Indicate by check mark whether the registrant files or will file annual reports under cover of Form 20-F or Form 40-F.
Form 20-F [ X ]      Form 40-F [   ]

Indicate by check mark if the registrant is submitting the Form 6-K in paper as permitted by Regulation S-T Rule 101(b)(1):       

Indicate by check mark if the registrant is submitting the Form 6-K in paper as permitted by Regulation S-T Rule 101(b)(7):       

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EXHIBIT INDEX

Exhibit No.		Description
99.1		Oncology Day presentation - Molecular Partners

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SIGNATURES

Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned, thereunto duly authorized.

		Molecular Partners AG
		(Registrant)
Date: December 15, 2021		/s/ PATRICK AMSTUTZ
		Patrick Amstutz
		Chief Executive Officer

Exhibit 99.1

 

 

Custom Built Biology for Patients 1 Oncology Day 2021 Molecular P artners A G, S witzerland (SIX: MOLN)

This presentation is not an offer to sell or a solicitation of offers to purchase or subscribe for shares of Molecular Partners AG, nor shall it or any part of it nor the fact of its distribution form the basis of, or be relied on in connection with, any contract or investment decision. This presentation is not an offering circular within the meaning of Article 652a of the Swiss Code of Obligations, nor is it a listing prospectus as defined in the listing rules of the SIX Swiss Exchange AG or a prospectus under any other applicable laws. Copies of this presentation may not be sent to countries, or distributed in or sent from countries, in which this is barred or prohibited by law. This document is not a prospectus or a prospectus equivalent document and investors should not subscribe for or purchase any securities referred to in this document. This document does not constitute a recommendation regarding the shares. This presentation contains specific forward - looking statements, beliefs or opinions, including statements with respect to the product pipelines, potential benefits of product candidates and objectives, estimated market sizes and opportunities as well as the milestone potential under existing collaboration agreements, which are based on current beliefs, expectations and projections about future events, e.g. statements including terms like “potential”, “believe”, “assume”, “expect”, “forecast”, “project”, “may”, “could”, “might”, “will” or similar expressions. Such forward - looking statements are subject to known and unknown risks, uncertainties and other factors which may result in a substantial divergence between the actual results, financial situation, development or performance of Molecular Partners AG and investments and those explicitly or implicitly presumed in these statements. There are a number of factors that could cause actual results and developments to differ materially from those expressed or implied by these statements and forecasts. Past performance of Molecular Partners AG cannot be relied on as a guide to future performance. Forward - looking statements speak only as of the date of this presentation and Molecular Partners AG, its directors, officers, employees, agents, counsel and advisers expressly disclaim any obligations or undertaking to release any update of, or revisions to, any forward looking statements in this presentation. No statement in this document or any related materials or given at this presentation is intended as a profit forecast or a profit estimate and no statement in this document or any related materials or given at this presentation should be interpreted to mean that earnings per share for the current or future financial periods would necessarily match or exceed historical published earnings per share. As a result, you are cautioned not to place any undue reliance on such forward - looking statements. Unless stated otherwise the information provided in this presentation are based on company information. This presentation is intended to provide a general overview of Molecular Partners AG’s business and does not purport to deal with all aspects and details regarding Molecular Partners AG. Accordingly, neither Molecular Partners AG nor any of its directors, officers, employees, agents, counsel or advisers nor any other person makes any representation or warranty, express or implied, as to, and accordingly no reliance should be placed on, the accuracy or completeness of the information contained in the presentation or of the views given or implied. Neither Molecular Partners AG nor any of its directors, officers, employees, agents, counsel or advisers nor any other person shall have any liability whatsoever for any errors or omissions or any loss howsoever arising, directly or indirectly, from any use of this information or its contents or otherwise arising in connection therewith. The material contained in this presentation reflects current legislation and the business and financial affairs of Molecular Partners AG which are subject to change and audit. 2 Disclaimer

R&D Day Speakers (and Intro to Agenda) Patrick Amstutz, PhD Chief Executive Officer, Molecular Partners Michael Stumpp, PhD Chief Operating Officer, Molecular Partners Daniel Steiner, PhD SVP Research, Molecular Partners Anne Goubier, DVM, PhD VP Biology, Molecular Partners Prof. Adrian Ochsenbein, MD The University of Bern Prof. Carsten Riether, PhD The University of Bern Nicolas Leupin, MD, PhD Chief Medical Officer, Molecular Partners Guest Speakers 3

Pioneering DARPin Therapies to Transform Lives 4 Overview: Pa t ri c k Amstu t z

2021 in Review: Corporate & Portfolio Growth • Ensovibep (Covid) from Phase 1 to POC data imminent • Activity on all variants of concern, to date • MP0317 (FAP x CD40) into Phase 1 • Initial data anticipated in H2 2022 • Nomination of MP0533 for the treatment of AML • ASH poster; Bern collaboration; Phase 1 initiation in 2022 • Ongoing assessment of additional antiviral DARPins • Updates following ensovibep data in H1 2022 • Completion of NASDAQ Listing • Ensuring ability to fund pipeline and discovery Molecular Partners: Our purpose is to transform the lives of people with serious diseases 5

DARPins: A Unique Class of Biologics 15 kDa 15 0 k Da Binding regions / specificities MONOCLONAL ANTIBODIES • High affinity and specificity • Large size: 150 kDa • Complex architecture; 4 proteins with 12 domains • Long half - life • Good safety & low immunogenic potential • High affinity and specificity • Small size: 15 kDa (1/10 of a monoclonal antibody) • Simple architecture 1 protein with 1 domain • Tunable half - life • Good safety & low immunogenic potential MONO - DARPin Binding region / specificity DARPin module Multi - specific DARPin Candidate 6

7 Pipeline Oncolo g y Discovery Oncology Op ht halmolo g y Infectious disease Pipeline CANDIDATE / FOCUS RESEARCH PRECLINICAL PHASE 1 PHASE 2 PHASE 3 RIGHTS Ensovibep – Covid Next Gen Covid Covid ambulatory – Empathy Future VoC* AMG506 / MP0310 FAP x 4 - 1BB Solid tumors MP0317 FAP x CD40 Solid tumors MP0533 CD3 x CD33+CD70+CD123 AML Abicipar VEGF wet AMD – Cedar & Sequoia Radio Ligand Therapy Solid tumors Platform Discovery Radical simplicity & Conditional Activation Additional Infectious Diseases * VoC = Variant of Concern

MP Strategy – Building on our Strengths Our candidates’ design aims to directly change the course of disease biology and allow testing in a model with high translatable value We aim to drive true patient value with early clinical read - outs We leverage the advantages of the DARPin technology to provide unique solutions to impact biology and bring value to patients We strive to collaborate with the best scientists and clinicians in the field from ideation to clinical trials TECHNOLOGY TARGET PATIENTS BIOLOGY T e c h n o l o g y Bio l o g y Target Patient 8

Local Agonists in Oncology: MP0310 (FAPx4 - 1BB) & MP0317 (FAPxCD40) • Tumor local activation of immune cells • Wider therapeutic window for combinations • Multi - specific DARPin leading to clustering upon co - engagement • MP0310: Amgen, MP0317: not partnered TECHNOLOGY TARGET PATIENTS BIOLOGY Early clinical rea d - out FAP on the tumor associated fibroblast 9 4 - 1BB or CD40 on the immune cell

Targeting Leukemic Stem Cell in AML: MP0533 (CD33+CD70+CD123 x CD3) • Avidity driven targeting of leukemic stem cells • Long - term control of AML • Tri - specific T - Cell engager with optimized binding affinities and geometry • University of Bern – Profs. Ochsenbein and Riether TECHNOLOGY TARGET PATIENTS BIOLOGY Early clinical rea d - out CD33, CD70, CD123 on the AML blast or LSC 10 CD3 on the T - cell

