These materials include express and implied "forward-looking statements," including forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward looking statements includ

From Serendipity to Rational Design

Taking Molecular Glue Degraders to New Heights | January 2022 Exhibit 99.1

These materials include express and

implied "forward-looking statements," including forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward looking statements include all statements that are not historical facts, and

in some cases, can be identified by terms such as "may," "might," "will," "could," "would," "should," "expect," "intend," "plan,"

"objective," "anticipate," "believe," "estimate," "predict," "potential," "continue," "ongoing," or the negative of these terms, or other comparable

terminology intended to identify statements about the future. Forward-looking statements contained in these materials include, but are not limited to, statements about our product development activities, including our expectations around the ongoing

development of our QuEENTM platform and in silico tools, the advancement of our pipeline and the various products therein, including -the timing for filing our IND for our GSPT1 program and the advancement of additional programs, the expansion of

our compound and degron libraries, our ability to identify additional molecular glue degraders, and our scientific predictions around clinical opportunities for our programs, including for GSPT1 program. By their nature, these statements are subject

to numerous risks and uncertainties, including the impact that the current COVID-19 pandemic will have on our development activities and operations, as well as those risks and uncertainties set forth in our Quarterly Report on Form 10-Q for the

third quarter ended September 30, 2021 filed with the US Securities and Exchange Commission, and any subsequent filings, that could cause actual results, performance or achievement to differ materially and adversely from those anticipated or implied

in the statements. You should not rely upon forward looking statements as predictions of future events. Although our management believes that the expectations reflected in our statements are reasonable, we cannot guarantee that the future results,

performance or events and circumstances described in the forward-looking statements will be achieved or occur. Recipients are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date such statements

are made and should not be construed as statements of fact. We undertake no obligation to publicly update any forward-looking statements, whether as a result of new information, any future presentations or otherwise, except as required by applicable

law. Certain information contained in these materials and any statements made orally during any presentation of these materials that relate to the materials or are based on studies, publications, surveys and other data obtained from third-party

sources and our own internal estimates and research. While we believe these third-party studies, publications, surveys and other data to be reliable as of the date of these materials, it has not independently verified, and makes no representations

as to the adequacy, fairness, accuracy or completeness of, any information obtained from third-party sources. In addition, no independent source has evaluated the reasonableness or accuracy of our internal estimates or research and no reliance

should be made on any information or statements made in these materials relating to or based on such internal estimates and research. Forward-Looking Statements

Monte Rosa Therapeutics Highlights

Taking molecular glue degraders (MGDs) to new heights World-class leadership & SAB with deep drug discovery know-how and development expertise in precision medicine Next-generation molecular glue-based targeted protein degradation platform

developing breakthrough small molecule drugs that selectively degrade therapeutically-relevant proteins Targeting the undruggable proteome via AI-based degron prediction & rational design of highly selective MGDs IND for GSPT1 program expected

in 2022 with clinical development planned in Myc-driven tumors Five disclosed programs targeting high unmet medical needs in oncology and non-oncology indications

World-Class Leadership Deep expertise

in molecular glue discovery, drug development and precision medicine Jullian Jones, Ph.D., J.D., MBA Chief Business Officer Markus Warmuth, M.D. Chief Executive Officer Ajim Tamboli, CFA Chief Financial Officer John Castle, Ph.D. Chief Data

Scientist Silvia Buonamici, Ph.D. SVP, Drug Discovery Biology Filip Janku, M.D., Ph.D. Chief Medical Officer Sharon Townson, Ph.D. Chief Technology Officer Owen Wallace, Ph.D. Chief Scientific Officer Phil Nickson, Ph.D., J.D. SVP, Head, Legal

Operations Jennifer Champoux, Vice President, Operations

Strong Cash Position and Investor

Support Over $455M raised since 2020 with top tier investors provides runway into late 2024 Aggregate IPO gross proceeds were approximately $255.6 million before deducting underwriting discounts and commissions and other offering expenses and

include an additional $33.3 million in gross proceeds the company received as part of its IPO from the full exercise of the underwriters' option to purchase up to an additional 1,755,000 shares of common stock at the public offering price of

$19.00 per share. Series A $32.5M April 14, 2020 Series B $96.0M September 14, 2020 Series C $95.0M March 11, 2021 IPO $255.6M* June 28, 2021 $367M Cash as of 9/30/21

Expanding Target Space through

Molecular Glue Degraders (MGDs) 3-10% of Proteome Uncharted Chemical and Target Space Drugging the Druggable Inhibitors Drugging the Undruggable MGDs Redrugging the Druggable PROTACs E3 Ligase UNDRUGGABLE TARGETS DRUGGABLE TARGETS E3 Ligase

The Next Generation of Precision

Medicine-based Small Molecule Drugs Selectively editing the human proteome with rationally designed MGDs Traditional small molecule inhibitors Therapeutic Antibodies RNAi, RNA Editing CRISPR/Gene Therapy MGDs Ability to access undruggable space

Cellular permeability Oral bioavailability Systemic distribution CNS Penetration Manufacturing scalability

