Agenda Welcome & Introduction Lloyd M. Segal, President & CEO Lunresertib Preliminary MYTHIC Monotherapy & Combination Therapy Clinical Trial Results Timothy Yap, MBBS, PhD, FRCP, Principal Investigator, MYTHIC Trial Con

Insight that enriches. Precision that

empowers. Lunresertib MYTHIC Clinical Trial Update October 13, 2023 Exhibit 99.1

Agenda Welcome & Introduction

Lloyd M. Segal, President & CEO Lunresertib Preliminary MYTHIC Monotherapy & Combination Therapy Clinical Trial Results Timothy Yap, MBBS, PhD, FRCP, Principal Investigator, MYTHIC Trial Conclusions & Lunresertib Development Plan Maria

Koehler, MD, PhD, Chief Medical Officer Upcoming Catalysts Lloyd M. Segal, President & CEO Q&A Repare Therapeutics Leadership & Dr. Yap

Disclaimer Statements contained in

this presentation regarding matters that are not historical facts are "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, as amended. Words such as "anticipates," "believes,"

"expects," "intends," "plans," "potential," "projects," "would" and "future" or similar expressions are intended to identify forward-looking statements. Each of these forward-looking statements involves

substantial risks and uncertainties that could cause actual results to differ significantly from those expressed or implied by such forward-looking statements. Forward-looking statements contained in this presentation include, but are not limited

to, statements regarding the initiation, timing, progress and results of our current and future preclinical studies and clinical trials, including specifically our clinical trials of lunresertib (RP-6306) and camonsertib; the expected timing

of program updates and data disclosures; the timing of filing INDs and other regulatory documents; the timing and likelihood of seeking regulatory approval for our product candidates; the competitive landscape for our product candidates; our

ability to identify and develop additional product candidates using our SNIPRx platform; and our estimates regarding expenses, future revenue, capital requirements, cash runway and needs for additional financing. These forward-looking

statements reflect our current beliefs and expectations. Many factors may cause differences between current expectations and actual results, including the duration and impact of the COVID-19 pandemic on our business and market volatility, unexpected

safety or efficacy data observed during preclinical or clinical studies, clinical site activation rates or clinical trial enrollment rates that are lower than expected, changes in expected or existing competition, changes in the regulatory

environment, and unexpected litigation or other disputes. These and other risks are described more fully in our filings with the Securities and Exchange Commission ("SEC"), including the "Risk Factors" section of our

Quarterly Report on Form 10-Q filed with the SEC on August 9, 2023, and other documents we subsequently filed with or furnished to the SEC. All forward-looking statements contained in this presentation speak only as of the date on which they were

made. Except as required by law, we assume no obligation to update any forward-looking statements contained herein to reflect any change in expectations, even as new information becomes available. This presentation also contains estimates and other

statistical data made by independent parties and by us relating to market size and growth and other data about our industry. This data involves a number of assumptions and limitations, and you are cautioned not to give undue weight to such

estimates. Neither we nor any other person makes any representation as to the accuracy or completeness of such data or undertakes any obligation to update such data after the date of this presentation. In addition, projections, assumptions and

estimates of our future performance and the future performance of the markets in which we operate are necessarily subject to a high degree of uncertainty and risk. Solely for convenience, the trademarks and trade names in this presentation may be

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Differentiated and expanding

clinical-stage pipeline Lunresertib: First-in-class oral PKMYT1 inhibitor (Phase 1/2) Camonsertib: ATR inhibitor (Partnered with Roche) Additional near-term clinical programs Potential across multiple tumor types Proprietary CRISPR-enabled SNIPRx

platform Focused on genomic instability and DNA damage repair within cancer cells Multiple clinical catalysts expected in 2023 and 2024 Cash runway into 2026 Developing Next-Generation Precision Oncology Therapeutics

