NASDAQ: IDYA

IDEAYA BiosciencesImproving LivesThrough Transformative Precision Medicines

November 2020

Certain statements in this presentation and the accompanying oral commentary are forward-looking statements. These statements relate to future events or the future financial performance of IDEAYA Biosciences, Inc. (the “Company”) and involve known and unknown risks, uncertainties and other factors that may cause the actual results, levels of activity, performance or achievements of the Company or its industry to be materially different from those expressed or implied by any forward-looking statements. In some cases, forward-looking statements can be identified by terminology such as “may,” “will,” “could,” “would,” “should,” “expect,” “plan,” “anticipate,” “intend,” “believe,” “estimate,” “predict,” “potential” or other comparable terminology. All statements other than statements of historical fact could be deemed forward-looking, including any expectations regarding the Company’s target discovery platform or new target validation efforts as creating opportunities for research and development initiatives; any projections of financial information, market opportunities, cash runway or profitability; any statements about historical results that may suggest trends for the Company's business; any statements of the plans, strategies, and objectives of management for development programs or future operations; any statements about the timing of preclinical research, clinical development, regulatory filings, manufacturing or release of data; any statements of expectation or belief regarding future events, potential markets or market size, or technology developments; and any statements of assumptions underlying any of the items mentioned. The Company has based these forward-looking statements on its current expectations, assumptions, estimates and projections. While the Company believes these expectations, assumptions, estimates and projections are reasonable, such forward-looking statements are only predictions and involve known and unknown risks and uncertainties, many of which are beyond the Company's control. These and other important factors may cause actual results, performance or achievements to differ materially from those expressed or implied by these forward-looking statements. The forward-looking statements in this presentation are made only as of the date hereof. For a further description of the risks and uncertainties that could cause actual results to differ from those expressed in these forward-looking statements, as well as risks relating to the business of the Company in general, see the Company's periodic filings with the Securities and Exchange Commission (the "SEC"), including its Annual Report on Form 10-K for the year ended December 31, 2019, its Quarterly Report on Form 10-Q for the quarter ended September 30, 2020, and any current and periodic reports filed thereafter. Except as required by law, the Company assumes no obligation and does not intend to update these forward-looking statements or to conform these statements to actual results or to changes in the Company's expectations.

This presentation concerns anticipated products that are under clinical investigation and which have not yet been approved for marketing by the U.S. Food and Drug Administration (FDA). It is currently limited by Federal law to investigational use, and no representation is made as to its safety or effectiveness for the purposes for which it is being investigated.

Safe Harbor Statement

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IDEAYA Biosciences Highlights

• Breakthrough Science on potential first-in-class Synthetic Lethality programs• Broad Pipeline of clinical and preclinical precision medicine oncology programs with

defined patient biomarkers • Proven Management Team with deep business and scientific experience has built leading

private and public oncology biotech companies • Pharma Collaborations and Strategic Partnerships with Pfizer and GlaxoSmithKline,

including ~$3 billion in potential cash milestones• Strong Balance Sheet with Capital Efficient Model anticipated to fund operations into

2024 through multiple clinical catalysts over multiple programs• NASDAQ: IDYA

Leading Synthetic Lethality focused biotechnology company advancing transformative precision medicine therapies for cancer patients

• Synthetic lethality occurs when the simultaneous perturbation of two genes results in cell death

• Synthetic lethal genetic interactions with tumor-specific mutations may be exploited to develop anticancer therapies

• Large-scale screening for cancer-gene-specific synthetic lethal targets in human cells has progressed through advances in RNA interference and CRISPR-Cas9 editing

Synthetic Lethality

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The Next Frontier in Precision Medicine Oncology

Synthetic Lethality provides a powerful approach to discover the next generation of precision medicine therapies for molecularly-defined patient populations, including MTAP-deletion (~15% of all solid tumors), BRCA/HRD, and high-MSI (16% CRC)

Reference: Charles Boone

Nature Reviews Genetics, Vol. 18, 2017, Hieter, et al

Indication Biomarker Preclinical IND Enabling Phase 1 Phase 2 Status Collaboration

