We caution you that this presentation contains forward-looking statements. All statements other than statements of historical facts contained in this presentation, including statements regarding our future results of ope

On a Journey to Erase Cancer Erasca

Corporate Presentation January 2023 Exhibit 99.1

We caution you that this presentation

contains forward-looking statements. All statements other than statements of historical facts contained in this presentation, including statements regarding our future results of operations and financial position, business strategy, research and

development plans, the anticipated timing, costs, design and conduct of our ongoing and planned preclinical studies and clinical trials for our product candidates, the potential benefits from our current or future arrangements with third parties,

the timing and likelihood of success of our plans and objectives, and future results of anticipated product development efforts, are forward-looking statements. In some cases, you can identify forward-looking statements by terms such as

"may," "will," "should," "expect," "plan," "anticipate," "could," "intend," "target," "project," "contemplates,"

"believes," "estimates," "predicts," "potential" or "continue" or the negative of these terms or other similar expressions. The inclusion of forward-looking statements should not be

regarded as a representation by us that any of our plans will be achieved. Actual results may differ from those set forth in this presentation due to the risks and uncertainties inherent in our business, including, without limitation: our approach

to the discovery and development of product candidates based on our singular focus on shutting down the RAS/MAPK pathway, a novel and unproven approach; we are early in our development efforts and have only five product candidates in clinical

development and all of our other development efforts are in the preclinical or development stage; the retrospective analysis of pooled clinical data for ERAS-007 and ERAS-601 covers multiple clinical trials with different designs, inclusion

criteria, and dosing regimens, which cannot be directly compared, and therefore may not be a reliable indicator of efficacy and safety data; interim results of clinical trials are not necessarily indicative of final results and one or more of the

clinical outcomes may materially change as patient enrollment continues, following more comprehensive reviews of the data and more patient data become available; potential delays in the commencement, enrollment, and completion of clinical trials and

preclinical studies; our dependence on third parties in connection with manufacturing, research, and preclinical and clinical testing; unexpected adverse side effects or inadequate efficacy of our product candidates that may limit their development,

regulatory approval, and/or commercialization, or may result in recalls or product liability claims; unfavorable results from preclinical studies or clinical trials; results from preclinical studies or early clinical trials not necessarily being

predictive of future results; the inability to realize any benefits from our current licenses and acquisitions and any future licenses, acquisitions, or collaborations, and our ability to fulfill our obligations under such arrangements; regulatory

developments in the United States and foreign countries; our ability to obtain and maintain intellectual property protection for our product candidates; our ability to fund our operating plans with our current cash, cash equivalents, and

investments; our ability to maintain undisrupted business operations due to the COVID-19 pandemic, including delaying or disrupting our clinical trials, manufacturing, and supply chain; unstable market and economic conditions having serious

adverse consequences on our business, financial condition and stock price; and other risks described in our prior filings with the Securities and Exchange Commission (SEC), including under the heading "Risk Factors" in our annual

report on Form 10-K for the year ended December 31, 2021, and any subsequent filings with the SEC. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof, and we undertake no

obligation to update such statements to reflect events that occur or circumstances that exist after the date hereof. All forward-looking statements are qualified in their entirety by this cautionary statement, which is made under the safe harbor

provisions of the Private Securities Litigation Reform Act of 1995. 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 you are cautioned not to give undue weight to such estimates. 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. These and other factors could cause results to differ materially from those expressed in the estimates made by the independent parties and by us. Disclaimer: Forward

Looking Statements & Market Data

Our name is our mission: to erase

cancer CNS = central nervous system 1 Number of patients alive and free of cancer or free from cancer progression 2-yrs after starting an Erasca regimen, as measured by disease-free survival (adjuvant setting) and progression-free survival

(metastatic setting) 2 Unaudited, as of September 30, 2022 Vision to one day erase cancer1 in at least 100,000 patients annually as a leading global oncology company Experienced leadership team and SAB with track record of serial successes Founded

by Jonathan Lim, MD & Kevan Shokat, PhD around disruptive idea to target RAS World class scientific advisory board of leading pioneers in RAS/MAPK pathway Team with deep experience in efficient planning and execution of global clinical trials

