mdna corporate overview | q1 2019filecache.investorroom.com/mr5ircnw_medicenna/163... ·...

TSX: MDNAOTCQB: MDNAF

©2018 Medicenna. All Rights Reserved.

Corporate Overview | Q1 2019

Forward-Looking Statements

Q1 2019 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 June 26, 2018. 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.

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Q1 2019 3

MDNA55 — LEAD PROGRAM SUPERKINE PLATFORM MDNA109

TARGETS IL4R: EXPRESSED IN GBMCompelling Phase 1/2a Data in rGBM

ORPHAN/FAST TRACK Orphan Drug (FDA, EMA)

Fast Track (FDA)

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

BEST IN CLASS IL-2 SUPER-AGONIST

PHASE 2B TRIAL NEARLY COMPLETE

Enrollment at 10 sites in the US including Centers of Excellence

4,000Brain tumor patients can be treated with 1 gram

of MDNA55

GROWING PIPELINE

Oncology, autoimmune andinflammatory

HIGH CD122 SELECTIVITY

250,000Annual incidence

of GBM and metastatic brain cancer2

2 BILLIONPotential market of MDNA55 market for brain cancer ($US)1,3

VALIDATED TARGETS

Industry transactions support further development

TUNABLE PKFc and Albumin Fusions

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.

Medicenna Corporate Overview

MDNA55A Powerful Molecular Trojan Horse Targeting Glioblastoma

> 300 Patient Biopsies Analyzed Show IL-4R Over-Expression1-7

5

Targeting the IL-4 Receptor in Brain Tumors

Glioblastoma

76%Mixed Adult

Glioma

>83%Mixed Pediatric

Glioma

76%Pediatric DIPG

71%

Medulloblastoma

100%Adult Pituitary

Adenoma

100%Meningioma

77%Normal Brain

Tissue

0%1. Joshi BH, et. al. Cancer Res 2001;61:8058-8061.2. Puri RK, et. al., Cancer Res 1996;56:5631-5637. 3. Kawakami M, et. al., Cancer. 2004 Sep 1; 101(5):1036-42. 4. Berlow NE, et al. PLoS One. 2018 Apr 5; 13(4):e0193565.

5. Joshi BH, et. al. British J of Cancer (2002) 86, 285 –291.6. Chen L, et al. Neurosci Lett. 2007 Apr 24; 417 (1):30-5.7. Puri S, et. al., Cancer. 2005 May 15; 103(10):2132-42.


IL-4R Predicts Poor Survival in GBM

6

Kohanbash G et al. Cancer Res 2013;73:6413-6423

IL4R +/+ (n=10); symptom-free survival = 55.5 daysSymptom-free survival = 90 daysIL4R -/- (n=15); symptom-free survival = 90 days

Survival in Subjects with GBM

-- No expression of IL-13Rα1 (n=32): mOS = 693 days-- High expression of IL-13Rα1 (n=65): mOS = 350 days

Survival in Glioma Mouse Model

Han J. and Puri R. J of Neuro-Oncology (2018) 136:463–474

Expression of IL-13Rα1 mRNA positively correlates with IL-4Rα indicating that these two receptors may form a complex in GBM.


7

TME-Infiltrating MDSCs Express IL-4R and Predict Poor Survival in GBM

MDSC gene signature (based on the combined positive expression of CD11b,CD33, CD45, CD244, and CXCR2) negatively correlates with GBM patientprognosis. Statistical significance of survival was based on log-rank analysis.

Otvos B et. al., (2016). Stem Cells 34:2026–2039Surface expression of IL-4Ra on tumor-infiltrating and splenic CD11b+/Gr-1+ MDSCs from GL26 tumor-bearing mice.