Lunresertib: First-in-class, oral,

small molecule, PKMYT1 inhibitor Combination therapy achieved strong anti-tumor activity across multiple tumor types and tested genotypes; 33% overall response at preliminary RP2D (N=18) 50% RECIST response observed in camonsertib combination

in largest cohort (gynecological tumors) at preliminary RP2D (N=10) Proof of concept established for monotherapy and camonsertib combination in MYTHIC Phase 1 trial Validated preclinical synergy hypothesis and patient selection approach from

proprietary SNIPRx platform Large, genomically defined potential patient population ~90K addressable population including CCNE1, FBXW7 and PPP2R1A Encouraging safety and tolerability profile observed for oral monotherapy and combination therapy

RP2D, recommended phase 2 dose

~90K patients across tumor types; ~65K

among top tumors CCNE1 amplification or inactivating mutations in FBXW7 and PPP2R1A Genetic alterations largely mutually exclusive Addressing unmet need in critical patient populations Top Tumors (New Advanced Cases, US+UK/EU4) Top Tumors (New

Advanced Cases, US+UK/EU4) Tumor Type Prevalence of Genes of Interest Eligible Patients Uterine 7,000 Ovarian 6,300 Stomach 9,000 Colorectal 24,500 Bladder 6,200 Cervical 1,300 Esophageal 4,500 Sarcoma1 1,200 Lung Squamous2 5,300 * Based on

estimated number of pts treated in 1st line, advanced setting for diagnosed and new recurrent patients (CancerMPact , Treatment Architecture, United States, 2021; accessed 5/19/23) and lesion prevalence (TCGA). 1 Soft Tissue Sarcoma only; 2

Squamous subtype of Non-Small Cell Lung Cancer only CCNE1 FBXW7 PPP2R1A Multiple

Lunresertib Preliminary Monotherapy

& Combination Therapy Clinical Trial Results Timothy Yap, MBBS, PhD, FRCP, Principal Investigator, MYTHIC Trial

Study principal investigator: Timothy

Yap, MBBS, PhD, FRCP Medical Oncologist and Physician-Scientist at the University of Texas, MD Anderson Cancer Center Professor, Department for Investigational Cancer Therapeutics (Phase 1 Program) Vice President, Head of Clinical

Development in the Therapeutics Division Primary research focuses on the first-in-human and combinatorial development of molecularly targeted agents and immunotherapies, and their acceleration through clinical studies using novel predictive and

pharmacodynamic biomarkers Main interests include the targeting of the DNA damage response with novel therapeutics, such as ATR and PARP inhibitors, as well as the development of novel immuno-therapeutics BSc degree in Immunology and Infectious

Diseases and MD from Imperial College London, UK

Speaker disclosures: Timothy Yap,

MBBS, PhD, FRCP I have the following relevant financial relationships to disclose: Employee of: University of Texas MD Anderson Cancer Center, where I am Vice President, Head of Clinical Development in the Therapeutics Discovery Division, which has

a commercial interest in DDR and other inhibitors (IACS30380/ART0380 was licensed to Artios) Consultant for: AbbVie, Acrivon, Adagene, Almac, Aduro, Amphista, Artios, Astex, AstraZeneca, Athena, Atrin, Avenzo, Avoro, Axiom, Baptist Health Systems,

Bayer, Beigene, BioCity Pharma, Blueprint, Boxer, Bristol Myers Squibb, C4 Therapeutics, Calithera, Cancer Research UK, Carrick Therapeutics, Circle Pharma, Clovis, Cybrexa, Daiichi Sankyo, Dark Blue Therapeutics, Diffusion, Duke Street Bio, 858

Therapeutics, EcoR1 Capital, Ellipses Pharma, EMD Serono, Entos, F-Star, Genesis Therapeutics, Genmab, Glenmark, GLG, Globe Life Sciences, GSK, Guidepoint, Ideaya Biosciences, Idience, Ignyta, I-Mab, ImmuneSensor, Impact Therapeutics, Institut

Gustave Roussy, Intellisphere, Jansen, Kyn, MEI pharma, Mereo, Merck, Merit, Monte Rosa Therapeutics, Natera, Nested Therapeutics, Nexys, Nimbus, Novocure, Odyssey, OHSU, OncoSec, Ono Pharma, Onxeo, PanAngium Therapeutics, Pegascy, PER, Pfizer,