DARPin Radio - Ligand Therapy , DARPin - Drug - Conjugates • Deep tumor penetration, low systemic exposure with high - tox payload • Deep response in hard - to - treat tumors • Small sized DARPin with high affinity coupled to a highly toxic payload (radio ligand) Novartis, a leader in the field of RLT: US$ 20 mio up - front, US$ 560 mio MS, to dd royalties TECHNOLOGY TARGET PATIENTS BIOLOGY Early clinical rea d - out Drug Payload Small & high affinity DARPin Radio Ligand Payload 11

Pipeline CANDIDATE / FOCUS RESEARCH PHASE 2 PHASE 3 R IG HT S Ensovibep – Covid Next Gen Covid 12 Pipeline Oncolo g y Discovery Oncology Op ht halmolo g y Infectious disease PRECLINICAL PHASE 1 Covid ambulatory – Empathy Future VoC* AMG506 / MP0310 FAP x 4 - 1BB Solid tumors MP0317 FAP x CD40 Solid tumors MP0533 CD3 x CD33+CD70+CD123 AML Abicipar VEGF wet AMD – Cedar & Sequoia Radio Ligand Therapy Solid tumors Platform Discovery Radical simplicity & Conditional Activation Additional Infectious Diseases * VoC = Variant of Concern

Abicipar – what's next? 13

Abicipar: Phase 3 Asset, Reviewing Data from AbbVie DARPin Advantage Target Patient Disease Biology Milestones • Growth/leakage of abnormal blood vessels beneath the retina • VEGF - A has been found to be a key molecule in numerous retinal diseases • VEGF - A inhibition has been established as a highly effective treatment for these diseases 14 • Higher affinity and inhibition of VEGF - A • Long half - life in the eye (PEGylated) • Small – higher molarity per mg • AbbVie returned all rights to Molecular Partners in Aug. 2021 • Full data currently under review • Meeting request with the FDA to discuss proposed path forward • Neovascular age related macular degeneration (nAMD) and diabetic macular edema (DME) • nAMD - More than 200,000 cases/year in the US • DME - Approximately 75,000 cases/year in the US

CEDAR & SEQUOIA Phase 3 using OCT as biomarker • Abicipar as effective as Lucentis • 10 injections instead of 25 (2 y) • Fixed Q12w regimen proven • Potential to simplify visits • OCT - ocular coherence tomography, a method to measure the thickness of the retina 15

Reducing Intraocular Inflammation (IOI) • CEDAR/SEQUOIA (Phase 3) • Much less IOI in 2 nd year (as Lucentis) • MAPLE (Phase 2, improved purity) • lower severity of IOI reported 16

Type of Syringe Identified as Likely IOI Contributor in vivo Ophthalmic - use 17

Abicipar Conclusions and Next Steps 18 • Increase benefit/risk ratio to address CRL • Plan to discuss with FDA in Q1/2022 • Establish precise need for additional clinical data/study • Further our understanding of potential timelines for re - submission • If proposals are feasible, discuss partnerships and appropriate vehicle to enact clinical plan • Acknowledging competitive landscape • Faricimab approval expected in Q1/22 • … and some set - backs in the field • Gene therapies • Brolucizumab • Establishing future development plan • With experts in the field • Demonstrate value - add of abicipar • IP protection well into 2030's

Our Platform and future products 19 Daniel Steiner

MP Strategy – building on our Strengths We strive to collaborate with the best scientists and clinicians in the field from ideation to clinical trials Our candidates’ design aims to directly change the course of disease biology and allow testing in a model with high translatable value We aim to drive true patient value with early clinical read - outs We leverage the advantages of the DARPin technology to provide unique solutions to impact biology and bring value to patients TECHNOLOGY TARGET PATIENTS BIOLOGY T ec hnology 20 Biology Target P a tient

DARPins: The Core of our Drug Engine Small size (15 kDa) DARPin KEY PROPERTIES Target p r o tein DAR Pin DARPin ADVANTAGE » Deep tissue penetration » High molar concentration » Turn - key multispecifics » Easy coupling of payloads » Ultra - high binding affinity and selectivity Rigid protein scaffold Simple & robust architecture DARPins are binding proteins derived from natural ankyrin repeat proteins 21

Our Platform in Action: Creating Ensovibep Isolation of 380 neutralizing anti - COVID mono - DARPin Generation of >100 tri - specific DARPin Candidates Functional screening and identification of Ensovibep WEEKS – 0 1 2 3 6 22

Creating MP0533: Unique Avidity - Driven Tumor Selectivity • The problem: Address AML tumor heterogeneity and reduce impact on healthy cells • The solution: DARPin platform allows to rapidly screen & iterate 100s of tri - specific T cell engagers to find the potency – selectivity – heterogeneity sweet spot MP05 3 3 Optim a l epitope Optimal affinity Optimal ori e n ta tion Optimal s pa c ing α - CD33 α - CD123 α - CD70 α - CD3 Pro j ect - spec if i c TAA binder Effector Function 23

Multi - DARPins are Offering a Broad Spectrum of Unique Solutions Multispecificity enabled possibilities Conditional activation Ensovibep High affinity for deep SARS - Cov - 2 inhibition and prevention of escape MP0310 & MP0317 Tumor localized clustering to activate effector cells in tumor only Immune ce l l Tumor associated cell MP0533 Avidity driven TCE for tumor - specificity and control of tumor heterogeneity T cell Tumor cell 24

Conditional Activation to Unlock full Potential of Potent Effectors Target binding activated Switch DARPin T - cell engager Tumor protease - activated ProDrug T - cell engager • Local activation via target “X” binding • No need for protease cleavage AACR 2021 • Local activation via protease cleavage • Key challenge: protease heterogeneity α - CD3 Blocker α - CD3 α - T A A T umor ce ll s I n active Blocker α - TAA Active 25

Expanding Multi - DARPins by Programming of Highly Potent Effectors Multispecificity enabled possibilities Conditional activation Delivery Vectors “radical simplicity” Ensovibep High affinity for deep SARS - Cov - 2 inhibition and prevention of escape MP0310 & MP0317 Tumor localized clustering to activate effector cells in tumor only Immune ce l l Tumor associated cell MP0533 Avidity driven TCE for tumor - specificity and control of tumor heterogeneity T cell Tumor cell SWITCH Programming highly potent effectors to omit off - tumor activity Tumor cell 26

Challenges of Standard Delivery Vectors of Potent Payloads mAB Peptide Size 150 kDa 1 - 2 kDa Affinity high (bivalent) low Specificity high limited High tumor load » concentration at site of action + + Deep tumor penetration » access site of action - + Long tumor retention » maintenance at site of action + - Limited normal tissue exposure » improved safety profile - + 27

Mono - DARPins as Ideal Delivery Vectors for Potent Payloads Efficient tumor targeting with limited systemic exposure t um or D r ug infusion I n f u sion s t opped Small size (15 kDa) fast extravasation & deep tumor penetration Small size (15 kDa) rapid systemic clearance High affinity (< 50 pM) long tumor retention Homogeneous access to tumor cells for killing Limited normal tissue exposure for improved safety Maintenance on tumor for complete local killing 28

