Bayer Pharma RD Event 2023

Agenda Pharmaceuticals R&D Event
Session Start/EDT Start/CEST Content Speaker
08:00 am 14:00 pm Welcome Oliver Maier

08:10 am 14:10 pm Transforming Bayer Pharma for Sustained Growth Stefan Oelrich
08:25 am 14:25 pm Reshaping Innovation at Bayer Pharma Christian Rommel
1 08:50 am 14:50 pm Making a Difference in Neurology & Rare Diseases
Christian Rommel
Leveraging a Unique Platform to Build a Presence in Immunology
08:55 am 14:55 pm Vividion Therapeutics: Removing the Boundaries of Druggability Aleksandra Rizo
09:15 am 15:15 pm Q&A (15 min) Stefan Oelrich, Christian Rommel, Aleksandra Rizo
09:40 am 15:40 pm Driving Leadership in Focus Areas of Oncology Dominik Ruettinger
10:00 am 16:00 pm Shaping new Treatment Paradigms in Cardiovascular Diseases Maria Borentain
10:25 am 16:25 pm Q&A (15 min) Dominik Ruettinger, Maria Borentain
2
10:40 am 16:40 pm BlueRock Therapeutics: Leading the way in PSC therapies Seth Ettenberg
11:00 am 17:00 pm Asklepios BioPharmaceutical: Pioneering AAV-based Gene Therapies R. Jude Samulski
11:20 am 17:20 pm Concluding Remarks Christian Rommel
3 11:35 am 17:35 pm Q&A and Closing Remarks (30 min) All

Transforming Bayer
Pharma for
Sustained Growth
Stefan Oelrich
Key Messages Today
1 2 3
Revised Expanding US Late-stage
innovation model footprint pipeline potential
Greater focus, streamlined Building US presence; From two to up to four
portfolio, emphasis on precision Expanding both R&D and blockbusters with a combined
medicine commercial footprint peak sales potential of €12bn
5 /// Bayer Pharmaceuticals R&D Event /// Boston /// June 28, 2023
We Have Taken Actions to Increase Focus, Quality and
Productivity of Our Innovation Model
Focus
Focus areas driven by value, differentiation, feasibility
Portfolio too broad for company size and competencies
Quality
Shift to breakthrough innovation leveraging scientific
Incremental innovation advances, platforms, precision medicine and AI
Productivity
Shift to value creation, asset-centric operating model,
Complex operating model leaner governance with renewed leadership team
Zeroing in on High Unmet Need With Great Value Potential
Optimizing our R&D focus to 4 broad therapeutic areas
Focus areas prioritized based on
Value & differentiation

Feasibility & risk
Bayer’s strengths Oncology Cardiovascular+1 Neurology & Immunology
Rare Diseases
1 including Precision Cardiovascular, Nephrology & Acute Care
We Have Expanded Our Capabilities And Pipeline Through
Strategic Acquisitions and Collaborations
INNOVATION ENGINE
Establishing Cell & Gene therapy platform through

acquisition of BlueRock and AskBio
Internal Gaining access to cutting-edge chemoproteomics

innovation platform through acquisition of Vividion
Collaborating with top academia, pharma partners

and biotech companies
LEAPS as a feeder of breakthrough technologies

External
innovation Platform
Companies ~ 100 deals signed in the last 4 years
innovation
People
Building US Footprint
Research & Development Commercial
Increased presence at the world’s most Expanding US commercial footprint reflecting new
vibrant Pharma innovation hubs products and pipeline assets with global rights
Increased R&D footprint in the US with Improved presence in oncology, in particular to

the acquisition of BlueRock, AskBio and support Nubeqa
Vividion
Ensuring Kerendia & Verquvo in cardio-renal
Established the Bayer Research and have appropriate marketing and sales support
Innovation Center in Cambridge/Boston
Nubeqa Has The Potential to Become The New Standard of Care
in Prostate Cancer Across Indications
Launch Performance Expanding to earlier prostate cancer settings
US Market Share1 Patient progression in prostate cancer
(Neo-) Nonmetastatic Metastatic

nmCRPC mHSPC Adjuvant BCR nmCRPC mHSPC
Drug
Sales treated ~145k ~86k ~47k ~76k
#1 43%
#2 25%
€0.5bn patient
2022
estimates2:
2028 2028 2019 2022 2025

Nubeqa Others Phase 3 ARASTEP ARANOTE
program: DaSL-HiCAP (ARAMON)4
ARAMIS ARASENS
(ARASEC)4
Ex-US, additional approvals will Committed to make Nubeqa available to a broad

drive further growth spectrum of prostate cancer patients
1
4
Source: IQVIA January 2023 3-month rolling market share, adjusted to reflect nmCRPC and mHSPC only 2 2030 Treated Estimates G7: US, EU5, J 3 Peak Sales Potential
Not label generating; supports ARASTEP/ARANOTE submission >€3bn
Peak3
Kerendia With Strong Launch Dynamics And The Option to
Broaden The Use in CKD And to Expand into HF
Launch Performance Expanding to additional indications
Global Patient Population3
US launch performance (monthly TRx)2
60.000
Entresto1 CKD
50.000
~700m people
40.000
Sales globally
€0.1bn
30.000
20.000
2022 HF Diabetes
10.000
~60m people ~480m
0 globally people globally
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 month
One of the strongest launch dynamics in CV despite initial

COVID restrictions Growing recognition of strong interlink between CKD and HF
Continued US market uptake with broad utility and Chronic Kidney Disease HF
relevance across GPs and specialists Non-
T2D T1D HFmr/pEF
China: NRDL Listing starting March 2023; granted diabetic
Extended Indication in China in mid-May, including CV FIGARO-DKD FINE-ONE FIND-CKD FINEARTS-HF

outcomes from FIGARO-DKD FIDELIO-DKD 2025 2026 2024
1 Entresto developed and commercialized by Novartis 2 Source: IQVIA TRx April 2023 3 Source: Vijay et al, 2021 4 Peak Sales Potential >€3bn
11 /// Bayer Pharmaceuticals R&D Event /// Boston /// June 28, 2023 Peak4
Elinzanetant as Investigational Non-hormonal Treatment Option in
The Menopause Market With Peak Sales Potential of >€1bn
Market Characteristics Elinzanetant
First, non-hormonal, once-daily, oral neurokinin-1,3

80% of women will ~60%1 of women with receptor antagonist
experience vasomotor menopausal syptoms
symptoms, with over half are not treated Differentiated, double mode of action
reporting moderate or
severe symptoms Phase II indicated significant and rapid improvement
in VMS and positive safety profile
1.2 billion women Current Status

menopausal or
postmenopausal
Four Phase III studies (OASIS-1 – OASIS-4)
by 2030
First Phase III data expected in H2 2023
Potential launch: 2025
>€1bn
Source: Market Research - IPSOS - Global VMS Women Segmentation
Peak2
1 2 Peak Sales Potential
Currently Un(der)treated Patients May Provide Asundexian a
Strong Entry Point Into The Anticoagulation Market
Market
Market Characteristics
Characteristics Asundexian
Innovative, once-daily, oral small molecule FXIa
Stroke prevention in AF Non-cardioembolic stroke inhibitor
~32m diagnosed AF ~27m diagnosed
patients in top 8 markets1 patients in top 8 markets1 Paradigm shift in thrombosis prevention, with the
potential to uncouple efficacy from bleeding risk
Standard of care: Standard of care:
DOACs (or VKA) Single/Dual APT Broad Phase II study program PACIFIC confirmed
Unmet need: 65%
consistent safety and near maximum FXIa
lower bleeding inhibition
with potential Continuous high
for efficacy recurrence despite
benefits vs. APT,and safety
SOC ~59M concerns with DAP
Current Status
people Unmet need: higher
efficacy without
increase in bleeding Two Phase III studies (OCEANIC-AF and
vs. SOC OCEANIC-STROKE)
U.S. FDA Fast Track Designation granted for both
indications
~1 in 3 patients in AF un(der)treated
with OACs mostly due to risk of bleeding Phase III data expected in H2 2025
>€5bn
Peak2
1 Top 8 markets: US, CN, JP, EU5; 2 Peak Sales Potential
Key Messages Today
1 2 3
Revised Expanding US Late-stage
innovation model footprint pipeline potential
Greater focus, streamlined Building US presence; From two to up to four
portfolio, emphasis on precision Expanding both R&D and blockbusters with a combined
medicine commercial footprint peak sales potential of €12bn
Reshaping
Innovation at Bayer
Pharma
Christian Rommel
Key Messages Today
We have reshaped our approach to innovation guided by value,

differentiation, feasibility, and our competencies.
We have streamlined our portfolio towards precision medicine,
with a narrower therapeutic area focus but a wider range of
modalities.
We will leverage partnerships, data science, new trial designs,
biomarker technologies, and improved governance to accelerate
our drug development processes and move to a higher, more
sustainable R&D productivity.
We are already starting to see a step change in the quality and
differentiation of our new molecular entities with the vast majority
offering the potential to be first- or best-in-class.
Patients and Society Need and Demand Transformational Change
HEALTH SYSTEMS UNDER PRESSURE ERA OF GROUND-BREAKING

SCIENTIFIC DISCOVERY
Ageing populations
Scientific breakthroughs
Increasing burden of Breakthrough

chronic diseases innovation is
needed
Data Science-driven R&D
Paying for value
REDEFINITION OF DISEASE
Precision treatments for homogeneous populations | Shifting to cure and prevention, holistic care beyond “the pill”
The New Face of Bayer Pharma R&D
Building on 160 years of innovation, we’ve significantly transformed our organization and shaped our strategy
New Bayer innovation strategy setting Extended capabilities Fast-tracked our ambition
the path for scientific leadership and and pipeline through through key R&D decisions
increased value for patients strategic acquisitions
• Diversified modalities • BlueRock • New R&D operating model

• Refocused therapeutic areas • AskBio • Leaner, simpler governance
• Increased R&D footprint in the US • Vividion • Rigorous portfolio health check
KEY FIGURES:
€3.2bn spend 5,800 FTEs at 25 NMEs and €9bn value increase ~100 deals signed
on R&D Bayer Pharma R&D 45 projects in of late-stage assets in the last 4 years
(including platform companies) development since 2021
Our People are Key for our Transformation and Future Success
Revamped leadership in action to transform our organization and unleash the potential of our people
UNLEASH R&D TALENT RED

REVAMPED R&D LEADERSHIP
RED
Precision
Oncology
Medicines
Attract, retain & engage diverse, 70% renewal of R&D
Regulatory
innovative talents Affairs Leadership team
Systematic talent up/re-skill
70% refreshment in
Foster open, bold, breakthrough next leadership level
innovation culture Drug
Discovery
Sciences
50:50 gender diversity ratio
including most senior levels
NEW WAYS OF WORKING & LEADING
Clinical Expanded geographic presence:
Develop.
US, China, Japan and Europe
Simplification of processes & governance Ops
Increased agility and collaboration

Shift to empowered, self organized Data
Science &
Chemical and
Pharmaceutical
teams, flow-to-work pools, etc. AI Development
Strategy & Leadership across innovation functions
portfolio
New to Bayer
New to the role
A Multi Faceted Innovation Engine to Unlock Value for Patients
Addressing need for breakthrough science with diverse research capabilities, technologies and talents
Internal
innovation
External
innovation Platform
Companies
innovation
Bolstering Science and Pipeline Through our Platform Companies
Balancing organizational synergies and scientific independence
BAYER R&D PLATFORM COMPANIES
Makes decision on Independently lead

⸗ Therapeutic and portfolio strategy BAYER PLATFORM ⸗ Platform strategy
⸗ Resource allocation R&D COMPANIES ⸗ Platform portfolio
⸗ Capability building ⸗ Technology and science
SYNERGIES
Cross-company interaction Building on respective Leverage Bayer’s Ensure scalable

and synergistic BD&L scientific capabilities expertise to accelerate and reliable product
activities to accelerate to expand early pre-clinical and clinical manufacturing
technology development pipeline development
/// Strategic & Change Communication /// Christiane Saborowski /// January 2022
Science & Portfolio People
Our Science & Portfolio Strategy Evolution
TARGETS INDICATIONS
Classical, well
“Undruggable”, new Mainly large Value driven
characterized
drug targets indications from large to rare
drug targets
TECHNOLOGIES PATIENT POPULATION
Small Mix of innovative, Broad Precise

molecules diverse modalities
INNOVATION FOCUS
Driven by
Diversified R&D Follow the
Mostly internal science & highest
ecosystem science
unmet needs
Innovation and Growth Potential as a Key Focus to Increase Value
Oncology
= Focus areas
Bubble size represents absolute

change in scales between 2022-
2028, in case of a positive CAGR
Source: Evaluate Pharma; incl. OTC sales; May 8, 2023; 1 Endorine includes Obesity; 2 gastro-Intestinal includes OTC
Refined Focus Areas with Highest Impact and Value Potential
Clear strategic mandates guiding decision making and resource allocation
Oncology Cardiovascular+ Neurology & Rare Diseases Immunology
Become a Top Remain Top player, shift Advance a competitive Build expertise
Oncology Company to precision medicine Cell & Gene therapy and portfolio
pipeline
Drive leadership in focus Enhance our leadership in Advance our pipeline to build
areas, accelerate growth precision cardiovascular, Drive and de-risk platform a presence and support other
through competitive early- nephrology and acute care with focus on first-in-market focus areas
stage pipeline potential
Targeting the Sweet Spot of Precision Medicine Across our Focus Areas
Through disease understanding and value potential assessment
Illustrative
Population
Address individual patients' needs to Large
achieve improved and sustainable indications
health by delivering transformative
medicines: the right treatment, to the
right patient, at the right time
Optimized outcomes by focusing on Subpopulations
highest unmet needs, value potential,
differentiation and risk mitigation
Rare
Open for disruption in large indications indications
Out of scope
Value
A Diverse and Innovative Modality Toolkit to Deliver our Ambition
Delivering innovative and competitive medicines in our focus therapeutic areas
Neurology &
Oncology Cardiovascular+ Rare Diseases Immunology
Small Molecules (SMOL)

