One Mission,
Inspired by
Patients:
Defeat Cancer.
February 2024

1

DECIPHERADISCLAIMER
This presentation has been prepared by
Deciphera Pharmaceuticals, Inc. for
informational purposes only and not for
any other purpose. Nothing contained inthis presentation is, or should beconstrued as, a recommendation,
promise or representation by Deciphera
Pharmaceuticals, Inc. or any director,
employee, agent, or adviser of Deciphera
Pharmaceuticals, Inc. This presentation
does not purport to be all-inclusive or tocontain all of the information you may
desire. Certain information contained inthis presentation relates to or is basedon studies, publications, surveys andother data obtained from third-party
sources and Deciphera Pharmaceuticals,Inc.’s own internal estimates andresearch. While Deciphera
Pharmaceuticals, Inc. believes thesethird-party sources to be reliable as ofthe date of this presentation, it has notindependently verified, and makes norepresentation as to the adequacy,
fairness, accuracy or completeness of,any information obtained from thirdparty sources. While Deciphera
Pharmaceuticals, Inc. believes its internal
research is reliable, such research has
not been verified by any independentsource.

Forward-Looking Statements
This presentation may contain forward-looking statements that are
based on our current expectations, estimates and projections about
our industry, our operations and financial performance, as well as
management’s beliefs and assumptions. Words such as“anticipates,” “expects,” “intends,” “plans,” “believes,” “seeks,”“estimates,” “may,” “will,” and variations of these words or similar
expressions are intended to identify forward-looking statements.
Such forward-looking statements are subject to various risks anduncertainties, including important factors that could cause actual
outcomes or results to differ materially from those indicated inthese statements. These statements include, without limitation, thepotential for our pre-clinical and/or clinical stage pipeline assets tobe first-in-class and/or best-in-class treatments, the ability to
become a multi-product, self-sustaining company, plans to continue
our geographic expansion of QINLOCK in European andinternational markets, our Phase 3 INSIGHT clinical study of
QINLOCK versus sunitinib in second-line GIST patients with
mutations in KIT exon 11 and 17/18, our expectations regarding theaggregate potential revenue opportunity for QINLOCK, our ability to
expand the market opportunity for QINLOCK in second-line GIST in
our INSIGHT Phase 3 study; the timing of our NDA and MAA
submission for vimseltinib, the potential revenue opportunity forvimseltinib, if approved, the commercial synergies between
QINLOCK and vimseltinib, plans to present additional data from our
Phase 3 MOTION study and Phase 1/2 study of vimseltinib, each in
TGCT patients, plans to initiate a Phase 2 study of vimseltinib inpatients with cGVHD, subject to FDA feedback; plans for our ongoing phase 1/2 study of DCC-3116 and to select a recommended
Phase 2 dose for at least one potential expansion cohort, subject tofavorable data; initiating a Phase 1 study of DCC-3084 in the firsthalf of 2024, submitting an IND for DCC-3009 in the first half of2024 and initiating a Phase 1 study in the second half of 2024, eachsubject to FDA feedback; clinical studies including status, progressand results, timing for clinical data readouts, planning efforts for
future clinical studies, NDA/MAA (and equivalent) filings andpotential additional approvals, research and discovery efforts
including the potential of our drug candidates, IND filings,
regulatory designations and programs, timing and likelihood of
success, plans and objectives of management for future operations,estimated patient populations, the market opportunity for our drug
and drug candidates and business guidance, including discovery,clinical and regulatory milestones, cash guidance, expectation

regarding our financial performance and business strategy, and thepotential impact of the Inflation Reduction Act (the “IRA”), speak onlyat the time this presentation was prepared. Such statements are
based upon the information available to us now and are subject tochange. We will not necessarily inform you of such changes. Thesestatements are not guarantees of future performance and are
subject to certain risks, uncertainties and assumptions that are
difficult to predict. Therefore, actual results could differ materiallyand adversely from those expressed in any forward-looking
statements as a result of various factors, including, among others,
the success of our commercialization efforts with respect to
QINLOCK, including our launch in key European markets, ourlimited experience as a commercial company, our ability to obtain,or any delays in obtaining, required regulatory approvals for our
drug and drug candidates, our reliance on sole source third-party
suppliers, our exposure to criminal sanctions, civil penalties,
contractual damages, reputational harm, and diminished profitsand future earnings from our relationships with customers andthird-party payors that are subject to applicable anti-kickback, fraud
and abuse, and other healthcare laws and regulations, and healthinformation privacy and security laws, our failure to obtain or
maintain adequate coverage and reimbursement for new orcurrent products, recently enacted and future legislation may
increase the difficulty and cost for us to obtain marketing approvalof and commercialize our drug candidates, the potential for
QINLOCK or any current drug candidates, such as vimseltinib andDCC-3116, or future drug candidates, if successfully developed andapproved, to cause undesirable side effects that limit thecommercial profile or result in other significant negative
consequences for approved products or delay or prevent further
development or regulatory approval with respect to drugcandidates or new indications, or cause regulatory authorities torequire labeling statements, such as boxed warnings, ourcompetition may discover, develop, or commercialize products
before or more successfully than we do, our estimates for market
opportunities for our approved drug and drug candidates, market
acceptance by physicians, patients, third-party payors, and others in
the medical community of QINLOCK, and of any future approved
drugs, such as vimseltinib or DCC-3116, if approved, our failure toobtain additional marketing approvals in other foreign jurisdictions,the potential for ongoing enforcement of post-marketing
requirements for QINLOCK and any drug candidate for which we
obtain marketing approval to subject us to substantial penalties,
including withdrawal of QINLOCK or any future approved productfrom the market, if we fail to comply with all regulatory
requirements, our assumptions in connection with the market
opportunity for the INSIGHT trial patient population including theaggregate potential revenue opportunity for QINLOCK, our ability tocomplete, and the costs and timing of completing, the development
and commercialization of our drug and drug candidates, oursuccess in enrolling patients in clinical trials, including in our clinical
trials of vimseltinib or DCC-3116, the potential for serious adverse
events or unacceptable side effects to be identified during thedevelopment of our drug or drug candidates, our ability to obtainor, if granted, retain orphan drug exclusivity for our drug or drugcandidates; our incurrence of significant operating losses since our
inception and our expectation that we will incur continued losses
for the foreseeable future and may never achieve or maintainprofitability, our ability to raise capital when needed, our reliance onthird parties to conduct our clinical trials and preclinical studies, ourreliance on third parties for the manufacture of our drugcandidates for preclinical testing and clinical trials, and for the
manufacture of QINLOCK for commercialization and clinical trials,
and our ability to enforce our intellectual property rights throughout
the world. New risk factors and uncertainties may emerge fromtime to time, and it is not possible to predict all risk factors anduncertainties. There can be no assurance that the opportunity willmeet your investment objectives, that you will receive a return of allor part of such investment. Investment results may vary significantly
over any given time period. The appropriateness of a particularinvestment or strategy will depend on an investor's individual
circumstances and objectives. Investors should independently
evaluate specific investments. For further information regardingthese risks, uncertainties and other factors, you should read the“Risk Factors” section of our Annual Report on Form 10-K for theyear ended December 31, 2023 filed with the Securities andExchange Commission (the “SEC”), and our other SEC filings.
© 2024 Deciphera Pharmaceuticals. The Deciphera logo and the
QINLOCK® word mark and logo are registered trademarks and the
Deciphera word mark is a trademark of Deciphera Pharmaceuticals,
LLC. Deciphera and One Mission, Inspired by Patients: Defeat
Cancer, are trademarks of Deciphera Pharmaceuticals, LLC. All
rights reserved. This presentation may contain trade names,
trademarks or service marks of other companies. Deciphera does
not intend the use or display of other parties’ trade names,
trademarks or service marks to imply a relationship with, orendorsement or sponsorship of, these other parties.

