viruses or CAR-T

Cells

Ex Vivo and/or combination with Adoptive Cell Therapy

Mutations to create IL-2 Super-antagonists (MDNA209)

Fc or Albumin Fusions for Long Acting MDNA-109FEAA

Fuse Checkpoint Inhibitors with cytokines

(CHeCK Cancer™)

Dual or TrispecificCytokines (TRiCK

Cancer™)

Fusion with Cytokines to Create New Class

of Synthekines

Superkine Targeting with Antibodies

(STAb Cancer™)

MDNA11 Next Steps

01

02

03

Q3 2020

MDNA55A Powerful Molecular Trojan Horse Targeting Glioblastoma

MDNA55 TreatmentDirect infusion

into tumorconvection enhanced

delivery (CED)

75%

INOPERABLE rGBM

24

Current Treatment Strategies for GBM are Ineffective

* Expression of the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is responsible for resistance to Temodar used in GBM treatment.

25%

OPERABLE rGBM

GBM IS UNIFORMLY FATAL – VIRTUALLY ALL TUMORS WILL RECUR (rGBM)


Glioblastoma (GBM) Background

• Uniformly fatal – virtually all tumors will recur

• New treatment strategies are needed

• The IL4 receptor (IL4R) is a potential target for GBM treatments – overexpressed in GBM cells and the tumor microenvironment

DIAGNOSIS

(85-90%)55% of GBM

Temodar-Resistant* RELAPSE

SURGERY RADIOTHERAPY TEMODAR ADJUVANT TEMODAR+

Q3 2020

25

MDNA55: A Dual Targeted Immunotherapy

MDNA55

Targets the IL4R expressed in brain tumors and in the tumor microenvironment (TME), but not the healthy brain

Highly Selective

Avoids collateral damage to healthy brain

Disrupts the TME

Targets IL4R positive cells in the TME, unblinding the tumor to the body’s immune system

Immune Memory Response

Anti-tumor immunity is initiated and remains active after MDNA55 is cleared

Targeting DomainCircularly Permuted Interleukin-4 (cpIL-4)

Lethal PayloadCatalytic domain of Pseudomonas Exotoxin A(FDA approved in 2018,Moxetumomab pasudotox)

ENDOCYTOSIS

FURIN PROTEASEADP RIBOSYLATION

Inhibit Protein Synthesis

CELL DEATH

NUCLEUS


MDNA55 All-Evaluable: Tumor Control Rate & Survival

26

92%

78% 74%

51%

26%20% 19%

14% 10% 10% 9% 6% 6% 2%

0% 0%-6%

-11%-16%-16%

-24%-24%-26%-28%

-39%-47%-48%

-55%-56%-59%

-71%-73%-74%-75%

-90%-98%

-100%

-80%

-60%

-40%

-20%

0%

20%

40%

60%

80%

100%

32 10 14 35 41 11 6 22 29 27 7 1 33 4 9 13 16 19 8 25 40 5 38 43 21 45 12 46 3 39 2 18 15 37 28 30 31 36 17 34 23

% C

hang

e in

SP

D (c

m2)

Subject #

Response from Nadir

Tumor Control Rate = 76% (31/41)

Best Response per Modified RANO (following initial PsP)

PDSD or better

0 10 20 300

50

100

Months From Start of MDNA55 Treatment

Per

cent

sur

viva

l MDNA55 (n=44)MDNA55 All-comers (n=44)mOS = 11.6 monthsOS-12 = 46%

*Tumor response based on radiologic assessment


Proposed Population shows > 100% improvement in survival when compared to Synthetic Control Arm (SCA)

27

MDNA55 Proposed Population: Tumor Control Rate & Survival

74%

51%

26%14% 10% 10% 6% 6% 2%

0% 0% -6% -11%-16%-16%-24%-26%-28%-39%-47%-48%-55%-56%-59%

-71%-74%-75%-90%-98%

-100%-80%-60%-40%-20%0%20%40%60%80%100%

32 14 41 22 29 27 33 4 9 16 19 8 25 40 5 38 43 21 45 46 3 39 2 18 15 37 28 30 36 17 34 23

% C

hange in S

PD

(cm

2)

Subject #

Response from Nadir

Tumor Control Rate = 81% (26/32)

PDSD or better

*Tumor response based on radiologic assessment

Best Response per Modified RANO (following initial PsP)

A Proposed Population (n=32) comprised of all IL4R High (irrespective of dose) as well as IL4R Low patients receiving the high dose