RNA targeting
Small Molecules Protein degraders
Peptides
Conjugates
Antibody Conjugates
Protein Therapeutics Multispecific antibodies
Monoclonal antibodies
Targeted Radiotherapy
Radiotherapy Antibody | SMOL | peptide
Covalent binders
Chemoproteomics Heterobifunctional degraders
Molecular glues
Pluripotent Stem Cells

Cell Therapy (PSCs)
Adeno-Associated Virus (AAV)

based gene therapy
Genetic Medicine CRISPR-based gene editing
Non-viral gene delivery

Combined with Bayer
in-house innovation
capabilities
26 /// Bayer Pharmaceuticals R&D Event /// Boston /// June 28, 2023 Bayer innovation capabilities Innovation capabilities added since 2019
Reshaping R&D Execution Through Data Science and AI
Exploiting increasing convergence of biology and technology to continuously optimize our portfolio
PRIORITIES PARTNERSHIPS
Dedicated Data Science & AI Accelerating drug discovery with

organization created in 2021 Google Cloud, applying machine
learning for Quantum chemistry
Uncovering new biology harnessing
the power of multi-modal data
Portfolio Schrodinger collaboration to co-
AI driven compound optimization optimization develop de novo design to
accelerate drug discovery
Automation and machine learning
accelerating clinical trials powered by
Partnership with Recursion to
real world data
strengthen digital drug discovery
and advance new therapies
Moving to Higher, Sustainable Level of R&D Productivity
Supported by key levers
INCREASE IN PTS REDUCTION OF COSTS DECREASE IN CYCLE TIMES
Moving toward precision medicine Digitization of clinical trials Improved governance and decision
making (fail / accelerate fast)
Improved validation of targets and Lean, innovative, adaptive clinical trial
translation to patient - target disease design in stratified population, as well Accelerate development from IND to
link as platform studies launch through tailored development
approaches
Strategic investments in new Reduction of in-vivo/wet lab work by
biomarker approaches applying prediction tools Unlock the potential of Real-World
Data with AI and Machine learning.
Improved patient profiling and New ways of working leveraging Automation and digitization enabling
selection using advanced Data organizational synergies decentralized trails
Science/AI approaches
Pursuing Industry Leading Innovation Across all Focus Areas
Selected assets with innovation, differentiation and high value profile
Program1 (Indication) Phase 0 Phase I Phase II Phase III
Asundexian (SPAF, Stroke) FDA fast track, FIC

Cardiovascular
including Precision CV,
Nephrology & Acute Care a2AP ant mAb (Ischemic Stroke) FIC
sGC Activator Oral FIC

(Chronic Kidney Disease)
mEGFR/HER2i (Lung Cancer) FIC/BIC
Oncology DGKalpha Inh. (Cancer) FIC
NRF2 Inh (Cancer) FIC
PSMA-SMOL-TAC (Prostate Cancer) FIC/BIC
Bemdaneprocel (Parkinson’s) FDA fast track, FIC

Neurology &
Rare Diseases AB-1005 (Parkinson’s) FIC
AB-1003 (LGMD2I/R9) BIC
Other Elinzanetant (Vasomotor Symptoms) BIC
1 Selected assets out of 40+ development projects

A Focused R&D Strategy to Deliver an Innovative, Differentiated and
Sustainable Pipeline
OUR FOCUS OUR PRIORITIES
4 core Therapeutic Areas Science & Portfolio Productivity

• Oncology
• Cardiovascular+ Launch elinzanetant and asundexian Excellence in execution to generate more
• Neurology & Rare Diseases Progress and accelerate high-value assets value and improve capital efficiency in R&D
• Immunology Focused investments in BD&L Shift to asset-centric operating model
Maximize impact from platform companies Increase agility and dynamic resource
6 modalities Unlock full potential of precision medicine allocation
Small molecules, Protein Accelerate data science & AI across R&D
Therapeutics, Radiotherapy, value chain
Chemoproteomics, Cell Therapy,
Genetic medicine
3 platform companies
AskBio, BlueRock, Vividion
Key Messages Today
We have reshaped our approach to innovation guided by value,

differentiation, feasibility, and our competencies.
We have streamlined our portfolio towards precision medicine,
with a narrower therapeutic area focus but a wider range of
modalities.
We will leverage partnerships, data science, new trial designs,
biomarker technologies, and improved governance to accelerate
our drug development processes and move to a higher, more
sustainable R&D productivity.
We are already starting to see a step change in the quality and
differentiation of our new molecular entities with the vast majority
offering the potential to be first- or best-in-class.
Making a Difference
in Neurology & Rare
Diseases
Christian Rommel
Bayer in Neurology & Rare Diseases
Opportunity to become leaders in transforming patient care
MARKET ATTRACTIVENESS BAYER’S KEY STRENGTHS
High unmet medical needs Enabled by our existing capabilities

Many underserved or previously intractable State-of-the-art technology platforms for cell
diseases with high unmet need and gene therapy
Bundling capabilities of strong in-house teams,
Paradigm shift in patient treatments platforms and partnerships in key technologies
Transition from symptomatic treatment to such as gene editing and lipid nanoparticles
transformative therapies addressing disease root Bayer know-how and experience across the
causes with long-lasting clinical benefit value chain
Neurology &
Infrastructure and upscaling know-how
Attractive growth market Rare Diseases
Exciting scientific breakthroughs in Neurology
and rapid advances in new modalities including Synergies with other therapeutic areas
CGT Opportunity to address unmet needs at the
~7000 known rare disease, 80% of which are intersection of cardiovascular and
genetic in origin ophthalmology to leverage synergies
Neurology and Rare Diseases Pipeline Overview
Significant proportion of our cell & gene therapy pipeline to enable potential medical advances in NRD
PRECLINICAL CLINICAL LEAD INDICATION STRATEGIC PRIORITIES
AB-1005 Parkinson’s
Further inclusion of
AB-1005 Multiple System Atrophy BlueRock and AskBio in
Bayer’s Innovation
AB-1001 Huntington’s ecosystem, leveraging
synergies while keeping
ACTUS-101 Pompe (LOPD) FDA fast track & ODD
USA/EU them largely independent
AB-1003 LGMD2i/R92 FDA fast track & ODD EU Build a competitive and
differentiated portfolio and
- de-risk assets and platform
approach in clinical stage
DA01 / Bemdaneprocel Parkinson’s FDA fast track
-
Once derisked, identify areas
for scale and growth
NRD Pipeline Overview - all platform companies’ therapeutic areas ex-NRD not shown
Leveraging a Unique
Platform to Build a
Presence in
Immunology
Christian Rommel
Bayer Entering Immunology
Significant unmet medical need despite rapid scientific advances
MARKET ATTRACTIVENESS BAYER’S KEY STRENGTHS
High unmet medical needs Enabled by our existing capabilities

Many underserved diseases Access to highly differentiated Vividion’s
Globally increasing incidence & prevalence chemoproteomics platform
Highly differentiated small molecules
library
Robust research innovation
Covalent and non-covalent small
Advancing disease understanding, biomarker
molecules, direct functional modulators,
research to drive future precision therapies
degraders
Rapidly accelerating assets in preclinical
Potential for long-lasting remission and clinical development
Immunology
Novel precision targets empowered by new
technology (incl. Machine Learning & AI) for
better disease understanding Synergies with other therapeutic areas
Relevant expertise enabling Bayer’s other
Attractive growth market strategic focus areas
Among top-growing pharma markets
Efficient clinical trials and attractive PTS
Immunology Early Pipeline Overview
Targeting central drivers of inflammation
PRECLINICAL CLINICAL LEAD INDICATION STRATEGIC PRIORITIES

Atopic Dermatitis
Leverage existing
capabilities to fully enable
RA-ILD
Vividion platform and
realize synergies with
Interferon dysregulation
Bayer R&D
Inflammatory Bowel Disease (IBD)
Develop strong foundation
Psoriatic arthritis, Psoriasis, IBD and accelerate data
generation to drive
TH-17/TH-1 autoimmune disease understanding
Alopecia and vitiligo
Augment early-stage
pipeline through attractive
Most autoimmune diseases
external innovation once
Psoriasis, IBD de-risked
Vividion
Therapeutics:
Removing the
Boundaries of
Druggability
Aleksandra Rizo
Key Messages Today
While hundreds of proteins are known to be drivers of

diseases, just ~10% can be drugged by current therapies
Chemoproteomics technologies can be used to selectively
target and bind to yet unaccessible proteins, thereby
removing today’s boundaries of druggability
Vividion has a world leading industrial scale
chemoproteomics platform based on a unique covalent
custom build library that can identify potent and selective
drugs in innovative and efficient way thereby unlocking the
full potential of small molecule therapies
Bayer’s strength in small molecules enables significant
synergies and ability to leverage Vividion’s platform
Vividion is advancing an attractive pipeline in Oncology
and Immunology with first program to enter the clinic in
2023
Company Overview
SCIENTIFIC FOUNDERS COMPANY PROFILE
BENJAMIN CRAVATT
Professor and Co-Chair,
Dept. of Molecular Medicine
The Scripps Research Institute
Member, Natl Academy of Sciences
2022 Wolf Prize in Chemistry
Small molecule drug
discovery and development
PHIL BARAN
Operations initiated in 2017
Chair, Chemistry
The Scripps Research Institute ~200 employees
McArthur Genius Award
Member, Natl. Academy of Sciences 8,000 m2 of lab/office space
in San Diego, CA
JIN-QUAN YU
Professor, Chemistry
The Scripps Research Institute
McArthur Genius Award
Bayer-Vividion Synergies
Bayer acquired Vividion in August 2021

Vividion’s unique chemoproteomics platform fits well with Bayer’s historical strength and expertise in small
molecules
Acquisition places Bayer and Vividion in a strong position to unlock undruggable targets and generate first-in-
class novel drug candidates for the benefit of patients
Through Bayer’s “Arm’s Length” operating model, Vividion operates autonomously and with full accountability to
develop and advance its portfolio and technologies
As a result of this structure, Vividion can maintain its entrepreneurial culture of a startup while accessing Bayer’s
global resources and strengths to accelerate transformation and advance new scientific breakthroughs
Limitations of Conventional Small Molecule Drug Discovery
100s of human proteins are known to All Human

cause disease Proteins
Disease
Only ~10% of these disease-causing Targets
proteins/targets are drugged by current
therapies1
Not yet
Despite advances in genomics, structural Drugged 10% 90%
biology, and high-throughput screening, drugged
most disease relevant targets are
inaccessible to conventional chemistry –
perceived as pocketless or undruggable
1 Source: Oprea et al.,Nature Reviews Drug Discovery, 17: 317-332, 2018.
Potential to Transform Small Molecule Drug Discovery
CHEMOPROTEOMIC
PLATFORM
TARGET BIOLOGY
MASS
SPECTROMETRY
CHEMISTRY
Vividion’s “Covalent First” Platform Expands Druggable Space
REVERSIBLE DRUG VIVIDION “COVALENT FIRST” DRUG
Target Covalent Target

Protein bond Protein
Drug Drug
Protein-small molecule
interaction surface
Drug-like potency and selectivity requires: Drug-like potency and selectivity requires:
Large contact surface between drug and protein Small contact surface and minimal polar interactions
Multiple specific types (polar) of interactions that guide covalent bond formation
Deep pockets Reactive amino acid (cysteine)

Shallow pockets
Drugs for targets within druggable classes Allows for druggability of all/any disease relevant targets
(e.g., enzymes, receptors) (e.g., enzymes, receptors, transcription factors, ubiquitin ligases)
Foundations of the Vividion Platform
1. THE CHEMISTRY 2. THE PLATFORM (ASSAY)

Unique Covalent Small Proteome-wide Footprinting of Small Molecule-
Molecule Library Target Interactions in Native Systems
VVD compounds are comprised of CELLS / LYSATES / TISSUE

2 distinct structural elements:
Target
Protein
Scaffold Cysteine-
reactive group
Diversity Diversity
Novel LC-MS/MS
pockets
The Innovation and Efficiency of the Vividion Drug Discovery Platform
VIVIDION “COVALENT FIRST” CHEMOPROTEOMICS APPROACH
Public
Databases Prioritize Targets
Propose and Evaluate
Many Targets
Relative Interest Level

Human
Genetics ATG16L1
IRF5 PKCO MyD88
IRF8 IFIH1 USP30
PRMT5
DTL
Structural KRAS
A20
HTT
GBA
Biology YAP1
SMRCA2 CRBN
STAT3 HUWE1 Actionable Hits 5. Evaluate results

Literature
Filtered for druggable classes CONVENTIONAL SMALL MOLECULE DISCOVERY APPROACH

Public
Target HTS Screen
Databases
Human
Genetics
Structural
Biology
Literature
Functional Assay Development Hits against a target
Industrial Scale Chemoproteomics Platform Accelerates
Discovery of Novel Shallow Pockets
INDIVIDUAL LIBRARY OF VIVIDION COMPOUNDS
Target 1 Most screening assays

only capable of
tracking one target at a
time, usually in
unnatural settings
INDIVIDUAL TARGET PROTEINS
Vividion technology
simultaneously tracks
small molecule
interactions against
1000s of targets in
natural settings to
discover potent and
selective compounds
at the same time
NO ENGAGEMENT 100% ENGAGEMENT
Range of Approaches to Modulate Undruggable Targets
First-in-class and/or Best-in-class Small Molecule Therapeutics
DIRECT FUNCTIONAL
Target MODULATORS (DFMs)
TARGETING Protein
FUNCTIONAL SITES “Silent“ Allosteric Inhibitors
Cysteine
Allosteric Activators
Functional
Cysteine Protein-protein Interaction
(PPI) Inhibitors
Target PROTEIN DEGRADERS