Multispecificity enabled possibilities Conditional activation Delivery Vectors “radical simplicity” RLT & DDC Small size – ultra high affinity for efficient delivery with limited systemic exposure Applying our DARPin Advantages to Address Disease Biology Ensovibep High affinity for deep SARS - Cov - 2 inhibition and prevention of escape New / Collaborations New New infectious disease MP0310 & MP0317 Tumor localized clustering to activate effector cells in tumor only Immune ce l l Tumor associated cell MP0533 Avidity driven TCE for tumor - specificity and control of tumor heterogeneity T cell Tumor cell SWITCH Programming highly potent effectors to omit off - tumor activity Tumor cell 29

Clinical Progress 30 MP0310 & MP0317 Nicolas Leupin

MP Strategy – Building on our Strengths Our candidates’ design aims to directly change the course of disease biology and allow testing in a model with high translatable value We aim to drive true patient value with early clinical read - outs We leverage the advantages of the DARPin technology to provide unique solutions to impact biology and bring value to patients We strive to collaborate with the best scientists and clinicians in the field from ideation to clinical trials TECHNOLOGY TARGET PATIENTS BIOLOGY T e c h n o l o g y 31 Bio l o g y Target Patient

• >900 patients dosed across all clinical programs, a new "record" for MP • Ensovibep, MP0310, and MP0317 all progressing well • Thousands of clinical samples analyzed, despite logistical challenges • Both in house and at external providers • ~15 clinical batches produced at various scales (up to >10'000 L) • Yielding hundreds of thousands of doses for clinical studies • Countless hours spent in video calls • Learnt how to say "you are on mute" politely 32 What We Achieved in 2021 – a Very Challenging & Successful Year @MP

Activated APC Toxicity of 4 - 1BB & CD40 Antibodies Has So Far Limited Their Activity CRS Liver To x icity Activated APC Re st i ng APC Tumor S t roma DARPin advantage: Increasing therapeutic window via a tumor - localized approach Systemic activation of immune cells leads to toxicity that limit treatment option Tumor Cells Tu mor Cells Tumor S t roma Activated APC 33

AMG 506 / MP0310: Localized Activation of 4 - 1BB • Patients with solid tumors, low T - cell tumor penetration and positive FAP expression • Patient populations where there are T - cell engagers in development, that can be boosted • Many solid tumors are surrounded by dense stromal tissue in which FAP expression is high • 4 - 1BB activation is a strong recruiter of T cells • Systemic administration of MP0310, with localized activation at site of disease • MP0310 is observed in tumor tissue, with no liver toxicity or systemic activation of immune cells • Tumor biopsies show tumor - localized immune response consistent with the MoA • Analyze data from ongoing phase 1 study, exploring weekly dosing. • Determine appropriate next steps DARPin Advantage Target Patient Disease Biology Expected Mi l e s to n es H SA D A R Pin FAP DARPin 4 - 1BB DARPin H SA D A R Pin 4 - 1BB DARPin 34

FAP – an Ideal Target for Tumor - localized Activity • FAP is expressed on activated cancer associated fibroblasts (CAFs) • Overexpression in the stroma of many solid tumors • Limited expression in normal adult tissues MP0310 (FAP - 4 - 1BB) Phase 1 human biopsy samples FAP is a clinically validated target for tumor - localization A ct i v ated APC 35

Baseline Post (C1D15) Time point Signature score (log2) 2 3 4 5 6 CD 8 T Cells Cytotoxicity IFN Gamma NK Cells T Ce lls TH1 Cells PD Activity in Paired Biopsies Supports AMG 506 / MP0310 MoA on 4 - 1BB Activation BLOOD TUM O R • In the blood, immune cells remain inactive (CD8 + & CD4 + T - cells, Treg, NKT, B - cells, NK) • In the tumor, T - cells and NK cells are activated 0 2 0 4 0 6 0 8 0 100 CD8 + T - cells: CD25 + % of CD8 + T - cells C 1D1 C 1D8 C 2D1 C 2D8 Treatment on C1D1 & C2D1 Note: C1D1 & C2D1 predose sample 36

Objectives of MP0310 - CP101 Study Primary Objectives • To define the safety and tolerability of MP0310 as monotherapy (with or without rituximab pre - treatment) in patients with advanced solid tumors • To determine the maximum tolerated dose ( MTD ) AND recommended expansion dose ( RED ) for MP0310 as monotherapy, based on biomarkers from biopsies • Cohorts (1 - 7): 0.015 - 12 mg/kg, completed to plan 37 Data to date: Best clinical response: • Part A: 1/21 pts PR (Pt 03 - 010); 10/21 pts SD; 10/21 pts PD; • Part B & C: Ongoing • 6 patients enrolled, analysis pending Drug safety: no DLT or SAEs; IRRs (mostly G2) in 28% of infusions => incomplete infusions in 10% of cases; clinically manageable » Peripheral cytokines: increased levels of CXCL9 and CXCL10 at DL3 - 6 (0.15 - 5 mg/kg) suggest enhanced IFNᵧ signaling » Peripheral immune cells: no activation observed

MP 0 3 1 7 38

MP0317: Localized Activation of CD40 • Solid tumor patients with positive FAP expression • Many patients still fail to benefit from current immunotherapy options, or relapse • CD40 is a potent activator of dendritic cells, macrophages, and B cells, and has long been considered an attractive immunotherapy target • Prior attempts at targeting CD40 have shown anti - tumor activity but remain hampered by toxicity issues • MP0317 is designed to activate CD40 in a context dependent manner, by anchoring to FAP and activating via clustering • Preclinical data show local activation of immune cells while limiting off target toxicity • FIH studies initiated in Q4 2021 • Initial data in H2 2022 • Rapidly explore expansion arms in phase 1b H SA D A R Pin FAP DARPin CD4 0 CD4 0 DARPin Advantage Target Patient Disease Biology Expected Mi l e s to n es 39

Competitive Environment is Favorable for MP0317 Phase II Localized effect w/in Immune system Non - localized approaches, mAB In v i tro In vivo Translational Preclinical Phase I APX005 / sotigalimab (IgG1) 13x ph1 & ph2 RP2D: 0.3 mg/kg (latest CRC neoadj, MEL 2 admin schedules, MEL +PD1+CTLA4) YH003 (IgG1 ??) ph1/2, NEW: ph2 MEL, PDAC 1L/2L & ph1 solid Ca -- +PD1, +CT, (+CTLA4) SEA - CD40 (IgG1), iv/sc NEW: ph2 MEL,NSCLC 1L/2L post PD1 // ph1 solid Ca & PDAC -- +PD1, +CT Mitazalimab/ADC - 1013 (IgG1) 2 ph1, NEW: ph2 PDAC , up - to 0.9mg/kg - +CT, pot. +PD1 Abbv - 927 (IgG1), IT/iv 3 ph1, NEW: PDAC -- +PD1, +OX40, +CT CDX - 1140 (IgG2) 1 ph1, 2 ph2, NEW 2 ph1: BC IT/iv -- +PD1, +CT, +RT, often +FLT3L , +vacc RP2D 1.5 mg/kg LVGN7409 (IgG1 ??) 3 ph1, solid Ca -- +PD1, +CD137, +CT NOTE: precise dev status GEN1042 4.1BBxCD40 (Fc silenced) Monovalent for CD40 & 4.1BB MP0317 FAPxCD40 RO7300490 FAPxCD40 -- +PD1 OvCa&Co, AML/MDS, EpCamxCD40 SL - 172 15 4 SIR P  x C D 40 YH008 PD1xCD40 L o c a lize d effect in tumour First generation attempts of CD40 in IO have been sub - optimal, Many hampered with systemic toxicity 40

