Insight that enriches. Precision that empowers. Corporate Presentation October 2023 Exhibit 99.2

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 referred to without the ® and ™ symbols, but such references should not be construed as any indicator that their respective owners will not assert their rights thereto.

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

Targeting the un-targetable through synthetic lethality Current Treatment Paradigm Genetic Alterations in Cancer Next Generation Therapeutics Specifically targeting and disrupting genes essential for cancer cell survival SNIPRx identifies and targets necessary genes to induce synthetic lethality Highly targeted & tumor-type agnostic approach Exploiting cancer cell genomic instability, including DNA damage repair Platform validated with established and expanding clinical-stage pipeline Targetable Gain-of-function ~29% Un-targetable Loss-of-function ~54% Un-targetable Gain-of-function ~17%

Enabling target identification & patient insights through SNIPRx® Predicted non-responders DRUG TARGET Small molecule inhibitor (clinical candidate) POTENTIAL SL DRUG TARGETS Viable VALIDATION NORMAL CELL CANCER-ASSOCIATED GENETIC LESION Predicted responders DRUG TARGET Viable Lethal SL genetic lesion STEP2 genetic alterations Lethal Select tumor lesion of interest Execute SNIPRx® CRISPR-Cas9 enabled screen campaign in isogenic cell lines Prioritize, select and validate druggable targets Develop potent and selective inhibitors Perform SNIPRx® Targeted Expansion of Patient Populations (STEP2) screens Conduct clinical trials in an enriched patient population

Expanding pipeline of precision oncology therapeutics PROGRAM TUMOR LESION DRUG TARGET PRECLINICAL PHASE 1 PHASE 2 PHASE 3 RIGHTS Camonsertib (RP-3500/ RG6526) ATM + 16 STEP2 lesions ATR Lunresertib (RP-6306) CCNE1, FBXW7 + others PKMYT1 RP-1664 Undisclosed Undisclosed RP-3467 Polθ Inhibitor BRCA1/2 + others Polθ SNIPRx® Platform Additional SL targets in advanced stages of development Discovery and validation of new SL precision oncology targets Ph2 TAPISTRY Ph1b/2 Morpheus-Lung Ph1/2 TRESR: Mono + PARP (talazoparib) Combo Ph1/2 ATTACC: PARP (olaparib/niraparib) Combo Ph1/2 TRESR: Gemcitabine Combo Ph2 CCTG ISTs Ph1 MYTHIC: Mono + Camonsertib Combo Ph1 MAGNETIC: Gemcitabine Combo Ph1 MINOTAUR: FOLFIRI Combo Ph1 Carboplatin/paclitaxel Combo IST

Driving shareholder value through strategic collaborations Global development and commercialization collaboration for Camonsertib Multi-target discovery collaboration leveraging SNIPRx® discovery platform $135M upfront ~$1.2B potential milestones High single-digit to high-teens royalties 50/50 U.S. co-development, profit/cost share and co-promotion option $65M upfront ~$3B potential milestones Royalties Both SL targets and “undruggable” targets outside our focus

Proven experience in drug discovery and development Leadership Team Scientific Founders Steve Forte, CPA Chief Financial Officer Michael Zinda, PhD Chief Scientific Officer Maria Koehler MD, PhD Chief Medical Officer Cameron Black, PhD Head of Discovery Philip Herman Chief Commercial, Portfolio Development Officer Daniel Bélanger Head of Human Resources Lloyd M. Segal President & CEO Kim A. Seth, PhD Chief Business Officer Daniel Durocher, PhD Developed CRISPR SL platform Deep DNA repair knowledge Lunenfeld-Tanenbaum Research Institute (LTRI) & professor at University of Toronto Agnel Sfeir, PhD DDR and cancer pathway investigator Pioneer in Polθ, genome instability Professor, MSKCC Frank Sicheri, PhD Globally recognized structural biologist, expert in eukaryotic cell signaling, drug mechanism of action LTRI & professor at University of Toronto