TARGETING Protein
NON-FUNCTIONAL SITES
“Silent“ Functionalize silent binders to
Cysteine enable targeted protein
(“SILENT LIGANDS”) Functional degradation
Cysteine
Continuous Library Expansion Allows for Pipeline Growth and
Durable Competitive Advantage
# Actionable Sites (pockets)

Screening &
iterative learning
Vividion unique
covalent chemistry
library
Proteome educated # Compounds in Library
library innovation
Unique Pipeline of First or Best in Class Programs
Pipeline Progress as of 2Q2023
Targets/Program1 Indication Enablement Lead-Op DC Enabling IND Enabling Clinical Entry
NRF2 (inhibitor) NRF2 dependent cancers
STAT3 (inhibitor) NSCLC, ALCL

ONCOLOGY
Kinase (PPI inhibitor) Mutated / amplified cancers
TF (degrader) mCRPC
Driver oncogene (inhibitor) Breast cancer
Restricted E3 (degrader) E3 expressing cancers
TF (inhibitor) Melanoma
STAT3 (inhibitor) PSA, PSO, IBD

IMMUNOLOGY
NRF2 (activator) IBD
Kinase (inhibitor) Psoriasis, IBD
TF (inhibitor) Alopecia and vitiligo
Dual TF (inhibitor) TH-17/TH-1 autoimmune
Adapter (inhibitor) Most autoimmune diseases
1 Multiple Roche-partnered programs in different stages of development; milestone payments can be expected per agreement
Targeting Traditionally Undruggable Transcription Factor NRF2 Enables
Two Distinct MOAs to Address Oncology and Immunology Diseases
KEAP1 (E3 LIGASE) REGULATES ONCOLOGY: NRF2 inhibitor

STABILTY OF NRF2 TO REDUCE
OXIDATIVE STRESS AND RESTORE Increase KEAP1-directed proteasomal degradation of NRF2
CELLULAR HOMEOSTASIS DRUG IMPACT Constitutive activation of NRF2 function enriched in multiple solid tumors (lung
ON PATHWAY sq/ad, esophageal sq/ad, head & neck, bladder cancer)
NRF2
NRF2 degradation Potential to broaden the patient population further (pan-cancer approach) in
inhibitor combination with SOC chemotherapy
KEAP1 OFF Upcoming milestone: VVD-037 expected to enter the clinic by end of 2023
Oncogenic and
cytoprotective gene
programs
IMMUNOLOGY: NRF2 activator
NRF2
Decrease KEAP1-directed proteasomal degradation and drive NRF2
Ub accumulation
Ub NRF2 Initial indication IBD where pre-clinical evidence demonstrates impact on all
Ub NRF2 three pathological domain levels (cytoprotective/tissue preservation,
NRF2 NRF2 ON
leukocyte trafficking and inflammatory mediator production)
activator Anti-inflammatory and

Potential for other inflammatory diseases where oxidative damage,
insufficient stress resistance and chronic inflammation contribute to the
NRF2 cytoprotective
programs underlying pathophysiology (e.g., COPD, NASH)
accumulation Upcoming milestone: Potential IND by end 2024
STAT3 is Traditionally Undruggable Transcription Factor That
Plays Key Roles in Multiple Oncology & Immunology Diseases
STAT3
ONCOLOGY
Prevents STAT3 DNA binding and blocks downstream gene transcription
Addresses primary checkpoint therapy resistance mechanism in genetically defined patient population
(LKB1 mutant lung adenocarcinoma)
Additional opportunity in T-cell lymphomas where STAT3 GOF mutation and/or high-pSTAT3 levels
supports STAT3 dependence
Upcoming milestone: VVD-850 potential IND by end of 2023
IMMUNOLOGY
Blockade of STAT3 DNA binding prevents both IL-6 cytokine family and IL-23 signaling for inhibition of
TH17 cell function with novel potential to simultaneously increase Treg frequency
Central role in multiple pathogenic cytokine signaling pathways hence potential to treat wide spectrum
Utilizing same mechanism/inhibitor in two different disease of human autoimmune diseases
areas offers potential to address multiple patient populations
Initial entry in psoriasis & psoriatic arthritis followed by IBD
Upcoming milestone: Potential IND by end of 2024
Key Messages Today
While hundreds of proteins are known to be drivers of

diseases, just ~10% can be drugged by current therapies
Chemoproteomics technologies can be used to selectively
target and bind to yet unaccessible proteins, thereby
removing today’s boundaries of druggability
Vividion has a world leading industrial scale
chemoproteomics platform based on a unique covalent
custom build library that can identify potent and selective
drugs in innovative and efficient way thereby unlocking the
full potential of small molecule therapies
Bayer’s strength in small molecules enables significant
synergies and ability to leverage Vividion’s platform
Vividion is advancing an attractive pipeline in Oncology
and Immunology with first program to enter the clinic in
2023
Driving Leadership
in Focus Areas of
Oncology
Dominik Ruettinger
Key Messages Today
Our Oncology R&D strategy is based on precision drug

development which enables fast identification of the most
promising targets and commercially viable programs
We focus on expanding the druggable target
pool, developing "kinder medicines", and
addressing resistance
We are rapidly building an early pipeline in precision
molecular oncology and next gen immuno-oncology
Targeted radiotherapies (TRT) provide another highly
attractive opportunity in oncology - we have a wealth of
expertise and experience
Oncology will Remain a Major Segment of the Pharma Market
and we have a Strong Foundation to Build on
Oncology opportunity
MARKET ATTRACTIVENESS BAYER'S KEY STRENGTHS
High unmet need Scientific and clinical expertise

SMOL chemistry and peptide therapeutics
Growing health burden, with cancer being the second Vividion as leaders in chemoproteomics
leading cause of death at present Targeted Radiotherapy (TRT)
GI, GU (notably prostate) and other
30M new cases annually expected by 2040
high unmet need cancers
One of the largest and fastest growing Commercial capabilities

segments Successfully launched several assets
2021-28 CAGR of 12%, expected to reach

>€300bn by 2028 Oncology
Disruptive innovation in Oncology
Access to “undruggable” targets, new biomarker
6 €1.8bn
approaches & diagnostic tools create numerous Approved 2022 Oncology
opportunities for new precision therapeutics medicines Revenue
Source: EvaluatePharma (July 2022), Pharmaprojects (Oct 2021); IQVIA Pharma Deals (January 2021); McKinsey analysis
Focus Where External Opportunity Meets Internal Strength
SCIENTIFIC FOCUS: PRECISION DRUG DEVELOPMENT (PROJECTED) UNMET NEED
Targeted Genitourinary (GU)

Radionuclide Prostate, Bladder,
Therapies (TRT) Renal cancers
Gastrointestinal (GI)
Colorectal, Liver,
Precision Gastric cancers
Molecular
Oncology (PMO) Lung Cancer
(NSCLC)
Next Generation
Other Tumors
Immuno-
with high unmet need
Oncology (IO)
Patient number
A Rapidly Expanding, Changing Patient Population
Patients are younger, diagnosed earlier, increasingly treatment resistant
TODAY FUTURE OUR FOCUS
High impact and kinder medicines

Higher selectivity for target
Expanding the pool of "druggable"
targets
Modalities/Targets working
regardless of mutational status,
pre-treatments e.g., TRT
Disease-centric drug development
= Early onset cancer patient = Early diagnosed patient = GI, GU, and lung Cancers (predicted = Cancer patient (cured)
(<50 years old) increase annual incidence > 20% )
Source: Nat Rev Clin Onc 2022;19:656 Nat Med 2023;29:1113 Cancer Research UK, https://www.cancerresearchuk.org/health-professional/cancer-statistics/worldwide-cancer/incidence, accessed June 2023
We aim to Meet the Needs of Cancer Patients with Precision Drug
Development
Identifying high impact and commercially viable programs earlier
Organizational
readiness
Precision Drug Development
Right Target Biology + Defined patient + Measurable impact Increase

productivity &
success rate
Fit for purpose modality of delivering
Leverage Bayer strengths in small molecules, biologics and TRT Precision
& Driven by value & differentiation

Medicines that
patients need
Considering elements such as FIC/BIC, pricing power, unmet need & competitive intensity
Oncology – Pipeline Update1 (as of Jun 16, 2023)
Rapidly building a balanced portfolio with 3 new clinical entries in 2023
Candidate medication Indication Modality Compound Origin Phase 02 Phase I Phase II Phase III
Darolutamide (AR Inhibitor) Prostate Cancer (mHSPC) (ARANOTE)
Adjuvant Prostate Cancer (DASL-HiCaP)3

Orion
Prostate Cancer with Biochemical Recurrence after Curative

Radiotherapy (ARASTEP)
Copanlisib (PI3K Inhibitor) Non-Hodgkin Lymphoma (CHRONOS-4) Bayer
Regorafenib (combi Nivolumab) (BAY 734506) Solid tumors (recurrent or metastatic) Bayer
mEGFR/HER2 Inhibitor (BAY 2927088) Advanced Non-small Cell Lung Cancer with EGFR Mutation Bayer/Broad Institute
and/or HER2 Mutation
DGKzeta Inhibitor (BAY 2965501) Advanced solid tumors Bayer/DKFZ
CCR8 Ab (BAY 3375968) Advanced solid tumors Bayer
Elimusertib (ATR Inhibitor) (BAY 1895344) Advanced solid tumors, Non-Hodgkin's Lymphoma, Mantle Bayer Focus
today
Cell Lymphoma
AhR Inhibitor (BAY 2416964) Advanced solid tumors Bayer/DKFZ
DGKalpha Inh (BAY 2862789) Cancer Bayer/DKFZ
PSMA TAC (BAY 3546828) Advanced Prostate Cancer Lantheus (prev. Progenics)
PSMA SMOL TAC (BAY 3563254) Advanced Prostate Cancer Noria Therapeutics/PSMA
Therapeutics
VVD NRF2 Inh (BAY 3605349) Cancer Vividion
VVD STAT3 Inh (BAY 3630914) Cancer Vividion
Protein Therapeutics Cell Therapy Contrast Agent Genetic Medicine Radiotherapy Small Molecule
1 Bayer and partner sponsored + 3rd party label enabling studies with first patient first visit 2 Pre-clinical selected assets on path to IND 3 Co-operative group trial led by Australian and New Zealand Urogenital and Prostate Cancer Trials Group (ANZUP)
mEGFR/HER2i (BAY 2927088): Targeting Underserved NSCLC
Mutations
Covalent and potent molecule with high selectivity for mutants over wild-type EGF receptor
UNMET NEED ADDRESSABLE PATIENT POPULATION

PHASE I
Exon 20 insertion (ex20ins) mutations in EGFR and HER2 in NSCLC are Indication Patients
associated with poor patient prognosis and resistance to first- and second- Advanced Non-small Cell Lung 1L - ~20K patients
generation TKIs Cancer with EGFR mutations or 2L ~9K patients
New therapies are also needed to overcome secondary resistance HER2 mutations 1L and 2L US, EU5 & Japan
mutations (eg EGFR C797X) to TKI therapy as well as toxicity from
wtEGFRi
ASSET POTENTIAL
Limited efficacy and tolerability of recently approved treatments for EGFR
exon20ins
Indication Asset Potential
Advanced Non-small Cell Lung
PROFILE & MODE OF ACTION Cancer with EGFR mutations or
HER2 mutation
<€500m €500m–€1bn >€1bn

Oral, reversible, potent TKI targeting EGFR and HER2 driver mutations,
including ex20ins and EGFR C797X acquired resistance mutations
High selectivity for mutant forms vs. wild-type EGFR CURRENT STATUS + NEXT MILESTONES
FPFV October 2021, ongoing expansion cohorts to complete in 2023
mEGFR/HER2i (BAY 2927088): Key Preclinical Data
Indicates potential for high clinical activity with reduced EGFR-mediated toxicities
PRECLINICAL DATA
PHASE I
Strong activity and selectivity for mutants vs. wild-type EGFR
Ongoing FiH trial in patients with advanced NSCLC harboring specific EGFR or HER2 mutations
BAY 2927088 is highly potent in EGFR/HER2

exon20ins and EGFR C797S in vitro and in vivo
BAY 2927088 is less potent on EGFR wild-type:

Treatment at efficacious dose does not affect
wild-type EGFR activity in murine skin – in
contrast to competitors
DGKa/z (BAY 2965501 / BAY 2862789): Inhibiting Diacylglycerol
Kinases to Overcome Immunosuppression
Highly selective DGK inhibitor for cancer immunotherapy with first-in-class potential

PHASE I
Most cancer patients do not derive clinical long-term benefit from immune Indication Patients
checkpoint inhibitors (ICIs) due to primary or acquired resistance. Advanced Non-small Cell Lung ~120k patients
Cancer, PD-1 US, EU5 & Japan
Multi-indication asset for immune sensitive tumors and potential to address Relapsed/Refractory
immune checkpoint inhibitors resistance
ASSET POTENTIAL
PROFILE & MODE OF ACTION Indication Asset Potential

NSCLC, PD-1 R/R
Modality: SMOL
DGK inhibition can overcome an immuno-suppressive tumor environment
with a differentiated mode of action: enhancement of suboptimal T cell <€500m €500m–€1bn >€1bn
priming against low-affinity tumor antigens and (re-) activation of silenced
T-cells
The inhibition of DGKz and DGKa with 2 highly selective NMEs represents CURRENT STATUS + NEXT MILESTONES
a First in Class and Best in Class multi-indication potential in immuno-
oncology with monotherapy and combination options
FPFV November 2022 (DGKz). Anticipated completion of dose
escalation mid of 2024
FPFV expected Q3 2023 (DGKa). Anticipated completion of dose
escalation H2 2024
DGKz (BAY 2965501): Key Preclinical Data
Highly selective DGK inhibitor for cancer immunotherapy with first-in-class potential
PRECLINICAL DATA
PHASE I
DGKΖ ACTS AS AN INTRACELLULAR ANTI-TUMOR ACTIVITY COMPLEMENTARY DGK INHIBITION INCREASES T-CELL
IMMUNE CHECKPOINT TO ANTI PD-L1 ANTIBODY ACTIVATION
2500
via enhancement of
suboptimal T-cell priming
2000
Vehicle against low-affinity tumor
tumor volume [mm³]