Industry leading portfolio focused on shutting down the RAS/MAPK pathway Naporafenib pan-RAFi with first-in-class potential for NRASm & other MAPK tumors ERAS-007 ERKi & ERAS-601 SHP2i with best-in-class potential for MAPK tumors ERAS-801,

CNS-penetrant EGFRi with first-in-class potential for EGFR-driven rGBM ERAS-3490, CNS-penetrant KRAS G12Ci with best-in-class potential in NSCLC Strong financial position with high quality investor base and industry visibility ~$365M in cash, cash

equivalents, and short-term marketable securities2; plus $100M equity financing announced on 12/9/2022 One of Fierce Biotech's 2021 "Fierce 15" most promising biotechnology companies

SAB includes world's leading

experts in the RAS/MAPK pathway Erasca co-founder. World expert in RAS who pioneered development of approaches to inhibit KRAS G12C (RAS-GDP) and active states of RAS (RAS-GTP) World expert in ERK, having studied nearly every ERK inhibitor that has

been or is being developed, as well as targeted therapies directed against KRAS, BRAF, and MEK mutations World expert in targeted oncology therapies who pioneered the development of Gleevec , which helped launched the precision oncology

revolution World expert in structure-based drug design; former head of research at Agouron and former head of Genentech's Research and Early Development (gRED) World expert in RAS/MAPK pathway signaling and identifying novel combination

therapies to shut it down Karen Cichowski, PhD George Demetri, MD Michael Varney, PhD Stephen Blacklow MD, PhD World expert in SHP2 who helped pioneer development of the first SHP2 inhibitor with Novartis Ryan Corcoran, MD, PhD World expert in

RAS/MAPK pathway with focus on the SHOC2 phosphatase complex as a unique regulatory node required for efficient pathway activation in the context of diseases such as cancer and RASopathies Pablo Rodriguez-Viciana, PhD Kevan Shokat, PhD

* Post-Osimertinib resistant population

shown for EGFRm NSCLC except for SCLC transformation ** Co-occurring activating MAPK pathway alterations exclude EGFR overexpression Source: SEER database (2020), ECIS database (2020), GLOBOCAN database (2020), The AACR Project GENIE Consortium

version 8.1 (2020), TCGA Research Network: https://www.cancer.gov/tcga, Tyner JW et al. (2018) PMID: 30333627, Brenner CW et al (2013) PMID: 24120142, Chen J et al. (2020) PMID: 32015526, and Ostrom QT, et al. (2020) PMID: 33123732 New cases

estimated worldwide per annum (thousands; numbers may not add up due to rounding) Blue ocean opportunities Red ocean opportunities Alterations GBM HNSCC NSCLC CRC Melanoma PDAC Other solid tumors AML US EU ROW Global EGFR*/FLT3 125 513 184 338 - - -

61 82 222 917 1,220 NF1 25 58 98 34 33 1.9 434 3.2 75 159 453 687 KRAS G12C - 2.8 240 57 - 5.1 45 0.1 36 82 232 350 KRAS G12D 0.2 4.7 68 238 0.5 178 201 1.3 65 171 456 692 RAS Q61X 0.4 23 35 80 69 32 155 4.1 51 106 242 399 RAS G13R - 9.4 5.9 5.5 2.1

- 14 0.5 3.6 8.1 26 37 Other RAS 0.6 31 162 452 4.4 211 331 13 112 291 800 1,203 BRAF V600E/K 2.0 1.9 23 180 93 1.4 158 0.4 63 127 271 461 BRAF Class 2 0.4 3.8 18 6.9 5.3 0.5 57 - 11 23 58 92 BRAF Class 3 0.1 0.9 12 17 2.5 - 29 0.2 6.1 15 40 61

Other BRAF - - 3.9 - 1.9 0.3 0.5 - 0.7 1.0 4.9 6.6 MEK 0.2 1.9 12 8.8 4.6 0.2 22 - 5.2 11 33 50 Co-occurring activating MAPK pathway alterations** 1.4 10 62 59 37 7.1 84 3.0 33 69 162 264 US 12 29 93 114 77 51 153 11 542 EU 34 76 194 398 116 124 324