2

DECIPHERA

ONE MISSION, INSPIRED BY PATIENTS: DEFEAT CANCER$1 billion in peak revenue for QINLOCK® (ripretinib) and vimseltinib provides path tobecoming self-sustaining company
QINLOCK®

Growing revenue globally in 4L GIST
with label expansion potential in 2L

Vimseltinib

Planned NDA and MAA filings for TGCT andnew clinical study in cGVHD

Focused Investment
in Pipeline
Financials

Clinical programs with first- or
best-in-class potential
Cash runway into 2H 2026

Notes: 2L=second line; 4L= fourth line; NDA=New Drug Application; MAA=Marketing Authorisation Application; TGCT=tenosynovial giant cell tumor; cGVHD=chronic graft versus host disease.

3

DECIPHERA

ROBUST PIPELINE OF SWITCH-CONTROL KINASE INHIBITORSRESEARCH

1

KIT Inhibitor

Vimseltinib
CSF1R Inhibitor

IND-ENABLINGULK Inhibitor

DCC-3084

Pan-RAF Inhibitor

DCC-3009
Pan-KIT Inhibitor

ISR Program
GCN2 Activator

PHASE 2

PHASE 3

REGULATORYSUBMISSIONAPPROVED+ GlobalApprovals

GIST ≥4th Line
GIST 2nd Line KIT Exon 11 + 17/18(INSIGHT Phase 3 Study)2
Submission to FDA andEMA planned3

TGCT (MOTION Phase 3 Study)
TGCT (Phase 1/2 Study)
cGVHD (Phase 2 Study)

DCC-3116

PHASE 1

Planned for 4Q 2024

+ KRASG12C Inhibitor (Sotorasib)+ KIT Inhibitor (QINLOCK)
Solid Tumors andHematologic Malignancies
GIST

IND planned for 1H 2024

Solid Tumors

Notes: ISR=Integrated Stress Response; BRAF=proto-oncogene b-RAF; CSF1R=colony-stimulating factor 1 receptor; EGFR=epidermal growth factor receptor; GCN2=general control nonderepressible 2; GIST=gastrointestinal stromal tumor;
G12C=single point mutation with a glycine-to-cysteine substitution at codon 12; KIT=KIT proto-oncogene receptor tyrosine kinase; RAF=rapidly accelerated fibrosarcoma; RAS=rat sarcoma gene; TGCT=tenosynovial giant cell tumor; cGVHD=chronic
graft versus host disease; IND=Investigational New Drug. ULK=unc-51-like autophagy-activating kinase; (1) Exclusive development and commercialization license with Zai Lab in Greater China for QINLOCK; (2) The patient population for the INSIGHT
study consists of second-line GIST patients with mutations in KIT exon 11 and 17 and/or 18 and the absence of mutations in KIT exon 9, 13, and/or 14 (also referred to as KIT exon 11 + 17/18 patients); (3) The Company expects to submit a New Drug
Application (NDA) to the U.S. Food and Drug Administration (FDA) for vimseltinib for the treatment of patients with TGCT in 2Q 2024 and a Marketing Authorisation Application (MAA) to the European Medicines Agency in 3Q 2024.

4

DECIPHERAEXPECTED 2024 MILESTONES✓

Continue enrolling INSIGHT pivotal Phase 3 study in 2L KIT exon 11+17/18 GIST patients(2024)
Published in Nature Medicine the INTRIGUE clinical results in 2L KIT exon 11+17/18 GIST
patients (January 2024)
Continue geographic expansion for 4L GIST in European and international markets(2024)

Vimseltinib
Submit NDA (2Q 2024) and MAA (3Q 2024) for TGCT and prepare for commercial
launchPresent additional results from Part 1 of Phase 3 MOTION study in TGCT (2Q 2024)
Present updated data from Phase 1/2 study in TGCT (2H 2024)
Initiate Phase 2 POC study in cGVHD (4Q 2024)

Early-Stage Pipeline
DCC-3116: Select recommended Phase 2 dose for expansion cohort(s) (2024)
DCC-3084: Initiate Phase 1 study (1H 2024)
DCC-3009: Submit IND to FDA (1H 2024) and initiate Phase 1 study (2H 2024)

Notes: 2L=second line; NDA=New Drug Application; LATAM=Latin America; cGVHD=chronic graft versus host disease; FDA=Food and Drug Administration; (1) Phase 2 study conditional and subject to FDA approval.

