August 2020

NASDAQ: IDYA

IDEAYA Biosciences

Improving Lives

Through Transformative

Precision Medicines

Safe Harbor Statement

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 June 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.

2

IDEAYA Biosciences Highlights

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

  • 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

3

Synthetic Lethality

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)

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

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

Reference: Charles Boone

4

IDEAYA's Precision Medicine Oncology Pipeline

Building the Leading Synthetic Lethality Biotech

Synthetic Lethality Pipeline

Indication

Biomarker

Preclinical

IND

Phase 1

Phase 2

Status

Collaboration

IDE397

Solid Tumors

MTAP

Targeting IND Q4 2020

(1)

MAT2A

PARG

Solid Tumors

Novel Biomarker

In vivo Efficacy

(2)

Polθ

Solid Tumors

HRD

In vivo Efficacy

(1)

WRN

Solid Tumors

High-MSI

Cell Activity

(1)

DDT

Solid Tumors

Novel Biomarker

Target Validation

  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

DDT = DNA Damage Target, WRN = Werner Helicase, Polθ = DNA Polymerase Theta, HRD = homologous recombination deficiency, MSI = microsatellite instability

Kinase Pipeline

Indication

Biomarker

Preclinical

IND

Phase 1

Phase 2

Status

Collaboration

GNAQ/11 Basket

GNAQ/11

Advancing Ph2 Basket (Non-MUM)

IDE196

Monotherapy

Ph2 Expansion in Skin Melanoma

PKC inhibitor

MUM

GNAQ/11

MEK Combo FPI (MUM) June 2020

(3)

MEK Combo

MEK Combo Enrollment Ongoing (MUM)

  1. Pursuant to Pfizer Clinical Trial Collaboration and Supply Agreement PKC = protein kinase C, MUM = metastatic uveal melanoma

5

= Target program milestone through 2020

IDEAYA and GSK Strategic Partnership

Landmark Partnership in Synthetic Lethality

Transformative Strategic Partnership

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

Key Partnership Terms

  • 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 %

MAT2A

  • 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

WRN Helicase

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

DNA Polymerase Theta

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

6

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

IDEAYA and GSK Strategic Partnership

Partnership Enables Strategic Combinations

Potential Combinations of IDEAYA SL + GSK Programs

Patient

Population

IDE397

MAT2A

Pol Theta

Small Molecule Inhibitor or

Protein Degrader

Werner Helicase

+

+

+

GSK3368715 (Ph 1)

MTAP

Type I PRMT

Deletion

Zejula™

BRCA/HRD

PARP

Dostarlimab (Ph 3)

MSI-H

PD-1

7

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

IDEAYA Synthetic Lethality Platform

Fully-Integrated Target, Biomarker, and Drug Discovery Capabilities

SL Target & Biomarker

Discovery & Validation

Dual CRISPR, CRISPR, siRNA Bioinformatics

Genetically Engineered Models

  • Potential 1st-in-class SL targets identified and validated, such as WRN
  • SL biomarker discovery has delivered multiple patient population hypotheses
  • 3 SL programs advanced to in vivo efficacy in target genetic settings

Drug Discovery

Structure Based Drug Design

Small Molecule Chemistry

Protein Degrader Capabilities

  • Crystal structures for all four SL programs obtained to enable SBDD
  • Potential best-in-class molecules discovered, including MAT2Ai, IDE397
  • Protein degraders advancing for selected targets

Clinical Biomarker

Genomics

Tissue Based (IHC, IF)

Liquid Biopsies

8

IDEAYA Team and Scientific Advisory Board

Scientific Thought Leaders in Synthetic Lethality and Precision Medicine Oncology

IDEAYA Executives & R&D Leadership

Yujiro Hata, M.B.A.

Michael Dillon, Ph.D.

Paul Stone, J.D.

Mark Lackner, Ph.D.

President, Chief Executive Officer, Director

SVP, Chief Scientific Officer

SVP, Chief Financial Officer

SVP, Head of Biology &

Head of Research

Translational Sciences

Mick O'Quigley, M.B.A.