IDE397MAT2A

Solid Tumors MTAP Targeting IND December 2020

PARG Solid Tumors Novel Biomarker In vivo Efficacy

Polθ Solid Tumors HRD In vivo Efficacy

WRN Solid Tumors High-MSI Chemistry SAR

DDT Solid Tumors Novel Biomarker Multiple DDT Targets and Biomarkers in Validation

IDEAYA’s Precision Medicine Oncology Pipeline

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Building the Leading Synthetic Lethality Biotech

Precision Medicine Pipeline

(1) Pursuant to GSK Collaboration, Option and License Agreement: MAT2A and WRN: 50/50 US Profits + ex-US Royalties; Polθ: Global Royalties(2) Pursuant to CRUK Evaluation, Option and License Agreement, with ongoing Collaborative Research; IDEAYA controls all Commercial Rights(3) Pursuant to Pfizer Clinical Trial Collaboration and Supply Agreement; IDEAYA retains all IDE196 Commercial Rights

DDT = DNA Damage Target, WRN = Werner Helicase, Polθ = DNA Polymerase Theta, HRD = homologous recombination deficiency, MSI = microsatellite instabilityPKC = protein kinase C, MUM = metastatic uveal melanoma

(1)

(1)

(1)

(2)

Indication Biomarker Preclinical IND Enabling Phase 1 Phase 2 Status Collaboration

IDE196PKC inhibitor

GNAQ/11 Basket Monotherapy GNAQ/11 Advancing Ph2 Basket (Non-MUM)

Ph2 Expansion in Skin Melanoma

MUMMEK Combo GNAQ/11 FPI (MUM) June 2020

Enrollment Ongoing (MUM)

MUMcMET Combo GNAQ/11 Targeting FPI (MUM) Late 2020 to Early 2021

(3)

(3)

Synthetic Lethality Programs

Kinase Programs

IDEAYA and GSK Strategic Partnership

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Landmark Partnership in Synthetic Lethality

• Validates IDEAYA Synthetic Lethality platform• Enhances collective leadership in Synthetic Lethality• Creates strategic combination opportunities

Transformative Strategic Partnership

• Targets: MAT2A, Pol Theta and Werner Helicase• Modalities: small molecule inhibitors & protein degraders• $100M cash upfront• $20M equity investment as direct private placement• $50M option exercise fee for MAT2A• 50/50 US profit share for MAT2A and Werner Helicase• 20% global development cost share for US profit share • Potential preclinical, clinical and sales milestones for each

licensed product • Royalties tiered high single-digit to sub-teen double digit %

Key Partnership Terms

DNA Polymerase Theta

• 50/50 US Profit Share and ex-US Royalties• 20% global development cost share• Cash payments upon preclinical, clinical and sales milestones

WRN Helicase

MAT2A

• Milestones and global royalties• Cash payments upon preclinical, clinical and sales milestones

• IDEAYA leads early clinical; GSK option to exclusive license• $50M Option Exercise Fee• 50/50 US Profit Share and ex-US Royalties• 20% global development cost share • Cash payments upon clinical and sales milestones

IDEAYA Form 8-K current report filed with the U.S. Securities and Exchange Commission on June 16, 2020

IDEAYA and GSK Strategic Partnership

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Partnership Enables Strategic Combinations

IDE397MAT2A

GSK3368715 (Ph 1) Type I PRMT+

Pol ThetaSmall Molecule Inhibitor or

Protein Degrader

Zejula™PARP+

PatientPopulation

MTAPDeletion

BRCA/HRD

Potential Combinations of IDEAYA SL + GSK Programs

IDEAYA Form 8-K current report filed with the U.S. Securities and Exchange Commission on June 16, 2020; GlaxoSmithKline Q2 2020 Earnings Presentation

Werner Helicase Dostarlimab (Ph 3)PD-1

+ MSI-H

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SL Target & Biomarker Discovery & Validation

Bioinformatics, including AI Algorithms

Dual CRISPR, CRISPR, siRNA

Genetically Engineered Models

Drug Discovery

Structure Based Drug Design

Small Molecule Chemistry

Protein Degrader Capabilities

• Potential 1st-in-class SL targets identified and validated, such as WRN, Pol Theta and PARG

• DECIPHER™ - Dual CRISPR SL Library in DDR in collaboration with UCSD

• PAGEO™ - Paralogous Gene Evaluation in Ovarian, in collaboration with Broad Institute