5

®
QINLOCK (ripretinib)

6

CONTINUED GROWTH IN THE US AND AROUND THE WORLD
Total Annual Revenue1$180

MILLIONSMILLIONS

$40

$96.1

$80
$60

$30

$41.8
$32.9

$33.2

$7.3

$8.6

$37.3

$25.6

$24.6

4Q 2022

1Q 2023

$46.7
$11.4

$9.1

$8.4

$20
$10

$40

↑42% YoY$50$134.0

$140
$100

$60

$163.4$160$120

Net Product Revenue

$28.9

$32.7

$35.3

3Q 2023

4Q 2023

$0

$20
$0
2021

2022

2023

U.S.

2Q 2023

Ex-U.S.

Notes: Full prescribing information is available at www.QINLOCK.com; YoY=Year over Year; (1) Total annual revenue includes net sales of QINLOCK and collaboration revenue.

7

| 4L GASTROINTESTINAL STROMAL TUMORSTRONG CLINICAL BENEFIT SEEN IN PHASE 3 INVICTUS STUDY
Progression-Free Survival1,2Overall Survival1,2

100

SECONDARY ENDPOINT: 0S

84%

60

1.0

40

MONTH
mPFS

MONTHS
mOS

80

HR=0.16(95% CI, 0.1-0.27)

MONTHS
mPFS

risk reduction ofdeath vs. placebo3

18.2
Overall Survival (%)

Progression-Free Survival (%)

6.3

59%

100

risk reduction ofprogression ordeath vs. placebo280Long-term Follow-up Analysis

QINLOCK 150 mg QD (n=85)

Placebo (n=44)20

HR=0.41(95% CI, 0.26-0.65)

60

6.3

40

MONTHSmOS

20

QINLOCK (n=85)
Placebo (n=44)

0

0
0

2

4

6

8

10

12

14

85
44

65
7

18

20

22

24

26

28

30

32

34

0

Time (months)

Number of patients at risk
QINLOCK
Placebo

16

4

8

12

Number of patients at risk
52
4

37
1

28
1

22
1

15
0

11

9

8

6

4

2

2

2

1

1

0

QINLOCK
Placebo

85
44

16

20

24

28

32

36

29
8

18
5

3
0

0

Time (months)
76
29

59
17

49
12

39
12

32
12

Notes: 4L=fourth-line; CI=confidence interval; HR=hazard ratio; mOS=median overall survival; OS=overall survival; PFS=progression-free survival; QD=daily; (1) Blay JY et al. Lancet Oncol. 2020;21(7):923-934.; (2) von Mehren M et al. Poster presented
at: ESMO Congress; September 16-21, 2021; Virtual. Poster 1540P

8

| 4L GASTROINTESTINAL STROMAL TUMORGLOBAL COMMERCIALIZATION CAPABILITIES OFFER SYNERGIES FORQINLOCK AND VIMSELTINIBQINLOCK now approved in >40 Countries
Direct Footprint• Direct commercialization in US and major European countries• Expansion to mid-sized European markets gated on market access

Partners• Zai Lab collaboration for Greater China• Distributors in Australia, Canada, Israel, New Zealand and Singapore

Complementary
Commercial Opportunities• Established relationships with physicians whotreat GIST and TGCT
• 70%-80% overlap in US prescribing physiciansfor GIST and TGCT• New distributor for Central and Eastern Europe
Notes: QINLOCK is approved for 4th line GIST in Australia, Canada, China, the European Union, Hong Kong, Iceland, Israel, Liechtenstein, Macau, New Zealand, Norway, Singapore, Switzerland, Taiwan, the United Kingdom, and the United States.

9

| 4L GASTROINTESTINAL STROMAL TUMORSIGNIFICANT PROGRESS MADE IN EUROPE TO ENABLE FUTURE LAUNCHESPOSITIONING QINLOCK FOR GROWTH
Finland

NorwaySwedenLaunched countries

Estonia
LatviaDenmark

Planned countries

Lithuania

IrelandGreat
Britain

Netherlands

PolandGermany

BelgiumPartnered countries

Czech Rep.

France*Austria
Switzerland*
Slovenia

Slovakia

Hungary
Croatia
Bosnia andHerzegovina

Italy

Romania

SerbiaBulgaria

Montenegro
Macedonia

Portugal

Spain

Albania
GreeceMalta

Cyprus

Notes: France and Switzerland under AP2 (post approval access program) and Art 71 (named patient sales) respectively. Price negotiations ongoing..

10

| 2L GASTROINTESTINAL STROMAL TUMORONGOING INSIGHT PHASE 3 STUDY

BTD
GrantedPHASE 3, RANDOMIZED, MULTICENTER, OPEN-LABEL STUDY
05 January 2024

Ripretinib versus sunitinibin gastrointestinal stromal
tumor: ctDNA biomarker
analysis of the phase 3
INTRIGUE trial1“The results of this exploratory
analysis suggest ctDNA sequencing
may improve the prediction of theefficacy of single-drug therapies, andsupport further evaluation of
ripretinib in patients with KIT exon
11+17/18 mutations…”

QINLOCK (n=36)

2:1 Randomization
Open-label Studyn=54

150 mg QD

Patients randomized to sunitinib arm
may crossover to QINLOCK arm after
PD

Sunitinib (n=18)

50 mg QD

Treatment
until diseaseprogression,unacceptabletoxicity, orwithdraw of
study consent(4 weeks on, 2 weeks off)

Primary Endpoint

PFS by IRR using mRECISTKey Secondary Endpoints
ORR by IRR using mRECISTOS

Notes: 2L=second-line; ctDNA=circulating tumor deoxyribonucleic acid; ECOG=Eastern Cooperative Oncology Group; GIST=gastrointestinal stromal tumor; IRR= individual research result; KIT=KIT proto-oncogene receptor tyrosine kinase;
mRECIST=modified Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 criteria; ORR=objective response rate; OS=overall survival; PD=progressive disease ; PFS=progression-free survival; QD=daily; (1) Heinrich, M.C., Jones, R.L., George, S.
et al. Ripretinib versus sunitinib in gastrointestinal stromal tumor: ctDNA biomarker analysis of the phase 3 INTRIGUE trial. Nat Med (2024). https://doi.org/10.1038/s41591-023-02734-5