Paul Barsanti, Ph.D.

Jason Throne, J.D.

VP, Development Operations

VP, Head of Drug Discovery

SVP, General Counsel

IDEAYA Scientific Advisory Board

Alan D'Andrea, M.D.

William Sellers, M.D.

Frank McCormick, Ph.D.

Trey Ideker, Ph.D.

IDEAYA SAB Chair

Broad Institute, Dana Farber, and Harvard, Professor

UCSF, Professor and former Director,

UCSD, Professor, Co-Director Cancer Genomes & Networks

Novartis, Former Head Oncology Research,

Helen Diller Cancer Center

Program, Research in Dual-CRISPR and SL interaction maps

Harvard Medical School, Professor

SL Project Drive initiative

Former President AACR; Founder and CSO, Onyx

Director, Center of DNA Damage and Repair, Dana Farber

Brian Daniels, M.D.

Elizabeth Swisher, M.D.

Jeffrey Hager, Ph.D.

Bristol Myers Squibb, Former SVP Global Development

University of Washington, Professor; Co-Leader, Breast and

Former Chief Technology Officer, IDEAYA

& Medical Affairs

Ovarian Cancer Research Program, Seattle Cancer Care Alliance

Principal Investigator on multiple PARP inhibitor trials

9

IDEAYA is Advancing the Next Generation of Synthetic Lethality Therapies

Today

PARP

HRD/BRCA

Lynparza (AZ)

Zejula (GSK)

Rubraca (Clovis)

Talzenna (Pfizer)

IDEAYA Synthetic Lethality Pipeline

MAT2A

WRN

Target Discovery

MTAP-Deletion

High-MSI

SL Targets

PARG

Polθ

Replication Stress

HRD

Novel Biomarker

HRD = Homologous Recombination Deficiency, MSI = Microsatellite Instability

10

MAT2A

MAT2A Inhibition is Synthetic Lethal with MTAP Deletion

MTAP Deletion Prevalence ~15% of all Solid Tumors

MTAP-MAT2A Synthetic Lethality Biology

Methionine

MAT2A is key enzyme that

produces SAM in cells

MTAP deletion leads

to MTA accumulationMAT2A MAT2A

inhibitor

MTA accumulation

partially inhibits PRMT5

Inhibition of MAT2A

MTA

results in reduction of

MTA

PRMT5

SAM, starving PRMT5

MTA

of its substrate

Protein Methylation

SAM

Loss of methylation function of PRMT5

results in defects in RNA splicing, gene

expression and genome integrity

MTAP Deletion Prevalence

Cancer Type

N

MTAP Deletions (%)

Glioblastoma

592

41

Mesothelioma

87

32

Esophageal

95

28

Bladder

411

26

Pancreatic

184

22

Melanoma

448

16

Lung Cancer (NSCLC)

1053

15

Head and Neck

523

14

Sarcoma

255

10

Esophagogastric

514

10

Diffuse Glioma

513

9

Breast

1084

3

Ovarian

585

3

Adrenocortical

92

3

Thymic

123

3

Hepatocellular

369

3

Renal non-clear cell

348

2

Data from The Cancer Genome Atlas in cBioPortal

11

IDEAYA MAT2A Inhibitors Demonstrate Synthetic Lethality in MTAP-/- Cell Lines & PD Modulation of SAM Levels

Structurally Enabled Lead Optimization

Synthetic Lethality in HCT116 Cell Line

  • IDB proprietary MAT2Ai co-crystal structure (1.33Å)
  • +17 high-resolutionco-crystal structures

Fold change (DMSO)

1.5

1.0

0.5

0.0

IDB361

HCT116 Parental HCT116 MTAP-/-

  • Lead series includes multiple compounds with nM potency and >5x IC50 ratio in HCT116 wt vs MTAP -/-

IDEAYA Data

-3-2-1 0 1 2

Concentration (µM)

IDEAYA Data

Consistent sensitivity across multiple MTAP-/- cell lines

IDEAYA Data

IC50 (uM)