Lunresertib (RP-6306)

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

Lunresertib: The only clinical-stage therapeutic targeting PKMYT1 Protein Kinase within the Wee1 kinase family Regulates cell cycle and is part of DNA damage repair-related signaling Inactivates CDK1 via phosphorylation of threonine14 (T14) holding the cell in S phase until ready to undergo mitosis CCNE1 amp or deleterious mutations in FBXW7 and PPP2R1A result in an extended S phase and reliance on PKMYT1 activity Inhibiting PKMYT1 in these genomic backgrounds may result in cell death via mitotic catastrophe STEP2 screen identified additional genes (FBXW7 and PPP2R1A) Initially identified CCNE1 amplification sensitive to PKMYT1 inhibition

~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

Evolving broad trial program: sponsored and collaborative PPP2R1A FBXW7 Recurrent solid tumors Key inclusion criteria: CCNE1 amplification or inactivating mutations Determine RP2D dose / schedule Progress to late-stage trials MAGNETIC: + Gemcitabine MYTHIC: + Camonsertib MINOTAUR: + FOLFIRI IST: + CCTG1 IST: + Carbo/paclitaxel2 Lunresertib Combination Therapy Selected tumors with FBXW7 loss Tumors with high rate of sensitivity genes Basket trial 1 Canadian Clinical Trial Group (CCTG) collaborations include NCT05605509 and NCT05601440. 2 SOC for 1st line ovarian cancer is carbo/paclitaxel (6 cycles) + PARPi maintenance therapy or carbo/paclitaxel with bevacizumab + bev maintenance therapy; this IST supports future potential 1st line combination studies as triplet therapy in patients with CCNE1 amplified tumors. Selected tumors with amplified CCNE1 Ovarian, Lung, Esophageal / Gastric Future Opportunities CRC, Other GI, Pan Tumor Endometrial, Bladder Breast, Sarcoma, Bile Duct 4 collaboration trials in advanced discussion

Lunresertib: MYTHIC Preliminary Phase 1 Trial Results (M1: Monotherapy) (M2: Camonsertib Combination Therapy) MONOTHERAPY Safe, well tolerated, and anti-tumor activity established (N=67) Recommended Phase 2 dose: 80 to 100mg twice daily in intermittent schedule CAMONSERTIB COMBINATION THERAPY Safe, well tolerated, and promising anti-tumor activity across tumors and lunresertib-sensitizing genomic alterations (N=59) 23.6% OR; 41.8% CBR in efficacy-evaluable patients (N=55)  33.3% OR; 50.0% CBR at preliminary RP2D range, across all tumors (N=18) 38.5% OR; 57.7% CBR in patients with heavily pre-treated gynecologic cancers (N=26); 50% RECIST response at preliminary RP2D (N=10) Preliminary recommended Phase 2 dose: Lunresertib 80mg twice daily and camonsertib 80mg once daily, dose/schedule optimization ongoing OR, overall response; CBR, clinical benefit rate; RP2D, recommended phase 2 dose.

Anti-tumor activity with lunresertib monotherapy FBXW7 PPP2R1A Baseline Left external iliac chain LN TA #1 – Week 6 Overall response: cPR (RECIST) RECIST target lesion decrease -41% Received therapy for 8.3 months Female 73 years old Metastatic recurrent uterine carcinosarcoma & One RECIST responder Mutations Further, 7 patients with <30% tumor shrinkage, and 2 patients with PFS > 6 and 14 months, respectively Lunresertib: 80mg BID-I Right paratracheal LN BID-I, twice daily, intermittent; cPR, confirmed partial response; LN, lymph node; RECIST, Response Evaluation Criteria in Solid Tumors; PFS, progression free survival; RP2D, recommended phase 2 dose; TA, tumor assessment. 3 prior lines of therapy

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.

