Disclaimer This presentation (including any oral commentary that accompanies this presentation) contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statemen

Closing In On Cancer January 9, 2020

Disclaimer This presentation (including

any oral commentary that accompanies this presentation) contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements contained in this presentation that do not relate to matters of

historical fact should be considered forward-looking statements, including without limitation statements regarding the impact our Biclonics platform can have on cancer, our product candidates' potential to treat certain types of tumors, the

timing of regulatory filings and the timing and anticipated data read outs or results from our clinical trials and our collaborations. These forward-looking statements are based on management's current expectations. These statements are neither

promises nor guarantees, but involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements

expressed or implied by the forward-looking statements, including, but not limited to, the following: we have incurred significant losses, are not currently profitable and may never become profitable; our need for additional funding, which may not

be available and which may require us to restrict out operations or require us to relinquish rights to our technologies or bispecific antibody candidates; potential delays in regulatory approval, which would impact our ability to commercialize our

product candidates and affect our ability to generate revenue; the unproven approach to therapeutic intervention of our Biclonics technology; our limited operating history; economic, political, regulatory and other risks involved with

international operations; the lengthy and expensive process of clinical drug development, which has an uncertain outcome; the unpredictable nature of our early stage development efforts for marketable drugs; potential adverse public reaction to the

use of cancer immunotherapies; potential delays in enrollment of patients, which could affect the receipt of necessary regulatory approvals; failure to obtain marketing approval internationally; failure to compete successfully against other drug

companies; potential competition from other drug companies if we fail to obtain orphan drug designation or maintain orphan drug exclusivity for our products; our reliance on third parties to conduct our clinical trials and the potential for those

third parties to not perform satisfactorily; our reliance on third parties to manufacture our product candidates, which may delay, prevent or impair our development and commercialization efforts; protection of our proprietary technology; our patents

being found invalid or unenforceable; potential lawsuits for infringement of third-party intellectual property; our ability to attract and retain key personnel; managing our growth could result in difficulties; and we may lose our foreign private

issuer status and incur significant expenses as a result. These and other important factors discussed under the caption "Risk Factors" in our Annual Report on Form 20-F filed with the Securities and Exchange Commission, or SEC, on April

3, 2019, and our other reports filed with the SEC, could cause actual results to differ materially from those indicated by the forward-looking statements made in this presentation. Any such forward-looking statements represent management's estimates

as of the date of this presentation. While we may elect to update such forward-looking statements at some point in the future, we disclaim any obligation to do so, even if subsequent events cause our views to change.

Designed by nature. Selected by Merus.

Merus: pioneering bispecific antibodies since 2006 4 clinical-stage bispecific antibodies in oncology Fully integrated discovery-to-manufacturing bi-/tri-specific technology platforms Sophisticated proprietary bispecific and trispecific technology

platforms Multiple clinical milestones anticipated in the next 12 months Discovery of novel modes of action based on target combinations and functional screening

Merus clinical pipeline, near term

milestones and program status PROGRAM TARGETS INDICATION / DRUG COMBINATION PRE-IND PHASE 1 PHASE 2 MILESTONE/STATUS MCLA-128 HER3 x HER2 NRG1 Solid tumors (monotherapy) Update expected around end of 2020 Metastatic Breast (combination in 2 cohorts)

Phase 2 Results in 2020 MCLA-117 CLEC12A x CD3 Acute Myeloid Leukemia (AML) Initial Data 1H 2020 MCLA-158 Lgr5 x EGFR Solid tumors Phase 1 Trial Ongoing MCLA-145 CD137 x PD-L1 Solid tumors Phase 1 Trial Ongoing MCLA-129 EGFR x c-MET Solid tumors IND

Enabling Studies Ongoing ONO-4685 PD-1 x CD3 Autoimmune disease Phase 1 Trial Ongoing . Undisclosed Autoimmune disease (ex- U.S.) (China)

Biclonics - designed to

look and perform like natural human antibodies BICLONICS - leveraging the attractive characteristics of natural antibodies Merus' Bispecific Antibodies are produced by a single cell Common Light Chain for unforced', natural

pairing with 2 different heavy chains Electrostatic attraction to efficiently drive formation of Biclonics Fc Modifications for Improved functionality (ADCC or silencing) IgG Format for efficient manufacturing and predictable in vivo behavior

We use large-scale functional screening

in cell-based assays to identify Biclonics with novel modes of action FUNCTIONAL SCREENING Biclonics - Selected in functional assays for differentiated activity HUMAN ANTIBODY GENERATION MeMo Transgenic Mouse We can create up

to 1,000 Biclonics against any target pair of choice PANEL GENERATION We use a proprietary transgenic mouse to generate panels of high-quality human antibodies