Can cer Cells Neutrophil CD8+ T - Cell B Cel l Dendriti c Cell M ac roph a ge CD40 Biology and Therapeutic Potential • Cell surface receptor member of the TNFRSF • Expressed broadly on Antigen Presenting Cells (B cells, DC and macrophages) as well as many non - immune cells and a range of tumors • CD40 is a central regulator of multiple pathways of both the innate and adaptive immune system  reduce the risk of immune escape • Potential for therapeutic activity in cold tumors by targeting the myeloid compartment  Ccomplementarity with T cell directed therapies NK C ell A nti ca nc er Abs ADAPTIVE IMMUNITY PD - 1 OX 4 0 G I T R 4 - 1 BB CD40L or CD40 agonist INNATE IMMUNITY CD40L or CD40 agonist CD40L or CD40 agonist CD4 0 CD4 0 41

MP0317 Activates all APCs in a FAP - dependent Manner in vitro anti - human CD40 mAb FAPxCD40 DARPin® - FAP FAPxCD40 DARPin® + FAP MFI CD86 20000 15000 10000 5000 10 - 4 10 - 3 10 - 2 10 - 1 10 0 10 1 10 2 concentration (nM) Monocytes + IL - 4 + GM - CSF DC 6000 40 30 20 10 TNFα (pg/ml) +FAP - F AP Monocytes Macrophages + GM - CSF Dendritic cells : Macrophages : B cells : 1 2 3 20 40 60 10 - 4 10 - 3 10 - 2 10 - 1 10 0 10 1 10 2 concentration (nM) % CD69 FAPxCD40 DARPin® - FAP FAPxCD40 DARPin® + FAP anti - human CD40 mAb 42 Presented at AACR 2021 Surrogate molecule mFAPxmCD 40 with similar properties : x DC activation FAP - specific x Mφ activation FAP - specific x B cell activation FAP - specific

0 50 40 30 20 10 Time after compound injection (h) % ID/ g mFAP x mCD40 0 50 40 30 20 10 50 µm 50 µm CTRL DARPin ® mFAP x mCD40 Published at AACR 2020 43 DARPin detection in the tumor by IHC SPECT - CT study 4 24 48 72 96 4 24 48 72 96 CTR DARPin Binding HSA but not FAP and CD40 % ID/ g 4 24 48 72 96 4 24 48 72 96 Muscle CTRL DARPin ® mFAP x mCD40 Biodistribution study Tumor CTRL DARPin ® mFAP x mCD40 MP0317: Localizes to MC38 - FAP Tumors

MC38 - FAP Colorectal cancer Time after tumor inoculation (days) Tumor growth (mm 3 ) MP0317 Shows Therapeutic Activity without Cytokine Release Efficacy Peripheral cytokine release Vehicle Neg. CTRL* mFAP x mCD40 mCD40 Ab Published at AACR 2020 44

e x - vivo : m F APxCD40 Activates DC i n t he TME CD86 on CD11c (MFI) CD54 on CD11c (MFI) 400000 300000 200000 100000 0 LN Tumor • Upregulation of co - stimulatory molecules on tumor Dendritic cells  potential for better T cell activation • Higher activity in Tumor vs LN, in contrast to aCD40 Presented at ESMO - IO 2021 45

mFAPxCD40 Increased CD8 T cell Infiltrate in the TME 0 5 1 0 1 5 % CD8+ T cells within total cells Anti - tumor activity Presented at ESMO - IO 2021 46

FAP Expression in Human Tumor Allows CD40 Mediated Immune Activation a - C D40 mAb CD 16 3 ↓ CD 8 0 ↑ Δ MF I CD 54 Δ M FI Δ MFI B cell activation - CD54 Macrophage repolarisation – inflammatory phenotype (CD80hi CD163lo) MP0317 x Macrophage repolarization is further supported by in vitro data 10 - 2 10 - 1 10 2 10 3 350 0 0 300 0 0 250 0 0 200 0 0 150 0 0 100 0 0 5000 0 10 0 10 1 MP0317 a - CD40 mAb * Presented at ESMO - IO 2021 47

48 MP0317 - CP101 Biomarker and Safety Trial Design Dose x6 x5 x4 x3 x2 x1 1 - 3pts 1 - 3pts 3 - 6pts 3 - 6 p ts 3 - 6pts 3 - 6pts 15pts Dose - Escalation MP0317 Monotherapy Expansion MP0317 Monotherapy T ime Next recommended dose level A d v anced solid tumors Obj ectives : • Safety • Local activity • No systemic reactivity Safety Expansion at Optimal/MTD monotherapy Ph1b c o m b i n a t i o n s

Identification and Screening of Potential Tumor Targets from MP0317 • The tumor immune score is correlated to response to aPD1. The FAP threshold is 20% > 2/3 score. + F AP CD40 49

CD40 Open for Multiple Combination (IO or Other) Tumor • Direct tumor killing • Release of tumor antigens • Debulking aids immune cell access • Timing with immunotherapy is important because immune cells can also be damaged PD - 1 or other IO Therapy T c Tumor • Removes suppression of T - cell responses by PD - L1 in the tumor C h emo / R a d io T h e ra p y C D 40 DC 50 Tn T c B Mo • Promotes B - cell activation • Improves tumor antigen presentation and T - cell priming • Reduces suppressive effect of macrophages on T cells • P romotes a n t i - tumour macroph a g e activity

Conclusions: Highly Differentiated Multi - Specific IO Assets 51 • Localized activity achieved with MP0310/AMG 506 • No systemic immune activation observed • Tumor local immune stimulation confirmed after 1 st dose • FAP “validated” as target in the TME of many solid tumors for DARPin IO agonists • Clinical work to establish optimal dosing regimen ongoing • H1 2022 data for review with MP and Amgen • MP0317 is at the intersection of the innate and adaptive immune system • Additional combination strategies possible with CD40 • Ongoing Phase 1 will provide critical information re: dosing, safety, and immune activation • Initial data in H2 2022

AML & MP0533 52 Prof. Adrian Ochsenbein, University Hospital Bern Prof. Carsten Riether, University Hospital Bern Dr. Anne Goubier, Molecular Partners

Universitätsklinik für Medizinische Onkologie, Inselspital Bern Prof. Carsten Riether, PhD Head of Research Department Medical Oncology, Inselspital, University Hospital Bern • PhD in Immunology, ETH Zurich • Post - doc in Tumorimmunology in the lab of Prof. A. F. Ochsenbein, University of Bern • Research focus on the identification of molecular and cellular mechanisms by which cells of the tumor microenvironment regulate cancer stem cells in leukemia and solid tumors. Anne Goubier DVM, PhD VP Biology, Molecular Partners • Doctorate in Veterinary Medicine, Ecole Vétérinaire de Nantes • PhD in Immunology, Université Claude Bernard Lyon 1 • Former CSO, Black Belt Therapeutics • VP Immunology, Tusk Therapeutics Prof. Adrian Ochsenbein, MD, EMBA Director Department Medical Oncology, Inselspital, University Hospital Bern • Trained in Experimental Oncology in the lab of Prof. Zinkernagel, University of Zürich • Translational Research in the lab of Prof. Greenberg, FHCRC, Seattle, USA • Research on Cancer Stem cells in the lab of Prof. Reya, UCSD, USA • Research focus on anti - tumoral immunity, interaction of immune cells with cancer (leukemia) stem cells, CD70/CD27

RD Day Molecular Partners Adrian Ochsenbein / Carsten Riether

Disclosures Molecular Partners: consultancy Argenx: research funding, consultancy, royalties Universitätsklinik für Medizinische Onkologie, Inselspital Bern

AML: Deadly Disease for About Half of the Patients 19,940 patients diagnosed 11,180 patients died US 2020 Patient are either cured or die within 1 - 2 y ea r s ( r api d , a g g r essi v e relapses) unmet need to cure more patients or s u b s t a n tially del a y the relapses MRD+ is driver of relapse (only partial eradication of leukemic stem cells) → for curative intent LSCs need to be fully eradicated, while leaving HSCs untouched