• Partnership Datasets• Public Databases

• Crystal structures for four SL programs obtained to enable SBDD

• Three SL programs advanced to in vivo efficacy in target genetic settings

• Potential best-in-class molecules discovered, including MAT2Ai, IDE397

• Protein degraders advancing for selected targets, including Pol Theta

Clinical Biomarker

Genomics – DNA and RNA Analysis

Proteomics – Protein Expression Profiling

Tissue (IHC, IF) and Liquid Biopsies Analysis

IDEAYA Synthetic Lethality Platform

• Translational biology research• Preclinical analysis of human

cell lines and model systems• Analysis of human clinical

samples and correlation with clinical trial outcomes

Fully-Integrated Target, Biomarker, and Drug Discovery Capabilities

Partnership DatasetsCancer Dependency Map – Broad InstituteFoundation Insights™ – Foundation Medicine

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IDEAYA Synthetic Lethality PlatformSynthetic Lethality Target and Biomarker Identification and Validation

DECIPHER™ Dual CRISPR SL Library in DNA Damage Repair (2)

PAGEO™Paralogous Gene Evaluation in Ovarian Cancer (1)

Public DatabasesIDEAYA data mining and analysis across data sets

Evaluation of SL targets in context of functionally redundant paralogous genes in ovarian cancer

Evaluation of DNA Damage Targets synthetic lethal with tumor suppressor or oncogenes

Novel Synthetic Lethality Platform and Data Integration• IDEAYA SL Platform integrates extensive proprietary and public data sets with orthogonal and complementary content• Bioinformatics enables identification and validation of synthetic lethal target / biomarker interactions across vast datasets• Robust SL interactions validated genetically (Dual CRISPR, paralogues, isogenic pairs, CRISPR/siRNA) and pharmacologically

(1, 2) IDEAYA Proprietary Libraries and Datasets – Strategic Collaborations with Broad Institute(1) and UC San Diego(2)

IDEAYA Team and Scientific Advisory Board

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Scientific Thought Leaders in Synthetic Lethality and Precision Medicine Oncology

IDEAYA Executives & R&D Leadership

IDEAYA Scientific Advisory Board

Yujiro Hata, M.B.A. President, Chief Executive Officer, Director

Paul Stone, J.D. SVP, Chief Financial Officer

Michael Dillon, Ph.D. SVP, Chief Scientific OfficerHead of Research

Mark Lackner, Ph.D.SVP, Head of Biology & Translational Sciences

Mick O’Quigley, M.B.A.VP, Development Operations

Paul Barsanti, Ph.D. VP, Head of Drug Discovery

Jason Throne, J.D.SVP, General Counsel

Alan D’Andrea, M.D.IDEAYA SAB ChairHarvard Medical School, ProfessorDirector, Center of DNA Damage and Repair, Dana Farber

William Sellers, M.D.Broad Institute, Dana Farber, and Harvard, ProfessorNovartis, Former Head Oncology Research, SL Project Drive initiative

Frank McCormick, Ph.D. UCSF, Professor and former Director, Helen Diller Cancer CenterFormer President AACR; Founder and CSO, Onyx

Trey Ideker, Ph.D.UCSD, Professor, Co-Director Cancer Genomes & Networks Program, Research in Dual-CRISPR and SL interaction maps

Jeffrey Hager, Ph.D.Former Chief Technology Officer, IDEAYA

Elizabeth Swisher, M.D.University of Washington, Professor; Co-Leader, Breast and Ovarian Cancer Research Program, Seattle Cancer Care AlliancePrincipal Investigator on multiple PARP inhibitor trials

Brian Daniels, M.D.Bristol Myers Squibb, Former SVP Global Development & Medical Affairs

IDEAYA is Advancing the Next Generation of Synthetic Lethality Therapies

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PARPHRD/BRCALynparza (AZ)Zejula (GSK)

Rubraca (Clovis)Talzenna (Pfizer)