11

| EXPLORATORY ANALYSIS FROM INTRIGUE STUDY IN 2L GIST

IMPRESSIVE ORR FOR QINLOCK IN KIT EXON 11+17/18 PATIENTS 1,2
Percent Change In The Sum Of Target Lesion Diameters

70
60

70

Sunitinib

QINLOCK

60

50

50

40

40

30

30

20

20

10

10

0

0

-10

-10

-20

-20

-30

-30
-40

-40
-50
-50
-60

Best Confirmed Response:
Partial Response (PR)-60

OBJECTIVE RESPONSE RATE
-70

-70
-80

Stable Disease (SD)
Progressive Disease (PD)-90

Not Evaluable (NE)
-100

-80

QINLOCKSUNITINIB

0%

44.4%

-90

VS.

3,4,5

-100

Notes: Data presented at the ASCO Plenary Series Session 2023; Full prescribing information is available at www.QINLOCK.com ; Deciphera data on file; 2L=second-line; (1) data cut off date of September 1, 2021; (2) for 2 patients in the sunitinib arm
and 1 patient in the ripretinib arm, no postbaseline disease assessment was available; (3) ORR was confirmed with follow-up imaging; (4) determined using modified Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 criteria; (5) response
difference=44.4%, 95% CI (23.0, 62.7), nominal p value 0.0001; (6) Heinrich, M.C., Jones, R.L., George, S. et al. Ripretinib versus sunitinib in gastrointestinal stromal tumor: ctDNA biomarker analysis of the phase 3 INTRIGUE trial. Nat Med (2024).
https://doi.org/10.1038/s41591-023-02734-5.

12

| EXPLORATORY ANALYSIS FROM INTRIGUE STUDY IN 2L GISTPFS STRONGLY FAVORS QINLOCK IN KIT EXON 11+17/18 PATIENTS 1PRIMARY ENDPOINT: PFS

78%

QINLOCK (n=27)

100

Progression-Free Survival (%)

Sunitinib (n=25)

risk reductionof progression
or death
vs. sunitinib

80

1.5

14.2

MONTHSmPFS

60

MONTHS
mPFS

40

20

+ Censored

0
0

3

6

9

12

15

18

21

24

27

MonthsNumber of Patients at Risk:
QINLOCK

27

23

19

14

13

9

7

1

0

Sunitinib

25

9

4

2

2

2

1

1

0

(median PFS of 14.2 months vs. 1.5 months; HR=0.22, 95% CI [0.11-0.44], nominal p value <0.0001)
Notes: Data presented at the ASCO Plenary Series Session 2023; Full prescribing information is available at www.QINLOCK.com ; Deciphera data on file; 2L=second-line; HR=hazard ratio; KIT=KIT proto-oncogene receptor tyrosine kinase;
mPFS=median progression-free survival; PFS=progression-free survival; (1) data cut off date of September 1, 2021; (2) Heinrich, M.C., Jones, R.L., George, S. et al. Ripretinib versus sunitinib in gastrointestinal stromal
tumor: ctDNA biomarker analysis of the phase 3 INTRIGUE trial. Nat Med (2024). https://doi.org/10.1038/s41591-023-02734-5

13

| EXPLORATORY ANALYSIS OF INTRIGUE STUDY IN 2L GIST

SUBSTANTIAL OS FOR QINLOCK IN KIT EXON 11+17/18 PATIENTS 1
LANDMARK ANALYSISSECONDARY ENDPOINT: 0S

number of patients alive at 30 months for
QINLOCK was estimated to be nearly twice
as sunitinib

QINLOCK (n=27)

100

Sunitinib (n=25)

QINLOCK

Overall Survival (%)

80

60%

VS.

At 30 MONTHSSUNITINIB30%

AT 30 MONTHS

NE

60

mOS

17.5

40

MONTHSmOS

20+ Censored

0
0

3

6

9

12

15

18

21

24

27

30

33

36

39

42

1

0

MonthsNumber of Patients at Risk:
QINLOCK

27

27

25

23

23

23

21

18

16

12

8

5

1

Sunitinib

25

20

18

16

16

15

10

8

8

6

5

2

0

(median OS of NE months vs. 17.5 months; HR=0.34, 95% CI [0.15-0.76], nominal p value 0.0061)
Notes: Data presented at the ASCO Plenary Series Session 2023; Full prescribing information is available at www.QINLOCK.com; Deciphera data on file; 2L=second-line; HR=hazard ratio; KIT=KIT proto-oncogene receptor tyrosine kinase; NE=not
estimable; OS=overall survival; (1) the data cut off date for the second interim analysis for overall survival was September 1, 2022; (2) Heinrich, M.C., Jones, R.L., George, S. et al. Ripretinib versus sunitinib in gastrointestinal stromal
tumor: ctDNA biomarker analysis of the phase 3 INTRIGUE trial. Nat Med (2024). https://doi.org/10.1038/s41591-023-02734-5

14

| 2L AND 4L GASTROINTESTINAL STROMAL TUMOROPPORTUNITY TO ADVANCE THE STANDARD OF CARE ACROSS MULTIPLE LINES
OF THERAPY
4L

2L3

Established 4L Standard-of-Care Across
All Mutations

Potential to Optimize 2L Therapy
Based on Secondary Mutations

6.3 mo. mPFS (HR=0.16)1
11.8% ORR

For exon 11+17/18 patients

mOS 18.2 mo. (HR=0.41)

14.2 mo. mPFS (HR=0.22)4~90% of prescribers cite QINLOCK as the
4L standard-of-care across all
mutations2✓ KIT exon 11✓ KIT exon 9✓ PDGFRA✓ Wild Type✓ Unknown mutational
status