18 1,285 Rest of World 109 555 635 964 60 264 1,053 57 3,696 Global 155 660 923 1,476 253 438 1,530 86 5,522 ~5.5m lives at stake annually worldwide with RAS/MAPK pathway alterations; 70+% of unmet needs are "blue oceans" with no

approved targeted therapies

Our singular focus is on the RAS/MAPK

pathway P P P Autophagy MAPK pathway ULK PI3K pathway RAS-GTP GRB2 SHP2 GAP GDP GTP P1 NF1 SOS1 RAF MEK PI3K AKT mTOR ERK RAS-GDP EGFR/ FLT3 Other RTKs MYC GEF Nodes targeted by Erasca Target upstream and downstream RAS/MAPK nodes with single agents

and clamp oncogenic drivers (MAPKlamp) with combinations 1 1 Target RAS directly with single agents and combinations with upstream, downstream, and escape route targeted therapies 2 2 2 Target escape routes enabled by other proteins or pathways to

further disrupt RAS/MAPK pathway signaling 3 3 Our Strategy Comprehensively shut down the RAS/MAPK pathway

Program/ Company Target Modality

Indication Discovery IND-enabling Phase 1 Phase 2 Phase 3 Erase Cancer Strategy Worldwide Rights Naporafenib BRAF/CRAF Pan-RAS Q61X tissue agnostic NRASm melanoma NF1 LOF, pan-RAS G13R, KRAS G12C, BRAF Class 2/3 solid tumors

ERAS-007* ERK1/2 RAS/MAPK altered tissue agnostic, NSCLC and GI Tumors ERAS-601* SHP2 RAS/MAPK altered tumors ERAS-801 EGFR EGFR altered GBM ERAS-3490 KRAS G12C KRAS G12C solid tumors ERAS-2/3

RAS-GTP RASm solid tumors ERAS-4 KRAS G12D KRAS G12D solid tumors ERAS-5 ULK RASm solid tumors ERAS-9 SOS1 RAS/MAPK altered solid tumors ERAS-10 RAS/MAPK RAS/MAPK altered cancers ERAS-11

MYC MYC & RAS/MAPK altered solid tumors ERAS-12 EGFR D2/D3 EGFR & RAS/MAPK altered solid tumors Affini-T KRAS G12V/D KRASm solid tumors * Together, ERAS-007 and ERAS-601 comprise our first innovative MAPKlamp

Also being evaluated in combo w/ G12Ci in KRAS G12C NSCLC and GI Tumors under Stand Up to Cancer grant large molecule protein degrader small molecule TCR T cell therapy investment SEACRAFT-2 (planned) HERKULES-1 / -2 / -3 SEACRAFT-1 (planned)

THUNDERBBOLT-1 AURORAS-1 FLAGSHP-1 Erasca's deep modality-agnostic RAS/MAPK pathway-focused pipeline SEACRAFT-3 (planned)

Our pipeline targets every node of the

RAS/MAPK pathway Note: MAPKlamp = ERAS-007 in combination with ERAS-601 and/or other agents P P P MAPK pathway ULK PI3K pathway RAS-GTP GRB2 SHP2 GAP GDP GTP P1 NF1 SOS1 RAF MEK PI3K AKT mTOR ERK RAS-GDP EGFR Other RTKS MYC GEF ERAS-9 ERAS-601

naporafenib ERAS-007 ERAS-10 ERAS-5 ERAS-11 ERAS-3490 ERAS-801 ERAS-12 ERAS-2/3/4

Erasca's clinical development

plan generates multiple ways to win for patients Indication Benchmark Regimen tested Erasca trial(s) HERKULES-2 Sub-study 11 EGFRm NSCLC post-osi ERAS-007 + osimertinib ORR 29%, mDOR 4.2 mos. HERKULES-3 Sub-study 13 BRAFm CRC EC-na ve ERAS-007

+ encorafenib + cetuximab ORR 20%, mDOR 6.1 mos. HERKULES-3 Sub-study 13 BRAFm CRC EC-treated ERAS-007 + encorafenib + cetuximab ORR ~2%, mDOR NA HERKULES-3 Sub-study 24 RASm CRC + KRASm PDAC ERAS-007 + palbociclib ORR ~2%, mDOR NA FLAGSHP-15

