MDNA Q3 2020 … · Medicenna Corporate Overview 1. BioXcel Strategic Analysis Report, 2014. 2. Globocan 2012: Estimated Cancer Incidence, Mortality and Prevalence Worldwide 2012

TSX: MDNAOTCQB: MDNAF

©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 in Canada, 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

3

Company Overview


TSX MDNA

OTCQB MDNAF

Headquarters Toronto, CA

Cash CDN$37.7 million (as of March 31, 2020)CDN$5.2 million over allotment exercised April 2020

Debt $0

Preferred Shares 0

Cash Runway Funded through 2022

Issued and Outstanding 48,672,810

Fully Diluted 59,994,140

“

”

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

“

4

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.

Q3 2020

MDNA55 - LEAD PROGRAM SUPERKINE PLATFORM CORPORATE SNAPSHOT

COMPELLING CLINICAL EFFICACY

Positive Phase 2b clinical data in 44 patients

END OF PHASE 2 MEETING

To be held in Q3 2020

250,000Annual incidence of GBM and

metastatic brain cancer2

ORPHAN/FAST TRACKOrphan Drug (FDA, EMA)

Fast Track (FDA)

4,000Brain tumor patients can be

treated with 1 gram of MDNA55

$2 BILLIONPotential market of MDNA55

market for brain cancer ($US)1,3

IL-2; IL-4; IL-13Tunable cytokines

NEAR TERM MILESTONES

MDNA11: BEST IN CLASS IL-2 SUPER-

AGONIST

EXCEPTIONAL CD122 SELECTIVITY

Boosts cancer killing immune cells without toxicity

WORLD CLASS EXPERTISE

Clinical and scientific advisors, collaborators and inventors

15 PATENT FAMILIESStrong technology platform

protection

Infinite Hope

MDNA55 Supported by a Pipeline of Superkines

5

Candidate Discovery Pivotal

MDNA55IL4 Toxin Fusion

MDNA19/11IL2 Super Agonist

Cancer Immunotherapies

MDNA413IL4/13 Super Antagonist

Solid Tumors

MDNA132IL13Ralpha2 selective IL13

Solid Tumors

Preclinical Phase 1 Phase 2

Recurrent GBM

Brain Metastasis

Newly Diagnosed GBM

Diffuse Intrinsic Pontine Glioma


6

Multiple Near-Term Value Inflection Milestones


End of Phase 2 Meeting with FDA

MDNA55

MDNA11 to be IND Ready

MDNA11

CORPORATE

Updated clinical data for MDNA55

Complete IND enabling studies

Initiate Phase 1 clinical trial

Nasdaq Listing

1H 2020 2H 2020 1H 2021

End of Phase 2 meetingwith FDA

Pre-IND meeting

MDNA55A Powerful Molecular Trojan Horse Targeting Glioblastoma

MDNA55 TreatmentDirect infusion

into tumor

convection enhanceddelivery (CED)

75%

INOPERABLE rGBM

8

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+

9

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

10

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

Medicenna Corporate OverviewQ3 2020

0 5 10 15 20 25 300

50

100

Duration from Relapse (months)

% S

urvi

val

Proposed Population (n=32)mOS 15.8 months; OS-12 62%

SCA (n=40)mOS 7.0 months; OS-12 18%

Proposed Population shows > 100% improvement in survival when compared to SCA

11

MDNA55 Proposed Population: Tumor Control Rate & Survival

p < 0.01HR 0.45

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


Improved Survival with MDNA55, Particularly in IL4R High Subjects

12

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) Kim et al., 2015; 3) Gliadel FDA Label 2018; 4) Stupp et al., 2012; 5) Brandes et al., 2016; 6) Taal et al., 2014; 7) Wick et al., 2017; 8) Friedman et al., 2009

Comparison of MDNA55 with FDA-approved Therapies for rGBM

13

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

14

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

MDNA109 PlatformIL-2 Super Agonist for Cancer Immunotherapy

Proleukin (hIL-2): first targeted immunotherapy

16

Improved IL-2 Variants are Needed

• Proleukin is approved for metastatic melanoma and renal cell carcinoma

• Proleukin is not efficient at binding CD122, therefore limiting activation of effector T cells and NK cells that attack tumors

• Proleukin preferentially stimulates the high-affinity receptor (CD25), causing:

• Extreme toxicity – hard to complete full course of therapy

• Treatment in Intensive Care Unit

• Frequent dosing (every 8 hours) for 9 days

Proleukin has very high affinity for CD25

High-affinity receptor

IL-2

(CD25)

(CD122)

(CD132)


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

17

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

200 X increase affinity to CD122


Evolution of MDNA109

18Q3 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 WT IL-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


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


THOR-707

MDNA11

MDNA11: Enhanced Selectivity and Potency Toward Immune Effector Cells

21

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

22

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

MDNA11 Inhibits Tumor Growth and Induces a Strong Memory Response

23

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

PilotNon-human Primate (Cynomolgus Monkey) Study

25

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 MDNA19 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


26

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

27

-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


28

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




29

MDNA11: Potential Best-in-Class IL-2 Superkine for Immunotherapy

PRODUCT CD122 POTENCY SAFETY HALF-LIFE IMMUNOGENICITY PROTEIN

VERSATILITY MANUFACTURING

Proleukin® Low Poor Minutes Low High Simple

NKTR-214 Low Better than IL-2 Hours Low Low Pegylation

ALKS 4230 Low Better than IL-2 Hours Low Low Simple

THOR-707 Low Better than IL-2 Hours N/A Low Pegylation

Neoleukin-201 Moderate Better than IL-2 N/A N/A N/A Pegylation

MDNA11 High Better than IL-2 13-25 Hours Low High Simple


30

IL-2 Superkine Program: Next Steps


Pre-IND meeting with US FDA (2H 2020)

Complete IND enabling studies in preparation for Phase 1 clinical trial (Q1 2021)

Initiate Phase 1 clinical trial (mid-2021)

MDNA109FEAA

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

31

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.

Q3 2020

MDNA55 - LEAD PROGRAM SUPERKINE PLATFORM CORPORATE SNAPSHOT

COMPELLING CLINICAL EFFICACY

Positive Phase 2b clinical data in 44 patients

END OF PHASE 2 MEETING

To be held in Q3 2020

250,000Annual incidence of GBM and

metastatic brain cancer2

ORPHAN/FAST TRACKOrphan Drug (FDA, EMA)

Fast Track (FDA)

4,000Brain tumor patients can be

treated with 1 gram of MDNA55

$2 BILLIONPotential market of MDNA55

market for brain cancer ($US)1,3

IL-2; IL-4; IL-13Tunable cytokines

NEAR TERM MILESTONES

MDNA11: BEST IN CLASS IL-2 SUPER-

AGONIST

EXCEPTIONAL CD122 SELECTIVITY

Boosts cancer killing immune cells without toxicity

WORLD CLASS EXPERTISE

Clinical and scientific advisors, collaborators and inventors

15 PATENT FAMILIESStrong technology platform

protection

Infinite Hope

Thank You!Elizabeth WilliamsChief Financial Officer

www.medicenna.com

Fahar Merchant, PhDPresident & CEO

Documents

MDNA Q3 2020 … · Medicenna Corporate Overview 1. BioXcel Strategic Analysis Report, 2014. 2. Globocan 2012: Estimated Cancer Incidence, Mortality and Prevalence Worldwide 2012