1

COMPANY

PRESENTATION

APRIL 2019

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MOLOGEN SNAPSHOT

• Based in Berlin, Germany; founded 1998

• Frankfurt Stock Exchange Prime Standard

• Approx. 50 employees

• One of the pioneers in immunotherapies in

cancer and HIV

• Core expertise: TLR9 agonists

• Lead compound: lefitolimod (phase III for

colorectal cancer, phase II for small-cell lung

cancer, phase I for HIV)

• EnanDIM® technology platform for the

development of additional compounds

Structure of lefitolimod

Structure of EnanDIM®

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TLR9 AGONISTS ACTIVATE BOTH INNATE AND ADAPTIVE

IMMUNE PATHWAYS AGAINST CANCER

• MOLOGEN’s TLR 9 agonists offer:

• Clearly proven mode-of-action in immune stimulation

• Systemic (sub-cutaneous) as well as local (intra-tumoral) administration

• Long-term treatment opportunity due to favorable safety profile

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TLR9 AGONISTS: RATIONALE FOR USE IN ONCOLOGY

• Lefitolimod monotherapy: maintenance therapy after first-line chemotherapy

• Initial chemotherapy leads to decrease in tumor burden and release of tumor-

associated antigens

• Lefitolimod reactivates the immune system to recognize said antigens and initiate

broad systemic anti-tumor response

• Lefitolimod combination therapy with checkpoint inhibitors:

• Checkpoint inhibitors decrease tumor-induced immune suppression but are

efficacious only in presence of sufficient general immune activity

• Lefitolimod causes a broad immune activation upstream of the checkpoint inhibitor

cascade and leads to an inflow of immune cells into tumor tissue (turning “cold”

tumors “hot”)

• Thus, lefitolimod increases therapeutic potential of checkpoint inhibitors

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PRODUCT PIPELINE: FOCUS ON CANCER IMMUNOTHERAPIES

WITH WIDE RANGE OF POTENTIAL INDICATIONS

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LEFITOLIMOD:

MODE-OF-ACTION IN ONCOLOGY

• The patient’s immune system generally polices the development of cancer cells;

Occasionally, cells evade that system, developing into cancer

• Lefitolimod reactivates the patient’s own immune system for anti-cancer surveillance

• Lefitolimod can work safely alongside other treatments leveraging the body’s own immune

surveillance system

Notes: mDC myeloid dendritic cell I NK cell natural killer cell I NKT cell natural killer T cell I pDC plasmacytoid dendritic cell

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Unique Molecular Structure

LEFITOLIMOD:

BEST-IN-CLASS TLR9-AGONIST

Superior Characteristics

Dumbbell-shaped DNA molecule

• No unnatural components due to covalently-

closed structure (116 nucleotides)

• 3 effective non-methylated CG motifs in each loop

• Stability against enzymatic degradation w/o chemical modification

• Unique immunomodulation profile

• Combination of efficacy & safety by design

• Large potential for clinical benefit

Broad immunologic activation combined

with favorable safety profile given lefitolimod’s

specific molecular composition

• Pure natural DNA

• Strong induction of Type I IFN response without triggering generalized inflammatory reaction

• Absence of toxicity seen with other chemically-modified TLR9 agonists

• Broad therapeutic window

• Systemic (s.c.) & intratumoraladministration

• High dosing schedules over prolonged periods of time

• Safety established with more than 20,000

administrations in over 460 subjects to date

Notes: Light blue area Motifs recognized by TLR9 receptor

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LEFITOLIMOD: PHASE II RESULTS IN mCRC SHOW CLEAR

EFFECT ON PFS AND GUIDE PHASE III DESIGN

• Phase II IMPACT trial allowed for optimized design of pivotal phase III

n=43 MGN1703

(n=29)

Placebo

(n=14)

HR=0.40 [95% CI: 0.19-0.84]