1500
antigens
1000
BAY 2965501 via (re-) activation of
aPD-L1
exhausted T-cells regardless
500 BAY 2965501
+ aPD-L1 of suppressive ligands in
0 tumor microenvironment
0 2 4 6 8 10 12 14
treatment days (e.g. PD-L1, TGFβ, PGE2)
Source: Offringa, Kirchhoff et al., AACR 2023
CCR8(BAY 3375968): Reactivating the Immune Response
Against Tumors
Depleting suppressive Tregs through CCR8 may overcome checkpoint inhibition resistance

PHASE I
Most cancer patients do not derive clinical long-term benefit from immune Indication Patients
checkpoint inhibitors (ICIs) due to primary or acquired resistance. Advanced solid tumors in >200K patients
Regulatory T cells (Tregs) are one of the key resistance mechanisms combination with ICI US, EU5 & Japan
hampering the efficacy of ICIs across many tumor types. - NSCLC,TNBC, Melanoma,
HNSCC
ASSET POTENTIAL
MODE OF ACTION
Advanced solid tumors in
Our CCR8 (chemokine receptor 8) antibody is designed to deplete tumor- combination with ICI
resident, activated regulatory T cells resulting in a (re-) activation of the - NSCLC,TNBC, Melanoma,
anti-tumor immune response. HNSCC
<€500m €500m–€1bn >€1bn
BAY 3375968 is expected to demonstrate a better efficacy and side effect
profile than other non-CCR8 Treg-targeting agents due to specific depletion
of tumor-infiltrating CCR8+ Tregs without impacting effector cells and CURRENT STATUS + NEXT MILESTONES
peripheral Tregs.
FPFV October 2022. Anticipated completion of dose escalation H2 2024
CCR8 Antibody (BAY 3375968): Key Preclinical Data
Depleting suppressive Tregs through CCR8 may overcome checkpoint inhibition resistance
PRECLINICAL DATA
PHASE I
An anti-mouse CCR8 surrogate antibody (Ab) showed strong in vivo response in monotherapy which was further improved by
combination with a checkpoint inhibitor anti-PD-L1 agent
In vivo tumor growth inhibition by CCR8 Ab and in combination with anti-PD-L1 In vivo survival by CCR8 Ab and in combination with anti-PD-L1
Arrows indicate the antibody treatment days
MC38 mouse model, MC38 mouse model

arrows indicate treatment
Targeted Radiotherapies (TRT) Offers a Specific Mode of Action
which Addresses Treatment Resistance in Areas of High Unmet Need
SPECIFIC MOA OF TRT CAN UNLOCK A BROAD OPPORTUNITY SPACE
DNA double-strand breaks Address tumor

=> no treatment resistance HNSCC
types that are not
druggable by ADCs
Melanoma
Potential to target
Breast stromal cells in tumor
Cross-fire effect to NSCLC
microenvironment
maximize tumor cell killing
Hem-onc
HCC
Pancreas Potential to overcome
RCC Stroma mechanisms of
resistance
Combination potential CRC
Bladder
with targeted therapies Ovarian
Cervix
(e.g. ICIs/DDRi’s) Prostate Target “cold” tumors
where IO does not
work or sensitize these
MARKET EXPECTED TO GROW TO $20BN BY 2030
Source: Nuclear Medicine Report & Directory 2021 and 2022 (Part 1, 2, 3) - MEDraysintell; TRT Market Sizing for Compass
We have the Right Expertise, Tools & Manufacturing Capabilities in
Place to Produce Best-in-Class TRT Precision Medicines
Strong scientific experience Through multiple iterations, we now Differentiated & fit for purpose
& expertise as well as have the toolkit to produce best-in- assets for high value patient
commercial capability class medicines augmented through populations of high unmet need
smart deals: Ratio & Bicycle
1
3
Linker 7 2
Pre-clinical P0 & P1
4 programs programs
Xofigo 2
(223RaCl2) Modality
Chelator
Launched in 2013 for mCRPC Highly differentiated mechanism of action Rapid expansion of programs expected
Several Lifecycle management achieved by synergistic design of components through internal discovery and external deals
activities ongoing
Key Messages Today
Our Oncology R&D strategy is based on precision drug

development which enables fast identification of the most
promising targets and commercially viable programs
We focus on expanding the druggable target
pool, developing "kinder medicines", and
addressing resistance
We are rapidly building an early pipeline in precision
molecular oncology and next gen immuno-oncology
Targeted radiotherapies (TRT) provide another highly
attractive opportunity in oncology - we have a wealth of
expertise and experience
Shaping new
Treatment Paradigms
in Cardiovascular
Diseases
Maria Borentain
Key Messages Today
CV diseases represent a significant health burden

and #1 leading cause of death with still high
unmet medical need
Our focus within cardiovascular include selected areas
within nephrology and acute care
Our R&D approach is based on three value pools with
an increasing focus in precision medicine: targeting
rare indications, subpopulations, and disruption in
large indications
Building on our strong heritage and expertise we will
continue to develop innovative therapies to address the
needs of patients with cardiovascular diseases
Bayer to Continue Leadership Position in CV
MARKET ATTRACTIVENESS BAYER'S KEY STRENGTHS
High unmet medical needs Record of success

Leading cause of death Industry leader in cardiovascular
Increasing disease burden and rising comorbidities Expertise along the entire value chain
Huge impact on healthcare systems and workforce Established global commercial footprint
Emerging trends Exciting recent and near-term launches

Novel drug modalities offer new opportunities Late-stage pipeline asset asundexian: Innovative,
Advanced tools like multi-omics enable precision medicine once-daily, oral small molecule FXIa inhibitor
Digital solutions enable early diagnosis and targeted Successful launch of Kerendia with LCM potential
treatment Cardiovascular,
Nephrology &
Attractive growth market Acute Care Strategic focus on precision CV
Worldwide market value of €65bn (2022) continuing
to grow at a steady pace Expertise available to address and internalize
scientific progress
Pharma industry underinvests in CV R&D in relation
to disease burden External collaborations & platform companies further
enhance our transition into precision CV
Huge opportunity in precision CV due to scientific
progress
CV: A Success Story set to Continue
Recent successes fuel our ambition for the future to help even more patients in need
Bayer has a strong R&D CV expected to drive future sales

and commercial of Bayer Pharma
record in CV
Asundexian2
(investigational FXIa inh.)
€4.5bn Worsening HFrEF T2D CKD, HFpEF SPAF, stroke

2022 & Stable HFrEF & ndCKD
Peak1 Peak1 Peak1
~€0.5bn >€3bn >€5bn
€0.8bn Bayer among the top leaders in CV

2022
We aspire to build on our R&D successes and
strengthen our CV leadership
1 Peak = Peak Sales Potential; 2 Late-stage pipeline asset
We Focus on Three Value Pools to Build on our Leadership in CV
Gradual shift from large indications to high value subpopulations and rare indications
PATIENT FOCUS DISEASE AREAS SELECTED INDICATIONS (INDICATIVE)
high
Subpopulations
Rare
Addressing the highest of larger
Disease
unmet medical need indications
for patients with Alport Heart Failure
rare diseases Cardiovascular Syndrome and Chronic
Unmet medical need

Kidney Disease
Catering to Disruption in
subpopulations of larger large indications
Nephrology
indications with high Stroke
unmet medical need Prevention
Opportunistic focus on Acute Care

real disruption in large
indications with highest
standard of care
low
low Patient population size high
Cardiovascular+ – Pipeline Update 1 (as of Jun 16, 2023)
Candidate medication Indication Modality Compound Origin Phase 02 Phase I Phase II Phase III
Finerenone (MR Antagonist) Heart Failure (HFmr/pEF) (FINEARTS-HF) Bayer
Non-diabetic CKD (FIND-CKD)
Vericiguat (sGC Stimulator) Heart Failure (HFrEF) (VICTOR3) Bayer
Asundexian (FXIa Inhibitor) Stroke Prevention in Atrial Fibrillation (OCEANIC-AF) Bayer

(BAY 2433334)
2⁰ Stroke Prevention
(OCEANIC-STROKE)
Major Adverse Cardiac Events Prevention (PACIFIC-AMI)
Congestive Heart Failure rAAV Gene Congestive Heart Failure AskBio
Therapy
(AB-1002 aka NAN-101)
sGC Activator Oral Chronic Kidney Disease (CKD) Bayer
(BAY 3283142)
Anti-a2AP Acute Ischemic Stroke; Pulmonary Embolism Bayer
(BAY 3018250)
sGC Activator Inhale Acute Respiratory Distress Syndrome Bayer
(BAY 1211163)
SEMA 3a Alport Syndrome Bayer/Evotec
(BAY 3401016)
Anti-coagulant Anti-coagulation Bayer
(BAY 3389934)
Protein Therapeutics Cell Therapy Contrast Agent Genetic Medicine Radiotherapy Small Molecule Focus today
Cardiovascular +: Including Precision Cardiovascular, Nephrology & Acute Care
1 Bayer and partner sponsored + 3rd party label enabling studies with first patient first visit 2 Pre-clinical selected assets on path to IND 3 Conducted by Merck & Co
Finerenone is a Potent, Highly Selective Non-Steroidal MRA
with Differentiated Profile
DIFFERENT BINDING MODES BETWEEN THE STEROIDAL PRECLINICAL DATA: RECEPTOR PROFILE, DRUG METABOLISM
MRAs AND THE NONSTEROIDAL FINERENONE1 AND TISSUE DISTRIBUTION OF FINERENONE2
Spironolactone Eplerenone Finerenone
MRA Class Steroidal Steroidal Non-steroidal
Potency High Low High
Selectivity Low Medium High
Metabolites Multiple, active No active No active
Tissue Kidney>>heart Kidney>heart

Balanced (1:1)
distribution3 (>6-fold) (~3-fold)
No sexual side effects including gynecomastia

Finerenone and steroidal mineralocorticoid receptor
antagonists differ in their molecular receptor binding mode Balanced kidney safety
resulting in distinct effects on gene expression
Low incidence of hyperkalaemia-related adverse events with
clinical impact and permanent treatment discontinuation4
Source: 1Kolkhof P, Nowack C, Eitner F. Curr Opin Nephrol Hypertens. 2015;24:417-424. 2Modified from: Kolkhof B, Borden SA. Mol Cell Endocrinol. 2012;350:310-317. 3 Determined in rodents. 4 Agarwal R, Filippatos G, Pitt B, Anker SD, Rossing P, Joseph A, Kolkhof P,
Nowack C, Gebel M, Ruilope LM, Bakris GL; FIDELIO-DKD and FIGARO-DKD investigators. Cardiovascular and kidney outcomes with finerenone in patients with type 2 diabetes and chronic kidney disease: the FIDELITY pooled analysis. Eur Heart J. 2022 Feb 10;
43(6):474-484. doi: 10.1093/eurheartj/ehab777. Erratum in: Eur Heart J. 2022 May 21;43(20):1989.
Large Integrated Program to Investigate Finerenone as a
Foundational Treatment for Chronic Kidney Disease (CKD)
Strong launch dynamics and the option to broaden the use in CKD
STUDY DATA ONGOING PHASE III STUDIES

Finerenone effective in reducing
PHASE III
Potential to Broaden the Use of

cardiovascular and renal events in patients with
Finerenone in CKD
T2D and CKD
Potential to Broaden
Non-diabetic CKD the Use of
Key results of the FIDELITY pooled analysis1: Finerenone in CKD
Composite Kidney
FIND-CKD: randomized, double-blind, placebo-
Composite CV Outcome
Outcome controlled, parallel-group, multicenter phase III trial
HR = 0.77 in CKD patients without diabetes
HR = 0.86 (95% CI 0.67-0.88), p=0.0002
(95% CI 0.78-0.95), p=0.0018 NNT 592 Phase III data expected in 2026
NNT 462
Relative risk reduction compared Relative risk reduction compared
to placebo to placebo
CKD in Type 1 Diabetes

FINE-ONE: randomized, double blind, placebo-
controlled, parallel-group, multicenter phase III trial
-14%
in CKD patients with type 1 diabetes (T1D)
-23%
Phase III data expected in 2025
Source: Agarwal, R. et al., data presented at ESC 2021
1 including > 13,000 randomized pts; 2at 36 months
Potential to Expand the Indication of Finerenone in Heart Failure
Phase 3 FINEARTS-HF with mildly reduced / preserved EF (HFmrEF/HFpEF ) is ongoing
UNMET MEDICAL NEED Clinical data suggest benefit of finerenone in heart failure
8
PHASE III
HF is the fastest-growing global CV disease Phase 3
Cumulative incidence (%)2