Today IDEAYA Synthetic Lethality Pipeline

MAT2AMTAP-Deletion

WRNHigh-MSI

Target DiscoverySL Targets

PolθHRD

PARGReplication Stress Novel Biomarker

HRD = Homologous Recombination Deficiency, MSI = Microsatellite Instability

MTAP Deletion PrevalenceMTAP-MAT2A Synthetic Lethality Biology

MAT2A Inhibition is Synthetic Lethal with MTAP Deletion

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MTAP Deletion Prevalence ~15% of all Solid Tumors

Data from The Cancer Genome Atlas in cBioPortal

Cancer Type N MTAP Deletions (%)Glioblastoma 592 41Mesothelioma 87 32Esophageal 95 28Bladder 411 26Pancreatic 184 22Melanoma 448 16Lung Cancer (NSCLC) 1053 15Head and Neck 523 14Sarcoma 255 10Esophagogastric 514 10Diffuse Glioma 513 9Breast 1084 3Ovarian 585 3Adrenocortical 92 3Thymic 123 3Hepatocellular 369 3Renal non-clear cell 348 2

MAT2A

MAT2Ainhibitor

MAT2A

Methionine

MAT2A is key enzyme that produces SAM in cells

SAM

PRMT5

MTAP

Protein Methylation

MTA

MTAMTA

MTAP deletion leads to MTA accumulation

MTA accumulation partially inhibits PRMT5

Loss of methylation function of PRMT5 results in defects in RNA splicing, gene

expression and genome integrity

Inhibition of MAT2A results in reduction of SAM, starving PRMT5

of its substrate

IDE397: MAT2A Development Candidate

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Differentiated Profile vs Agios Compounds; Selective for MTAP-/- Cell Lines

IDE397 demonstrates greater in vivo efficacy at 5 to 10mg/kg

• More potent vs. AGI-25696 at 1/30th to 1/60th the dose in MTAP-deletion models

IDE397 has not caused liver injury or increased unconjugated bilirubin

• Liver injury not observed in tox studies• Not an inhibitor of UGT1A1

IDE397 has favorable physical properties, including solubility

• AG-270 observed non-linear exposure >200mg QD (GI absorption)

Targeting IND in December 2020

IDE397 vs Agios Compounds IDE397 is Selective for MTAP-/- Cell Lines

IDEAYA Data

Increased dependence on MAT2A gene knockdown

Incr

ease

d se

nsiti

vity

to

IDE3

97 tr

eatm

ent

MTAP-/- cell lines are sensitive to IDE397MTAP WT cell lines are insensitivePharmacological inhibition correlates with MAT2A genetic knockdown

MTAP WT MTAP-/-

Log1

0 GI

50 (µ

M)

-1.0 -0.5 0.0 0.5

DepScore (RNAi)

BFTC909

LMSU

SNU449

HuPT3

COLO741

NCIH838

KP4

BxPC3

RT112

SW780

SKMEL5SW1573

Log1

0 IC

50 (µ

M)

0 3 6 9 12 150

300

600

900

1,200

1,500

Study Day

Mea

n Tu

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Vol

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(mm

3 )± S

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Vehicle

IDE397 10 mg/kg QD

First doseDay 1

IDE397: MAT2A Development Candidate

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Enhanced In Vivo Efficacy in MTAP-/- Engineered and Endogenous Models

HCT 116 MTAP-/- Model

IDEAYA Data

0 3 6 9 12 150

100

200

300

400

500

600

Study Day

Mea

n Tu

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(mm

3 )± S

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Vehicle

IDE397 5mg/kg QDHCT-116 MTAP-/-

First dose Day 1

IDEAYA Data

KP4 Endogenous MTAP-/- Model

IDEAYA Data

Enhanced In Vivo Efficacy vs Agios

-100

-80

-60

-40

-20

0

20

Tum

or g

row

th in

hibi

tion

(%)

HCT-116 MTAP-/-

IDE397

5mpk

AGI-25696

100mpk

300mpk

IDE397 In Vivo Efficacyin HCT116 model at 1/20th to 1/60th of the dose, and in KP4 model at 1/30 of the dose of Agios MAT2A compound

Published AG-270 preclinical dose is typically 200 mg/kg QD

IDE397 PD Modulationin HCT116 model: IDE397 significantly reduces tumor SAM levels at 5 mg/kg

Dose-Dependent Efficacy in MTAP-/- Endogenous NSCLC ModelIDE397 Demonstrates Monotherapy Tumor Regression

In Vivo Endogenous NSCLC MTAP-/- Model

IDEAYA Data

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7 14 21 280

500

1000

1500

2000

NSCLC model

Days Post Inoculation

Mea

n Tu

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Vol

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(mm

3 )± S

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.