HER2 x HER3 Biclonics Clinical

Tumor Blocks primary tumor cell growth

and escape to HER2/EGFR targeted therapy Block HER3 Blocks HER3 signaling even in high neuregulin tumor environments Enhanced ADCC Mediates tumor elimination by immune killer cells Dock HER2 Docks to HER2 expressed on tumor cells to efficiently

block HER2:HER3 dimer formation Combinations with HER2 targeted therapies possible Combination Unique DOCK & BLOCK mechanism of action potently inhibits neuregulin (NRG)-driven tumor growth KILL TUMOR CELLS MCLA-128

Preclinical efficacy demonstrated,

well-tolerated in patients Please Refer to https://merus.nl/publications/ for full data presented. Refer to ASCO poster 2018 and AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics 2019 SAFETY AND TOLERABILITY IN

PHASE 1/2 TRIAL MCLA-128 Dosing: 750 mg ranging from q1w-q3w 117 PATIENTS EVALUATED* Single agent well tolerated Low risk for immunogenicity SUPERIOR ACTIVITY SHOWN IN PRECLINICAL MODELS * As of Jan. 2019 DOCK ONTO HER2 & BLOCK NRG1 -DRIVEN

HER/HER3 DIMER FORMATION PI3K/AKT Cell proliferation/survival DOCKS BLOCKS NRG1 Fusions MCLA-128

Novel therapeutic paradigm for NRG1

Fusion cancers NRG1 FUSIONS ARE FOUND ACROSS MULTIPLE SOLID TUMOR TYPES Lung Breast Kidney Gallbladder Pancreas Prostate Ovarian Sarcoma Bladder Colorectal Nasopharyngeal MCLA-128

BLOCKS TUMOR GROWTH IN NRG1 FUSION PDX MODEL Projections of NRG1 Fusions occurrence (incidence) are based on limited published information Tumor type Incidence (%) Lung 0.3 - 3.0 Pancreas 0.5 - 1.5 Other < 1.0 PI3K/AKT Cell

proliferation/survival NRG1 FUSIONS STIMULATE TUMOR CELL GROWTH NRG1 Fusions Estimated MCLA-128

Active in NRG1 fusionPOS cancers

PDAC (ATP1B1-NRG1): 52-year-old male* Clinical Proof of Concept Established Clinical Trial Ongoing * Data was presented on October 27, 2019, at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics by investigators

from the Memorial Sloan Kettering Cancer Center in a presentation titled "Clinical proof-of-concept for MCLA-128, a bispecific HER2/3 antibody therapy, in NRG1 fusion-positive cancers" MCLA-128

Phase 1/2 in NRG1 solid tumors,

Phase 2 in metastatic breast cancer (combo) DESIGN ENDPOINTS STATUS NRG1 Solid Tumors (Monotherapy) Phase 1/2 Study Cohort 1: NRG1+ Pancreatic cancer Cohort 2: NRG1+ NSCLC Cohort 3: NRG1+ Other solid tumors Dose: 750mg every 2 weeks Safety

Anti-tumor activity Enrollment ongoing Metastatic Breast Cancer (MBC) Phase 2 Study in combination with 2 cohorts in MBC Cohort 1: HER2+ (MCLA-128 + Herceptin + Chemo) Cohort 2: ER+/HER2low (MCLA-128 + Hormone Therapy) Dose: 750mg every 3 weeks

Clinical benefit at 24 weeks To be presented at a medical conference in 2020 WHOLLY-OWNED TARGETS INDICATION / DRUG COMBINATION PRE-IND PHASE 1 PHASE 2 MCLA-128 HER3 x HER2 NRG1 Solid tumors (monotherapy) Metastatic Breast (2 cohorts) MCLA-128 MRUS

CD3 x CLEC12A Biclonics

Clinical Programs MCLA-117

CLEC12A Expressed by tumor (stem)

cells in ~ 90-95% of AML patients Expression restricted to hematopoietic system = potential less off-tumor toxicity CD3 Low affinity CD3 arm and silenced Fc for controlled T cell activation to reduce toxicity and improve biodistribution MCLA-117

efficiently activates and redirects T cells to kill CLEC12A-expressing acute myeloid leukemia (stem) cells T Cell T cell engager for acute AML addressing a potential first-in-class target Tumor Cell ENGAGE T CELLS AND KILL TUMOR CELLS

MCLA-117 efficiently activates and

redirects T cells to kill CLEC12A-expressing AML(stem) cells Designed to spare the formation of platelets and red blood cells during therapy Active across AML patient subpopulations Potent activation of T cells in preclinical studies Day 0 +

MCLA-117 84% blasts 5% T cells 5% blasts 84% T cells Day 10 MCLA-117 MEDIATED ACTIVATION OF T CELLS AND KILLING OF TUMOR CELLS >60-fold T Cell Expansion >90% AML Tumor Cell Killing MCLA-117