Our Rational Approach to Unleash the

Full Potential of MGDs Beyond cereblon Beyond the canonical degrome Unraveling the canonical degrome Expanding the Degradable Proteome Neosubstrates - E.g. IKZF1 MGD E.g. Lenalidomide Cereblon

QuEEN Discovery Platform

Quantitative and Engineered Elimination of Neosubstrates

Degron encyclopedia QuEEN

Discovery Platform: A Target-Centric Approach to MGDs Cereblon binding (pIC50) 5 7 Molecular weight (Da) 190 300 Degron discovery using proprietary AI-powered algorithm Rationally designed, diverse and growing library engaging a variety of degrons

Proprietary MGD library Accessing a large pool of undruggable targets with a diverse MGD library Sequence Topology Surface 1000s of proteins across multiple degrons GlueomicsTM toolbox Specialized suite of in vitro and in silico assays to discover,

optimize and advance MGDs as clinical candidates Protein fold-change; (log2) p-value

A Rich, Differentiated Target Space

Across Protein Domains and Diseases Degron-containing domains Broad disease landscape Many highly credentialed targets >85% degrons have unique sequence >75% undruggable Diverse protein domains and classes Degron Encyclopedia >3000 proteins

containing a predicted loop degron Predicted degrons

Increasing MGD scaffold diversity

Library design and expansion Increasing Novelty and Structural Diversity to Match the Target Space Scaffold evolution Tanimoto similarity 0.6 1 Design focused on optimal drug-like properties High structural diversity and novelty Current library size

20K MGDs 0.8 MGD library is derived from > 400 unique low molecular weight scaffolds with favorable CRBN binding affinities 0.4 Lenalidomide (reference point) Cereblon binding (pIC50) 5 7 Molecular weight (Da) 190 300

Multiple points of contact for

dialing in selectivity and potency MGDs are rationally designed to exploit key contacts to selectively engage different neosubstrates MGDs Reprogram the Cereblon Surface Remodeled MGD-CRBN surface enables selective engagement of neosubstrates

Effective ternary complex generation involves MGD-cereblon interactions MGD-neosubstrate interactions CRBN-neosubstrate interactions MGDs reshape the cereblon surface through different exit vector geometries Neosubstrates are engaged selectively

through unique interactions with both MGD and cereblon MGD MGD Neosubstrate E3 ligase MGD

in vitro screens Glueomics

Toolbox Accelerates Identification of MGDs Multiple assays enable rapid identification and validation of MGDs for novel targets Chemoproteomics - proximity Protein fold-change; (log2) p-value Turbo-ID Cellular Biochemical Proteome-wide expression

TMT Proteomics to evaluate: Proteome-wide changes in protein levels MGD selectivity Protein fold-change; (log2) p-value

Rhapsody, QuEEN's in silico

Engine A suite of proprietary AI-powered algorithms to design, discover and develop MGDs Taking MGD discovery in silico to accelerate discovery Creation and E3 ligase docking of novel MGDs, expanding our library to engage more targets Ternary

complex models enabling MRT scientists to engineer and optimize selective MGDs Computational screening identifying and prioritizing hits inducing binding and selective degradation in silico library generation in silico ternary complex models in

silico MGD screening Neosubstrate E3 ligase MGD E3 ligase Novel in silico MGDs MGD library Neosubstrate E3 ligase

Targets Clinical Path Leveraging a

Leading Drug Discovery Platform Purpose-built to discover and develop a wide landscape of therapeutically-relevant MGDs Undruggable and inadequately drugged degron-containing proteins High level of target validation, preclinically and clinically

Programs with biomarker-based patient selection strategy and clear path to the clinic Opportunity for rapid clinical PoC for MOA and efficacy Address high unmet needs Potential to address a wide range of therapeutically-relevant proteins in oncology

and beyond Create synergies within therapeutic areas Monte Rosa's High-Value Proprietary Pipeline Patient Benefit

Monte Rosa Pipeline Rapidly

advancing wholly owned MGD programs targeting undruggable proteins Oncology Autoinflammation Oncology / immunology Genetic diseases GSPT1 NSCLC, SCLC and other MYC-driven Malignancies CDK2 Ovarian Cancer, Breast Cancer NEK7 Inflammatory Diseases

VAV1 T and B Cell Malignancies, Autoimmune Disease Discovery Target / Program Indication(s) IND filing mid-2022 BCL11A SCD, -Thalassemia Next Anticipated Milestones Ownership Undisclosed Multiple IND-Enabling Clinical IND-Enabling Studies Lead

Targeting Myc-driven Tumors and

Their Addiction to Protein Translation GSPT1 is a key regulator and vulnerability of Myc-induced translational addiction To sustain growth, Myc-driven tumors are addicted to protein translation Myc regulates the expression of key genes related to

protein translation, including the master regulator 4EBP1 and eIF4E This addiction to protein translation creates a dependency to the translation termination factor GSPT1 a degron-containing protein GSPT1 MGDs exploit this vulnerability by:

Disrupting protein translation output Reducing Myc-oncogenic signaling Myc hijacks the cellular protein translation machinery creating a vulnerability to GSPT1