44.4% ORR
ctDNA
AnalysismOS not estimable (HR=0.34)

sunitinib

Notes: 2L=second-line; 4L=fourth-line; HR=hazard ratio; mOS=median overall survival; mPFS=median progression-free survival; (1) Updated data on the INVICTUS Study presented at the ESMO Congress 2021; Full prescribing information isavailable at www.QINLOCK.com; Overall survival data includes all time periods, including dose escalation. Placebo arm includes patients taking placebo who, following progression, were crossed-over to QINLOCK treatment; The long-term
follow-up analysis was conducted approximately 19 months from the data cutoff date in the primary analysis and was not powered to show statistical significance; (2) Deciphera ATU survey, 1Q 2022; approximate % of GIST Treaters agreeing tostrongly agreeing that QINLOCK is the standard of care for 4L+ advGIST patients; % of GIST treaters stating their likelihood to prescribe QINLOCK across GIST mutational types.; (3) Use of QINLOCK in the 2nd line setting for patients with GIST
with exon 11 + 17/18 mutations is subject to positive INSIGHT phase 3 study and approval by regulatory authorities; (4) Deciphera Data on File. Data cut off date of September 1, 2021; (5) Heinrich, M.C., Jones, R.L., George, S. et
al. Ripretinib versus sunitinib in gastrointestinal stromal tumor: ctDNA biomarker analysis of the phase 3 INTRIGUE trial. Nat Med (2024). https://doi.org/10.1038/s41591-023-02734-5

15

| 2L GASTROINTESTINAL STROMAL TUMOR

A 2L KIT EXON 11+17/18 INDICATION ESTIMATED TO DOUBLE QINLOCK U.S.
PEAK REVENUE POTENTIAL 1
QINLOCK Estimated U.S. Peak Revenue ($MM)1$400$175-$200MM Incremental Peak
Revenue for 2L Indication

$350
$300

New QINLOCK-treated patients in 2L1
More months of therapy per patient
Net price growth

($MM)

$250
$200

$350-$400MM Total U.S.
Peak Revenue1$175-$200MM Peak Revenue for
4L Indication

$150
$100

Modest volume growth as average DOT
matures
Net price growth$50$0
2L KIT exon 11+17/18
indication and 4L indication

Notes: Full prescribing information is available at www.QINLOCK.com; 2L=Second-Line; 4L=Fourth-Line; DOT=Duration of Therapy; (1) These estimates are based on management's current expectations and assumptions, including, without
limitation, estimates of net price growth over time, adoption of ctDNA testing for GIST patients, estimates of on-label adoption, the potential for unpromoted off-label usage and reasonable expectations of the potential impact of the Inflation
Reduction Act (the full impact of which is still under review) and an assumption of a second-line approval in GIST patients with mutations in KIT exon 11 + 17/18; estimates are inherently uncertain and are subject to a wide variety of assumptions,risks and uncertainties that can cause actual results to differ materially. (1) Estimate assumes positive results of INSIGHT study.

16

GROWTH OPPORTUNITIES AHEAD BUILDING ON STRONG MOMENTUM$163.4M in total revenue in 2023
42% YoY growth in net product revenue (4Q 2023)

Growth in 2024 expected from increasing
treatment duration and geographic expansion
Inclusion in NCCN guidelines for select 2L patients
may impact unpromoted use based on
independent physician decision
Significant future growth opportunity in 2L GIST inpatients with mutations in KIT exon 11+17/18
subject of ongoing Phase 3 INSIGHT study

Notes: 2L=second line; YoY=Year over Year

17

VIMSELTINIB

18

VIMSELTINIB | OVERVIEWPOTENTIAL BEST-IN-CLASS TREATMENT FOR TGCT

Vimseltinib is an oral, switch-control TKI specifically designed to
selectively and potently inhibit CSF1R

Successful pivotal Phase 3 MOTION study and Phase 1/2 study
positions vimseltinib as potential differentiated therapy toaddress high unmet medical need
NDA and MAA submissions expected in 2Q 2024 and 3Q 2024
Large market opportunity in tenosynovial giant cell tumor(TGCT) with strong commercial synergies with QINLOCK
New growth opportunity in chronic graft versus host disease(cGVHD); Phase 2 study planned to initiate in 4Q 20241

Notes: CSF1=colony-stimulating factor 1; CSF1R=colony-stimulating factor 1 receptor; TKI=tyrosine kinase inhibitor; NDA=New Drug Application; MAA=Marketing Authorisation Application; (1) Phase 2 study conditional and subject to
FDA approval.

19

VIMSELTINIB | TENOSYNOVIAL GIANT CELL TUMORSIGNIFICANT UNMET MEDICAL NEED

Locally aggressive tumor with substantial
morbidity including severe pain, limited
function, swelling, and stiffness

Many patients are not amenable to surgery or
have disease recurrence after one or more
surgeries

Only FDA approved therapy has a black box
warning and REMS program due tohepatotoxicity risks limiting adoption; rejectedby EMA“The impact is huge. You
get really limited by thetumor….What bothers
me the most are thepain symptoms…Youcontinuously take pain
meds to fight the pain.
— TGCT patient”

Notes: FDA=U.S. Food and Drug Administration; EMA=European Medicines Agency; REMS=Risk Evaluation and Mitigation Strategies; TGCT=tenosynovial giant cell tumor;

20

VIMSELTINIB | PHASE 3 MOTION STUDY OF PATIENTS WITH TGCTA MULTICENTER, RANDOMIZED, PLACEBO-CONTROLLED, DOUBLE-BLIND STUDYDOUBLE-BLIND PERIODPart 1: Eligible study participants wereassigned to receive either vimseltinib ormatching placebo for 24 weeks.

OPEN-LABEL PERIODPart 2: A long-term treatment

phase in which all participants may
receive open-label vimseltinib.