20

15

10

5

4

3

2

1.0

0.8

0.6

0.4

0.2

0.0

KP4

RT112/84

SW780

H647

BXPC3

MTAPnull

HCT116

WT

HCT116

PD Modulation:

SAM Levels in

HCT116 Cell Line

IDEAYA Data

12

IDE397: MAT2A Development Candidate Nominated

Targeting IND in Q4 2020

In Vivo Efficacy in HCT 116 MTAP-/- Model

IDE397

600

Vehicle

HCT-116MTAP-/-

(5 mg/kg)

IDE397 5mg/kg QD

demonstrates

S.E.M.

500

greater tumor

400

growth

3

)±

inhibition at

(mm

1/60th the dose

Volume

300

vs AGI-25696

Published AG-

Tumor

200

270 preclinical

Mean

dose is typically

100

200 mg/kg QD

0

0

3

6

9

12

15

First dose Day 1

Study Day

IDEAYA Data

Tumor Pharmacodynamic Effect

20

Significant reduction in tumor SAM

HCT-116MTAP-/-

levels with IDE397 at 5 mg/kg

IDE397

AGI-25696

0

Tumor SAM HCT-116MTAP-/-

5

100

300

(%)

S.E.M.

5000

mpk

mpk

mpk

-20

4000

growthTumorinhibition

SAMTumor(ng/g)

1000

3000

-40

2000

-60

Mean

0

-80

Vehicle

IDE397 5 mg/kg

-100

IDEAYA Data

13

IDE397: MAT2A Development Candidate Nominated

Differentiated Profile vs Agios Compounds

Efficacy in Endogenous MTAP-/- Model (KP4)

1,500 Vehicle

IDE397 10 mg/kg QD

)± S.E.M.

1,200

3

(mmVolume

900

Mean Tumor

600

300

First dose

0

Day 1

0

3

6

9

12

15

Study Day

IDB397 demonstrates efficacy at 1/30th of the dose of Agios MAT2A compound (see data)

IDEAYA Data

1,500

1,250

mm3)

1,000

Volume

750

79% TGI

Tumor

P = 2e-31

Average

500

250

+/- S.E.M.

0

15

20

25

30

35

Days post implant

Vehicle

MAT2Ai III 300 mg/kg

Keystone Symposium 2017

Agios Data

IDE397 vs Agios Compounds

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

IND-enabling studies initiated and targeting Q4 2020 IND

14

IDE397 Demonstrates Monotherapy Tumor Regression in an MTAP-Deleted Endogenous NSCLC Model

IDE397 produced dose-dependent efficacy in a NSCLC model with regression (TGI >100%) at 30 mg/kg

In Vivo Endogenous NSCLC MTAP (-/-) PDX Model

Volume

2000

S.E.M.

1500

MeanTumor

±

1000

)

3

(mm

500

0

7

14

21

28

Days Post Inoculation

Vehicle control

3 mg/kg IDE397

10 mg/kg IDE397

30 mg/kg IDE397

IDEAYA Data

15

PARG

PARG Synthetic Lethality Program

Candidate Biomarkers: Replication Stress/HRD/Novel Biomarker

PARG Biology

Poly(ADP-ribose) glycohydrolase (PARG) regulates DNA repair mechanisms

PARG hydrolyzes PAR chains in final step of DNA Damage Repair (DDR) cycle

Cancer Research

August 2019

Dysfunction of Poly(ADP-ribose) Glycohydrolase Induces a Synthetic Lethality Effect in Dual Specificity Phosphatase 22-deficient Lung Cancer Cells

PARG & DNA Replication Vulnerabilities

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

Sasaki et al., Cancer Res, Aug 2019, 79:3851-3861; Jain et al, Cancer Res Jul 2019;79:4491-4502; Pillay et al., Cancer Cell Mar 2019, 35, 519-533

16

PARG Synthetic Lethality Program

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

PARG Drug Discovery Program

PARG Inhibitor In Vivo PD and Efficacy Data

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

Significant tumor PAR accumulation observed in vivo

(ng/ml) ± S.E.M.