Vehicle control3 mg/kg IDE39710 mg/kg IDE39730 mg/kg IDE397

IDE397 In Vivo Efficacyis being evaluated in over 40 patient derived xenograft (PDX) models with homozygous MTAP deletions in solid tumors, including in NSCLC

PARG Synthetic Lethality Program

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Candidate Biomarkers: Replication Stress/HRD/Novel Biomarker

Pillay et al., Cancer Cell Mar 2019

March 2019

DNA Replication Vulnerabilities Render Ovarian Cancer Cells Sensitive to Poly(ADP-ribose) Glycohydrolase Inhibitors

PARGi demonstrate cell viability effects in ovarian cell lines resistant to PARPi

PARG & DNA Replication VulnerabilitiesPARG Biology

PARG

Poly(ADP-ribose) glycohydrolase (PARG) regulates DNA repair mechanismsPARG hydrolyzes PAR chains in final step of DNA Damage Repair (DDR) cycle

IDB-PARG Potency

Biochemical IC50 7 nM

PAR Foci cell EC50 50 nM

Cell Viability EC50 510 nM

• Extensive research in PARG biology and chemistry

• Multiple collaborations ongoing to refine patient selection biomarker strategy

IDEAYA has discovered potentPARG inhibitors SAR guided by structure-based drug design

PARG Inhibitor In Vivo PD and Efficacy DataPARG Drug Discovery Program

PARG Synthetic Lethality Program

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Drug Discovery on Potential 1st in Class DDR Synthetic Lethality Target

IDEAYA PARG inhibitors demonstrate in vivo TGI in a model with a replication stress gene signature

Significant tumorPAR accumulation observed in vivo

IDEAYA Data IDEAYA Data

0 4 8 12 16 20 241

10

100

1000

10000

100000

0

2000

4000

6000

8000

10000

Time post dose (h)

Plas

ma

conc

entr

atio

n (n

g/m

l)±

S.E.

M.

pg PAR/mg protein

± S.E.M.

IDB-PARG plasmaconcentration

protein adjusted viability IC50

Tumor PAR accumulation

1st dose - 0 hrs2nd dose - 8 hrs

7 14 21 280

500

1000

1500

2000

2500

Days post inoculation

Mea

n Tu

mor

Vol

ume

(m

m3 )±

S.E

.M.

Vehicle controlIDB-PARG

TGI = 47%

• IDEAYA-proprietary Novel Synthetic Lethality Biomarker

• IDB-PARG demonstrates differentiated activity relative to PARP inhibitor niraparib

• Targeting PARG development candidate in 2021

PARG Synthetic Lethality Program

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IDB-PARG Demonstrates In Vivo Tumor Regression in PDX Model

Robust Monotherapy Activity Observed in Multiple PDX Models

IDEAYA Data

Vehicle

0 7 14 21 28 350

250

500

750

1000

PDX-1

Study Day

Mea

n Tu

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(mm

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1st dose Day 1

IDB-PARGVehicle

0 7 14 21 28 350

250

500

750

1000

PDX-2

Study Day

Mea

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1st dose Day 1

IDB-PARG

Project Drive: Werner is essential in MSI-high cancer cell lines

Werner Syndrome Helicase is Required for the Survival of Cancer Cells with Microsatellite Instability

IDEAYA Publication

• Discovery: multiple hit discovery campaigns using a range of screening formats and compound libraries completed

• Screening: robust suite of biochemical and biophysical assays to identify WRN inhibitors and differentiate false positives

• Structurally Enabled: crystal structure of WRN helicase domain solved

• Lead Series: identified a lead series with <10 nM IC50 potency in a Werner helicase biochemical assay

• >10,000x potency improvement obtained through ongoing SAR

Werner Helicase Drug DiscoveryWerner Helicase Biomarker

WRN

Werner Helicase Synthetic Lethality Program

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Candidate Biomarker: High-MSI (15% GI Cancers and 16% CRC) 1