International
Study with
35 Sites

2:1 Randomization
Enrollment Complete(n=123)

Placebo (n=40)(24 weeks)

Assessed the efficacy and safety ofvimseltinib for the treatment of patientswith TGCT not amenable to surgery1

Primary Endpoint

Vimseltinib (n=83)
30 mg BIW (24 weeks)

Phase 3 MOTION Study

Objective Response Rate (ORR)

Open-Label
Study
Patients had the option
to continue onor cross over tovimseltinib 30 mg BIW

Secondary Endpoints
ORR per Tumor Volume Score
Mean Change From Baseline (CFB) in
Active Range of Motion (ROM)Mean CFB in PROMIS-PF
Mean CFB in Worst Stiffness NRS
Mean CFB in EQ-VAS
BPI-30 Response Rate in Worst Pain

Notes: BIW=twice weekly; TGCT=tenosynovial giant cell tumor. PROMIS=Patient-reported Outcomes Measurement Information System; worst stiffness by Numeric Rating Scale (NRS), worst pain response rate by Brief Pain Inventory (BPI). (1) Primaryand secondary endpoints at Week 25.

21

VIMSELTINIB | PHASE 3 MOTION STUDY OF PATIENTS WITH TGCTSTUDY MET PRIMARY AND ALL SIX KEY SECONDARY ENDPOINTSKey Secondary Endpoint

ORR at Week 25 by RECIST v1.1

ORR at Week 25 by Tumor Volume Score (TVS)
80%

40%

40%

30%

ORR at Week 25
p<0.0001
Placebo

20%

Vimseltinib

0% 40%

10%

0%

Placebo

67%

70%
60%
50%
40%
30%

ORR at Week 25
p<0.0001
Placebo

20%

0%

0%
Vimseltinib

n=83 (95% CI: 29%, 51%)

Vimseltinib

0% 67%

10%0%n=40 (95% CI: 0%, 9%)Response Rate by TVS (%)

Response Rate by RECIST (%)

50%

Primary Endpoint

Placebon=40 (95% CI: 0%, 9%)Vimseltinib

n=83 (95% CI: 56%, 77%)

Notes: Results are based on a data cutoff date of August 22, 2023. Endpoints evaluated by blinded independent radiologic review (IRR). ORR=Objective Response Rate by Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 Complete
Response = 4 (5%); Partial Response = 29 (35%).
ORR by TVS Complete Response = 4 (5%); Partial Response = 52 (63%). A response by TVS is defined as a ≥50% reduction in the tumor volume relative to baseline.

22

VIMSELTINIB | PHASE 3 MOTION STUDY OF PATIENTS WITH TGCTKEY SECONDARY ENDPOINT: ACTIVE RANGE OF MOTION

Improvement in ROM at Week 25 (%)

25%

Improvement in Active Range of Motion (ROM)

18.4%

20%

15%
Improvement difference of 14.6%
between vimseltinib and placebo(95% CI: 4.0%, 25.3%); p=0.0077

10%

5%

~5X

IMPROVEMENTROM
AT WEEK 25

3.8%

IN

0%
Placebo n=38
Baseline of 62.9%

Vimseltinib n=79
Baseline of 63.0%

Notes: n=number of patients with a baseline ROM value. Active ROM is measured for the affected joint as a percentage of a normal reference range as defined by the American Medical Association. The mean change from baseline at Week 25 wascompared between the two treatment arms.

23

VIMSELTINIB | PHASE 3 MOTION STUDY OF PATIENTS WITH TGCTFAVORABLE SAFETY AND TOLERABILITY PROFILE FOR VIMSELTINIB
Treatment Emergent Adverse Events (TEAEs) in ≥15% of Patients
Preferred Term n (%)

Vimseltinib (n=83)

Placebo (n=391)

All Grades

Grade 3/4

All Grades

Grade 3/4

Periorbital edema^

37 (45%)3 (4%)

5 (13%)

0

Fatigue^27 (33%)0

6 (15%)

0Face edema^

26 (31%)1 (1%)

3 (8%)

0Pruritus^

24 (29%)2 (2%)

3 (8%)

0

Headache^23 (28%)1 (1%)

10 (26%)0Asthenia^

22 (27%)

1 (1%)

9 (23%)

1 (3%)

Nausea^21 (25%)0

8 (21%)

1 (3%)CPK increased

20 (24%)8 (10%)

00

AST increased

19 (23%)0

1 (3%)0

Arthralgia^

16 (19%)0

6 (15%)

1 (3%)Rash^

16 (19%)02 (5%)0Rash maculopapular^

16 (19%)1 (1%)

00

Edema peripheral^

15 (18%)0

3 (8%)

0Hypertension

14 (17%)

4 (5%)

4 (10%)

1 (3%)

Diarrhea

10 (12%)0

8 (21%)

1 (3%)•

No evidence ofcholestatic
hepatotoxicity forvimseltinib•

Serum enzyme
elevations wereconsistent with the
known mechanismof action of CSF1R
inhibitors•

5/83 (6%)
treatment
discontinuation
due to TEAEs in thevimseltinib arm

Notes: (1) Does not include one patient randomized to placebo that did not receive study drug.

TEAE incidence is based on maximum grades per CTCAE v5.0. The only Grade 4 adverse events were CPK Increased observed in two patients. TEAEs leading to dose interruption were 44 (53%) and dose reduction 35 (42%).
^ Denotes adverse events without Grade 4 criteria per CTCAE v5.0.

24

VIMSELTINIB | PHASE 1/2 STUDY OF PATIENTS WITH TGCTAN INTERNATIONAL, MULTICENTER, OPEN-LABEL PHASE 1/2 STUDYPHASE 1 (DOSE ESCALATION)
A pharmacologically guided 3 + 3 design, todetermine the recommended Phase 2 dose (RP2D)
and the maximum tolerated dose

PHASE 2 (EXPANSION)
Study to evaluate the safety, tolerability, and preliminary efficacy in two TGCT expansion cohorts
Recommended Phase 2 dose of 30 mg twice weekly with no loading dose

COHORT A (n=46)

COHORT 5 (n=8)
Loading Dose30 mg QD x 5 days

30 mg twice weekly

COHORT 8 (n=12)
Loading Dose30 mg QD x 3 days

Dose

10 mg QDCOHORT 9 (n=12)
Loading Dose

20 mg QD x 3 days

TGCT patients with no prior anti-CSF1/CSF1R therapy(previous therapy with imatinib or nilotinib is allowed)

Dose

Dose

6 mg QD

RP2D

30 mg twice
weeklyPHASE 2 (n=65)
COHORT B (n=19)
TGCT patients with prior anti-CSF1/CSF1R therapy (previous
therapy with imatinib or nilotinib alone would not be eligible)

Cohort B ACTIVE AND NOT RECRUITING
Notes: Data presented as of data cutoff of June 27, 2023; CSF1=colony-stimulating factor 1; CSF1R=colony-stimulating factor 1 receptor; QD=once daily; RP2D=recommended Phase 2 dose; TGCT=tenosynovial giant cell tumor.