Grimwade et al., Blood 2010 AML is a Heterogeneous Disease Universitätsklinik für Medizinische Onkologie, Inselspital Bern

Pathogenesis and Biology of AML Patel, et al., NEJM 2012; TCGA NEJM 2013. 200 clinically annotated cases 23 genes commonly mutated 237 genes mutated in 2 or more cases

2017 European Leukemia Net Stratification by Genetics Döhner et al. Blood 2017;129:424 - 447. Ge n etic R isk Group Subset Favorable • t(8;21)(q22;q22); RUNX1 - RUNX1T1 • inv(16)(p13.1q22) or t(16;16)(p13.1;q22); CBFB - MYH11 • Mutated NPM1 without FLT3 - ITD (normal karyotype) • Bialleli c m u t a t e d C EB P A (norma l k ar y o t y pe) Intermediate • Mutated NPM1 and FLT3 - ITD high (normal karyotype) • Wild - type NPM1 without FLT3 - ITD or FLT3 - ITD low (normal karyotype) • t(9;11)(p22;q23); MLLT3 - MLL • Any cytogenetics not classified as favorable or adverse Adverse • inv(3)(q21q26.2) or t(3;3)(q21;q26.2); GATA2.MECOM(EVI1) • t(6;9)(p23;q34); DEK - NUP214 • t(v;11)(v;q23); KMT2Arearranged • Monosomy 5 or del(5q); monosomy 7; - 17p; complex karyotype (≥3 abnormalities) • Mutated RUNX1 • M utated AS X L1 • M utated T P53 Patel et al. NEJM 2012 March 22; 366(12):1079 - 89. Revised Risk Stratification of Patients with AML on the Basis of Integrated Genetic Analysis

Treatment for AML patients Universitätsklinik für Medizinische Onkologie, Inselspital Bern curative intention palliative intention Induction Induction ? « 3 +7» • hypomethylating agents (HMA) • + BCL 2 inhibitor venetoclax Further consolidation or autologous HSCT Allogeneic HSCT

Treatment for AML patients Universitätsklinik für Medizinische Onkologie, Inselspital Bern curative intention palliative intention Induction Induction ? « 3 +7» • hypomethylating agents (HMA) • + BCL 2 inhibitor venetoclax Further consolidation or autologous HSCT Allogeneic HSCT

Universitätsklinik für Medizinische Onkologie, Inselspital Bern History of FDA approved AML therapy 2020 2018 Sept. 2020 Azacitidine (maintenance) Nov. 2018 Gilteritinib, V eneto c l a x , Glasdejib July 2018 Ivosidenib 2017 Aug./Sept 2017 Gemtuzumab ozga m ici n , C P X - 351, Enasidenib Apr. 2017 Midostaurin No approvals over 15 years 2010 No approvals over 20 years 2000/20 0 2 Jun. 2010 Ge m tuzu m a b ozogamicin withdrawn May 2002 Idarubicin May 2000 Ge m tuzu m a b ozogamicin 1973 / 19 7 7 1977 First BM transpla n t 1973 Cytarabine/ D aunorubicin

Universitätsklinik für Medizinische Onkologie, Inselspital Bern CD33 and CD123 as single therapeutic targets in AML Expression: Treatment approaches: CD123 • on blasts and LSCs > 90% patients • on virtually all healthy myeloid and progenitor cells, megakaryocytes, B cell subsets as well as endothelial cells. • Flotetuzumab : humanized BiTE; FDA - orphan drug. ongoing phase I/II clinical trials (NCT02152956), (NCT04158739). • Other CD123 x CD3 bispecific antibodies in early - phase : Vibecotamab (XmAb 14045, NCT02730312), SAR440334 (NCT03594955), APVO436 (NCT03647800), and JNJ63709178 (NCT02715011) • IMGN632, CD123 - targeting antibody - drug conjugate, : phase Ib/II in combination with standard of care (Ven/Aza) or monotherapy MRD+ AML ( NCT04086264 ) • CD123 - targeting CAR T cells : Autologous CD123 - specific CAR - T cells are under investigation (NCT02159495) for R/R AML. Few reports using CD123 CAR T cells have shown muted effectiveness in patients compared to pre - clinical models. Toxicity: • Cytokine - release syndrome • on - target off - leukemia toxicity: CAR T cell infusion was accompanied by serious adverse events; CRS CD 3 3 Expression: • on blasts and LSCs > 90% patients • on virtually all healthy myeloid and progenitor cells Treatment approaches : • Gemtuzumab ozogamicin (GO, Mylotarg) : CD 33 - targeting antibody - drug conjugate ; approved treatment in combination with daunorubicin and cytarabine for newly diagnosed CD 33 - positive AML • AMG 330 , AMG 673 and AMV 564 : BiTE molecules . Ongoing Phase I/II studies (NCT 02520427 , NCT 03224819 , NCT 03144245 ) Toxicity: • The on - target off - leukemia toxicity is a major side effect observed in the clinical practice and in clinical trials investigating CD 33 - targeting therapies Alternatives : • Combination of CD33 with other antigens. Dual CD33 - CLL1 CAR - T Therapy in R/R AML (NCT05016063) • Gene editing: A first - in - human trial will be initiated that combines an alloHSCT utilizing genetically modified, CD33 - negative HSCs with CD33 - directed CAR - T cells

Universitätsklinik für Medizinische Onkologie, Inselspital Bern activated lymphocytes dendritic cells MHC C D 70 C D 27 SS T CR B and T cells HSCs S S S S SS • proliferation • anti - apoptotic signals • effector function • memory function . CD70/CD27 signaling ..... .. induces T cell expansion and differentiation of effector cells Hendriks J. Nat Immunol. 2003 .. improves secondary expansion of effector cells and CTL memory Matter M. EJM, 2005, Matter M. EJM 2008 .. increases resistence of HIV specific CTL to exhaustion Ochsenbein AF 2004. J Exp. Med. .. induces immunopathology and aquired immuno - deficiency in chronic LCMV infection Matter M. 2006. J Exp Med. … induces regulatroy T cells and promotes tumor progression Claus C. 2012. Cancer Research … provides a negative feedback signal to leukocyte differentiation during immune activation Nolte M. 2010. Nat. Immunol.

Universitätsklinik für Medizinische Onkologie, Inselspital Bern Elevated levels of soluble CD27 correlate with poor prognosis in AML Riether et al, J Exp Med 2017; 214:359 – 80 Parameter HR (95% CI) P - value sCD27 2.17 (1.34 – 3.50) 0.0016 Risk group 1.69 (1.29 – 2.38) 0.0024 Age 1.03 (1.01 – 1.05) 0.0050 sCD27 (U/mL) 1200 800 400 H e a lthy A ML **** 0 Mean **** P<0.0001 Survival (%) 100 50 0 0 500 CD27 low (n=87) CD27 high (n=50) Threshold: 577 U/mL 1000 1500 2000 OS (days) *** P<0.001

Universitätsklinik für Medizinische Onkologie, Inselspital Bern Cusatuzumab: Swimmer plot T r an s plant 0 6 12 18 24 C usa tu z u ma b monotherapy EOT due to PD EOT due to AE EOT due to transplant Treatment duration (months) Ongoing Time to response PR CRi CR * Data cut - off: February 2019 PR = partial remission CR = complete remission CRi = complete remission with incomplete hematologic recovery EOT = end of treatment PD = progression of disease AE = adverse event NCT03030612 Cusatuzumab doses ID Sex Risk BR C1 F Adv. CRi Cohort 1 C2 M Int. CR 1 mg/kg C3 M Int. CR C4 Cohort 2 M Fav. CR C5 F Int. CR 3 mg/kg C6 F Adv. PR C7 Cohort 3 M Int. CR C8 F Int. CR 10 mg/kg C9 M Adv. CRi C10 M Adv. CR Cohort 4 C11 F Adv. CR 20 m g /kg C12 M Fav. PR Riether et al, Nat. Med. 2020; 26; 1459 - 1467