Log-rank test p=0.009

Phase 1/2 Solid Tumors

Safety

Pharmacokinetics

Pharmacodynamics

Dosing regimen

Phase 2 IMPACT mCRC

Safety

Pharmacodynamics

PFS signal

Responder characteristics

Phase 3 IMPALA mCRC

Aim: Significant OS benefit

vs standard-of-care

Ongoing, data expected

H2-2019

• Progression-free survival (PFS) in mCRC

patients who responded to first-line

chemotherapy

• Selected as inclusion criteria for Phase III

• Additional potential biomarkers chosen as

stratification factors in Phase III

IRR

, In

dependent

Radio

logic

al R

evie

w

Source: Schmoll et.al. Cancer Res Clin Oncol 2014, 140(9); 1615-1624

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LEFITOLIMOD: PIVOTAL PHASE III IN mCRC

ONGOING TO CONFIRM MEANINGFUL CLINICAL BENEFIT

• Primary endpoint: Overall survival (OS)

• Structure: Open, randomized, controlled, two-arm, multinational

• Size: 540 patients, 122 sites, 8 EU countries

• Readout: After 365 events

• Design: Maintenance therapy in patients with partial or complete response to 1st

line chemotherapy vs. local standard of care

• Timeline: Recruiting completed, readout predicted for H2-2019

PD

Lefitolimod

Trial Treatment Period

Re-Induction

Induction

chemo

12–30 weeks

(Standard

1st line chemo)

PR / CR Screening/

Randomization

Control

groupPD

Lefitolimod

with

induction

chemo

Induction

chemo

PD

Start of

2nd line

PD

Maintenance

Notes: Chemo chemotherapy | PR partial response | CR complete response | PD progressive disease

• IMPALA was designed for achieving regulatory approval on significant OS benefit

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LEFITOLIMOD: SMALL-CELL LUNG CANCER PHASE II SHOWED

POSITIVE RESULTS IN TWO SUBGROUPS OF PATIENTS

• Results provide significant guidance for defining pathway to approval

IMPULSE: Exploratory phase II trial with 103 patients with extensive disease small-cell lung cancer

(SCLC); control group: local standard of care

• Primary endpoint “overall survival” not met in the overall study population

• Positive results in two pre-defined and clinically relevant subgroups of patients with clear overall

survival benefit in comparison to the control arm:

1. Patients with a low count of activated B cells. Hazard ratio: 0.53

2. Patients with reported Chronic Obstructive Pulmonary Disease (COPD),

a frequent comorbidity. Hazard ratio: 0.48

• Final results presented at ESMO 2018 (EUROPEAN SOCIETY FOR MEDICAL ONCOLOGY) and

published in “Annals of Oncology“1

1 Thomas et.al., Ann Oncol 2018, 29(10): 2076-2084

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LEFITOLIMOD: SMALL-CELL LUNG CANCER PHASE II SHOWED

SUBSTANTIAL OS BENEFIT IN CLEARLY DEFINED SUBGROUPS

Overall survival (OS) in a pre-defined patient subgroup – low number of activated B cells

Subgroup characteristics in line with TLR9 mode-of-action

OS is the time after randomization to death. Patients without event are censored at the date of last information available from the patient

23 23 18 13 9 7 4 4 2 0

15 14 10 4 2 1 1 1 0

Patients at riskLEFITOLIMOD (MGN1703)

CONTROL

0 90 183 270 365 455 548 638 730 793 820

Time to Event [days]

0.0

0.2

0.4

0.6

0.8

1.0

Ove

rall S

urv

ival

Censored

CONTROLLEFITOLIMOD (MGN1703)

1.0

0.8

0.6

0.4

0.2

0.0

0 90 183 270 365 455 548 638 730 820

Time to event (days)

Overa

ll surv

ival

LefitolimodControl

23 23 18 13 9 7 4 4 2

15 14 10 4 2 1 1 1 0

Lefitolimod

Control

Patients

at risk

0

793

n=38

Lefitolimod

(n=23)

Control

(n=15)

Median OS

[95% CI]