KRASwt/ NRASwt/ BRAFwt CRC ERAS-601 + cetuximab ORR 20%, mDOR 5.4 mos. THUND- ERBBOLT-1 EGFR altered rGBM ERAS-801 monotherapy ORR 7-8% mDOR 3.9 mos. HERKULES-2 Sub-study 22 KRAS G12C NSCLC ERAS-601 + sotorasib ORR 36%, mDOR 10 mos. ERAS-3490

AURORAS-1 HERKULES-1 RAS/MAPK altered solid tumors ERAS-007 + ERAS-601 (our first MAPKlamp) SOC is largely chemo 100% of CRC FLAGSHP-15 HPV-negative HNSCC ERAS-601 + cetuximab ORR 13%, mDOR 5.8 mos. SEACRAFT-1 RAS Q61X solid tumors naporafenib +

trametinib SOC is largely chemo SEACRAFT-2 NRASm melanoma post-IO naporafenib + trametinib ORR 7%, mDOR 4.1 mos. 1 Completed enrollment; data in H1 2023 2 Closed from further enrollment due to prioritization of other opportunities Focus of

presentation 3 Sep. 2021: Announced CTCSA with Pfizer for encorafenib (Braftovi ) Mar. 2022: Announced CTCSA with Lilly for cetuximab (Erbitux ) Nov. 2022: Announced CTCSA with Pierre Fabre for encorafenib (Braftovi ) 4 Oct.

2022: Announced CTCSA with Pfizer for palbociclib (Ibrance ) 5Jul. 2022: Announced CTCSA with Lilly for cetuximab (Erbitux ) BRAFm CRC EC-na ve BRAFm CRC EC-treated KRASwt/ NRASwt/ BRAFwt CRC EGFR altered rGBM RAS/MAPK altered

solid tumors HPV-negative HNSCC RAS Q61X solid tumors NRASm melanoma post-IO

Erasca's clinical-stage

programs could address unmet needs in up to 1.7 million patients annually in the US and Europe SEACRAFT-3/HERKULES-1: BRAF Class 2/3 * Addressable patient population, US and Europe ('000s; numbers may not add up due to rounding) ERAS-801

Naporafenib Napo + ERAS-007 or ERAS-601, ERAS-007 + ERAS-601, or Napo + ERAS-007 + ERAS-601 Erasca pipeline agents ERAS-007 ERAS-601 483 1,221 Source: * Post-Osimertinib resistant population shown for EGFRm NSCLC except for SCLC transformation

Source: SEER database (2020), ECIS database (2020), The AACR Project GENIE Consortium version 8.1 (2020), TCGA Research Network: https://www.cancer.gov/tcga, Tyner JW et al. (2018) PMID: 30333627, Brenner CW et al (2013) PMID: 24120142, Chen J et

al. (2020) PMID: 32015526, and Ostrom QT, et al. (2020) PMID: 33123732 466 ERAS-3490

P P P Autophagy MAPK pathway ULK

PI3K pathway RAS-GTP GRB2 SHP2 GAP GDP GTP P1 NF1 SOS1 RAF MEK PI3K AKT mTOR RAS-GDP EGFR/ FLT3 Other RTKs MYC GEF Erasca's naporafenib pan-RAFi could address unmet needs in approximately 500k patients in the US and Europe ERK BRAF CRAF

naporafenib Addressable Patient Pop. Tumor Type RAS Q61X Solid Tumors 157,000 NF1 Loss-of-Function 234,000 BRAF Class II/III Solid 55,000 TOTAL 500,000 NRASm Melanoma 54,000 tissue agnostic indication Note: Addressable patient population rounded to

Naporafenib is a potent and

selective inhibitor of BRAF and CRAF with sub-nanomolar IC50 potency and most advanced pan-RAFi in development Source: Monaco K-A, Delach S, et al. LXH254, a Potent and Selective ARAF-Sparing Inhibitor of BRAF and CRAF for the Treatment of