Piper-Sandler, Pliant Therapeutics, Prolynx, Radiopharma Theranostics, Repare, resTORbio, Roche, Ryvu Therapeutics, SAKK, Sanofi, Schrodinger, Servier, Synnovation, Synthis Therapeutics, Tango, TCG Crossover, TD2, Terremoto Biosciences, Tessellate

Bio, Theragnostics, Terns Pharmaceuticals, Tolremo, Tome, Thryv Therapeutics, Trevarx Biomedical, Varian, Veeva, Versant, Vibliome, Voronoi Inc, Xinthera, Zai Labs and ZielBio Grant/Research support from: Acrivon, Artios, AstraZeneca, Bayer,

Beigene, BioNTech, Blueprint, BMS, Boundless Bio, Clovis, Constellation, Cyteir, Eli Lilly, EMD Serono, Forbius, F-Star, GlaxoSmithKline, Genentech, Haihe, Ideaya ImmuneSensor, Insilico Medicine, Ionis, Ipsen, Jounce, Karyopharm, KSQ, Kyowa, Merck,

Mirati, Novartis, Pfizer, Ribon Therapeutics, Regeneron, Repare, Rubius, Sanofi, Scholar Rock, Seattle Genetics, Tango, Tesaro, Vivace and Zenith Stockholder in: Seagen

PKMYT1 was identified as a strong

synthetic lethal partner to CCNE1 amplification1 1Gallo et al. CCNE1 amplification is synthetic lethal with PKMYT1 kinase inhibition. Nature. 2022; 604 (7907): 749-756. SNIPRx SL hits are LoF mutations that are essential for fitness in

CCNE1-O/E cells but not their wild type counterparts. STEP2 (SNIPRx Targeted Expansion of Patient Populations ) hits are LOF mutations that are essential for fitness in lunresertib treated cells but not the vehicle treated

controls. PKMYT1, protein kinase, membrane associated tyrosine/threonine 1; SNIPRx, SyNthetic Lethal Interactions for Precision Therapeutics platform; PP2A, protein phosphatase 2A. Chemogenomic screen identified novel sensitizers to

PKMYT1i FBXW7 PPP2R1A Inactivating mutations in FBXW7, E3 ubiquitin ligase, increase cyclin E levels and replication stress. Hotspot inactivating mutations in PP2A phosphatase increase replication stress. Cyclin E overexpression (O/E) drives

premature S-phase entry, overloads the DNA replication machinery, resulting in genome instability Synthetic lethal score (CCNE1-O/E cells) Essentiality score (RPE1 WT cells) PPP2R1A FBXW7 PKMYT1i sensitivity score PKMYT1i sensitivity score

Genome-wide CRISPR-Cas9 screen

Lunresertib: Potent and selective

first-in-class PKMYT1 inhibitor Potency Enzyme potency (IC50, nM) 3 HCC1569 CDK1 T14 phosphorylation (IC50, nM) 20 HCC1569 cell viability (EC50, nM) 19 PKMYT1 selectivity over WEE1 (cell-based ) >100-fold ADME Properties CYP inh (3A4, 2D6,

2C9, 1A2, 2C19) all >30 M Hepatocytes: rat, dog, human Clint ( L/min/106cells) 28, <6, <6 Human plasma protein binding 79% Rat PK (%F, t1/2) 44%, 2.6h Dog PK (%F, t1/2) 74%, 5.5h

Lunresertib profile: Highly potent and selective inhibitor PanLabs Lead Profiling screen on 68 assays showed no significant activity at 10 M No activity (>100 M) in patch clamp assays for hERG, hNaV1.5, and hCaV1.2 ion channels

Favorable pre-clinical PK profile Low potential for clinical drug-drug interactions Parameter Lunresertib ADME, absorption, distribution, metabolism, excretion; CDK, cyclin-dependent kinase; cClint , intrinsic clearance CYP inh, cytochrome P

inhibition; EC50, half maximal effective concentration; F, bioavailability; h, hour; IC50, half-maximal inhibitory concentration; min, minute; PK, pharmacokinetics; PKMYT1, protein kinase, membrane associated tyrosine/threonine 1; Thr, threonine.