300.0 days

[189.0; 526.0]

231.5 days

[171.0; 272.0]

HR [95% CI] 0.53 [0.26; 1.08]

• Strong OS benefit in pre-defined subgroup forms basis for future development

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LEFITOLIMOD:

SMALL-CELL LUNG CANCER: OUTLOOK

Next steps

Detailed expert discussions of results and further development options

Design of future development program toward approval in EU & US

• Single-agent maintenance treatment in clearly defined subgroup of SCLC patients

• Combination with checkpoint inhibitors

Scientific advice in EU & US to de-risk / educate development approach

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LEFITOLIMOD: BREAK-THROUGH POTENTIAL FOR

COMBINATIONS WITH CHECKPOINT INHIBITORS

• Lefitolimod is ideally suited to overcome the limitations of checkpoint inhibitor therapy

• In mouse tumor models, combination with lefitolimod clearly improved the anti-tumor

effect of checkpoint inhibitors:

• Increased immune cell activation

• Reduced tumor growth further compared to either compound as monotherapy

• Clearly prolonged survival

• Promising potential for the combination of lefitolimod with checkpoint inhibitors

• First preclinical confirmation of combination of lefitolimod with checkpoint inhibitors in

treatment of cancer

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LEFITOLIMOD AND CHECKPOINT INHIBITORS:

ONGOING AND FUTURE CLINICAL STUDIES

Combination study lefitolimod with ipilimumab (Yervoy®) in solid tumors

• Collaboration with MD Anderson Cancer Center, Texas, US

• First combination trial of lefitolimod with ipilimumab (Yervoy®, Bristol-Myers Squibb)

• Phase I study in patients with advanced solid tumors

• Evaluation of safety and tolerability of combination

• Exploration of efficacy signals and effects on tumor micro-environment

Further combination studies lefitolimod / checkpoint inhibitors in solid tumors

• In advanced planning in cooperation with leading clinical centers

• First results show beneficial effect on tumor micro-environment

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Lefitolimod substantially enhances effect of checkpoint inhibitors in different mouse models

Notes: Experimental details: CT 26 colon carcinoma model, 11 intra-tumoral injections of

lefitolimod, 4 intra-peritoneal injections of mouse-specific aPD-1 antibody

0 10 20 30 40 50 60 70

0

500

1000

1500

2000

2500

3000

Days

Mean

tu

mo

r vo

lum

en

[m

m3]

Lefitolimod + aPD-1

Lefitolimod

ControlaPD-1

0 10 20 30 40 50 60 700

20

40

60

80

100

Days

Su

rviv

al

[%]

Control

aPD-1

Lefitolimod

Lefitolimod + aPD-1

Vehicle

Vehicle

• PRE-CLINICAL SETTING • FIRST CLINICAL RESULTS

LEFITOLIMOD AND CHECKPOINT INHIBITORS:

RESULTS

First results from Phase I trial in combination with

ipilimumab show:

• Increased T cell infiltration into tumor

• No dose-limiting toxicities at maximum dose

• two patients with stable disease

Source: SITC 2018 poster. Reilly et. al. Data from Phase I trial at MD Anderson Cancer

Center

CD8+ T cell infiltration into tumor in 5 patients

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DEVELOPMENT OF LEFITOLIMOD IN HIV

TEACH – Phase I trial with first application of lefitolimod in HIV

• Phase I trial at University Hospital Aarhus, DK (readout summer 2017)

• Activation of relevant immune cell population makes lefitolimod intriguing treatment option

for reduction of viral reservoir in HIV

• Results:

• Remarkable immunostimulatory potency

confirmed

• Lefitolimod enhanced type-I IFN response

in the sigmoid colon, direct proof of systemic

effect without inflammation

• Eradication of HIV viral reservoir in single-agent

setting not achieved

• First clinical trials exploring TLR9 agonists’ potential in fighting HIV

Upregulation of type-I-interferon

induced gene MX1

Lefitolimod induces strong immune

response in colon tissue of HIV

patients

Source: Krarup et.al. Mucosal Immunol. 2017;11(2):449-61.