25

VIMSELTINIB | PHASE 1/2 STUDY OF PATIENTS WITH TGCTROBUST ANTI-TUMOR ACTIVITY INCREASING OVER TIME
Phase 1 (Escalation)

Percent change in the sum of diameters in target
lesions from baseline to the post-baseline nadir

100

80

80
60

BEST OVERALL ALL COHORTSRESPONSE

72%

40

40
20

0

0

-20

-20

-40

-40

-60

-60

-80

-80

COHORT 5
30 mg BIW

COHORT 8
10 mg QD

BEST OVERALLRESPONSE

60

20

-100

Phase 2 (Expansion)

100

COHORT 9
6 mg QD-100

COHORT A

COHORT B1

64% 44%

ORR AT WEEK 25
COHORT A

38%

COHORT A

COHORT B

30 mg BIW

30 mg BIW

Notes: Results are reported for patients with TGCT with a data cutoff of June 27, 2023; BIW=twice weekly; QD=once daily; ORR=Objective Response Rate by Response Evaluation Criteria in Solid Tumors (RECIST) v1.1; (1) Previously treated withspecific anti-CSF1/CSF1R agents

Complete Response (CR)

Partial Response (PR)

Stable Disease (SD)26

VIMSELTINIB | PHASE 1/2 STUDY OF PATIENTS WITH TGCTINCREASING DURATION OF THERAPY AND DURABLE RESPONSES
Phase 1 (Escalation)

Phase 2 (Expansion)#

MEDIAN TREATMENT
DURATIONMEDIAN TREATMENT
DURATIONCOHORT A

ALL COHORTS

21.0 MONTHS

25.1 months

48% ACTIVE
COHORT A PATIENTS

47% ACTIVE PATIENTSCOHORT B
7.3 MONTHS

74% ACTIVE
COHORT B PATIENTSMEDIAN DURATION OF RESPONSE(months) (min, max.):
NR (0.03+, 25.4+)

MEDIAN DURATION OF RESPONSE(months) (min, max.):
NR (4.0+, 21.0+)(months) (min, max.):
NR (3.8+, 45.2+)

Cohort 5 (30 mg BIW)
Cohort 8 (10 mg QD)
Cohort 9 (6 mg QD)

0

5

10

15

20

25

30

35

40

45

Cohort A (30 mg BIW)
Cohort B (30 mg BIW)

50

0

5

Months on Study

10

15

20

25

30

35

Months on Study

Notes: Results are reported for patients with TGCT with a data cutoff of June 27, 2023. NR=not reached by Kaplan-Meier analysis. + indicates response is ongoing.

Complete Response (CR)

Partial Response (PR)

Ongoing

Not Evaluable

Stable Disease (SD)# From Local Data

27

VIMSELTINIB | PHASE 1/2 STUDY OF PATIENTS WITH TGCTFAVORABLE SAFETY AND TOLERABILITY PROFILE FOR VIMSELTINIB WITH LONGTERM FOLLOW UPTreatment Emergent Adverse Events (TEAEs) in ≥15% of Patients Receiving Vimseltinib
Phase 1/2 Combined: All Patients(n=95)

Preferred Term n (%)

All Grades

Grade 3/4

Blood CPK increased

63 (66%)39 (41%)

Periorbital edema^45 (47%)0

Headache^37 (39%)0

Fatigue^35 (37%)2 (2%)

Myalgia^28 (29%)3 (3%)

Nausea^28 (29%)0

AST increased

27 (28%)4 (4%)

Arthralgia^

27 (28%)2 (2%)

Asthenia^

23 (24%)

1 (1%)

Edema peripheral^

23 (24%)0Rash maculopapular^

21 (22%)

1 (1%)

Face edema^21 (22%)0Pruritus^

20 (21%)0

Diarrhea

19 (20%)1 (1%)Rash^

18 (19%)0

COVID-19

18 (19%)0Hypertension

15 (16%)6 (6%)

Lipase increased

15 (16%)

4 (4%)

Amylase increased

15 (16%)

3 (3%)

ALT increased

15 (16%)

1 (1%)•

No evidence ofcholestatic
hepatotoxicity•

Serum enzyme
elevations wereconsistent withthe knownmechanism ofaction of CSF1R
inhibitors•

9/95 (9%)
treatment
discontinuation
due to TEAEs in
combined Phase
1/2

Notes: Results are reported for patients with TGCT with a data cutoff of June 27, 2023. TEAE incidence is based on maximum grade per CTCAE v4.03. TEAEs were summarized in n=95 patients with TGCT across all cohorts in the Phase 1/2 study. One
patient from Phase 1 and one patient from Cohort A discontinued and enrolled into Cohort B. The only Grade 4 adverse events were CPK increased.
^ Denotes adverse events without Grade 4 criteria per CTCAE v4.03.