Lunresertib monotherapy inhibits

xenograft growth across doses and schedules HCC1569 CCNE1 amplified Breast Cancer CDX model 5-on/2-off, 5 days on / 2 days off; BID, twice daily; Lunre, lunresertib.

PKMYT1 and ATR inhibitors synergize

to enhance anti-tumor activity1 Lunresertib-sensitizing alterations engage ATR through replication stress Combination of ATR and PKMYT1 inhibition enhances CDK1 activation and premature mitosis 1ANE poster B057: Gallo et al. Preclinical development

of PKMYT1 and ATR inhibitor combinations. ATR, ataxia telangiectasia and Rad-3 related; CDC25, cell division cycle-25; CDK, cyclin-dependent kinase; CHK1, checkpoint kinase 1; PKMYT1, protein kinase, membrane associated tyrosine/threonine 1.

Lunresertib and camonsertib

combination treatment is active in CCNE1 amplified or FBXW7 altered tumor models Combination treatment drives tumor regressions at sub-efficacious single-agent doses *Additional internal Repare data, not shown. Free drug exposure of 5-10 mg/kg

dose in mouse (AUC or Cmin) are comparable to that at the respective human RP2Ds. 5-on/2-off, 5 days on / 2 days off; 3-on/4-off, 3 days on / 4 days off; AUC, area under the curve; BID, twice daily; Cam, camonsertib; Lunre, lunresertib;

QD, once daily; RP2D, recommended phase 2 dose. DLD1 Colorectal Cancer FBXW7 Knockout CDX model OVCAR3 Ovarian Cancer CCNE1 amplified CDX model Camonsertib alone has limited activity in CCNE1 and FBXW7 altered PDX models*

MYTHIC: PKMYT1 inHIbition for the

treatment of Cancers (N=126) Module 1: Single agent lunresertib Primary endpoints: Safety and tolerability RP2D, schedule Other endpoints: PK PD in paired tumor biopsies Preliminary antitumor activity Kinetics of ctDNA Module 1 initiated Apr 2021

Data snapshot Sept 5, 2023 Module 2: Lunresertib with camonsertib Module 2 initiated May 2022 Study is ongoing NCT04855656 Patients 12 y with solid tumors resistant/intolerant to standard therapy Local NGS report (tissue or plasma)* Tumors

with CCNE1 amplification**, deleterious FBXW7 or PPP2R1A alterations*** ECOG PS of 0-2 Hgb 9 g/dL Platelets 100 K/uL ANC 1.5 K/uL Inclusion criteria: 67 patients 59 patients * NGS report centrally reviewed and annotated

by Precision Oncology Decision Support (PODS) Group at MDACC. ** CCNE1 amplification (Copy number 6). *** Up to 5 patients with endometrial cancer without these alterations were eligible in Module 1. ANC, absolute neutrophil count;

ctDNA, circulating tumor DNA; ECOG PS, Eastern Cooperative Oncology Group Performance Status; Hgb, hemoglobin; NGS, next generation sequencing; PD, pharmacodynamics; PK, pharmacokinetics; RP2D, recommended phase 2 dose.

MYTHIC: Patient demographics

Parameter (Lun alone) N=67 (Lun + Cam) N= 59 Sex, n (%) Male Female 17 (25.4) 50 (74.6) 15 (25.4) 44 (74.6) Age (years) Median (range) 65 years, n (%) 60 (15, 81) 25 (37.3) 65 (16, 81) 30 (50.8) ECOG PSa, n (%) 0 1/2 21 (31.3) 44 (65.7) /1

(1.5) 23 (39.0) 35 (59.3) / 0 Prior lines of therapy, n (%) 0 1-2 3-4 5 1 (1.5) 21 (31.3) 25 (37.3) 20 (29.9) 0 24 (40.7) 24 (40.7) 11 (18.6) Prior platinum, n (%) 58 (86.6) 51 (86.4) Parameter (Lun alone) N=67 (Lun + Cam) N=59 Tumor types, n