100000

IDB-PARG plasma

10000

concentration

10000

Tumor PAR accumulation

8000

PAR/mg pg

protein adjusted viability IC50

1000

6000

Plasma concentration

100

4000

.M.E.S ± protein

10

2000

1

0

0

4

8

12

16

20

24

1st dose - 0 hrs

Time post dose (h)

2nd dose - 8 hrs

  • Extensive research in PARG biology and chemistry
  • Multiple collaborations ongoing to refine patient selection biomarker strategy

IDB-PARG Potency

Biochemical IC50

7 nM

PAR Foci cell EC50

50 nM

Cell Viability EC50

510 nM

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

2500

Vehicle control

Volume

IDB-PARG

S.E.M.

2000

1500

Mean Tumor

) ±

TGI = 47%

3

1000

(mm

500

0

7

14

21

28

IDEAYA Data

IDEAYA Data

Days post inoculation

17

PARG Synthetic Lethality Program

IDB-PARG Demonstrates In Vivo Tumor Regression in PDX Model

Robust Monotherapy Activity Observed in Multiple PDX Models

  • IDEAYA-proprietaryNovel Synthetic Lethality Biomarker
  • Targeting PARG development candidate in 2021

PDX-1

1000

Vehicle

S.E.M.)±

IDB-PARG

±S.E.M.)

750

3

3

(mm

(mm

VolumeTumor

500

VolumeTumor

Mean

250

Mean

0

0

7

14

21

28

35

1st dose Day 1

Study Day

PDX-2

1000

Vehicle

IDB-PARG

750

500

250

0

0

7

14

21

28

35

1st dose Day 1

Study Day

IDEAYA Data

18

WRN

Werner Helicase Synthetic Lethality Program

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

Werner Helicase Biomarker

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

IDEAYA Publication

Cell Press, iScience, March 2019, Hager et al

Werner Helicase Drug Discovery

  • 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: 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

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

Project Drive

IDB-WRN1

ATPase IC50 = ~30 M

IDB-WRN2

ATPase IC50< 10 nM

IDEAYA Data

IDB-WRN1

120

IDB-WRN2

Inhibition

60

>10,000x

100

Percent

80

40

20

0

.00001

.0001

.001

.01

.1

1

10

100

1000

0

0

0

0

0

Compound (uM)

19

Werner Helicase Synthetic Lethality Program

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

WRN Inhibitor Cellular PD and Viability

  • PD-marker:dose dependent increase of DNA damage marker γH2AX demonstrated at 48 hours
  • Cell viability: MSI-highspecific cell viability effect observed across multiple cell lines; no effect in MSS cell lines
  • Target Milestone: In

vivo efficacy data in 2020

WRN Inhibitors Phenocopy Genetic Knockdown

WRN siRNA

WRN inhibitor

IDEAYA Data

IDEAYA Data

20

Polθ Synthetic Lethality Program

Candidate Biomarker: BRCA/HRD

Polθ Inhibitor Cell Viability

Polθ Inhibitor In Vivo Activity

PolQ

Percent of DMSO treated control

100

50

0

0.001

0.01

0.1

1

10

100

DLD1 DLD1(-/-BRCA2)

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

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

1250

) ±S.E.M.

1000

3

(mm

750

Vehicle

IDBPOLQ 100 mg/kg QD Niraparib 45 mg/kg QD

IDBPOLQ 100mg/kg QD + Niraparib 45 mg/kg QD

Polθ-1 (M)

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

  • Regressions observed for all animals dosed with combination in the study
  • All treatments well-tolerated, with body weights similar to control at end of study

Volume

500

Tumor

Mean

250

0

7

14

21

28

1st dose on Day 1

Study Day

IDEAYA Data

IDEAYA Data

21

IDE196

IDE196 Phase 1/2 Clinical Program Summary

PKC Inhibitor Targeting GNAQ/GNA11 Hotspot Mutation Tumors

Metastatic Uveal Melanoma (MUM)