Universitätsklinik für Medizinische Onkologie, Inselspital Bern • CD70 has a unique expression pattern on activated immune cells and on AML LSCs • Blocking the CD70/CD27 signaling pathway eliminates LSCs • Treatment with HMA upregulates CD70 on LSCs • cusatuzumab monotherapy reduces AML blasts and LSCs within 2 weeks of therapy • Different strategies to target CD70 are currently under investigation: CAR - T cells; bi - (tri - ) specific antibodies • Although cusatuzumab reduced LSCs, all patients in the phase Ib/II trial relapsed Summary I

Universitätsklinik für Medizinische Onkologie, Inselspital Bern Leukemia: a Paradigmatic Stem Cell Disease Bonnet et al. Nature Medicine 1997; 3, 730 - 737 • Self - renewing • Therapy - resistant • Quiescent Leukemia Stem Cells Bla s ts Unlimited r egene r a ti o n

Universitätsklinik für Medizinische Onkologie, Inselspital Bern Leukemic SC Numbers and Stem Cell Signatures are negative Predictors for Survival in AML van Rhenen et al. Clin. Cancer Research 2005; 11:6520 – 6527 Pearce et al. Blood 2006; 107:1166 – 1173. Gentles et al. JAMA 2010; 304:2706 – 2715. Eppert et al. Nature Medicine 2011; 17:1086 – 1093 Stanley et al. Nature 2016; 540(7633):433 - 437

Universitätsklinik für Medizinische Onkologie, Inselspital Bern How Can We Study the Effect of a Treatment on LSCs? 1. Colony formation assay (ex vivo) 2. Re - platings assays (ex vivo) 3. Gold - standard : Patient - derived xenograft model 4. Next - generation RNA sequencing analysis

Universitätsklinik für Medizinische Onkologie, Inselspital Bern Blockade of CD70/CD27 Signaling reduces Stem Cell Function X αCD70 = F c - d i m i n i s h e d blocking version of cusatuzumab wi th o u t ADCC potential Riether et al. J Exp Med; 214, 359 - 380

Universitätsklinik für Medizinische Onkologie, Inselspital Bern Cusatuzumab kills leukemic stem cells NCT0303 0 6 1 2 Mean > ***P<0.001 Stem cell frequency (fold change vs. diagnosis) Diagnosis Monotherapy Reduction in leukemic stem cell frequency : *** 1.0 0.8 0.6 0.4 0.2 0.0 Riether et al. Nat Med 2020; 26, 1459 - 1467

Universitätsklinik für Medizinische Onkologie, Inselspital Bern Identification of Targets for the Treatment of AML Patients van Rhenen et al. Clin. Cancer Research 2005; 11:6520 – 6527 ; Pearce et al. Blood 2006; 107:1166 – 1173 ; Gentles et al. JAMA 2010; 304:2706 – 2715 ; Eppert et al. Nature Medicine 2011; 17:1086 – 1093 ; Stanley et al. Nature 2016; 540(7633):433 - 437 ; Perna et al. Cancer Cell 2017; 32, 506 – 519 New therapies must aim at the elimination of leukemia stem cells Targeting various surface proteins simultaneoulsy may increase specificity Commercial In development IDH1 F L T3 IDH2 BCL2 CD70 CD 1 23 CD33 CD 4 7 HDAC

Universitätsklinik für Medizinische Onkologie, Inselspital Bern CD33 and CD123 as single therapeutic targets in AML Expression: Treatment approaches: CD123 • on blasts and LSCs > 90% patients • on virtually all healthy myeloid and progenitor cells, megakaryocytes, B cell subsets as well as endothelial cells. • Flotetuzumab : humanized BiTE; FDA - orphan drug. ongoing phase I/II clinical trials (NCT02152956), (NCT04158739). • Other CD123 x CD3 bispecific antibodies in early - phase : Vibecotamab (XmAb 14045, NCT02730312), SAR440334 (NCT03594955), APVO436 (NCT03647800), and JNJ63709178 (NCT02715011) • IMGN632, CD123 - targeting antibody - drug conjugate, : phase Ib/II in combination with standard of care (Ven/Aza) or monotherapy MRD+ AML ( NCT04086264 ) • CD123 - targeting CAR T cells : Autologous CD123 - specific CAR - T cells are under investigation (NCT02159495) for R/R AML. Few reports using CD123 CAR T cells have shown muted effectiveness in patients compared to pre - clinical models. Toxicity: • Cytokine - release syndrome • on - target off - leukemia toxicity: CAR T cell infusion was accompanied by serious adverse events CD 3 3 Expression: • on blasts and LSCs > 90% patients • on virtually all healthy myeloid and progenitor cells Treatment approaches : • Gemtuzumab ozogamicin (GO, Mylotarg) : CD 33 - targeting antibody - drug conjugate ; approved treatment in combination with daunorubicin and cytarabine for newly diagnosed CD 33 - positive AML • AMG330, AMG 673 and AMV564 : BiTE molecules. Ongoing Phase I/II studies (NCT02520427, NCT03224819, NCT03144245) Toxicity: • The on - target off - leukemia toxicity is a major side effect observed in the clinical practice and in clinical trials investigating CD 33 - targeting therapies Alternatives : • Combination of CD33 with other antigens. Dual CD33 - CLL1 CAR - T Therapy in R/R AML (NCT05016063) • Gene editing: A first - in - human trial will be initiated that combines an alloHSCT utilizing genetically modified, CD33 - negative HSCs with CD33 - directed CAR - T cells

Universitätsklinik für Medizinische Onkologie, Inselspital Bern MP0533 Reduces Colony Formation of Primary Human LSCs ex vivo

Universitätsklinik für Medizinische Onkologie, Inselspital Bern • Various targetable surface antigens in AML have been identified (e.g. CD33, CD123, CLL - 1, CD70). • Therapeutic approaches targeting most of these antigens have been shown to reduce leukemia burden and induce remission in a fraction but not all patients. • Major problem: on - target off - leukemia toxicity is a major side effect observed in the clinical practice. • Potential solution: Targeting several tumor antigens to induce specificity and reduce side - effects. • Ongoing collaboration work: • Assessment killing of SOC - resistant/refractory LSCs • Combination with SOC and assessment of LSC and HSC killing Summary II

MP 0 5 3 3 77 Anne Goubier

MP0533: Tri - specific T - cell Engager for AML DARPin Advantage Target Patient Disease Biology Expected Mi l e s to n es • FIH clinical studies in 2022 • Avidity driven multispecific DARPin, targeting 3 TAA's, engaging CD3 • T cell are activated only when 2 or more TAA's are bound • Should allow for broader therapeutic index with reduced safety issues • Persistence of LSCs is the driver of relapse • “MRD+ status” refers to low level disease and can be detected by immunophenotypic or molecular markers • Current T - cell engager approaches are limited by on - target toxicity (not clean targets) • ~20,000 people are diagnosed with AML every year • Over 50% of patients die in the first year • High relapse rates CD3 3 CD 3 CD7 0 CD12 3 78