Phase 1 Trial DESIGN ENDPOINTS

STATUS Single-arm, open-label, dose escalation w/ safety dose expansion Up to 50 patients with relapsed / refractory AML Starting dose determined using MABEL dose escalation requirements Protocol amended July 2019 to allow for the exploration of

higher doses Primary Endpoints: safety, tolerability Secondary Endpoints: PK/PD, anti-tumor response, clinical benefit Ongoing in Europe and the U.S. Preliminary anti-tumor activity has been observed Initial data expected at medical conference 1H

2020 TARGETS INDICATION / DRUG COMBINATION PRE-IND PHASE 1 PHASE 2 MCLA-117 CLEC12A x CD3 Acute Myeloid Leukemia (AML) MCLA-117 MRUS Fully Owned

Lgr5 x EGFR Biclonics Clinical

Potently blocks EGFR signaling in

Wnt dysregulated solid tumors Potential to be first colorectal cancer treatment to block growth of tumors with RAS mutations (~50% of patients), a high unmet need Lgr5 Expressed by intestinal cancer initiating cells Identified through Merus

functional screening and organoid discovery methods Preclinical data shows higher potency than Cetuximab EGFR Blocks growth in Wnt dysregulated tumors including RASmut Tumor KILL TUMOR CELLS ADCC-enhanced MCLA-158

Superior growth inhibition and

selectivity of tumor versus healthy tissue KILLING OF ORGANOIDS FROM TUMOR TISSUE > 100-fold Dose (log g/ml) -3 0 50 100 Cetuximab Tumor Colon MCLA-158 Cetuximab Normal Colon MCLA-158 -3 -1 0 1 2 Organoid Size Superior SELECTIVITY for

tumor- derived orgnoids % Survival Days Elapsed P=0.0001 0 10 20 30 0 50 100 INHIBITION OF ORGANOID GROWTH Superior ACTIVITY compared to Cetuximab MCLA-158 No antibody Cetuximab MCLA-158 MCLA-158 is active in xenograft models that are resistant to

treatment with Cetuximab Unlike Cetuximab, MCLA-158 discriminates between organoids derived from tumor and healthy tissue

Phase 1 Trial DESIGN ENDPOINTS

STATUS Global open-label, multicenter dose escalation w/ safety dose expansion phase Patients with solid tumors Initial focus on metastatic colorectal cancer Primary endpoint: safety and tolerability of defined dose Secondary endpoint: single-agent

preliminary anti-tumor activity Dose escalation is ongoing. Amended protocol to allow for the exploration of higher dose cohorts. Acceptable safety profile with no observed dose limiting toxicities to date. TARGETS INDICATION / DRUG COMBINATION

PRE-IND PHASE 1 PHASE 2 MCLA-158 Lgr5 x EGFR Solid tumors MCLA-158 MRUS Fully Owned

CD137 x PD-L1 Biclonics

Clinical Programs MCLA-145

Recruit, activate and prevent

exhaustion of tumor-infiltrating T cells CD137 Potent activation of tumor infiltrating T cells dependent on PD-L1 expressing tumor cells and macrophages PD-L1 Targeting to PD-L1 positive cells in the tumor Blocking of T cell inhibitory PD-1/ PD-L1

interactions in tumor Attracting T cells into the tumor Triple action for potent and durable T cell activation in the tumor micro-environment TUMOR-INFILTRATING T CELL REVIVAL T Cell Tumor MCLA-145

Binds to PD-L1 and CD137 Preclinical

work demonstrates recruitment of T cells into the tumor blocking of inhibitory PD-1/PD-L1 axis potent T cell activation Potential to overcome the known side effects of CD137 agonists in development Demonstrated Potent T Cell Activation MCLA-145

preclinical data presented at AACR 2019 PRIMARY T CELL TRANSACTIVATION ASSAY ^ Urelumab Analog ^ ^ * * Atezolizumab Analog + MCLA-145

Phase 1 trial initiated in May 2019

DESIGN ENDPOINTS STATUS Global open-label, multicenter dose escalation with dose expansion phase Patients with advanced solid tumors Primary endpoint: dose finding, safety and tolerability Secondary endpoint: single-agent preliminary activity IND

cleared January 2019 First patient dosed May 9, 2019 TARGETS INDICATION / DRUG COMBINATION PRE-IND PHASE 1 PHASE 2 MCLA-145 CD137 x PD-L1 Solid tumors MCLA-145 Merus US Rights Incyte ex-US Rights

The new Triclonics platform

for additional differentiated modes of action Designed by nature. Improved by Merus. Common light chain for unforced pairing with 3 (different) VH regions The BICLONICS Beginning Our existing foundation 1:1:1 or 2:1 format for new

biology/modes of action Next Generation TRICLONICS Platform for 2 or 3 different targets Linker diversity for added functionality

Closing In On Cancer