Responses to combination observed across tumor types and lunresertib-sensitizing alterations * One response evaluable patient became uPR and four patients had responses confirmed after the Sept. 5, 2023 cutoff, data as of Oct. 6, 2023. Relevant patient tumor co-mutations †BRCA1 rearrangement and ‡BRCA2 biallelic loss. +Treatment ongoing. BL, baseline; cPR, confirmed partial response; RECIST, Response Evaluation Criteria in Solid Tumors; TL, target lesion; Tx, treatment; uPR, unconfirmed partial response. RECIST and tumor marker responses occurred early despite heavily pre-treated, relapsed/refractory patient population Tumor type Genotype Response Best % change in TL from BL Therapy (weeks) Lines of prior Tx/ prior platinum Endometrial PPP2R1A/FBXW7 cPR -55.9 30.4 3/Y PPP2R1A/CCNE1 cPR -53.0 18.1 2/Y FBXW7 cPR* -100.0 11.1+ 3/Y FBXW7 uPR -39.6 16.0 3/Y FBXW7 uPR* -44.7 11.4+ 3/Y Ovarian CCNE1 cPR* -70.2 21.4+ 2/Y CCNE1† cPR* -30.8 12.6+ 3/Y CCNE1 CA-125 -16.9 29.0+ 9/Y CCNE1 CA-125 -23.1 37.0+ 2/Y CCNE1 CA-125 13.6 12.9+ 5/Y Cervical PPP2R1A cPR* -44.4 11.0+ 1/Y Colorectal FBXW7 cPR -43.3 27.6 3/Y Bile duct CCNE1 cPR -35.0 28.1 2/Y Breast  FBXW7‡ uPR -43.8 18.1 2/N

*Efficacy evaluable patients only (≥1 post-baseline tumor assessment). Other tumor types include cervical (n=1), esophageal (n=1), GI (n=1), liver (n=1), lung (n=3), melanoma (n=1), osteosarcoma (n=1), pancreatic (n=2), and upper GI (n=1). CBR: overall response or time on treatment ≥ 16 wk w/o progression; CRC, colorectal cancer; RECIST, Response Evaluation Criteria in Solid Tumors (RECIST) Gynecologic Cancer InterGroup (GCIG); MRR, molecular response rate; OR, overall response based on RECIST or GCIG CA-125 response; RP2D, recommended phase 2 dose. Frequent and deep tumor reductions with lunre + cam combination across multiple tumor types In evaluable patients*, across all tumors/doses: OR: 23.6% (n=55)    CBR: 41.8% (n=55) MRR: 50.0% (n=24) At preliminary RP2D, across all tumors: OR: 33.3% (n=18)   CBR: 50.0% (n=18) CA-125 response Treatment ongoing + Tumor type: Ovarian Endometrial CRC Bile Duct Breast Other Best change from baseline in tumor size (%) 100 −80 80 60 40 20 0 −20 −40 −60 −100

Most patients with gynecologic cancers had tumor reductions with combination treatment * Gynecologic cancers: ovarian, endometrial, and cervical cancers. Data represent the efficacy evaluable population (≥1 post-baseline tumor assessment). CBR, clinical benefit rate; OR, overall response based on RECIST or GCIG CA-125 response; MRR, molecular response rate; PR, partial response; RECIST, Response Evaluation Criteria in Solid Tumors ; Gynecological Cancer InterGroup (GCIG); RP2D, recommended phase 2 dose. Across all doses (n=26): Overall response: 38.5%; RECIST Response: 26.9% CBR: 57.7%; MRR: 8/10 (80%) At preliminary RP2D (n=10): Overall response: 60%; RECIST Response: 50% CBR: 70% Patients had 1-9 prior therapies (median=3); treatment ongoing in 11 patients; enrollment in expansion cohorts at RP2D continues Meaningful tumor reductions and durable clinical benefit observed in heavily pre-treated patients PR Tumor marker response Treatment ongoing Gynecologic cancers* Efficacy evaluable patients Weeks of treatment 0 4 8 12 16 20 24 28 32 36 40 Best change from baseline in tumor size (%) CA-125 response Treatment ongoing + 60 40 20 0 −20 −40 −60 −80 −100 At preliminary RP2D