Requisites for an Ideal AML Therapeutic Solution • An ideal AML therapeutic solution should: • Achieve control of the disease by eliminating LSCs • Cover tumor heterogeneity by targeting multiple antigens • Increase the therapeutic window: optimal dose levels with limited side effects • Limited killing of healthy HSCs • Reduced CRS 79

The DARPin Solution: a Trispecific CD3 Engager DARPin For Specific killing of all LSCs and blasts via avidity - driven T cell engagement Minimal effect on healthy cells Single targets Low affinity engagement Efficient attack of heterogenous cancer cells CD3 engager : demonstrated potency in hematological malignancies Targeting 3 TAA in order to: • Ensure tumor - specificity via avidity - driven T cell activation • Control tumor heterogeneity 100% 0% 1 TAAs Dose Therapeutic Window 80 Resp o nse 2 or 3 TAAs

CD33, CD123 & CD70: Optimal Targets to Maximize Efficacy and Selectivity • Clinically validated targets • Co - expression pattern of CD70, CD33 and CD123 on LSCs and AML blasts • Differentiates LSCs and AML blasts from healthy cells  optimal selectivity • Covers tumor heterogen e ity  opti m al efficacy LSCs and blasts CD33 - CD123 - CD70 Trispecific CD3 engager DARPin C D 123 C D 70 C D 33 CD7 0 CD 12 3 CD 3 3 CD3 81

CD123/CD70/CD33 co - expression differentiates LSCs and AML Blasts Allowing for or avidity - driven specific T cell killing of LSCs and blasts LSCs Blasts HSC Lymphocytes Inflamed EC Myeloid cells pDCs Basophiles CD70 Low Low Neg /Low Variable Neg Neg Neg Neg CD123 High High Low Neg Medium Low/ Medium High High CD33 High High Medium Neg Neg High/ Medium Low Medium Theoretical A v idi t y - b ased killing* Yes Yes Limited No No Limited Limited Likely * Assuming equivalent affinity for CD33, CD123 and CD70 Eliminating LSC and Blast through avidity - driven selective targeting should be doable and will allow ▪ Treating frail patients thanks to a higher safety profile ▪ Increasing dose and thus deepening responses for long term control of the disease 82

10 12 1 10 10 3 5 100 From the Idea to MP0533: Exploiting DARPin Platform Versatility Allows Screening for Function Sweet Spot Screening of multi - domain DARPins Functional M ulti - D A RPin ca ndida tes Screening of multi - domain DARPins Multi - DARPin lead molecule Library used to generate binders against TAAs Identified functional DARPin modules to each TAA Multiple It eration s C D 70 C D 123 C D 33 Binding to TAAs CD3 e n g a g e s w i th T - cells HSA f or h al f - li f e extension MP0533 : a multi - domain, multi - specific, half - life extended DARPin Recombination of DARPin modules: TAA1 x TAA2 x TAA3 x CD3 Affinity & format & half - life optimization Recombination of DARPin modules α - C D 70 α - C D 123 α - C D 33 α - CD3 A M L - spec if i c TAA binders Effector Function 83

MP0533: a DARPin Solution for AML Patients? 1. Validation of the avidity - driven T cell mediated killing concept • Can MP0533 induce killing of cells expressing 2 or 3 TAA while sparing cells with 1 TAA? 2. Demonstration of MP0533 efficacy against AML • Is the level of TAA expressed by AML blasts sufficient for MP0533 - induced killing? • Are patient T cells fit and numerous enough for MP0533 to induce AML blasts killing? • Is MP0533 also potent in vivo? 3. Demonstration of MP0533 enhanced therapeutic window • Can MP0533 induce LSCs killing while sparing HSCs? • Can MP0533 preserve healthy blood cells and show reduce cytokine release? MP0533 CD70 DARPin CD123 DARPin CD33 DARPin Binding to TAAs CD3 DARPin Effector func t ion HSA DARPin f or ha lf - li f e extension 84

10 - 2 10 - 1 10 0 10 1 10 2 10 3 10 4 10 5 0 2 5 5 0 7 5 1 0 0 M P 0 53 3 Concentration [pM] % cell killing CD 3 3 + C D 123 + C D 7 0 + CD33+CD70+ CD123+CD70+ CD33+CD123+ CD33+ C D 12 3 + CD70+ MP0533 Induces Specific Killing of AML Cells Expressing 2 or 3 TAAs TAAs expressed on Molm - 13 cells MOLM - 13 cells WT or KO for CD70, CD33 and/or CD123 + Healthy donor T cells (E:T = 5:1) MP0533 or controls 48 hours Tumor cell killing T cell activation C D 123 C D 70 C D 33 85

MP0553 Induces Potent T - Cell Mediated Killing of AML Blasts As compared to CD123 - DART and CD33 - Bite 10 - 3 10 - 2 10 - 1 5 0 2 5 7 5 1 0 0 BMMC AML - Mean of 3 donors 10 0 10 1 10 2 10 3 10 4 10 5 pM %viable tumor cells CD33 - BITE C D 123 - D A R T MP0533 Primary AML samples + Healthy donor T cells (E:T = 4:1) MP0533 or controls 48 hours Tumor cell killing T cell activation CIDp780007007 CIDp780004612 CIDp780004 ABC LSC+Blasts BMMC AML - TAA expression BMMC AML – Tumor killing Mean values for 3 donors 86

MP0533 Induces AML Killing by Patients’ Own T Cells Despite lower frequency and expected lower quality of T cells *No unspecific killing with NB - CD3 control (not shown) MP0533 CD 12 3 - D A R T First line 87 R e l a pse Primary AML samples ( no addition of healthy T cells ) MP0533 or controls 120 hours Tumor cell killing

MP0533 Shows in vivo Efficacy Against Established MOLM - 13 Tumors As compared to CD33 - Bite Day - 2 Day 0 Day 8 HuPBMCs M O L M - 13 T reatme n t Start MP0533 3 times per week for 2 weeks (6 injections) CD33 - bite or vehicle daily for 2 weeks (14 injections) 0 50 0 100 0 150 0 200 0 250 0 MOLM - 13 tumor growth T u mo r v o l u m e (mm 3 ) V e h i cl e 0 2 0 4 0 6 0 8 0 10 0 TNF alpha in serum TNF - alpha [pg/mL] Vehicle DARPin CD3 control MP0533 CD3xCD33 BiTE TNF α in serum Effica c y S a fety 88

0 1 0 0 1 0 0 1 0 1 1 0 2 5 5 0 7 5 1 0 0 % colony count M P 0 5 3 3 100 10 C D 1 2 3 - CD 3 DART 100 10 CD 3 3 - C D 3 BiTE 1 [pM] L S C H S C MP0533 Shows Preferential Killing of CD34+ LSCs over HSC Larger therapeutic window as compared to CD123 - DART and CD33 - bite L S C H S C CD 3 3 CD1 2 3 CD 7 0 Median Target Expression (delta MFI) 89 20 0 0 40 0 0 60 0 0 K illing >50 %H S C s K illing >50 %H S C s Killing of sorted CD34+ LSC or HSC by colony formation assay using allogenic T - cells (E:T of 1:1, 4 d) / CFU counted after 2 weeks semi - solid media