TME-MDSCs show 12-fold increase in IL-4R⍺expression compared to splenic myeloid cells

p < 0.001

Kamran N, et. al., (2017). Mol Ther 25:232-248


MDNA55: A Powerful Molecular Trojan Horse

8

Targeteddelivery of toxin

Tumor Targeting Domain

Circularly Permuted Interleukin-4 (cpIL-4)

ENDOCYTOSIS

FURIN PROTEASEADP RIBOSYLATION

Inhibit Protein Synthesis

CELL DEATH

NUCLEUS

Tumor Killing “Cytotoxic” DomainCatalytic domain of Pseudomonas Exotoxin A (PE)

• Potently toxic to tumor cells

• Simultaneously purges the tumor microenvironment (TME)

• Bypass the BBB via convection enhanced delivery (CED)

Medicenna Corporate OverviewQ1 2019

MDNA55 Treatment

Direct infusion into tumor

convection enhanceddelivery (CED)

75%

INOPERABLE rGBM

9

Treatment Pathway for GBM

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

STANDARD OF CARE FOR PATIENTS WITH GBM

DIAGNOSISADJUVANT TEMODARSURGERY

(85-90%) 55% of GBM Temodar-Resistant*

RADIOTHERAPY TEMODAR

RELAPSE

25%

OPERABLE rGBM

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

MDNA55 treatment can also provide benefit in newly diagnosed and

operable rGBM settings

Q1 2019

Open-Label Single Arm Study in 52 Recurrent GBM Patients (NCT02858895)

10

MDNA55-05 Phase 2b Study Design Summary

DIAGNOSIS PLANNING TREATMENT FOLLOW UP

Q1 2019

Optimization: High-flow Image Guided CED Improves Distribution

Q1 2019 Medicenna Corporate Overview 11

PAST STUDIES1st Generation CED

CURRENT STUDIES2nd Generation High-flow CED

Image-guided catheter placement

New catheters prevent backflow

Real-time monitoring ensures

tumor coverage

Inaccurate catheter placement

Drug leakage due to backflow

Inadequate tumor coverageTumor Drug Coverage

Saito and Tominaga (2012), Neurol Med Chir (Tokyo) 52, 531

Sampson et al, Congress for Neurosurgery, Oct 9-11, 2017

3D IMAGE FROM PATIENTIN CURRENT CLINICAL STUDY

Reduced Treatment Duration from 4 Days to 1 Day

12

Promising Survival at Low Doses of MDNA55 Compared to Approved Therapies for rGBM

Monotherapy Population (n)Survival

mOS (mos.) OS-6 OS-9 OS-12MDNA55-05

Low Dose Cohorts* rGBM (n=27) 11.8 89% 59% 46%

Avastin1 rGBM (n=50) 8.0 62% 38% 26%

Lomustine1 rGBM (n=46) 8.0 65% 43% 30%

Temozolomide2 rGBM (n=31) 5.6 NA NA NA

Temozolomide3 rGBM (n= 792) NA 65% NA 36.4%

MDNA55-05High Dose Cohorts Currently enrolling

1 Taal et al, Single-agent bevacizumab or lomustine versus a combination of bevacizumab plus lomustine in patients with recurrent glioblastoma (BELOB trial): a randomised controlled phase 2 trial. Lancet Oncol 2014 Aug;15(9):943-532 Kim et al., Outcome of salvage treatment for recurrent glioblastoma. J Clin Neuroscience 22 (2015) 468–473, 2015.3 Chen et al., The efficacy of temozolomide for recurrent glioblastoma multiforme (Meta-analysis). Eur J Neurol, 2013 Feb; 20(2):223-30.


0 200 400 600 800 1000 12000

50

100

Days Elapsed

Perc

ent R

elap

sed

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IL-4R Positivity is Associated with More Aggressive Disease

Time to 1st Relapse from Initial Diagnosis

IL-4R H-Scores (range 0-300)

Median time to 1st Relapse from Initial

Diagnosis

≤ 75 16.7 mos

> 75 10.3 mos


Shorter Time to Relapse from Initial Diagnosis

0 100 200 300 400 500 600 7000

50

100

Days elapsed

Perc

ent s

urvi

val

H-Score 0 - 75 (n=11)H-Score > 75 (n=13)