Early response in recurrent FBXW7 mutated colorectal adenocarcinoma FBXW7 Male 63 years old Recurrent colorectal adenocarcinoma Mutation Lunre 240mg QD 3/4 Cam 80mg QD 3/4 Overall response: cPR (RECIST) RECIST target lesion decrease -43.3% Received therapy for 27.6 weeks Left para-aortic lymph node Baseline TA - 6 weeks TA - 12 weeks Pre-treatment On-treatment ctDNA Dynamics pCDK1-Thr14 ƔH2AX Gene alteration: ALK p.L1118F APC p.A1485fs APC p.E984* FANCA p.L1167F FBXW7 p.R505C H3F3A p.HA114HG TP53 p.R213* Allele frequency Time on treatment (days) 3/4, 3 days on/4 days off; cPR, confirmed partial response; ctDNA, circulating tumor DNA; RECIST, Response Evaluation Criteria in Solid Tumors; QD, once daily; RP2D, recommended phase 2 dose; TA, tumor assessment; Thr, threonine. 3 prior lines of therapy TP53 mut

Gradual response heralded by CA-125 decrease; recurrent CCNE1 amplified ovarian cancer Overall response: cPR (RECIST) RECIST target lesion decrease -70.2% Therapy ongoing  for >21 weeks Female 56 years old High grade serous ovarian carcinoma Amplification RP2D: Lunre 80mg BID 3/4 Cam 80mg QD 3/4 CCNE1 Baseline 6 wks 12 wks T01 Peritoneum T02 Peritoneum Pelvis 18 wks Tumor assessment Size Size Size Images not available in RECIST report Images not available in RECIST report No visible lesion reported  No visible lesion reported  ctDNA dynamics Allele frequency Time on treatment (days) ARID1B p.Q122_Q128dup CIC p.N1133fs RET p.EV62DL TP53 p.R280* Gene alteration: CA-125 dynamics 3/4, 3 days on/4 days off; cPR, confirmed partial response; ctDNA, circulating tumor DNA; RECIST, Response Evaluation Criteria in Solid Tumors; QD, once daily; RP2D, recommended phase 2 dose. 2 prior lines of therapy TP53 mut

Prompt response in recurrent cervical carcinosarcoma with a PPP2R1A mutation Female 66 years old Recurrent cervical carcinosarcoma Mutation RP2D: Lunre 80mg BID 3/4 Cam 80mg QD 3/4 T01 Lymph node external iliac left PPP2R1A Baseline 6 weeks 12 weeks Tumor assessment CA-125 dynamics Overall response: cPR (RECIST) RECIST target lesion decrease -44.4% Therapy ongoing at 11 weeks 3/4, 3 days on/4 days off; BID, twice daily; CN, copy number; cPR, confirmed partial response; RECIST, Response Evaluation Criteria in Solid Tumors; QD, once daily; RP2D, recommended phase 2 dose; TA, tumor assessment. 1 prior line of therapy MYC amp TP53 mut

Camonsertib (RP-3500 / RG6526)

Camonsertib: Potential best-in-class ATR inhibitor Expanded potential with combination therapy Proof of concept established in Phase 1/2 monotherapy trial Durable antitumor activity in combination with PARP inhibitors and gemcitabine; meaningful clinical benefit in ovarian cancer Demonstrated synthetic lethal interaction of ATR and a network of genes identified by SNIPRx and STEP2 process Global development and commercialization collaboration with Roche; Initially advancing TAPISTRY Phase 2 and Morpheus Lung Phase 1b/2 trials

Potential across additional patient populations Top 10 Tumor Types* with Highest Prevalence of ATM Deficiency Top 10 Tumor Types* with Highest Prevalence of ATM Deficiency or STEP2 Genomic Alterations Source: *TCGA; Not weighted for tumor prevalence