Su

rviv

al P

rob

abili

ty

32.0 31.0 20.0 12.0 5.0 1.0 0.033.9 25.7 10.5 5.5 5.1 3.8 3.6

MDNA55SCA

Duration from Relapse (months)0 10 20 30

0.0

0.2

0.4

0.6

1.0

0.8

Group(weighted n)

mOS(months)

MDNA55 (n=32) 15.7

SCA (n=33.86) 7.2

p = 0.1177HR = 0.523

(95% CI 0.30, 0.91)

Q3 2020

Improved Survival with MDNA55, Particularly in IL4R High Subjects

28

All subjects (n=44)

mOS is 11.6 months; ~ 50% increase

compared to null hypothesis of 8.0

months based on FDA-approved

therapies. OS-12 is 46%.

IL4R High + IL4R Low High Dose (n=32)

mOS is 15 months; OS-12 is 55%

IL4R High + IL4R Low High Dose

Subgroups

Improved outcomes also seen in

unmethylated MGMT (n=17), low

steroid use (n=12)

1) Brada et al., 2001; 2) Gliadel FDA Label 2018; 3) Stupp et al., 2012; 4) Wick et al., 2017; 5) Friedman et al., 2009; 6) Reardon et al., 2020; TTF = Tumor Treating Fields; HD = High Dose

Comparison of MDNA55 with FDA-approved Therapies for rGBM


29

Safety Profile (n=118) shows MDNA55 is safe and well tolerated

• No deaths attributed to MDNA55

• No systemic toxicity

• No clinically significant laboratory abnormalities

• Drug-related adverse events were primarily neurological/aggravation of pre-existing neurological deficits characteristic with GBM and have generally been manageable with standard measures.

• Maximum Tolerated Dose established at 240 μg

• No evidence of a differential rate of neurological toxicities between doses of MDNA55 used in the current study (up to 240 µg) and a range of higher doses explored in previous studies (up to 900 μg)


Brain Cancer Represents a Significant Market Opportunity

Tumor Type Annual Incidence1 Projected Market2

Recurrent Glioblastoma (rGBM) 33,300 $650M

Metastatic Brain Cancer3 91,500 $1.30B

Pediatric Glioma 3,800 $50M

Total 133,500 $2.0B

30

1. GLOBOCAN 2012 http://globocan.iarc.fr/Default.aspx2. U.S., Europe and Japan3. Metastatic Brain Cancer numbers from colon, breast and kidney cancer only

Market Size Estimated at $2B Annually


Brain Cancer Next Steps End of Phase 2 Meeting

with FDA in Q3 2020

Infinite Hope31

Visionary Medicines


1. BioXcel Strategic Analysis Report, 2014.2. Globocan 2012: Estimated Cancer Incidence, Mortality and Prevalence Worldwide 2012.3. Decision Resources, Inc Glioblastoma Report, Sept 2013.

MDNA11: IL-2 SUPERKINE NEAR TERM MILESTONES CORPORATE SNAPSHOT

BEST IN CLASS IL-2 SUPER-AGONIST

EXCEPTIONAL CD122 SELECTIVITY

Boosts cancer killing immune cells without toxicity

EXCELLENT PHARMCOKINETIC

PROFILEVast improvement over Proleukin

COMPELLING CLINICAL EFFICACY

Positive Phase 2b clinical data in 44 glioblastoma (GBM) patients

ORPHAN/FAST TRACK

Orphan Drug (FDA, EMA) Fast Track (FDA)

$2 BILLIONPotential market of MDNA55 for

brain cancer ($US)1,3

SAFETY PORTION OF MDNA11 PHASE 1

MONOTHERAPY STUDYExpected completion in H2 2021

15 PATENT FAMILIESOffer strong protection for

proprietary technology platforms

WORLD CLASS EXPERTISE

Clinical and scientific advisors, collaborators and inventors

MDNA55: TARGETS IL4R

MDNA55 END OF PHASE 2 MEETING

To be held September 29, 2020

EXPERIENCED MANAGEMENT TEAM

C-suite has combined 6+ decades of experience in biotech/pharma

PRE-IND MEETING WITH FDA FOR MDNA11

In H2 2020

Q3 2020

Thank You!Elizabeth WilliamsChief Financial Officer

www.medicenna.com

Fahar Merchant, PhDPresident & CEO

Documents

MDNA Q3 2020 September...Conc (pM) pSTAT5+ (%) Signaling in CD8+ T Cells rhIL-2 MDNA11 0.01 0.1 1 10 100 1000 10000 100000 0 20 40 60 80 100 Conc (pM) pSTAT5+ (%) MDNA11 MDNA11 rhIL-2