IDB-WRN1ATPase IC50 = ~30 µM

IDB-WRN2ATPase IC50 < 10 nM

IDEAYA DataProject Drive

Cell Press, iScience, March 2019, Hager et al

0

20

40

60

80

100

120

Compound (uM)

Perc

ent I

nhib

ition

IDB-WRN1

0.000

10.0

01 0.01 0.1 1 10 10

010

00

0.000

01

IDB-WRN2

>10,000x

1 Cancer Res., November 1998

WRN Inhibitors Phenocopy Genetic KnockdownWRN Inhibitor Cellular PD and Viability

WRN inhibitor

WRN siRNA

Werner Helicase Synthetic Lethality Program

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Candidate Biomarker: High-MSI (15% GI Cancers and 16% CRC) 1

IDEAYA Data

• PD-marker: dose dependent increase of DNA damage marker γH2AX demonstrated at 48 hours

• Cell viability: MSI-high specific cell viability effect observed across multiple cell lines; no effect in MSS cell lines

• Target Milestone: In vivo efficacy data in 2020

IDEAYA Data

1 Cancer Res., November 1998

Polθ Inhibitor In Vivo ActivityPolθ Inhibitor Cell Viability

PolQ

• Combination of Polθi with niraparib enhances activity of niraparib in DLD1 BRCA2-/- xenograft model

• Regressions observed for all animals dosed with combination in the study

Polθ Synthetic Lethality Program

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Candidate Biomarker: BRCA/HRD

IDEAYA Data

IDEAYA Polθ ATPase inhibitors show cell viability effects in DLD1 BRCA2-/- cell lines

Advancing preclinical research for small molecule inhibitors and protein degraders

IDEAYA Data

0.001 0.01 0.1 1 10 1000

50

100

Polθ-1 (µM)

Perc

ent o

fD

MSO

trea

ted

cont

rol DLD1

DLD1(-/-BRCA2) Combination of Polθi and niraparib demonstrates tumor regression in DLD1 BRCA2-/- xenograft model

134% TGI

86% TGI

55% TGI

0 7 14 21 28

250

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Mea

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1st dose on day 1

VehicleIDB-PolθiNiraparibIDB-Polθi + Niraparib

MUM Indication: Focus on Clinical Combinations

IDE196 + MEK – FPI June 2020

IDE196 + cMET – Target FPI Late 2020 / Early 2021

Pfizer Clinical Trial Collaboration and Supply Agreement

Metastatic Uveal Melanoma (MUM)IDE196 Combination Therapies

IDE196

IDE196 Phase 1/2 Clinical Program Summary

• IDE196 Combination Therapies: MUM Indication Study goals are to identify tolerated combo dose and enhance clinical activity in MUM

– IDE196 BID Monotherapy in MUM (30 pts), ~73% Disease Control Rate & ~13% ORR (AACR 20191)– IDE196 + MEK inhibitor preclinical synergy demonstrated in uveal melanoma (AACR 20202)– IDE196 + cMET inhibitor preclinical synergy and retrospective analysis of human clinical samples support cMETi combination 3

IDE196 + MEK (binimetinib) – interim data anticipated 2021 IDE196 + cMET (crizotinib) – FPI anticipated late 2020 / early 2021

• IDE196 Monotherapy: GNAQ/GNA11 Basket Trial (Non-MUM) Phase 2 expansion in Skin Melanoma with 100% DCR and 1 confirmed PR (by RECIST V1.1) in first 4 evaluable patients Interim monotherapy data anticipated 2021; targeting to provide together with IDE196 / binimetinib combination interim data

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PKC Inhibitor Targeting GNAQ/GNA11 Hotspot Mutation Tumors

GNAQ/11 Basket (Non-MUM): Evaluating Monotherapy

Ph2 Expansion in Skin Melanoma (July 2020)

In 4 evaluable Skin Melanoma patients observed 100% DCR and 1 confirmed PR by RECIST Guidelines (version 1.1)

GNAQ/GNA11 Basket Trial (Non-MUM)IDE196 Monotherapy

1 Novartis Data 2, 3 IDEAYA Data

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IDE196 Monotherapy Confirmed PR by RECIST Guidelines (version 1.1) in Metastatic Skin Melanoma Patient with GNAQ Q209L Hotspot Mutation