MP0533 Demonstrates Reduced Cytokine Release and Hemotoxicity As compared to CD123 - DART Addition of test molecules Blood draw healthy donor C y tokine analysis R o tating wheel Blood sampling 0 - 2 - 4 - 8 - 24h Cell counts 1 1 0 0 150 0 0 300 0 0 450 0 0 I F N γ 0.001 0.01 0.1 nM AUC 0 - 24h 1 1 0 0 100 0 0 80 0 0 60 0 0 40 0 0 20 0 0 T N Fα 0.001 0.01 0.1 nM AUC 0 - 24h 1 1 0 0 5 0 0 10 0 0 15 0 0 I L 6 0.001 0.01 0.1 nM AUC 0 - 24h 1 1 0 5 0 0 11 0 0 10 0 0 9 0 0 8 0 0 7 0 0 6 0 0 Platelet count 0.001 0.01 0.1 nM AUC 0 - 24h 1 1 0 1 4 2 4 2 2 2 0 1 8 1 6 WBC count 0.001 0.01 0.1 nM AUC 0 - 24h Fl o t e t u z u m a b MP0533 N B - C D 3 90 *NB = Non - Binding to TAAs CD 1 2 3 - D A R T

MP0533: a DARPin Solution for AML Patients 1. Validation of the avidity - driven T cell mediated killing concept x • Can MP0533 induce killing of cells expressing 2 or 3 TAA while sparing cells with 1 TAA? 2. Demonstration of MP0533 efficacy against AML x • Is the level of TAA expressed by AML blasts sufficient for MP0533 - induced killing? • Are patient T cells fit and numerous enough for MP0533 to induce AML blasts killing? • Is MP0533 also potent in vivo? 3. Demonstration of MP0533 enhanced therapeutic window x • Can MP0533 induce LSCs killing while sparing HSCs? • Can MP0533 preserve healthy blood cells and show reduce cytokine release? MP0533 CD70 DARPin CD123 DARPin CD33 DARPin Binding to TAAs CD3 DARPin Effector func t ion HSA DARPin f or ha lf - li f e extension 91

MP0533: a Unique DARPin Solution for AML Patients • An ideal AML therapeutic solution should: • Ensure long term control of the disease by eliminating LSCs x • Control tumor heterogeneity by targeting multiple Ag x • Increase the therapeutic window: optimal dose levels for efficacy with limited side effect • Limited killing of healthy HSCs x • Reduced CRS x Phase 1 clinical trial initiation H2 2022 92

Pa t ri c k Amstu t z 93 Co n clusions

MP Strategy – Building on our Strengths Our candidates’ design aims to directly change the course of disease biology and allow testing in a model with high translatable value We aim to drive true patient value with early clinical read - outs We leverage the advantages of the DARPin technology to provide unique solutions to impact biology and bring value to patients We strive to collaborate with the best scientists and clinicians in the field from ideation to clinical trials TECHNOLOGY TARGET PATIENTS BIOLOGY T e c h n o l o g y Bio l o g y Target Patient 94

How we Select Targets for Optimized Risk/Reward Probability of Success Differentiation OUR PURPOSE: Transform the lives of people with cancer by delivering truly innovative therapies Novel Biology Novel Biology on Validated Targets V alidated Targets 95

Pipeli n e CANDIDATE / FOCUS RESEARCH PHASE 2 PHASE 3 R IG HT S Ensovibep – Covid Next Gen Covid AMG506 / MP0310 FAP x 4 - 1BB MP0317 FAP x CD40 MP0533 CD3 x CD33+CD70+CD123 Abicipar VEGF Radio Ligand Therapy Platform Discovery 96 Pipeline Inflection Points Discovery Oncology Op ht halmolo g y Infectious disease Radical simplicity & Conditional Activation Additional Infectious Diseases Solid tumors PRECLINICAL PHASE 1 Covid ambulatory – Empathy Future VoC* wet AMD – Cedar & Sequoia Solid tumors A M L Solid tumors * VoC = Variant of Concern Oncolo g y

Pipeline CANDIDATE / FOCUS Ensovibep – Covid Next Gen Covid AMG506 / MP0310 M P0317 M P0533 Abicipar Radio Ligand Therapy Platform Discovery Pipeline Inflection Points Oncolo g y Discovery Oncology Op ht halmolo g y Infectious disease Radical simplicity & Co Additional Infectious D RESEARC H P R E C L I N I C AL P H ASE 1 P H ASE 2 PHASE 3 R IG HT S Covid ambulatory – Empathy Future VoC* Solid tumors Solid tumors AML wet AMD – Cedar & Sequoia Solid tumors nditional Activation iseases Empathy read out part A (400 pt) read out Q1/22 Candidate ready for future VoC Weekly Dosing H1/22 Initial Results H2/22 FIH H2/22 FDA feedback H1/22 Additional DARPin programs identified in 2022 Outlook – virology deep dive post Empathy read out Cash to 2024 Collaboration set - up 97

My Key Takeaways • DARPin leadership and Product Strategy in place • Strong cross - functional execution: Technology & Biology & Medical • Continued collaboration to leverage outside expertise AND • Creation of molecules where we control our full destiny: » MP0533 = first DARPin with real potential to generate clinical data for POC in - house (ideally registrational) 98

THANK YOU 99

Molecular Partners AG Wagistrasse 14 8952 Zürich - Schlieren Switzerland www.molecularpartners.com T +41 44 755 77 00 100

Ensovibep Protects Against Omicron 101

Covid Pseudotype Inhibition – From Wilde - Type to Omicron 1 2 0 1 0 0 80 60 40 20 0 0 1 0 - 1 1 0 0 1 0 1 1 0 2 1 0 3 1 0 4 1 0 5 n o v ir u s Concentration (ng/ml) Wild Type Relative infection (%) 1 2 0 1 0 0 80 60 40 20 0 0 1 0 - 1 1 0 0 1 0 1 1 0 2 1 0 3 1 0 4 1 0 5 n o v ir u s Concentration (ng/ml) Om i c r o n Relative infection (%) Ensovibep R EG N 109 3 3 R EG N 109 8 7 AZD8895 AZD1061 LY - CoV555 LY - CoV016 B r ii - 1 9 6 B r ii - 1 9 8 S 309 102

Ensovibep Remains Fully Active Against Omicron Pseudotype 103 Neutralization of ensovibep and a panel of monoclonal antibodies in VSV - pseudotype assays containing the Omicron variant spike protein with >30 substitutions. Wild Type Omicron 1 Compound IC 50 (ng/mL) IC 50 (ng/mL) fold change to wt ensovibep 1.6 2.2 1.4 REGN10933 3.2 >1000 >100 REGN10987 3.3 >1000 >100 LY - CoV555 13 >1000 >100 LY - CoV016 6.4 >1000 >100 S309 23 72 3.1 AZD8895 0.6 415 >100 AZD1061 5.5 237 43 Brii - 196 9.5 392 41 Brii - 198 52 30 0.6 IC 50 : green: <10 ng/mL; orange: 10 - 100 ng/mL; dark orange: 100 - 1000 ng/mL; red: >1000 ng/mL fold change to wt: green: <10 - fold; orange: 10 - 100 - fold; red: >100 - fold 1 Set of mutations: A67V, Δ69 - 70, T95I, G142D, Δ143 - 145, Δ211, L212I, ins214EPE, G339D, S371L, S373P, S375F, K417N, N440K, G446S, S477N, T478K, E484A, Q493R, G496S, Q498R, N501Y, Y505H, T547K, D614G, H655Y, N679K, P681H, N764K, D796Y, N856K, N969K, L981F.

C onfidential 104 DARPin – Radio - Ligand Therapeutics New collaboration with Novartis

105 Radio - Ligand Therapeutics Collaboration • NIBR established as world leader in the RLT field • RLTs - the potential to deliver targeted radiation to tumor cells anywhere in the body • DARPins – small size and high specificity & affinity may offer an advantage in RLT’s, which often require a highly specific delivery vehicle • Both parties to collaborate on the discovery and optimization of the therapeutic candidates • Novartis would be responsible for all clinical development and commercialization activities • $20 million upfront to Molecular Partners, total potential milestone payments of up to $560 million, and up to low double - digit percent of royalties.