IL4R+ Subjects Show Better Survival Outcomes Following Treatment with MDNA55

IL-4R H-Scores

(range 0-300)OS-6

(n=24)OS-9

(n=24)OS-12(N=21)

≤ 75 73% 36% 30%

> 75 100% 69% 55%

Survival from Start of MDNA55 Treatment

16Q1 2019 Medicenna Corporate Overview

15

MDNA55 Presents a Promising Benefit-Risk Profile Especially in IL-4R+ Recurrent GBM

Time to 1st Relapse from Initial Dx (median)

All Subjects 11.3 months

IL-4R+ Subjects 10.3 months

IL-4R- Subjects 16.7 months

Survival After Treatment with MDNA55

mOS (mos.) OS-6 OS-9 OS-12

All Subjects 11.8 89% 59% 46%

IL-4R+ Subjects 15.2 100% 69% 55%

IL-4R- Subjects 8.5 73% 36% 30%

IL-4R+ is associated with more aggressive disease

MDNA55 improves survival outcomes in IL-4R+ rGBM


MDNA55 Brain Cancer 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

16

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

MDNA109: IL-2Super Agonist for Cancer Immunotherapy

A High Potency Agonist for CD122: Preferentially Activates Effector Cells

18

CD25 Limits Immuno-Oncology Potential of IL-2

VS

• Expressed on activated T cells, Treg, and pulmonary endothelium• Treg abrogate anti-tumor responses• Pulmonary endothelial cells mediate toxicity (vascular leak

syndrome)• Affinity <10 pM for IL-2

IL-2R⍺(CD25)

High-affinity receptor

• Expressed on effector cells that can recognize and attack tumor cells (naïve T cells, NK cells, and CD8 Tcells)

• Mediates anti-tumor effect• Affinity 1 nM for IL-2

IL-2

IL-2Rβ(CD122) IL-2Rγc

Intermediate affinity receptor


MDNA109: >1000-fold Higher Affinity for CD122 (IL-2Rβ) Than Native IL-2

19

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

• CD122 affinity is key 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 CD122-CD132 (ɣc)

IL-2 23 500-1000 0.6

MDNA109 2-20 0.5 0.04

Similar affinity to

CD25

>1000 X increase affinity to

CD122

15 X increase affinity to

intermediate affinity IL2R


MDNA109 More Potent and Less Toxic then Wild-type IL-2

20


Reduced Adverse Effects in Vivo

Selective Expansion of CD8+ T Cells in Vivo

10

5

0

15

Cel

ls p

er s

plee

n (x

106 )

0.20

0.15

0.10

0.25Pu

lmon

ary

wet

wei

ght (

g) 0.30

PBS IL-2

MDNA109

Anti-tumor response against pulmonary B16F10 nodules. B6 mice received 3x 105 B16F10 cells intravenously, followed by five daily injections of either PBS, 20 μg IL-2, or 20 μg MDNA109, starting three days after tumor injection. Shown are photographs of fixed whole lungs on day 16 after tumor injection.


21

MDNA109 Shows Superior Efficacy in Syngeneic Mouse Cancer Models


C57BL/6 mice were injected either subcutaneously with 106 B16F10 melanoma cells, 2.5x106 murine colon carcinoma 38, or 106 Lewis lung carcinoma followed by daily injections of either PBS, 20 mg IL-2, or 20mg MDNA109 for 5 days once subcutaneous tumor nodules became visible and palpable. Shown is mean tumor volume in mm3 (+/-s.d.) versus time upon tumor inoculation. Error bars represent SEM., P values refer to comparisons of wild type with the other treatment modalities. *P,0.05; **P,0.01; ***P,0.001.


5 10 15 20 25 30 35 40 450

500

1000

1500

2000

Days Post-Implant

Mea

n Tu

mor

Vol

ume

(mm

3 )

PBSanti-PD-1MDNA109 (5 ug q.d.)MDNA109 (25 ug q.d.)anti-PD-1 + MDNA109 (5 ug q.d.)anti-PD-1 + MDNA109 (25 ug q.d.)