Clinical Background CT Scan at Baseline and 20 Weeks

20 weeks

Baseline• Nivo, ipi, and pembro treatment through 2016 and 2017; progressed with liver metastases in 2018

• Restarted nivo in combination with radiation to liver lesions in 2018, and then T-VEC to cutaneous lesions in 2019

• Subsequent progression followed by adoptive T-cell therapy (TIL) May 2019; confirmed progression noted Feb 2020

• Started on IDE196 400mg BID Feb 2020

• PR (-31.1%) at 8 weeks, sustained at 20 weeks (-37%) with reduction in target liver lesion and inguinal lymph node

• Ongoing treatment with IDE196

IDEAYA Data as of 8/1/2020

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IDE196 Potential Addressable Market Solid Tumors Having GNAQ/11 Hotspot Mutations

3.5

2.5

0

1

2

3

4

5

6

7

IDE196 GNAQ/GNA11 Hotspot Population

MUM GNAQ/11 Other Solid Tumors (Hotspot)

(Patients in 1,000’s)

US and EU5~3.5 K GNAQ/11 Metastatic Uveal Melanoma (MUM)~2.5 K GNAQ/11 Other Solid Tumors (Hotspot)

0

1000

2000

3000

4000

5000

6000

7000

(Patients)

GNAQ/11: The Cancer Genome Atlas (TCGA), IDEAYA AnalysisROS1 Advanced NSCLC: Turning Point Therapeutics 11/2019 corporate presentation, prevalence estimates (160,000 US + 117,000 EU5) x 2% mutation rateHRASm HNSCC estimates: KURA Oncology 11/2019 corporate presentation (2,900-4,700 patients US)FGFR2 rearrangements in cholangiocarcinoma: Incyte 6/2019 press release (~2,000-3,000 patients US/EU/JPN)TRK fusion: LOXO 11/2018 corporate presentation Ex 99.2 (2,500-3,000 patients US) 4L GIST estimates: Deciphera 11/2019 corporate presentation (~2,100 patients US)

GNAQ/11 Hotspot Patients in US & EU5 Rare Oncology Indication Comparables

Indication Biomarker Preclinical IND Enabling Phase 1 Phase 2 Target Milestones Through 2021 Collaboration

IDE397MAT2A

Solid Tumors MTAP IND December 2020Phase 1 Initiation H1 2021

PARG Solid Tumors Novel Biomarker Development Candidate 2021

Polθ Solid Tumors HRD Development Candidate 2021

WRN Solid Tumors High-MSI Lead Optimization 2021

DDT Solid Tumors Novel Biomarker Multiple DDT Programs in Chemistry Optimization

IDEAYA’s Precision Medicine Oncology Pipeline

25

Precision Medicine Pipeline

= Target Program Milestone through 2021(1) Pursuant to GSK Collaboration, Option and License Agreement: MAT2A and WRN: 50/50 US Profits + ex-US Royalties; Polθ: Global Royalties(2) Pursuant to CRUK Evaluation, Option and License Agreement, with ongoing Collaborative Research; IDEAYA controls all Commercial Rights(3) Pursuant to Pfizer Clinical Trial Collaboration and Supply Agreement; ; IDEAYA retains all IDE196 Commercial Rights

DDT = DNA Damage Target, WRN = Werner Helicase, Polθ = DNA Polymerase Theta, HRD = homologous recombination deficiency, MSI = microsatellite instability PKC = protein kinase C, MUM = metastatic uveal melanoma

(1)

(1)

(1)

(2)

Indication Biomarker Preclinical IND Enabling Phase 1 Phase 2 Target Milestones Through 2021 Collaboration

IDE196PKC inhibitor

GNAQ/11 Basket Monotherapy GNAQ/11 Phase 2 Basket (Non-MUM) Enrolling

Interim Data 2021

MUMMEK Combo GNAQ/11 MEK Combo Phase 2 Expansion

Interim Data 2021

MUMcMET Combo GNAQ/11 cMET Combo Phase 1 and Phase 2 Expansion

Enrollment Ongoing

(3)

(3)

Synthetic Lethality Programs

Kinase Programs

Target Milestones Through 2021