MAPK-Driven Tumors. 2021. PMID: 33355204; Ramurthy S, Taft BR, et al. Design and Discovery of N-(3-(2-(2-Hydroxyethoxy)-6-Morpholinopyridin-4-Yl)-4-Methylphenyl)-2-(trifluoromethyl)isonicotinamide, a Selective, Efficacious, and Well-Tolerated RAF

Inhibitor Targeting RAS Mutant Cancers: The Path to the Clinic. 2020. PMID: 31059256 Assay Value (nM) Biochemical CRAF IC50 (IC50) 0.1 Biochemical BRAF IC50 (IC50) 0.2 Biochemical ARAF Inhibition (IC50) 6.4 Biochemical activity of naporafenib

against RAF kinase family Biochemical activity of naporafenib across 456 kinases (KINOMEscan)

Naporafenib has been dosed in more

than 500 patients to date, establishing its safety, tolerability, and preliminary PoC in multiple indications Source: Novartis Non-Confidential Materials; PoC = proof-of concept P P P MAPK pathway ULK PI3K pathway RAS-GTP GRB2 SHP2 GAP GDP GTP P1

NF1 SOS1 RAF MEK PI3K AKT mTOR ERK RAS-GDP EGFR Other RTKs MYC GEF CDK4/6 Study (Trial #) Description N Ph 1 FIH study (LXH254X2101) Naporafenib dose escalation in patients with RAS/MAPK-driven solid tumors 142 Ph 1b combo dose finding (LXH254X2102)

Dose-finding study (+ rineterkib, trametinib, or ribociclib) in patients with NRASm melanoma, KRASm or BRAFm NSCLC 241 Ph 2 combo study (LXH254C12201) Evaluating efficacy (+ rineterkib, trametinib or ribociclib) in patients with NRASm or BRAF V600X

melanoma 134 Platform study (ADPT01C12101) Exploring triplet combination of naporafenib + dabrafenib + rineterkib in BRAF V600X CRC 7 Total size of safety database > 500 patients (includes monotherapy and combinations) trametinib naporafenib

rineterkib ribociclib

Preliminary clinical PoC in NRAS

Q61X melanoma and KRAS Q61X NSCLC supports development in RAS Q61X tissue agnostic solid tumors (SEACRAFT-1) Strong antitumor activity, with confirmed ORR = 44% 15 out of 16 patients had confirmed codon Q61X melanoma (1 patient had no data) Source:

LXH254X2102 Ph 1b combination data from Novartis Non-Confidential Materials; PoC = proof-of-concept KRASm NSCLC NRASm Melanoma ORR in Q61/G13R mutated group (n=4) = 75% Confirmed/unconfirmed RECIST responses shown

Current standard of care post-IO for

NRASm metastatic melanoma is chemotherapy with 7% ORR and 1.5m PFS 1 NEMO trial (Lancet Oncol (2017) 18: 435-445.); IO = immuno-oncology Front line Second line plus IO mono or combo Ex: nivolumab, pembrolizumab, nivolumab + ipilimumab Post-IO

therapy is predominantly chemo Binimetinib (MEKi) is not approved; recommended by US NCCN but not by EU guidelines Improvement in ORR and DCR of binimetinib vs. dacarbazine translated to improvement in PFS SOC1 ORR DCR PFS OS Dacarbazine 7% 24% 1.5m

10.1m Binimetinib 15% 56% 2.8m 11.0m

Phase 1 in NRASm melanoma:

naporafenib 200mg BID + trametinib 1mg QD showed strong anti-tumor activity De Braud et al AACR 2022 (Trial LXH254X2102, NCT02974725). ^ NEMO trial initially limited to 1 prior therapy later amended to allow more than 1 line. Range not available. *

95% confidence interval. ORR: objective response rate. DCR: disease control rate (ORR + stable disease). ORR 47% (21%-73%)* DCR 80% (n=15) Regimen (n) Median Prior Therapy ^ ORR * DCR Dacarbazine (133) 1 7% (3-13) 25% Binimetinib (269) 1 15% (11-20)

58% Napo 200mg BID + Trame 1mg QD (15) 2 (1-7) 47% (21-73) 80%