IDE196 + MEK Combo

MUM Indication: Focus on Clinical Combinations IDE196 + MEK Combo FPI (June 2020)

Pfizer Clinical Trial Collaboration and Supply Agreement IDE196 + MEKi (binimetinib) Preclinical Synergy

GNAQ/GNA11 Basket Trial (Non-MUM)

IDE196 Monotherapy

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)

  • IDE196 + MEK inhibitor Combo: MUM Indication
    • Study goals are to identify tolerated combo dose and enhance clinical activity in MUM
      • AACR 20191: IDE196 BID Monotherapy in MUM (30 pts), ~73% Disease Control Rate & ~13% ORR
      • AACR 20202: IDE196 + MEK preclinical synergy demonstrated in uveal melanoma
    • Interim data anticipated late 2021 to early 2022
  • IDE196 Monotherapy: GNAQ/GNA11 Basket Trial (Non-MUM)
    • Phase 2 expansion in Skin Melanoma with 100% DCR and 1 confirmed PR (by RECIST 1.1) in first 4 evaluable patients
    • Interim data anticipated H1 2021

1 Novartis Data 2 IDEAYA Data

22

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

Clinical Background

  • 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

CT Scan at Baseline and 20 Weeks

Baseline

20 weeks

23IDEAYA Data as of 8/1/2020

IDE196 Potential Addressable Market

Solid Tumors Having GNAQ/11 Hotspot Mutations

GNAQ/11 Hotspot Patients in US & EU5

Rare Oncology Indication Comps

7

(Patients in 1,000's)

6

52.5

4

3

23.5

1

0

IDE196 GNAQ/GNA11 Hotspot Population

MUM

GNAQ/11 Other Solid Tumors (Hotspot)

US and EU5

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

(Patients)

7000

6000

5000

4000

3000

2000

1000

0

GNAQ/11: The Cancer Genome Atlas (TCGA), IDEAYA Analysis

ROS1 Advanced NSCLC: Turning Point Therapeutics 11/2019 corporate presentation, prevalence estimates (160,000 US + 117,000 EU5) x 2% mutation rate

HRASm 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)

24

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)

IDEAYA's Precision Medicine Oncology Pipeline

Target Milestones Through 2021

Synthetic Lethality Pipeline

Indication

Biomarker

Preclinical

IND

Phase 1

Phase 2

Target Milestones Through 2021

Collaboration

IDE397

Solid Tumors

MTAP

IND Q4 20

(1)

MAT2A

Phase 1 Initiation H1 2021

PARG

Solid Tumors

Novel Biomarker

Development Candidate 2021

(2)

Polθ

Solid Tumors

HRD

IND 2021

(1)

WRN

Solid Tumors

High-MSI

In vivo Efficacy 2020

(1)

DDT

Solid Tumors

Novel Biomarker

Chemistry Optimization

  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

DDT = DNA Damage Target, WRN = Werner Helicase, Polθ = DNA Polymerase Theta, HRD = homologous recombination deficiency, MSI = microsatellite instability

Kinase Pipeline

Indication

Biomarker

Preclinical

IND

Phase 1

Phase 2

Target Milestones Through 2021

Collaboration

GNAQ/11 Basket

GNAQ/11

Phase 2 Basket (Non-MUM) Enrolling

IDE196

Monotherapy

Interim Data H1 2021

PKC inhibitor

MUM

GNAQ/11

MEK Combo Phase 2 Expansion

(3)

MEK Combo

Interim Data Late 2021 to Early 2022

  1. Pursuant to Pfizer Clinical Trial Collaboration and Supply Agreement PKC = protein kinase C, MUM = metastatic uveal melanoma

25

= Target program milestone through 2021

Attachments

  • Original document
  • Permalink

Disclaimer

IDEAYA Biosciences Inc. published this content on 12 August 2020 and is solely responsible for the information contained therein. Distributed by Public, unedited and unaltered, on 12 August 2020 10:12:15 UTC