9/10 cures

1/10 cures

0/10 cures

22

MDNA109 Synergizes with Anti-PD-1 Immunotherapy

• MDNA109 and anti-PD-1 are not fully efficacious alone

• Dose-dependence observed with monotherapy and anti-PD1

• Combination treatment sufficient to cure most mice

• Increased efficacy of combination was well-tolerated

C57BL/6 mice were implanted with 106 MC38 murine colon tumor cellssubcutaneously above hind limb. When tumor reached approximately 125mm3,animals were randomized into groups and dosing was initiated by intraperitonealinjections; q.d. = daily.

**

**

**

***

Combination Therapy Produces Robust Dose-Dependent Responses in Colon Cancer Model


0 10 20 30 40 50 60 70 80 900

500

1000

1500

2000

2500

Study Day

Tum

or v

olum

e (m

m3 )

23

TxStart

***

****

***

*

• MDNA109 and anti-CTLA4 (10 mg/kg IV q4d x 3)are not fully efficacious alone

• Significant response observed in combination with anti-CTLA4; sufficient to cure most mice

• Increased efficacy of combination was well-tolerated

• MDNA109 can synergize with checkpoint inhibition to fully unleash the immune system against cancer

MDNA109 Synergizes with Anti-CTLA-4 Immunotherapy

MDNA109 and IL2 administered daily x5 for 2 cycles; anti-CTLA4 administered twice weekly for two cycles; average tumor volume at treatment start was 18 mm3; asterisks indicate significant differences as compared to Isotype control group (*p<0.05; **p<0.01; ***p<0.001; ****p<0.0001).

Combination Therapy Produces Robust Tumor Responses in CT26 Colon Cancer Model


30 40 50 60 70 80 900

500

1000

1500

2000

Days Post 1st Implant

Tum

or v

olum

e (m

m3 )

Day of Implant

Tumor Re-challenge Shows Sustained Benefit with MDNA109 + Anti-CTLA-4

24

Secondary challenge

Primary challenge

1 2

MDNA109 + Anti-CTLA4 (n=8)IL-2 + Anti-CTLA4 (n=6)

30 40 50 60 70 80 900

500

1000

1500

2000

Days Post 1st Implant

Tum

or v

olum

e (m

m3 )

Day of Implant

1 CR (17%)4 deaths

4 CR (50%)1 PR (13%)


0 20 40 60 80 1000

20

40

60

80

100

Days Post Implant

Per

cent

sur

viva

l

MDNA109 + Anti-CTLA-4 Immunotherapy Improves Survival

25

Tumor re-challenge

(Day 32)

Start of Dosing(Day 7)

MDNA109 and IL2 were administered daily x5 for 2 cycles; anti-CTLA-4 administered twice weekly for two cycles*Asterisks indicate statistically significant difference as compared to Isotype group (*p<0.05; **p<0.01; ***p<0.001; ****p<0.0001).

********

**

****

****


MDNA109 is Not Immunogenic

26

Antibody titers from terminal serum samples fromBalb/c mice. Vehicle group (n=8), Proleukin group(n=8) and MDNA109 group (n=8).

Antibody titers from terminal serum samples fromC57BL/6 mice. Vehicle group (n=10), Proleukingroup (n=10) and MDNA109 group (n=10).

Isotype Proleukin MDNA1090

500

1000

1500

Treatment Groups

Ant

ibod

y Ti

ter

Isotype

Proleukin

MDNA109

Isotype IL-2 MDNA1090

500

1000

1500

Ant

ibod

y Ti

ter

IsotyperhIL-2

MDNA109

Treatment GroupsTreatment Groups

Vehicle Proleukin MDNA109

Treatment Groups

Vehicle IL-2 MDNA109


MDNA109-Fc Has Similar In Vivo Potency But Superior PK Profile

27

• An optimized dose and schedule for the extended PK variant of MDNA109 has been identified

• MDNA109-Fc (0.75mg MDNA109/kg) enables effective B16F10 tumor control with a biweekly schedule, a similar schedule as anti-PD-1 antibodies used in mice