Expanding clinical development through Roche collaboration Note: Camonsertib monotherapy TRESR Module 2 expansion phase to be integrated into partnered clinical development plans under Roche IND Repare Trials Roche Collaboration TRESR Phase 1/2 Monotherapy (M1) + Talazoparib (M3) + Gemcitabine (M4) ATTACC Phase 1/2  + Olaparib / Niraparib TAPISTRY Phase 2 (Initiation expected 2H 2023) Morpheus Lung Phase 1b/2 Robust clinical program potential

Camonsertib: TRESR & ATTACC Phase 1/2 Trial Results MONOTHERAPY Favorable safety profile (N=120) Proof-of-concept established in ovarian cancer 25% OR; 75% CBR; 8+ months PFS Clinical benefit in patients with BRCA1/2 mutations COMBINATION THERAPY Clinically meaningful anti-tumor activity in combination with all leading PARP inhibitors Confirmed efficacy in platinum- and PARPi-resistant cancers 48% overall CBR (N=90) 32% OR; 58% CBR; ~7 months PFS in advanced ovarian cancer (N=19) OR, overall response; CBR, clinical benefit rate; PFS, progression free survival

Anti-tumor activity in ovarian cancer with monotherapy *Platinum refractory/resistant: progression on platinum or a platinum-free interval of <6 mo. CBR: OR or ≥16w on therapy without progression 25% Overall response (5/20*) 35w Median PFS 75% Clinical benefit rate (CBR) 90% (18/20) patients had prior PARPi 85% (17/20) patients platinum refractory/ resistant* Time on Treatment (wk) – Ovarian Time to Disease Progression or Death – Ovarian

Time on Treatment (wk) – BRCA1/BRCA2 Module 1 subjects with > 100mg/day dose levels Percent change from baseline in target lesions (BRCA1/BRCA2) Module 1 subjects > 100mg/day dose levels Clinically relevant benefit in patients with BRCA1/2 mutations with monotherapy CBR (OR or ≥16w on therapy without progression) was 48% for BRCA1 population, and 36% for BRCA2 14% Overall response in BRCA1/2 (RECIST, 5/37) 43% CBR for BRCA1/2 tumors 48% CBR for post-PARPi BRCA1/2 tumors

Durable clinical benefit observed with combination therapy Similar benefit observed in patients with platinum-resistant tumors (ORR 12%, CBR 49%) and non-platinum-resistant tumors (ORR 13%, CBR 46%) Benefit observed across multiple tumors, regardless of previous PARPi treatment 48% overall CBR (N=90) Included patients from efficacy analysis set. ORR is based on overall response as best response of confirmed or unconfirmed CR or PR per RECIST v1.1 criteria or confirmed CA-125 response per Gynecological Cancer Intergroup; CBR is based on overall response or ≥16 weeks on treatment without progression; MRR is based on ctDNA molecular response as >50% decline in mVAF assessed by GuardantINFINITY or Tempus xF gene panel for patients with detectable somatic alterations. CBR, clinical benefit rate; CR, complete response; PR, partial response; ORR, overall response rate; RECIST, Response Evaluation Criteria in Solid Tumors.

Upcoming milestones 2H 2024 2H 2023 1H 2024 Camonsertib Phase 2 TAPISTRY trial initiation Lunresertib + carboplatin/paclitaxel combination Phase 1 IST initiation RP-1664 and RP-3467 (Polθi) focused investor event RP-1664 clinical trial initiation Initial lunresertib + FOLFIRI combination Phase 1 data RP-3467 (Polθi) clinical trial initiation Lunresertib + gemcitabine combination Phase 1 data Lunresertib + camonsertib combination Phase 1 data (expansion cohorts)

Developing Next-Generation Precision Oncology Therapeutics 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

Insight that enriches. Precision that empowers. Corporate Presentation October 2023