(%) Endometrialb Colorectal Ovarian Breast Lung Otherc 23 (34.3) 11 (16.4) 11 (16.4) 3 (4.5) 0 19 (28.4) 17 (28.8) 13 (22.0) 11 (18.6) 3 (5.1) 3 (5.1) 12 (20.3) Most common genotypesd, n (%) CCNE1 FBXW7 PPP2R1A PPP2R1A and CCNE1 PPP2R1A and FBXW7

FBXW7 and CCNE1 Unselected endometriale 31 (46.3) 21 (31.3) 12 (17.9) 0 1 (1.5) 0 2 (3) 20 (33.9) 23 (39.0) 13 (22.0) 1 (1.7) 1 (1.7) 1 (1.7) 0 Similar patient characteristics in monotherapy and combination therapy cohorts aOne each, pediatric

patient in monotherapy and combination with Lansky Performance Status score 80 and 90, respectively. bIncludes uterine serous carcinoma, carcinosarcoma, clear cell carcinoma, endometrioid cOther tumor types in monotherapy: esophageal

(n=2), head and neck (n=3), leiomyosarcoma (n=2), osteosarcoma (n=3) and one each (bladder, brain, cervical, gallbladder, GI, gastroesophageal junction, kidney, melanoma, vulvar); combination therapy: gastroesophageal (n=2), bile duct (n=2),

pancreatic (n=2), one each (cervical, liver, melanoma, osteosarcoma, upper GI, and vulvar). d4 patients in lun + cam cohort also had ATRi-sensitizing alterations: 2 biallelic and 2 of unknown allelic status. eEndometrial patients without CCNE1,

FBXW7, or PPP2R1A mutation. Cam, camonsertib; ECOG PS, Eastern Cooperative Oncology Group Performance Status; GI, gastrointestinal; Lun, lunresertib.

Multiple doses/schedules of

lunresertib tested Adaptive BOIN design, sufficient cohort sizes to establish MTD/RP2D QD dose tested first, once half-life known, BID dose was then tested Continuous and intermittent schedules showed similar activity in preclinical efficacy models

DLT: reversible rash Intermittent weekly schedule minimized rash** Exposure with and without food was similar at preliminary RP2D 5mg to 600mg QD Continuous daily N=34 60mg & 80mg BID Continuous daily N=20 60mg to 140mg BID Intermittent weekly*

N=13 80mg to 100mg BID Intermittent weekly* N=8 Preliminary RP2D range * 5 days on/2 days off and 3 days on / 4 days off were evaluated. ** Investigation of the mechanism of rash ongoing BID, twice daily; BOIN, bayesian optimal interval; DLT,

dose-limiting toxicity; MTD, maximum tolerated dose; QD, once daily; RP2D, recommended phase 2 dose

TRAEs in 15% of patients, n

(%) All Grades G3 G4 All Grades G3 G4 Rash* 23 (34.3) 5 (7.5) 0 4 (50.0) 0 0 Nausea/Vomiting 21 (31.3) 1 (1.5) 0 2 (25.0) 0 0 Anemia 15 (22.4) 4 (6.0) 0 1 (12.5) 0 0 Fatigue 15 (22.4) 1 (1.5) 0 3 (37.5) 0 0 Lunresertib monotherapy: Treatment

related adverse events (TRAEs) Safety profile encouraging Infrequent Grade 3 and no reported Grade 4 TRAEs across all doses evaluated Preliminary RP2D range (80-100mg BID, intermittent) demonstrates encouraging tolerability profile Favorable

tolerability, with manageable AEs Dose reductions limited to 14.9% of patients Rash* improves, as early as 48 hours, with supportive care or lunresertib interruption * Rash terms included: dermatitis contact, eczema, erythema, flushing,

pruritis, rash, rash erythematous, rash maculopapular, rash pruritic, skin exfoliation. BID-I, twice daily, intermittent; G, grade; RP2D, recommended phase 2 dose. All Patients N=67 Limited and reversible low-grade toxicity in

monotherapy is encouraging for combination therapies Preliminary RP2D 80-100mg BID-I N=8

Target PK exposures achieved with