0 5 10 150

1000

2000

3000

Study Day

Tum

or v

olum

es (m

m3 )

Saline IP QD

MDNA109 1 mg/kg IP QD

MDNA109-Fc 2 mg/kg SQ BIW

B16F10 tumor model

Subcutaneous administration• Subcutaneous MDNA109-Fc is an advantageous administration approach for a future immunotherapy drug• Checkpoint inhibitors, Proleukin and competitor IL-2 therapies (NKTR-214, ALKS 4230) all require IV infusion, with

lengthy administration and monitoring time in the clinic• Subcutaneous administration offers fast and convenient administration that is typically preferred by patients for

common targeted cancer therapies (Stoner, 2014, PMID: 25015302; Jin, 2015, PMID: 26170642)

C57BL/6 mice implanted with 3 x 105 B16F10 cells subcutaneously in the right flank. Tumors were allowed to grow for 7 days prior to the initiation of the study. Average tumor volume was 70 mm3 when the animals were randomized. Treatment started on day 7. MDNA109 and IL2 were administered daily; MDNA109-Fc was administered twice weekly.

Treatment Start

****


Additional MDNA109 variants with optimized PK/PD properties

28

Widening the Therapeutic Window of MDNA109

STAT5 Phosphorylation Assay Using Human PBMCs

Optimized variants that retain high potency towards CD8+ T cells and NK cells but decreased Treg activity (decreased CD25 binding).

****

*** ***


MDNA109 Product Concept: IL-2 variants improved drug profile

29

MDNA109: A Best-in-Class IL-2 Cytokine for Cancer Immunotherapy

PRODUCT MANUFACTURING CD122 POTENCY

PROTEIN VERSATILITY HALF-LIFE SAFETY IMMUNOGENICITY

Proleukin® Simple Low High Minutes Poor Low

NKTR-214 Complex Low Low Days Better than IL-2 Low

ALKS 4230 Simple Low Low Minutes to hrs Better than IL-2 N/A

Synthorins Complex Low Low Potentially Days N/A Potentially High

MDNA109-Fc Simple High High Potentially Days

Better than IL-2 Potentially Low


Leading the Way

31

Financial Snapshot


• Cash and cash receivable balance at September 30, 2018: CDN$3.0 million• Financing completed December 2018: CDN$4.0 million• Available to be drawn under CPRIT grant: up to US$4.1 million • Received to date from CPRIT grant: US$10.0 million• No Debt, No Preferred Shares

Issued and Outstanding28,578,137

Fully Diluted*36,153,562

* Fully diluted includes 3,294,105 warrants with a CND$2.00 exercise price and 2,250,000 stock options with a weighted average exercise price of CDN$2.09

TSX: MDNAOTCQB: MDNAF

Seasoned Management and Experienced Board


Management TeamFahar Merchant, PhD Chairman, President & CEOFormer CEO Sophiris Bio (TSX); Former Director, President & CTO at KS Biomedix (LSE); Founder, President & CEO of Avicenna Medica and IntelliGene Expressions

Elizabeth Williams, CPA,CA Chief Financial OfficerFormer VP Finance & Admin and interim CFO at Aptose (TSX and Nasdaq); Previously with Ernst & Young

Martin Bexon, MD Head of Clinical DevelopmentFormer Medical Director at CSL Behring; Medical Director at Hoffman La Roche (UK and Switzerland)

Nina Merchant, MESc. Chief Development OfficerFormer SVP Development at Sophiris Bio; Formerly VP Development at KS Biomedix (LSE); Previously at Avicenna Medica, IntelliGene, Pharmacia and Sanofi Pasteur

Shafique Fidai, PhD Head of Corp DevelopmentFormer VP of Business Development at Sophiris Bio; Formerly with Xenon Pharma, Chromos

Board of DirectorsFahar Merchant, PhD Chairman, President & CEO

Albert Beraldo, CPA, CA Independent DirectorFounder, President and CEO of Alveda Pharmaceuticals until its acquisition by Teligent, Inc. (NASDAQ: TLGT); Former President and CEO of Bioniche (TSX).