HR = 0.68
with approximately ~60m HF patients FIGARO- (95% CI, 0.54-0.86), p=0.0013 Placebo: 173/3666 (4.7%)
6
worldwide DKD:
Reduced 4
About 50% of HF patients have HF with risk of
LVEF ≥ 40%. They suffer from a high CV HF-related 2 Finerenone: 120/3686 (3.3%)
mortality rate (42% within 5y of diagnosis) death or
despite SoC first HHF1 0
0 6 12 18 24 30 36 42 48
Months since randomisation
Renal dysfunction and HFmrEF/pEF
frequently coexist, due to shared
comorbidities and factors impacting Phase 2 CV hospitalisation4 CV death4
macrovascular and microvascular circulation ARTS-HF3:
Cumulative probability of
Cumulative probability of
30 Eplerenone 8 Eplerenone
CV hospitalisation (%)
Reduced 25 Finerenone 1020 mg Finerenone 1020 mg
risk of CV 6
CV death (%)
20
hospitalization 15 4
UPCOMING DEVELOPMENT MILESTONES and CV death 10
vs eplerenone 2
5
Phase 3 data expected in 2024 0 0
Day Day Day Day Follow Day Day Day Day Follow
0 30 60 90 -up5 0 30 60 90 -up5
1 First hospitalisation for HF defined as first event after randomisation; 2 Source: cumulative incidence calculated by Aalen–Johansen estimator using deaths due to other causes as competing risk. Filippatos G, et al. Circulation 2022;145:437–447
3 Both phase 2a study ARTS and phase 2b study ARTS-HF were in HFrEF, 4 Source: Kolkhof P, et al. Handb Exp Pharmacol 2017;243:271–305; 2. Filippatos G, et al. Eur Heart J 2016;37:2105–2114; 5 30-day period after cessation of study drug
FXI(a) Inhibitors Are a Promising And Distinct New Class of Drugs
For Thrombosis Prevention
Separating thrombosis protection from haemostasis via selective modulation of the coagulation system
Mode of Action1-3 Patients with genetically higher FXI levels show

increased risk of ischemic stroke4
Ischemic stroke Cases Controls OR p-value

subtype^x (N) (N) 95% CI
Cardioembolism 3,071 28,722 0.0003
Large artery
2,454 28,880 0.02
atherosclerosis
Small vessel
2,736 27,588 0.69
occlusion
Undetermined
4,755 25,292 0.0002
cause
0,1 1 10
Paradigm shift in thrombosis prevention, with the
potential to uncouple efficacy from bleeding risk Favors control Favors genetically
FXI levels higher FXI levels
FXa, activated Factor X; FXI(a), activated Factor XI, FXII(a), activated Factor XII; TF, tissue factor.
Source: 1 Piccini JP et al. Lancet 2022;399:1383–1390. 2 Fredenburgh JC, Weitz JI. Hamostaseologie 2021;41:104–110. 3 Gailani D et al. J Thromb Haemost 2015;13:1383–1395. 4 Gill D et al. Stroke 2018;49:2761–2763
Phase III Decision for Asundexian Strongly Backed by Results
From PACIFIC Phase II Program
Innovative, once-daily, oral small molecule FXIa inhibitor
Study Data: PACIFIC-AF Study Data: PACIFIC-STROKE

Bleeding: Asundexian at near maximum FXIa inhibition showed Bleeding: no significant increase vs. Placebo on
lower rates of observed bleeding versus apixaban in PACIFIC-AF top of Antiplatelet/Dual Antiplatelet
Efficacy: too few events to draw conclusion
Proportion of participants with bleeding event, % of patients1 Recurrent stroke and TIA in patients with any extra-/intracranial
10.4% atherosclerosis2
0.16 (0.01-0.99) 0.39 (0.18-0.85)
8.0%
8.1%
3.5% 3.9%
2.4%
3.1%
0.4%
Asundexian Apixaban
50mg
ISTH major bleeding or clinically relevant non-major bleeding Asundexian Placebo
ISTH minor bleeding 50 mg
All bleeding
Broad Phase II study program PACIFIC confirmed

consistent safety at near maximum FXIa inhibition1
Source: 1 Piccini JP, Caso V, Connolly SJ, Fox KAA, Oldgren J, Jones WS, Gorog DA, Durdil V, Viethen T, Neumann C, Mundl H, Patel MR; PACIFIC-AF Investigators. Safety of the oral factor XIa inhibitor asundexian compared with apixaban in patients with atrial
fibrillation (PACIFIC-AF): a multicentre, randomised, double-blind, double-dummy, dose-finding phase 2 study. Lancet. 2022 Apr 9;399(10333):1383-1390. doi: 10.1016/S0140-6736(22)00456-1. Epub 2022 Apr 3. PMID: 35385695. Data presented at ACC 2022 and
ESC 2022. 2 Data presented at ESC in August-2022 in Barcelona, and ESOC May-2023 in Munich (data on file)
OCEANIC Phase III Program
Study program well on track
The OCEANIC program consists of two Phase III studies
OCEANIC-AF OCEANIC-STROKE
Patients with atrial fibrillation Patients with non-cardioembolic ischemic stroke

Active comparator-controlled trial (apixaban) Placebo-controlled trial
# of patients ~18,000 patients # of patients ~9,300 patients
Minimum treatment period 9 months Minimum treatment period 3 months
Primary efficacy endpoint: stroke or systemic embolism Primary efficacy endpoint: ischemic stroke
Primary safety endpoint: ISTH major bleeding Primary safety endpoint: ISTH major bleeding
First patient first visit: Q4 2022 First patient first visit: Q1 2023
Data expected: H2 2025 Data expected: H2 2025
Started in Dec 2022 (~27,000 patients, across 40 countries)

First topline data expected H2 / 2025
The NO/sGC/cGMP Pathway is a Key Modulator of Patho-Mechanisms in
Cardiovascular and Renal Function
Bayer has a strong 20+ year legacy in sGC
UNMET NEED PROFILE & MODE OF ACTION

PHASE I
Impairment of the NO/sGC/cGMP signaling can cause Oxidative stress results in heme-oxygenation and heme-
cardiovascular, cardiopulmonary and cardiorenal free sGC (soluble Guanylyl Cyclase)
diseases
Oxidative stress is a hallmark of CKD/DKD and there Oxidized/ heme free sGC limits the activity of Nitric Oxide
is a need to reduce progression to end-stage renal (NO) and therefore impairs cGMP signaling
disease (ESRD) and CV mortality Re-activation of sGC is expected to restore regulation of
Inactivation of sGC disrupts the local regulation of perfusion in affected organs
perfusion, resulting in ischemia, the main cause of
end-organ damage in diabetes patients sGC activators specifically
Binds and activates oxidized/ heme free sGC
Independent from and additive to endogenous NO
Source: Stasch & Hobbs, Handb Exptl Pharmacol 2009; Follmann et al., Angew. Chem. Int. Ed. 2013;52:9442-9462 Sandner, Biol Chem. 2018 Jun 27;399(7):679-690; Sandner et al., Handb Exptl Pharmacol 2021
sGC Activator Front-Runner Runcaciguat Confirmed Strong
UACR Reduction of the Drug Class
In various experimental models, soluble guanylyl cyclase (sGC) Phase 2 CONCORD Study2:
activators1 Runcaciguat demonstrated beneficial effects in patients with CKD & advanced CVD
Lowered blood pressure A reduction in UACR was observed in all strata and significant UACR reductions were
Decreased proteinuria seen in patients with diabetes on top of RAASi and on top of SGLT2 inhibitors
Improved renal outcomes The small reduction in SBP with runcaciguat suggests that improvement in UACR is
not driven by changes in BP
These sGC activators did so in a dose-dependent manner, in A small reduction in eGFR was observed with runcaciguat
diabetic, as well non-diabetic, CKD models
Runcaciguat was well tolerated
Change in albuminuria, patients with Change in albuminuria, patients with

DKD without SGLT2i DKD using SGLT2i
80 80
40 40
0 0
-40 -40
-80 -80
Runcaciguat Placebo
Source: 1 Hahn MG et al. J Med Chemistry 2021;64:5323–5344; 2Ron T. Gansevoort et al. Oral presentation ERA 2023 Data show estimated mean percent change and 95% confidence interval (ANCOVA) for the PPS.
sGC Activator Oral (BAY 3283142)
Preclinical pharmacodynamic data confirm comparable profiles of BAY3283142 and runcaciguat in CKD
PRECLINICAL DATA ADDRESSABLE PATIENT POPULATION

PHASE I
BAY3283142 vs Runcaciguat preclinical comparison Indication Patients

Progressive CKD Rat Model (ZSF-1) Chronic Kidney CKD is a progressive condition that
Disease affects >10% of the general
population worldwide, amounting to
Urine Protein / Creatinine
~700 million individuals1

Asset Potential

Chronic Kidney Disease
<€500m €500m–€1bn >€1bn
Preclinical model shows BAY328 is highly effective in CKD prevention

(decrease in proteinuria and glomerulopathy) Upcoming Development Milestones
BAY3283142 pharmacokinetics with favorable Peak/Trough profile
Initiation of Phase 2 program
allows for once daily dosing
Source: 1 Vijay et al, 2021

Anti-a2AP (BAY 3018250)
Timely vessel opening represents a high unmet medical need in acute ischemic stroke (AIS) and
pulmonary embolism, areas without innovation for more than 2 decades
UNMET NEED PROFILE & MODE OF ACTION
PHASE I
Current thrombolytic drugs have shown limited efficacy and Fibrinolysis

notable hemorrhagic complication rates
Active lysis of acute embolic or thrombotic clots without
Surviving patients often experience significant sustained increasing risk of bleeding by blocking the endogenous
disability Plasmin inhibitor a2Ap
tPA
The clinical and economic burden of AIS is considered high
and still rising clot
Plasmin dissolution
>2 million patients hospitalized with AIS in US, EU4
and JP
Average healthcare cost of stroke per person

estimated at ~US$140k in US α2-Antiplasmin
function blocking
Incidence of PE is still rising and comes with high mortality
(a2Ap) anti-a2Ap antibody
as well as considerable economic burden BAY 3018250
>500k patients hospitalized with AIS US, EU4 and JP,
expected to increase to 700K by 2030
Potential for significant differentiation vs SoC with a profile that
In EU and US deaths are expected to be around 600k allows use in a broad eligible population based on efficacy coupled
by 2030. Average healthcare costs are US$12-20k in with no increase in bleeding profile
the US
Potential to be the first in class, effective thrombolytic with no increase in bleeding risk and a wider
treatment window
PHASE I
In animal models, BAY 3018250 demonstrated to be an effective Indication Patients

thrombolytic with no increased bleeding risk. Acute Ischemic Stroke; AIS: 500k (US, EU4, UK, JP)
Pulmonary Embolism PE: 250k (US, EU4 and JP)
1. Accelerates clot dissolution on a PE model
2. Increased clot dissolution in a venous thromboembolism model
3. In vivo bleeding experiments do not indicate an increased risk
of bleeding Asset Potential

Clot Lysis Bleeding Time
Acute Ischemic Stroke;
60.000 1.200 Pulmonary Embolism
in vivo clot lysis (rFU AUC)
50.000 1.000
40.000 800 <€500m €500m–€1bn >€1bn
time [secs]
30.000 600
20.000 400
10.000
Upcoming Development Milestones
200
0 0
Control tPA BAY3018250 Control tPA BAY3018250 Decision to move to Phase 2 in H2 2023
1 mg/kg 1 mg/kg
Sema3A mAB1 for Alport patients
Aiming to delay disease progression and onset of end-stage renal disease

PHASE I
Rare genetic kidney disease with progressive loss of filtration Indication Patients (rare orphan
capacity, leading to end stage renal disease and dialysis early with disease)
the need for kidney transplant in 4th/5th decade Alport 1 in 5,000 – 10,000 (globally)
Progressive hearing-loss (frequent)
Variable vision impairment (less frequent) Asset Potential
PROFILE & MODE OF ACTION
Semaphorin-3A (Sema3A) is an extracellular guidance protein and a Alport
well-known regulator of the actin cytoskeleton
<€500m €500m–€1bn >€1bn
Alterations of the actin cytoskeleton, particularly of podocytes, are a
key pathophysiological feature of Alport Syndrome
Sema3A is upregulated in injured human kidneys and implicated in the Upcoming Development Milestones
development and progression of acute and chronic kidney diseases
Sema3A antibody blocks Sema3A activity Start of Phase 1 with first dosing of healthy
subjects in June 2023
Study data expected in 2024
1 Compound Origin: Bayer / Evotec
Sema3A mAB1 for Alport patients
First to market potential in Alport syndrome – a rare genetic disease
PRECLINICAL DATA
PHASE I
Evidence of Sema3A in kidney disease

Therapeutic efficacy of Sema3A inhibition
in Alport mouse model
400 n.s. n.s. n.s. **** **** ****
1500
uPCR [%] increase from baseline

**
relative mRNA expression [AU]
control
300
1000
200
+Sema3A
500
100
0
healhy Alport 0
healthy Alport baseline day 28
healthy Alport Alport + compound dose 1 Alport + compound dose 2
Sema3A is upregulated in Sema3A induces detrimental changes in
injured mouse kidneys primary human kidney cell morphology Sema3A inhibition significantly reduced proteinuria
progression in Alport mice
1 Compound Origin: Bayer / Evotec
Key Messages Today
CV diseases represent a significant health burden

and #1 leading cause of death with still high
unmet medical need
Our focus within cardiovascular include selected areas
within nephrology and acute care
Our R&D approach is based on three value pools with
an increasing focus in precision medicine: targeting
rare indications, subpopulations, and disruption in
large indications
Building on our strong heritage and expertise we will
continue to develop innovative therapies to address the
needs of patients with cardiovascular diseases
BlueRock
Therapeutics:
Leading the way in
PSC Therapies
Seth Ettenberg
Key Messages Today
A new frontier of cellular medicine was launched with

the commercialization of cell therapies for hematological cancers
Pluripotent stem cell (PSC) derived therapies with the potential to
broaden the impact of cellular medicine beyond cancer are the
next frontier.
BlueRock is one of the leaders of this next field, with end-to-end
capabilities for delivering innovative PSC-based therapies
Near-term OpCT-001 IND filing for the treatment of
primary photoreceptor diseases (e.g., retinitis pigmentosa,
cone/rod dystrophies)
Advancing bemdaneprocel for Parkinson’s Disease into
phase 2 clinical development based on positive readout of
our phase 1 study
Bayer and BlueRock are working to change the future
of medicines by replacing the cells that are lost to diseases
The Cell Therapy Market Is Expected to Reach >USD25bn by 2026
HISTORY OF FDA CELL THERAPY APPROVALS1 NUMBER OF CELL THERAPIES IN CLINICAL
DEVELOPMENT TODAY2
Informa, June 2023
CAR-T ~640 cell therapies in
Non-genetically modified cells 73 clinical development
158 CAR-Ts across TAs
Anticipated regulatory decisions 1
2 6 Non-CAR-Ts
224 Multiple ongoing phase 3
137
47 trials for approved CAR-T
Phase 1 Phase 2 Phase 3 (e.g., label expansion)
Only unapproved agents in clinical development included
2 2
1 1
GLOBAL SALES OF CELL THERAPIES3 (USDbn)
2017 2018 2019 2020 2021 2022 2023
FDA Approved Cellular and Gene Therapy Products
Forecast
25,6
First cell therapy approved in 2017, majority of currently