MRT-2359 is a potent inducer of

GSPT1-cereblon proximity MRT-2359 is a selective GSPT1-directed MGD MRT-2359 is a Potent and Selective GSPT1-directed MGD GAPDH IKZF1 IKZF3 ZFP91 CK1a GSPT1 - 0.3 3 30 30 30 6hr post treatment in MM1S and Kelly (SALL4) - - - - + - - - - - - + SALL4

1hr post treatment Protein fold-change; (log2) p-value MRT-2359, mM Bortezomib MLN-4924 Proximity - Turbo ID Ternary complex model in vitro data CRBN binding, Ki 113 nM Ternary complex, EC50 < 7 nM Degradation, DC50 80 nM Degron MRT-2359

Myc-Driven NSCLC lines are Highly

Sensitive to MRT-2359 Myc-driven NSCLC cell lines are sensitive to MRT-2359 Each dot represents a cell line MRT-2359 induces GSPT1 degradation in all cell models, but selective killing in high N-Myc lines only Viability GSPT1 western blot at 6 hr

(N-Myc high) and 24 hr (low). 72 hr viability assay (CTG) GSPT1 degradation Myc-driven Non-Myc-driven

MRT-2359 Affects N-Myc Pathway only

in Myc-driven Cells GSPT1 N-Myc 0.03 0.3 3 - 0.03 0.3 3 0.03 0.3 3 Tubulin 0 6 hr 24 hr 48hr MRT-2359 ( M) Myc-driven (NCI-H1155) - - 0.03 0.3 3 - GSPT1-directed MGD degradation affects translation, a critical vulnerability of Myc-driven cells

Non-Myc-driven (NCI-H2023) N-Myc not detected GSPT1 N-Myc 0.03 0.3 3 - 0.03 0.3 3 0.03 0.3 3 Tubulin 0 6 hr 24 hr 48hr MRT-2359 ( M) - - 0.03 0.3 3 -

Oral dosing of MRT-2359 shows

anti-tumor activity and regressions in NCI-1155 Dose- and time-dependent degradation of GSPT1 is associated with N-Myc downregulation MRT-2359 Induces Tumor Regressions in N-Myc-driven Xenograft Models Similar observations in other high N-Myc

expression models (ABC-1, NCI-H1770) Day 5 1 mg/kg 10 mg/kg MRT-2359 plasma concentration N-Myc protein level GSPT1 protein level

MRT-2359 Anti-tumor Activity in L-

and N-Myc-positive NSCLC PDXs Tumor progression to 800 mm3

Targeting Myc-positive Tumors with

MRT-2359 Potential indications and patient stratification hypotheses Patient diagnosed incidence #s, major markets (US, EU and JP): Decision Resources Group (DRG) Patient stratification %s: Schaub - Cell Systems 2018; Mass -Vall s -

Exp. Op. therapeutic targets 2020; Sesques and Johnson - Blood 2016 Non-small cell lung cancer 352K patients (LUAD + SCC) - 7-10% L-Myc overexpression/amplification Diffuse large B-cell lymphomas 67K patients - 30% N-Myc

overexpression/amplification c-Myc amplification c-Myc translocation/rearrangement Triple-neg breast cancer 68K patients - 30% Ovarian cancer 63K patients - 64% Other c-/L-/N-Myc driven tumors Bladder cancer Uterine cancer Neuroendocrine

lung cancer, Lu-NET Neuroendocrine prostate cancer, NEPC Small cell lung cancer 66K patients - 50%

Early Phase Clinical Development

Dose Level 1 MTD or RDE Expansion cohorts Dose escalation BOIN design Lung cancer (NSCLC, SCLC), solid tumors with L-/N-Myc amplification and diffuse large B-cell lymphomas SCLC - Enriched for high L-/N-Myc expression NSCLC - Enriched

for high L-/N-Myc expression Dose Level 2 Dose Level X Solid tumors - L-/N-Myc amplification Dose Level 3

Targeting Myc-addicted Tumors with

MRT-2359 IND-enabling activities have been initiated Rationally designed potent and selective GSPT1-directed MGD Favorable drug-like properties and ADMET profile Orally bioavailable development candidate Robust antitumor activity in vivo in multiple

tumor models IND-enabling activities ongoing Patient stratification hypothesis developed and being validated IND filing expected in mid-2022

NEK7 (NIMA-Related Kinase 7) as a

Target for Inflammatory Disease NEK7 is an essential regulator of the inflammasome Pyroptosis Gasdermin D Active NLRP3 inflammasome Cytokines secretion Pro-IL-1 Pro-IL-18 IL-18 IL-1 NEK7 NLRP3 Pro-Caspase-1 ASC N-terminal C-terminal

N-terminal Caspase-1 N-terminal Therapeutic hypothesis: Diseases with over-activated or mutated NLRP3 inflammasome NEK7 licenses NLRP3 assembly in a kinase independent manner NEK7-deficient macrophages are severely impaired in IL-1 and IL-18

secretion Clinical opportunity: First-in-class NEK7 degraders for Over-activated NLRP3 inflammasome: metabolic pathologies, cardiovascular diseases, inflammatory issues and neurologic disorders NLRP3 activating mutations: Cryopyrin-associated