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DEVELOPMENT OF LEFITOLIMOD IN HIV: FUTURE TRIAL

TITAN - lefitolimod in combination with virus-neutralizing antibodies in HIV

• Collaboration with University Hospital Aarhus and Rockefeller Institute

• Funded by a grant from Gilead Sciences to University Hospital Aarhus

• Planned start: spring 2019

• Aiming to study the combined effect of lefitolimod and broadly neutralizing antibodies

on the viral reservoir in HIV patients

• Potential to make meaningful impact on patients’ lives

• Combining TLR9 agonists and broadly neutralizing antibodies in fighting HIV

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3rd party TLR9 agonists

FOLLOW-UP MOLECULES ENANDIM®:

NEXT-GENERATION TLR9 AGONISTS

• Linear molecules

• Simple, cost-effective

production

• Stability through chemically

modified structure

• Usually unfavorable

risk / benefit ratio

Lefitolimod

• Stability through closed,

dumbbell-shaped structure

• Complex production

• Only natural DNA

components

• Good safety and

tolerability profile

EnanDIM®

• Linear molecules; stability

through specific feature

• Simple, cost-effective

production

• No chemical modifications,

only natural DNA components:

• Good safety and

tolerability profile

expected

Notes: EnanDIM® Enantiomeric DNA-based ImmunoModulator | DNA sequence essential for function (so-called “CG motifs”) |

new structural feature in EnanDIM® providing protection against degradation | phosphorothioate backbone (chemical modification)

• Two lead candidates from EnanDIM® platform technology: one for oncology, one for HIV

• Highly convincing anti-tumor effects in various tumor models as monotherapy and in combination with checkpoint inhibitors

• Start of clinical development planned for 2019

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ENANDIM®: SUMMARY HIGHLIGHTS

EnanDIM® family

• TLR9 agonist platform technology with promising safety profile

• Two distinct lead candidates for separate development in oncology and HIV

• Anti-tumor effect in multiple murine tumor models as single-agent

• Anti-tumor effect of anti-PD-1 enhanced by EnanDIM® in pre-clinical models

• Proven modulation of tumor micro-environment

• Optimal combination partner for checkpoint inhibitors (CPI)

• Enhancement of CPI efficacy → reduction of CPI dose → reduction of toxicity

• Potential to break resistance to CPI → re-sensitization towards CPI

• Status: IND-ready in 2019

• EnanDIM® platform promises broad potential in immunotherapy strategies

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ENANDIM®: PRE-CLINICAL HIGHLIGHTS (I)

EnanDIM® candidates show

• strong enhancement of checkpoint inhibitor effect in different tumor models

EnanDIM® candidates show

• beneficial modulation of tumor micro-environment

Murine model of colon carcinoma (CT26):

Combination of EnanDIM® and aPD-1

improves survival in comparison to aPD-1

monotherapy

EnanDIM® leads to strong infiltration of

T cells into the tumor in comparison to

vehicle control

• EnanDIM® platform offers huge potential in single-agent and combination setting

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• EnanDIM® platform offers huge potential in single-agent and combination setting

ENANDIM®: PRE-CLINICAL HIGHLIGHTS (II)

Induction of persistent anti-tumor immune memory

• EnanDIM® platform offers huge potential in single-agent and combination setting

• EnanDIM® candidates show dramatic anti-tumor effect and induction of sustained

immune memory against tumors in single-agent setting

• Immune memory protection extends beyond the initial challenge tumor cell line!

10 animals were initially inoculated with EMT-6

breast cancer cells. All 8 surviving animals were

protected against re-challenge with EMT-6 breast

cancer cells, and also against a subsequent

challenge with CT26 colon carcinoma cells.