17,5
approved cell therapies still CAR-T based for hematological
malignancies
Cell therapies expected to remain one of the fastest growing 11,1
therapeutic options in the pharmaceutical sector
6,7
Key considerations for successful commercialization: 3,9
streamlining supply chain and administration logistics 1,4 2,4
0,6 0,9
patient and caregiver support
innovative payment solutions 2018 2019 2020 2021 2022 2023 2024 2025 2026
Cord Blood approvals not included in approved therapies

Sources: 1 FDA Approved Cellular and Gene Therapy Products 2 Pharma Intelligence, Informa 3 EvaluatePharma, Oct. 2022 for pipeline and sales/ forecast
BlueRock Therapeutics is a Leader in PSC Biology,
Bringing Therapies From Bench to the Clinic
MISSION: To discover and develop new cell therapies that change the way disease is treated and improve patients’ lives
Cell Replacement Engineered Cells
REPLACE RESTORE REVERSE ENGINEER DELIVER TREAT

CELLS FUNCTION DISEASE CELLS PAYLOAD RARE & COMMON
FOUNDING SCIENCE FOUR SITES ACROSS USA, Canada and Germany
Lorenz Studer, MD Gordon Keller, PhD Bruce Blazar, MD Cambridge (HQ) New York Toronto Berlin
MSK Cancer University Health University of Immunology Research Neurology Research Cardiac research Support for clinical
Center Network Minnesota Clinical & Regulatory Platform technology Device and programs and coordination
Pilot cGMP facility formulations of regulatory processes in
Genome Biology Pilot cGMP facility Europe
Focus on four disease areas (Neurology, Cardiology, Immunology, Ophthalmology)

Within the Cell Therapy Space, Pluripotent Stem Cells Have the
Broadest Therapeutic Potential
AUTOLOGOUS VERSUS
ALLOGENEIC CELL THERAPY SOURCES FOR CELL THERAPY ADMINISTRATION
Cell therapy is the administration of Final cell product can be

cells into a patient that are derived Adult Harvestable Cells: administered in different ways,
from the patient (autologous) or a Harvested from adult donor depending on the therapeutic
healthy donor (allogeneic) approach and indication
Limited available quantities, difficulty in
Autologous access and cell expansion
Examples include: Systemic delivery
Isolated T-cells for CAR-T therapy Examples include:
MSCs Intravenous
HSCs
Direct delivery to target area:

Pluripotent Stem Cells (PSC): Examples include:
Allogeneic
Can differentiate into any cell type in the Intracranial
body Spinal cord
Allogeneic PSCs with unlimited potential for Heart
expansion and scalability Eye
Source: 1 El-Kadiry 2021. Frontiers in Medicine, p.2340.
Pluripotent Stem Cells Have the Potential to Restore Lost Cellular
Function and Introduce New Functions to Address Multiple Diseases
THERAPEUTIC POTENTIAL OF PSCs EXAMPLES OF TARGET DISEASE AREAS
Differentiated cell Parkinson’s Disease

to restore lost Heart Failure
function Retinitis Pigmentosa
Geographic Atrophy (AMD)
Reprogram
blood cells
Pluripotent Cell
Oncology
Engineered to
Alzheimer‘s Disease
introduce new
functions Metabolic Diseases
Autoimmune Diseases
Source: El-Kadiry 2021. Frontiers in Medicine, p.2340.
BlueRock Has End-to-end Capabilities in PSC Technology
CORE FOUNDATIONAL EXPERTISE IN BRINGING CELL COMMERCIAL MANUFACTURING

REPROGRAMMING TECHNOLOGY THERAPY TO THE CLINIC CAPABILITIES
Donor material fully consented for Thorough understanding and ability to Commercial scale production of
commercial use differentiate cells into specified cryopreserved product
medicines at scale, reproducibly
Proprietary, non-integrating, high- Technology transfer to commercial
efficiency reprogramming Demonstrated ability to bring manufacturing facility in Berkeley
technology; deep analytics differentiated cells into clinical (Bayer)
development
Defined cGMP-compliant processes,
including master cell banking
Ongoing Partnerships for Continued Advancement of PSC
Therapies
PARTNERSHIP GOALS ONGOING PARTNERSHIPS
Technologies to accelerate pipeline execution
Enabling technologies to bolster platform
Capabilities and programs to enhance pipeline
Partnerships enables BlueRock to continually push the boundaries of

PSC-based therapies
BlueRock’s Pipeline Addresses Areas of High-Unmet Needs
AREA TARGET DISEASE CELL TYPE DISCOVERY PRECLINICAL IND-ENABLING CLINICAL
Parkinson’s Disease Dopaminergic Neuron Bemdaneprocel

Neurology
Demyelinating Disorders Oligodendrocyte v
Lysosomal Storage Disorders Microglia
Photoreceptor Precursor Cell

Primary Photoreceptor Disease
Ophthalmology
OpCT-001
(PRP)
Early / Intermediate Dry AMD Retinal Pigment Epithelium (RPE)
Late Dry AMD / GA PRP + RPE

Cardiology
Heart Failure Cardiomyocyte

Immunology
& Oncology
Oncology Myeloid
Autoimmune Disease Regulatory T Cell
Focus today
Primary Photoreceptor Disease is a Group of IRDs That Lead to
Irreversible Vision Loss in Children and Adults
Primary Photoreceptor Diseases (PPD) Background CURRENT TREATMENTS AND UNMET NEED
A group of inherited retinal disorders (IRDs) that specifically affect the Over 200k1 patients are currently affected with primary
function / structure of the photoreceptor cells (cone, rods) in the retina photoreceptor disease
Includes Retinitis Pigmentosa, cone and cone-rod dystrophies; ~65% of There are no specific treatment options available, management is
all IRDs focused on supporting patients as vision loss progresses (guide
dogs, visual aids)
GENETIC CAUSES OF INHERITED RETINAL DISORDERS (IRDs) Most therapies in development only target specific genetic mutations
CELL THERAPY APPROACH
BlueRock’s cell therapy can potentially treat an

entire class of diseases
OpCT-001 will be evaluated for patients with
Retinitis Pigmentosa as well as cone and
cone-rod dystrophies
1 US, EU4 + UK
Source: Rattner, A. et. al. Annu. Rev. Genet. 2009, Kantar Health, 2020 and Luxturna PI 4 BR Analysis
BlueRock’s Ophthalmology Ambition: Restoring Vision by Replacing
Degenerated Tissue in the Retina with Functional Cells
ANATOMY OF THE HUMAN EYE PSC DERIVED RETINAL CELL DIFFERENTIATION
Retinal pigment epithelium (RPE)

Human PSC
Single layer of cells, essential for

maintaining vision
Changes in the RPE can impair Retinal OpCT-001
visual function and lead to Progenitor
Cell
retinopathy (i.e., RP, AMD, SD) RPE Photoreceptor
Progenitor Progenitor Cell
Cell (PRP Cell)
Photoreceptors in the retina
Convert light into nerve signals

RPE Cell Bipolar Horizontal Ganglion Amacrine Muller Cone Rod
Rods: responsible for vision at cell cell cell cell Glia
low light levels
Future programs
Cones: active at higher light
levels, responsible for color vision In focus of BlueRock’s pipeline
Source: Yang, et al., 2021. Frontiers in pharmacology, 12, p.727870.
OpCT-001 – Cell Therapy for PRP Cell Replacement
OpCT-001 cells engraft and display characteristics of

functional photoreceptors ADDRESSABLE PATIENT POPULATION
In addition to phenotypic maturation, transplanted photoreceptors begin to show physical maturation Indication Patients
including the formation of inner and outer segments and the trafficking of rhodopsin to outer segments
Primary Photoreceptor Disease US, EU4/UK, ~200k
Opsin protein expression

Outer
segment
Inner and outer segment
RODS CONES
formation ASSET POTENTIAL
Rods traffic rhodopsin to
Inner
outer segments
segment Indication Asset Potential
Outer segments are stable
long-term Primary photoreceptor disease
Outer Segment Formation
<€500m €500m–€1bn >€1bn
STATUS AND UPCOMING DEVELOPMENT

MILESTONES
IND submission in the next 12 months
Rat model
Parkinson's Disease is a Progressive, Neurodegenerative Condition
Defined by Dopaminergic Neuron Loss and Motor Impairment
PD Motor Symptoms Caused by Loss of DA Neurons

Healthy dopamine Current Treatments and Unmet Need
Healthy PD Patient
neurons (DA) in the PD is the second most common neurodegenerative
brain make the Presynaptic
neurotransmitter Terminal disorder in the US
dopamine critical for Limited treatment options available as patients progress
several brain Dying
functions, including Neuron
Medications, effective at early stages, become less and less
movement Dopamine effective with disease progression
Loss of DA cells
results in less Significant unmet need for longer-lasting therapies that will
dopamine and leads alter the disease trajectory
to Parkinson’s
Disease Postsynaptic
Terminal
Bemdaneprocel is being developed as a one-time cell therapy that will provide dopaminergic neurons to
the brain to restore lost dopaminergic function
The goal is to alter disease progression and reverse symptoms over time, so patients remain independent and
live a life that is not defined by their diagnosis
Source: Song 2016. Frontiers in aging neuroscience, 8, p.65.; Kalia 2015. The Lancet. 386(9996), 896-912.; Bridi 2018. Frontiers in neuroscience, 12, p.80.
All Patients from Phase 1 Trial have Completed 1-Year Follow-up
Bemdaneprocel Surgical Procedure
Burr hole Tracts for

Phase 1 Study Summary cell delivery
• Multi-center, open label, Phase I trial

Trial Design assessing bemdaneprocel authentic cell
therapy for Parkinson’s Disease
• Subjects with PD (male/female)

Enrollment • Patients diagnosed ≥3 and ≤15 years ago
Criteria • Responsive to L-dopa, but inadequate relief
of motor symptoms
• Safety, tolerability, PET-imaging for cell

Objectives
survival at years 1 & 2 Surgery Overview
• Preliminary efficacy (motor, non-motor) at
years 1 & 2 Single burr hole per hemisphere with three tracts for cell delivery
Bemdaneprocel custom procedure minimizes needle passes and
• Two cohorts - low and high doses burr holes to decrease surgical risk and optimize coverage
Dosing • Immunosuppression for 12 months following
transplantation
Sources: ct.gov NCT04802733
Bemdaneprocel is the First PSC-derived Dopaminergic Cell Therapy
with Positive Data in PD
TOPLINE PHASE 1 RESULTS ADDRESSABLE PATIENT POPULATION
The study met the primary endpoint; bemdaneprocel was well tolerated Indication Patients
with no major safety issues by all twelve patients in both the low and high Parkinson’s Disease US ~1 million
dose cohorts through one year
Feasibility of transplantation, and evidence of transplanted cell survival
and engraftment in both cohorts was demonstrated through one year. ASSET POTENTIAL
Detailed phase 1 trial data from primary and secondary endpoints will be
presented at the 2023 International Congress of Parkinson’s Disease and
Movement Disorders (MDS) taking place in Copenhagen from Aug. 27 – Indication Asset Potential
31, 2023 Parkinson’s Disease
Phase 1 Study Endpoints

<€500m €500m–€1bn >€1bn
Primary Endpoint:
Safety and tolerability at 1-year post-transplant
Secondary Endpoints (1- and 2-year post transplant): STATUS AND UPCOMING
Evidence of cell survival – F-DOPA PET
DEVELOPMENT MILESTONES
Changes in motor function – Changes in MDS-UPDRS III
Q3 2023 planned presentation of Phase 1 data in a medical meeting
Changes in waking hours in “OFF” state Phase 2 clinical study expected to begin enrolling patients in H1 2024
Continued safety and tolerability
BlueRock is a Leader in the Development of PSC-derived Therapies
2023 & Beyond
PARKINSON'S DISEASE OPHTHALMOLOGY HEART FAILURE
Report Ph1 results of bemdaneprocel IND filing for OpCT-001 Demonstration of PoC in large
animal models
Initiate bemdaneprocel Ph 2 study Initiate FIH study
IND filing for cardiomyocytes
Advance follow-on PD
program (DA02)
Asklepios
BioPharmaceutical:
Pioneering AAV-
based Gene
Therapies
R. Jude Samulski
Key Messages Today
Highly attractive market:

Gene therapy market expected to grow significantly
until the end of the decade
Pioneer in AAV-based gene therapy:
Unparalleled pipeline, talent and manufacturing
capabilities
Robust therapeutic pipeline:
Balanced portfolio addressing monogenic and pathway
disorders
Scalable platform for continued growth and innovation:
Building a platform enables to extend the field of
application of the technology to multiple diseases
FDA January 21, 2019
We anticipate that by 2020 we will be receiving more than

200 INDs per year, building upon our total of more than
800 active cell-based or directly administered gene therapy In the case of gene therapy, it’s similarly a
INDs currently on file with the FDA. product innovation that has marked an
And by 2025, we predict that the FDA will be approving 10 inflection point in the development of
to 20 cell and gene therapy products a year based on an these therapies, and a surge in new
assessment of the current pipeline and the clinical success product activity. In this case, it was the
rates of these products [....] advent of safe and effective vectors for the
We’re working to expand our review group dedicated to the delivery of gene therapy products, such as
evaluation of these applications to keep pace with the rapid the adoption of adeno-associated virus
expansion in new product development. Our eventual goal (AAV) vectors.
is to add about 50 additional clinical reviewers to the group
charged with overseeing the clinical investigation,
development, and review of these products
The Gene Therapy Market is Expected to Reach €17bn in 2028
Gene therapies in clinical development today1 Gene Therapy sales [2021-2028; €bn]2
Phase 1 Phase 2 Phase 3