William W. Li, M.D. Independent DirectorCEO, President and Co-Founder of the Angiogenesis Foundation. Executive strategic consultant to pharma in drug development and major investment banks. Director of Leap Therapeutics (NASDAQ)

Chandra Panchal, PhD Independent DirectorFounder, Chairman and CEO of Axcelon; Former Co-Founder, President and CEO of Procyon Biopharma Inc. (TSX); Former Senior Executive VP of Business Development at Ambrilia Biopharma Inc. (TSX).

Andrew Strong, JD Independent DirectorPartner at Pillsbury Winthrop Shaw Pittman — leading the Life Sciences Team in Houston, TX. Formerly CEO of Kalon Biotherapeutics. Director of Ashford Hospitality Prime (NYSE)

Nina Merchant, M.E.Sc Director, Chief Development Officer

32

World Class Advisors and Collaborators

Q1 2019 Medicenna Corporate Overview 33

Clinical and Scientific Advisors Collaborators and InventorsJohn Sampson, MD, PhD, MBADuke UniversityChair CAB and Expert in CNS immunotherapy and Drug Delivery to the Brain

David Reardon, MDDana Farber/HarvardClinical Director: Novel treatments for CNS Cancers

Krys Bankeiwicz, MD, PhDUniv of California San FranciscoProf of Neurosurgery: Expert in Convection Enhanced Delivery

Guido Kroemer, MD, PhDUniversity of ParisChair: SAB and Expert in Cancer Immunotherapy

Amy Heimberger, MDMD Anderson Cancer CenterProfessor of Neurosurgery and expert in GBM Immunotherapy

Sam Denmeade, MDJohn Hopkins UniversityProfessor of Oncology: Targeted therapies for cancer

Raj Puri, MDUSFDADirector at CBERInventor of MDNA55

Aaron Ring, MD, PhDYale UniversityAsst. Prof Immunobiology & Cancer BiologyCo-Inventor of IL-2 Superkines

Chris Garcia, PhDStanford UniversityCo-Inventor of IL-2, IL-4 and IL-13 Superkines

Haya Loberboum Galski, PhDHebrew University of JerusalemInventor of Fully Human Payloads

34

Multiple Near-Term Value Inflection Milestones


MDNA55• Complete enrollment in Phase 2b rGBM trial• Report rGBM Phase 2b interim top-line results• End of Phase 2 meeting with FDA• Commence Phase 2a clinical trial in newly diagnosed brain cancer

MDNA109• Select lead candidate with extended half life• Complete dose range finding studies for pre-IND meeting with FDA• Complete IND enabling studies in preparation for Phase 1 clinical trial

Phase 2 clinical results for MDNA55

in rGBM

MDNA109 to be IND Ready

Q1 2019 35

MDNA55 — LEAD PROGRAM SUPERKINE PLATFORM MDNA109

TARGETS IL4R: EXPRESSED IN GBMCompelling Phase 1/2a Data in rGBM

ORPHAN/FAST TRACK Orphan Drug (FDA, EMA)

Fast Track (FDA)

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

BEST IN CLASS IL-2 SUPER-AGONIST

PHASE 2B TRIAL NEARLY COMPLETE

Enrollment at 10 sites in the US including Centers of Excellence

4,000Brain tumor patients can be treated with 1 gram

of MDNA55

GROWING PIPELINE

Oncology, autoimmune andinflammatory

HIGH CD122 SELECTIVITY

250,000Annual incidence

of GBM and metastatic brain cancer2

2 BILLIONPotential market of MDNA55 market for brain cancer ($US)1,3

VALIDATED TARGETS

Industry transactions support further development

TUNABLE PKFc and Albumin Fusions

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.

Medicenna Corporate Overview

Thank You!Fahar Merchant, PhDPresident and Chief Executive [email protected]

mdna corporate overview | q1 2019filecache.investorroom.com/mr5ircnw_medicenna/163... ·...

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