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MGN1601: ALLOGENEIC CELL-BASED CANCER VACCINE

• Allogeneic therapeutic cancer vaccine

• Used off the shelf – no patient-specific CMC needed

• Consisting of

• a proprietary human cancer cell line

• … which is genetically modified fourfold by MOLOGEN’s vector technology MIDGE®

• … and given in combination with MOLOGEN’s TLR9 agonists

• Has shown promising signals in a Phase I/II trial in renal cell carcinoma patients

• Off-the-shelf therapeutic cancer vaccine as novel immunotherapeutic approach

ASET trial: single-arm phase I/II in 19 renal cell

carcinoma patients

• Median OS:

115.3 weeks (per protocol group) vs 24.8

weeks (intent to treat group)

• Two patients had no progression after 12

weeks and continued treatment for more than

48 weeks without progression

• Favorable safety and tolerability profile

Notes: CMC chemistry, manufacturing, and control

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LEFITOLIMOD: LICENSE AGREEMENT WITH ONCOLOGIE

INC. FOR ASIAN TERRITORIES

• Feb 2018: MOLOGEN signed a license and initial co-development agreement with

ONCOLOGIE for lead compound lefitolimod:

• License for China, Hong Kong, Macao, Taiwan, and Singapore

• Co-development: Leveraging innovative biomarker technologies from ONCOLOGIE

• ONCOLOGIE INC. (www.oncologie.international):

• Objective to develop personalized medicine in immuno-oncology

• Dedicated to biomarker-driven development of large and small molecules

• Strong leadership of industry veterans

• Headquartered in Boston, U:S., with operations in Boston and Shanghai

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20%

7%

3%

3%

67%

Global Derivative Trading GmbH, DE

Deutsche Balaton Aktiengesellschaft, DE

SIGNAL IDUNA Krankenversicherung a.G., DE

Axxion S.A., LUX

Freefloat

EXECUTIVE BOARD

AND CURRENT SHAREHOLDER STRUCTURE

Dr Matthias Baumann

CMO

• About 30 years industry expertise

• R&D and corporate leadership positions in

pharma, CRO and biotech

• Boehringer Mannheim, Roche, FOCUS,

NOXXON

Shareholder Structure

as of February 2019 (estimates)

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DISCLAIMER

This presentation does not constitute an offer to buy shares or other securities of MOLOGEN AG and doesnot replace the prospectus. This announcement does not contain or constitute an offer of, or the solicitationof an offer to buy or subscribe for, securities to any person in the United States of America (the “UnitedStates”), Australia, Canada or Japan or in any jurisdiction. The securities referred to in this announcementwill not be and have not been registered under the U.S. Securities Act of 1933, as amended (the “U.S.Securities Act”) and may not be offered or sold in the United States absent registration or an applicableexemption from registration requirements under the U.S. Securities Act. There will be no public offer of thesecurities in the United States. Subject to certain exceptions, the securities referred to in this announcementmay not be offered or sold in Australia, Canada or Japan, or to, or for the account or benefit of, any national,resident or citizen of Australia, Canada or Japan. The offer and sale of the securities referred to in thisannouncement has not been and will not be registered under the U.S. Securities Act or under the applicablesecurities laws of Australia, Canada or Japan. There will be no public offer of the securities in the UnitedStates.

Note about risk for future predictionsCertain statements in this presentation contain formulations or terms referring to the future or futuredevelopments, as well as negations of such formulations or terms, or similar terminology. These aredescribed as forward-looking statements. In addition, all information in this presentation regarding plannedor future results of business segments, financial classification numbers, developments of the financialsituation, or other financial or statistical data contains such forward-looking statements. The companycautions prospective investors not to rely on such forward-looking statements as certain prognoses ofactual future events and developments. The company is neither responsible nor liable for these forward-looking statements. It is not responsible for updating such information, which only represents the state ofaffairs on the day of publication.

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CONTACT

Investor Relations

Phone: +49-30-841788-37

Fax: +49-30-841788-50

investor@mologen.com

www.mologen.com

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COMPANY

PRESENTATION

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