CAGR
+43%
245 247 30 ~500 14

17
11
7
4
1 1 2
2021 2022 2023 2024 2025 2026 2027 2028
Majority of approved gene therapies are based on AAV vector technology

First AAV gene therapy approval in 2017; number of gene therapy approvals is expected to increase significantly until 2030,
resulting in strong anticipated sales growth
Shaping of access models, policies and payer environment are crucial to sustainable success
Source: 1 ASGCT Q1/2023 report; 2 Evaluate Pharma Feb 2023 , Fx rate based on central financial 1.01US$ = 1€
AskBio is a Pioneer in AAV-based Gene Therapy with Unparalleled
Pipeline, Talent and Manufacturing Capabilities
FIRST
Founded in 2001 by R. Jude Samulski, Sheila Mikhael and

Xiao Xiao who pioneered the AAV gene therapy field
Dedicated to developing life-saving medicines that can
potentially cure genetic diseases
to clone AAV for to deliver to treat DMD to deliver AAV
~7,000 rare diseases are known to date; ~80% of rare therapeutic AAV and Pompe to the brain
diseases are genetic in origin purposes intrathecally patients
PILLAR I PILLAR II PILLAR III TRANSLATE INTO
TECHNOLOGY MANUFACTURING CLINICAL PROMISING

DEVELOPMENT
THERAPEUTIC
Renowned toolbox Distinguished Strong translational
PIPELINE
(capsids, regulatory manufacturing capabilities expertise, combined with
elements, gene editing) (cell line/infrastructure) academic network
AskBio Built Industry Leading Manufacturing Facilities and
Technologies, which are Crucial to Bring Gene Therapies to Patients
Gene therapy manufacturing overview
Viralgen Clinical – GMP Manufacturing TAAV – no-end DNA (neDNA)1

San Sebastian, Spain San Sebastian, Spain / Hampton UK
Stable Packaged Inducible
Cell Line Promoters
Increases yields Increases productivity
Pharmaceutical grade Turns off genes during mfg
Plasmid
Pro10™ Alternative
Novel manufacturing 2
Cell Line
technologies at every stage
Serum free Shorter cycle time
Scaled up to 2,000 liters Improved yields Fewer bacterial
Higher throughput contaminants
Yields of 10^17
In-house control Lower cost
Unmatched batch purity

Viralgen Commercial – Production Capacity Reliable consistency RTP HQ – Additional production capacity
San Sebastian, Spain Durham, NC
1 neDNA is made using technology licensed from Touchlight IP Ltd; 2 Technology licensed from Touchlight IP Ltd
AskBio Industry Leading Platforms
CELL LINES &

AAV CAPSIDS PROMOTERS & REGULATION GENE EDITING TOOLS MANUFACTURING
Tissue-specific targeting Precise cell targeting Enhanced gene editing Scaled, integrated
technology manufacturing (Pro10™ cell
Engineered chimeric capsids On/off expression control line and plasmid alternative)
AskBio’s Technology and Pipeline is a Key Innovation Engine for
Bayer’s CVD, Neurology and Rare Disease Ambition
Platform Asset1 Pre-clinical Phase I

Parkinson’s Disease (AB-1005)
Gene CNS Multiple System Atrophy (AB-1005)

therapy Huntington’s Disease (AB-1001)
platform
(AAV1) CV Congestive Heart Failure (AB-1002)
Pompe Disease (ACTUS-101)

Neuro-
muscular Limb Girdle Muscular Dystrophy 2i (AB-1003)
1 Excludes partnered programs
Balanced Portfolio Addressing Monogenic and Pathway Disorders
MONOGENIC PATHWAY
DISORDERS DISORDERS
MONOGENIC DISORDERS PATHWAY DISORDERS
Mutation occurs in the DNA sequence of a single gene. Caused by mutations in several genes and can be
compounded by environmental factors such as smoking or diet
Most monogenic disorders are rare diseases such as
Pompe disease, Huntington’s disease, hemophilia Common examples include heart disease, cancer
and cystic fibrosis. and type 2 diabetes
Historically the first to be targeted by gene therapy Require more complex therapeutic approaches than
monogenic disease-targeting therapies, which are mainly gene
Smaller patient populations addition (or augmentative) gene therapies
Larger patient populations
Midbrain Infusion of AAV2-AADC
Dopamine
Pathways
Serotonin
Pathways
 Dopaminergic
neurons in the
midbrain (SNc, VTA)
project to multiple
brain regions
 Goal of gene
Substantia
delivery Nigra
= restore dopamine
synthesis in midbrain Ventral
dopaminergic
neurons Tegmental Raphe nucleus
Area Locus coeruleus
AAV2-AADC: 5 Children Subsequently Learned to Walk
Independently
SUBJECT 10 (BASELINE) - AGE 4.5 YEARS 3 YEARS POST-GT - AGE 7.5 YEARS
Building a Therapeutic Platform Enables to Extend the Field of
Application of the Technology to Multiple Diseases
VALIDATION IN SINGLE GENE DEFECT EXPANSION TO LARGER MARKET SIZES
WITH SAME TECHNOLOGY
Parkinson’s Disease Gene Therapy (AB-1005) MONOGENIC
DISORDERS
PATHWAY
DISORDERS
DISEASE & UNMET MEDICAL NEED OUR APPROACH
Parkinson’s Disease is the most common movement The AB-1005 vector expresses a neurotrophic factor
disorder caused by the progressive neurodegeneration of (GDNF) essential for the development and survival of
dopaminergic neurons dopaminergic neurons
Limited symptomatic treatment options available AB-1005 aims to slow, stop or reverse disease
progression by restoring function and providing
Dopaminergic medications, effective at early neuroprotection to susceptible dopaminergic neurons
stages, become less and less effective with disease
progression Restored dopaminergic tone potentially results in the
improvement of motor control including restored ability to
Deep brain stimulation (DBS) carries the risk of perform activities of daily living. Possible improvements
infections, stroke, seizures, is costly and typically on the non-motor symptoms of PD and the function of
requires follow-up maintenance surgeries neuronal networks are being assessed.
No approved treatments to slow or change the course of Surgical Delivery:
disease progression One-time bilateral delivery
of AB-1005 via minimally
invasive, MRI-monitored
neurosurgery
Parkinson’s Disease Gene Therapy (AB-1005) MONOGENIC
DISORDERS
PATHWAY
DISORDERS
Turning back the clock on Parkinson’s disease
ADDRESSABLE PATIENT
CLINICAL DATA
POPULATION
PHASE Ib
Neurologist rated improvements in Patient-reported recovery of motor performance Indication Patients

motor performance OFF time improved by 52% Parkinson’s Disease US ~1 million
50
–– Part III Motor OFF-med
40
ASSET POTENTIAL
UPDRS score (points)
MDS-UPDRS Score
30
–– Part III Motor ON-med Indication Asset Potential
20 Parkinson’s Disease
18-month clinical data shows marked motor
improvement compared to natural history
10 <€500m €500m–€1bn >€1bn
–– Part II Activities of Daily Living Functional effects are progressive, similar to NHP
studies: Ongoing improvements reported beyond 6
0 months, unlike brief improvement in other CGTs or
placebo effects
UPCOMING DEVELOPMENT
g
h
nin
lin
Clinically meaningful improvements consistent

t
t
on
on
on
se
ee
MILESTONES
m
with anticipated MoA – neuron regrowth and

Ba
r
12
18
Sc
progressive restoration of dopamine function

Initiation of randomized, double-blinded, sham-
surgery controlled Phase 2 RESTORE-PD study
Multiple System Atrophy (MSA) Gene Therapy MONOGENIC
DISORDERS
PATHWAY
DISORDERS
AB-1005 (AAV2-GDNF) already well tolerated in Parkinson´s Disease patients1

AAV2
MSA is a fast-progressing disease Mode of action: Surgical Delivery:
with symptoms similar to Restore and One-time bilateral
Parkinson’s maintain brain cell delivery via
function by MRI-monitored
a-synuclein aggregation in the brain neurosurgery
expression of
Glial dysfunction and loss of GDNF in the basal
neurotrophic factors (GDNF) ganglia
GDNF2
Neuroinflammation
3 Why GDNF for MSA:

Onset: Mid-life 76% loss of GDNF in MSA post-mortem tissue4
Prognosis: Death ~8-10 years after diagnosis Degeneration of the dopaminergic neurons causes parkinsonian
Epidemiology (US & EU): Prevalence ~35K, incidence ~4.5K per year features in MSA
Improve “sick-but-not-dead” neurons by GDNF restoration to
Unmet medical need: No disease-modifying therapy
Enhance dopamine production
SoC: Symptom management Increase neurite density
Clinical competition: Several clinical programs addressing α-synuclein Reduce α-synuclein accumulation
Attenuate neuroinflammation
1 Product has been applied in Phase 1 and Phase 1b studies for Parkinson’s disease already; 2 Glial cell line-derived neurotrophic factor; 3 Source: Kühnel et al 2022, 4 Source: Goldstein et al 2019
Multiple System Atrophy (MSA) Gene Therapy MONOGENIC
DISORDERS
PATHWAY
DISORDERS
MSA is an adult-onset, spontaneously occurring rare neurodegenerative disease

PHASE I
MSA is pathologically defined by glial cytoplasmic inclusions Indication Patients

(GCIs) containing ⍺-synuclein Multiple system atrophy US/EU ~ 35k
AAV2-GDNF delivery in a GM1 knock-out transgenic mouse

attenuated the accumulation of ⍺-synuclein in the substantia ASSET POTENTIAL
nigra.1
Multiple system atrophy
<€500m €500m–€1bn >€1bn
UPCOMING DEVELOPMENT MILESTONES
Recruitment & dosing of Phase 1 RESTORE-MSA study
Source: Figure modified from Hadazcek et al 2015
Limb-girdle Muscular Dystrophy 2I/R9 Gene Therapy MONOGENIC
DISORDERS
PATHWAY
DISORDERS
AB-1003: Mitigate the Molecular Pathobiology and Improve Functions
Limb-girdle muscular dystrophy 2I/R9 (LGMD2I/R9) is a Single-time systemic administration of AB-1003 contains
monogenic, rare disease. a normal FKRP gene and uses an AAV9 capsid and the
Syn-100 promoter.
Autosomal recessive muscular dystrophy is caused by
mutations in the gene for fukutin-related protein (FKRP), Self-complementary AAV technology to target and
needed for glycosylation of α-dystroglycan (α-DG). express FKRP protein, predominantly in skeletal
muscle, diaphragm and cardiomyocytes.
LGMD2I/R9 patients are prone to cardiac fibrosis, respiratory Syn-100 muscle-specific promoter enables
complications, and dysphagia that may lead to early death. relatively low doses
The management of LGMD2I/R9 is supportive. No disease- Non-clinical safety and bioactivity data from two different
modifying treatments are approved. disease mouse models demonstrated FKRP expression
in target tissues and functional improvements
Limb-girdle Muscular Dystrophy 2I/R9 Gene Therapy MONOGENIC
DISORDERS
PATHWAY
DISORDERS
Innovative Clinical Trial Design to Support Accelerated Development and Regulatory Approval

PHASE I/II
Robust Bioactivity in Preclinical Dose Range Finding Study Indication Patients

Limb-Girdle (LGMD2I/R9) ~7k worldwide
Evaluation Low dose High dose
Muscle strength >75% of wild-type >90% of wild-type
Exercise distance >75% of wild-type >90% of wild-type
ASSET POTENTIAL
Mean Serum CK levels Comparable to wild-type Comparable to wild-type

Part I of a Phase 1/2 study has started in Q1 2023:
Limb-Girdle (LGMD2i)
Double-blind, randomized, placebo-controlled design (N=10) to
establish safety, tolerability, and preliminary efficacy
<€500m €500m–€1bn >€1bn
Part I will build the foundation for the registrational Part II of the
clinical study.
• Dosing the First Subject

• Completion of Part I Enrollment
Congestive Heart Failure Gene Therapy MONOGENIC
DISORDERS
PATHWAY
DISORDERS
AB-1002 (AAV2i.8.I-1c): improves intracellular calcium cycling, decreases fibrosis and reverses remodeling
HF is a high prevalent disease, especially in the Western AB-1002 targets a subset of advanced HFrEF patients
world (NYHA III) who have non-ischemic etiology.
For HFrEF well established guidelines are in place for Abnormal calcium cycling secondary to a decrease in the
treatment of those in earlier stages of the disease. Sarcoplasmic reticulum calcium ATPase (SERCA2a) and
In patients with end stage heart failure, mortality is 50% at an increase in protein phosphatase 1 activity in heart
5 years, and limited therapeutic options are available. failure.
No disease modifying treatment available for any AB-1002 uses gene therapy to deliver a critical protein: a
stages of CHF constitutively active form of inhibitor 1 of c which when
expressed improves intracellular calcium cycling,
decreases fibrosis and reverses remodeling.
These cellular/molecular effects improve the overall
function of the failing heart and the functional status of
the patient.
Congestive Heart Failure Gene Therapy MONOGENIC
DISORDERS
PATHWAY
DISORDERS
AB-100 (AAV2i.8.I-1c): Preliminary results suggest clinically meaningful improvements
CLINICAL DATA ADDRESSABLE PATIENT POPULATION

PHASE I
Eight subjects with non-ischemic congestive heart failure (CHF) treated; Indication Patients
7 of the 8 subjects completed primary follow up (12 months)
Chronic Heart Failure US/EU5 ~ 1.6 million
No product- or delivery-related serious adverse events at either tested
dose
Study participants in both cohorts exhibit directionally favorable efficacy
results as evidenced by
ASSET POTENTIAL
1. New York Heart Association (NYHA) class reduction
2. Left Ventricular Ejection Fraction (LVEF) increase
3. Peak oxygen consumption (VO2 max) improvement
Chronic Heart Failure
4. Quality of life assessment improvement.
<€500m €500m–€1bn >€1bn

• Completion of Cohort 1 Expansion of Phase 1 with 3 additional
subjects
• Initiation of GenePPhit: A phase II, adaptive, randomized, double-
blind, placebo controlled, multicenter trial
People
The Individual AskBio Sites Contribute Their Respective

Competency Strongholds to the End-to-End Development Platform
AskBio competence distribution
Key Messages Today
Highly attractive market:

Gene therapy market expected to grow significantly
until the end of the decade
Pioneer in AAV-based gene therapy:
Unparalleled pipeline, talent and manufacturing
capabilities
Robust therapeutic pipeline:
Balanced portfolio addressing monogenic and pathway
disorders
Scalable platform for continued growth and innovation:
Building a platform enables to extend the field of
application of the technology to multiple diseases
Concluding Remarks
Christian Rommel
Key Takeaways
1 2 3 4
Seize the Clear focus on Execute Ready to move
opportunity for value & Innovation to the next phase
more impact differentiation strategy of our history
Building on our long legacy and Through rigorous assessment Our R&D strategy is already We are building a truly
learnings, world-class expertise and prioritization, we now up and running – we have a differentiated high-value
and differentiating modalities have a sharper focus on the clear strategic focus, the pipeline, delivering patient
and platforms, we have an areas of greatest unmet platforms, the strategic impact, and delivering on our
opportunity to increase the need and highest potential partners, the modalities and bold Pharma ambition.
scale of our impact for where we can make a the capabilities to deliver at Following a thorough portfolio
patients and for Bayer. difference by targeting the pace – we are positioned to pruning, the vast majority of
our (pre)clinical NME’s have
sweet spot of precision succeed.
the potential to be first- or
medicine.
best-in-class, today.
Appendix: Pharmaceuticals – Pipeline Overview1 (as of June 16, 2023)
Phase 02 Phase I Phase II Phase III
DGKalpha Inh (BAY 2862789) Elimusertib (ATR Inhibitor) (BAY 1895344) Regorafenib (combi Nivolumab) (BAY 734506) Copanlisib (PI3K Inhibitor)
Solid tumors (recurrent or metastatic) Non-Hodgkin Lymphoma (CHRONOS-4)
PSMA TAC (BAY 3546828) AhR Inhibitor (BAY 2416964)
Asundexian (FXIa Inhibitor) (BAY 2433334) Darolutamide (AR Inhibitor)
Major Adverse Cardiac Events Prevention (PACIFIC-AMI)
PSMA SMOL TAC (BAY 3563254) mEGFR/HER2 Inhibitor (BAY 2927088) Prostate Cancer (mHSPC) (ARANOTE)
Adjuvant Prostate Cancer (DASL-HiCaP)
Zabedosertib (IRAK4 Inh.) (BAY 1834845)
VVD NRF2 Inh (BAY 3605349) DGKzeta Inhibitor (BAY 2965501) Atopic Dermatitis (DAMASK)
Prostate Cancer with Biochemical Recurrence after Curative
Radiotherapy (ARASTEP)
VVD STAT3 Inh (BAY 3630914) CCR8 Ab (BAY 3375968) Gadoquatrane (High Relaxivity Contrast Agent) Finerenone (MR Antagonist)
(BAY 1747846) Heart Failure (HFmr/pEF) (FINEARTS-HF)
Anti-coagulant (BAY 3389934) Congestive Heart Failure rAAV Gene Therapy Magnetic Resonance Imaging (HRCA-PAT) Non-diabetic CKD (FIND-CKD)
(AB-1002 aka NAN-101)
Next Generation Liver MRI Runcaciguat (sGC Activator) (BAY 1101042) Vericiguat (sGC Stimulator)
(BAY 3393081) sGC Activator Oral (BAY 3283142) Non-prolif. Diabetic Retinopathy (NPDR) (NEON-NPDR) Heart Failure (HFrEF) (VICTOR3)
Asundexian (FXIa Inhibitor)
Stroke Prevention in Atrial Fibrillation (OCEANIC-AF)
sGC Activator Inhale (BAY 1211163) 2⁰ Stroke Prevention (OCEANIC-STROKE)
SEMA 3a (BAY 3401016) Elinzanetant (Neurokinin-1,3 Rec Antagonist)

Vasomotor Symptoms (OASIS)
Bemdaneprocel (Parkinson’s Disease Cell Therapy)
(BRT-DA01) Aflibercept 8mg (VEGF Inhibitor)
Retinal Vein Occlusion (QUASAR)
Parkinson‘s Disease rAAV Gene Therapy
(AB-1005 aka AAV2-GDNF-PD)
Multiple System Atrophy rAAV Gene Therapy
(AB-1005 aka AAV2-GDNF-MSA)
Submissions
Pompe Disease rAAV Gene Therapy (ACTUS-101)
Oncology Aflibercept 8mg (VEGF-Inhibitor)
Huntington‘s Disease rAAV Gene Therapy EU, JP, US4: Diabetic Macular Edema (DME)
Cardiovascular+5 (AB-1001 aka BV-101) EU, JP, US4, CN: Neovasc. Age-rel. Macular Degen. (nAMD)
Neurology & Rare Diseases LGMD2I/R9 rAAV Gene Therapy

(AB-1003 aka LION-101)
Immunology GPR84 Antagonist (BAY 3178275)
Others
New molecular entity
Life cycle management Protein Therapeutics Cell Therapy Contrast Agent Genetic Medicine Radiotherapy Small Molecule
1 Bayer and partner sponsored + 3rd party label enabling studies with first patient first visit 2 Pre-clinical selected assets on path to IND 3 Conducted by Merck & Co 4 US submission made by Regeneron 5 Including Precision Cardiovascular, Nephrology & Acute Care
Appendix: Abbreviations (1/4)
AAV Adeno-associated virus CGT Cell and gene therapy

Ab Antibody CHF Congestive heart failure
ADC Antibody-drug conjugate CI Confidence interval
AF Atrial fibrillation CKD Chronic Kidney Disease
AI Artificial intelligence CMC Chemistry, manufacturing and controls
AIS Acute ischemic stroke COPD Chronic Obstructive Pulmonary Disorder
ALCL Anaplastic large cell lymphoma CRC Colorectal cancer
AMD Age-related macular degeneration CV Cardiovascular
APT Antiplatelet therapy DA Dopamine
AR Androgen receptor DAPT Dual Antiplatelet Therapy
BCR Biochemical relapse DBS Deep brain stimulation
BD&L Business Development & Licensing DC Development Candidate
BIC Best in class DDRi DNA damage repair inhibitors
bn billion DFMs Direct Functional Modulators
BP Blood pressure DGK Diacylglycerol Kinases
CAGR Compound Annual Growth Rate DKD Diabetic Kidney Disease
CAR-T Chimeric antigen receptor modified T cells DMD Duchenne Muscular Dystrophy
cGMP Current good manufacturing practice DNA Deoxyribonucleic acid
135 /// Bayer Investor Relations /// Pharma R&D Event /// June 2023
DOACs Direct oral anticoagulants GP General practitioner

eGFR estimated glomerular filtration rate GU Genitourinary
EGFR Epidermal Growth Factor Receptor HCC Hepatocellular Carcinoma
ESRD End-stage renal disease HER2 Human epidermal growth factor receptor 2
EU5 France, Germany, Italy, Spain, United Kingdom HF Heart failure
fAD familial Altzheimer’s disease HFF Hospitalization heart failure
FDA U.S. Food and drug administration HFmrEF Heart failure with midrange ejection fraction
FIC First in class HFpEF Heart failure with preserved ejection fraction
FIH First-in-Human HFrEF Heart Failure with reduced Ejection Fraction
FKRP Fukutin-related protein HNSCC Head and neck squamous cell carcinoma
FPFV First Patient First Visit HR Hazard ratio
FTE Full Time Equivalent HSCs Hematopoietic stem cells
GA Geographic Atrophy HTS High throughput screening
GCIs Glial cytoplasmic inclusions IBD Inflammatory Bowel Disease
GDNF Glial cell line-derived neurotrophic factor ICIs Immune checkpoint inhibitors
GI Gastrointestinal IND Investigational New Drug
GM1 GM1 gangliosidoses Inh Inhibitor
GOF Gain of function IO Immuno-Oncology
IRDs Inherited retinal disorders NHP Nonhuman primate

ISTH International Society on Thrombosis and Hemostasis nmCRPC non-metastatic castration resistant prostate cancer
LCM Life Cycle Management NME New Molecular Entity
LC-MS/MS Liquid chromatography tandem mass spectrometry NNT Number needed to treat
LGMD2i/R9 Limb-Girdle Muscular Dystrophy NO Nitric Oxide
LOPD Late onset Pompe Disease NRD Neurology and Rare Diseases
LVEF Left Ventricular Ejection Fraction NRLD National Reimbursement Drug List
m million NSCLC Non small cell lung cancer
mCRPC Metastatic castration resistant prostate cancer NYHA New York Heart Association
MDS Movement Disorders ODD Orphan drug designation
mHSPC Metastatic hormone sensitive prostate cancer OSM Oncostatin M
MOAs Mode of action OTC Over-the-counter
MRA Mineralocorticoid Receptor Antagonist PD Parkinson’s Disease
MSA Multiple System Atrophy PD-L1 Programmed Cell Death Ligand 1
MSCs Mesenchymal stem cells PPD Primary Photoreceptor Diseases
NASH Non-alcoholic steatohepatitis PPI Protein-protein Interaction
ndCKD Non-diabetic chronic kidney disease PRP Photoreceptor Precursor Cell
PSA Psoriatic arthritis SPAF Stroke Prevention In Atrial Fibrillation

PSC Pluripotent Stem Cells sq/ad squamous/adenocarcinoma
PSO Psoriasis T1D Type 1 diabetes
PTS Probability of Technical Success T2D Type 2 diabetes
RA-ILD Rheumatoid arthritis associated interstitial lung disease TA Therapeutic areas
RCC Renal cell carcinoma TF Transcription Factor
R&D Research & Development TH T helper
RED Research & Early Development TKI Tyrosine kinase inhibitor
RNA Ribonucleic acid TNBC Triple Negative Breast Cancer
ROS1 C-ros oncogene 1) TRT Targeted radiotherapy
RP Retinitis Pigmentosa TRx Total prescriptions
RPE Retinal pigment epithelium UACR Urine Albumin Creatinine Ratio
RTP HQ Research Triangle Park Headquarter Ub Ubiquitin
SD Stargardt's disease VKA Vitamin K Antagonists
sGC Soluble guanylate cyclase VMS Vasomotor symptoms
SGLT2i Sodium-glucose Cotransporter-2 inhibitors VTA Ventral tegmental area
SMOL Small Molecule VVD Vividion
SOC Standard of Care WW Worldwide

Bayer Pharma RD Event 2023

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Agenda Pharmaceuticals R&D Event

Session Start/EDT Start/CEST Content Speaker

08:00 am 14:00 pm Welcome Oliver Maier

09:40 am 15:40 pm Driving Leadership in Focus Areas of Oncology Dominik Ruettinger

3 11:35 am 17:35 pm Q&A and Closing Remarks (30 min) All

Focus areas prioritized based on

Value & differentiation

1 including Precision Cardiovascular, Nephrology & Acute Care

Establishing Cell & Gene therapy platform through

Internal Gaining access to cutting-edge chemoproteomics

Collaborating with top academia, pharma partners

LEAPS as a feeder of breakthrough technologies

Research & Development Commercial

Increased R&D footprint in the US with Improved presence in oncology, in particular to

US Market Share1 Patient progression in prostate cancer

(Neo-) Nonmetastatic Metastatic

2028 2028 2019 2022 2025

Ex-US, additional approvals will Committed to make Nubeqa available to a broad

One of the strongest launch dynamics in CV despite initial

Extended Indication in China in mid-May, including CV FIGARO-DKD FINE-ONE FIND-CKD FINEARTS-HF

First, non-hormonal, once-daily, oral neurokinin-1,3

1.2 billion women Current Status

We have reshaped our approach to innovation guided by value,

HEALTH SYSTEMS UNDER PRESSURE ERA OF GROUND-BREAKING

Increasing burden of Breakthrough

Data Science-driven R&D

Paying for value

• Diversified modalities • BlueRock • New R&D operating model

UNLEASH R&D TALENT RED

Increased agility and collaboration

BAYER R&D PLATFORM COMPANIES

Makes decision on Independently lead

Cross-company interaction Building on respective Leverage Bayer’s Ensure scalable

Our Science & Portfolio Strategy Evolution

TECHNOLOGIES PATIENT POPULATION

Small Mix of innovative, Broad Precise

Bubble size represents absolute

Oncology Cardiovascular+ Neurology & Rare Diseases Immunology

Small Molecules (SMOL)

Pluripotent Stem Cells

Adeno-Associated Virus (AAV)

Genetic Medicine CRISPR-based gene editing

Non-viral gene delivery

Dedicated Data Science & AI Accelerating drug discovery with

INCREASE IN PTS REDUCTION OF COSTS DECREASE IN CYCLE TIMES

Asundexian (SPAF, Stroke) FDA fast track, FIC

sGC Activator Oral FIC

mEGFR/HER2i (Lung Cancer) FIC/BIC

Oncology DGKalpha Inh. (Cancer) FIC

NRF2 Inh (Cancer) FIC

PSMA-SMOL-TAC (Prostate Cancer) FIC/BIC

Bemdaneprocel (Parkinson’s) FDA fast track, FIC

AB-1003 (LGMD2I/R9) BIC

Other Elinzanetant (Vasomotor Symptoms) BIC

1 Selected assets out of 40+ development projects

OUR FOCUS OUR PRIORITIES

4 core Therapeutic Areas Science & Portfolio Productivity

We have reshaped our approach to innovation guided by value,

MARKET ATTRACTIVENESS BAYER’S KEY STRENGTHS