28

VIMSELTINIB | PHASE 3 STUDY AND PHASE.1/2 STUDY OF PATIENTS WITH TGCTPLANNED REGULATORY SUBMISSIONS: NDA IN Q2 2024 AND MAA IN Q3 2024
PHASE 1/2 STUDY UPDATEPIVOTAL PHASE 3 MOTION STUDY

Results demonstrate strong clinical benefit, welltolerated safety profile, and long duration of treatment

Met its primary and all key secondary endpoints anddemonstrated a well-tolerated safety profile

Best Overall Response:•

72% (Phase 1) and 64% (Phase 2 Cohort A)

Median Treatment Duration:•

25.1 months (Phase 1), 21.0 months (Phase 2 Cohort A)

Active Patients on Treatment:•

Primary Endpoint ORR at Week 25:•

40% for vimseltinib vs. 0% for placebo (p<0.0001)

Key Secondary Endpoints:
Statistically significant and clinically meaningful improvement
across all key secondary endpoints, including:•

67% for vimseltinib vs. 0% for placebo (p<0.0001) ORR by
Tumor Volume Score•~5X improvement in active range of motion vs. placebo(p=0.0077)

47% (Phase 1) and 48% (Phase 2 Cohort A)

Vimseltinib was well-tolerated and the safety profile was consistent with previously disclosed data with no evidenceof cholestatic hepatotoxicity
Notes: ORR=Objective Response Rate by Response Evaluation Criteria in Solid Tumors (RECIST) v1.1; NDA=New Drug Application; MAA=Marketing Authorisation Application

29

VIMSELTINIB | TENOSYNOVIAL GIANT CELL TUMOREXTENSIVE POLYPHARMACY USED TO MANAGE DISEASE MORBIDITY IN THE U.S.
Rx Therapies Received by U.S. TGCT Patients (n=~1,400)1

Any pain or steroid medication

U.S. Incident TKI-treated Patient Share1

85%

Pain medications (oral)

68%

27%
Steroids (oral)

42%

Pain medications (parenteral)

36%

Steroids (parenteral)

35%

TKI

Imatinib (off-label)
Pexidartinib

60%

13%

Other TKI (off-label)

52%~75% of TKI-treated patients have painor steroid medications in their history1

Average Durationof Therapy1• Imatinib ~18 months• Pexidartinib ~10 months

Notes: TKI=tyrosine kinase inhibitor. (1) Deciphera internal analysis of U.S. claims data; eligible patients defined as diagnosed, Rx-treated, and recently engaged with a medical oncologist; claims data span 2012-2022; estimates shown are for 2022;
estimates are inherently uncertain.

30

VIMSELTINIB | TENOSYNOVIAL GIANT CELL TUMORSIGNIFICANT OPPORTUNITY TO BENEFIT PATIENTS WITH TGCT
E.U. Opportunity

U.S. Opportunity

1,400 Incident Patients1$700MM+ U.S. TAM2
Seen by Oncologists

9,000
PrevalentPatients1

1,300
Incident
Patients1
Seen by Surgeons▪ Comparable
incidence andrecurrence rates in
Europe3▪ No approved
therapies

Notes: TAM=total addressable market; (1) Deciphera internal analysis of U.S. claims data; eligible patients defined as diagnosed, Rx-treated, and recently engaged with a medical oncologist (or a surgeon); claims data span 2012-2022; estimates
shown are for 2022; prevalent estimate includes incident patients; estimates are inherently uncertain; (2) Total addressable market calculated as estimated Rx-treated patient incidence x 24 months duration x current pexidartinib WAC price andassumes opportunity at steady state. (3) Mastboom et al. Acta Orthopaedica. 2017;88(6):688-694

31

VIMSELTINIB | TENOSYNOVIAL GIANT CELL TUMORHIGHLY DIFFUSE U.S. MARKET WITH SIGNIFICANT PRESCRIBER OVERLAP
Higher Volume HCPs

Lower Volume HCPs

Incident Rx-treated patients

~500

~900

Healthcare providers

~150

~700

Incident Rx-treated patients / HCP~3~1

HCP academic % / community %60% / 40%

30% / 70%

TKI treatment rate

~50%

~50%

TKI prescriber overlap with GIST

>80%

>70%

16%

Imatinib (off-label)

TKI patient share (all HCPs)

35%
54%
11%

13%

Pexidartinib
Other TKI (off-label)

71%

Imatinib (off-label)
Pexidartinib
Other TKI (off-label)

Notes: TKI=tyrosine kinase inhibitor; HCP=healthcare provider; GIST=gastrointestinal stromal tumor; (1) Deciphera internal analysis of U.S. claims data; eligible patients defined as diagnosed, Rx-treated, and recently engaged with a medical
oncologist; claims data span 2012-2022; estimates shown are for 2022; estimates are inherently uncertain.

32

VIMSELTINIB | TENOSYNOVIAL GIANT CELL TUMOR

LIFE-LONG DISEASE BURDEN IMPACTS HOW PATIENTS FEEL AND FUNCTION
Liza, 341 – Surgery, Pain/Steroid Rx

Engagement with oncologist

Surgery

Treatment
Pain Rx

Pain/steroid Rx

Steroid Rx

TKI RxTKI Rx“I will be in pain, at least part of the day, every day until I die andsometimes that is really hard to deal with.”

SurgeryDavid, 501 – Surgery, Pain/Steroid Rx, TKI Rx

Engagement with oncologist

Surgery
Pain/steroid Rx
TKI Rx“[After my first recurrence], I called my wife to tell her I had to go
through this all over again. I was pretty devastated at that point.”

2018

2019

2020

2021

2022

Notes: TKI=tyrosine kinase inhibitor; (1) Illustrative patient cases based on insights from U.S. claims data (data span 2012-2022) and patient market research (2023).

33

VIMSELTINIB | TENOSYNOVIAL GIANT CELL TUMOR

MARKET RESEARCH HIGHLIGHTS THE POTENTIAL FOR VIMSELTINIB TO DELIVER A
BEST-IN-CLASS PROFILE AND ESTABLISH A NEW STANDARD OF CARE
Relative Scoring of Key Product Attributes
Clinical Attribute

Vimseltinib

Pexidartinib

Preferred Systemic Treatment For TGCT
Imatinib

100%

Tumor Response
Efficacy(Objective Response, CBR)

PROs

Limited Data

(Improvement in Pain & Stiffness)

Grade 3/4 AEs
SafetyNot Reported
in TGCT

Hepatotoxicity
Discontinuation Rates

Vimseltinib(Due to any TEAEs)

Highly Compelling

Moderately Compelling

20 out of 20 TGCT
treaters surveyed
selected vimseltinib as
their preferredtreatment10%0%Pexidartinib

Imatinib

Less Compelling

TGCT Treater Sentiments on Vimseltinib Profile
CLINICAL PROFILE

CLINICAL ACTIVITY“This is very impressive data. Well over half the patients responded tothe medication with excellent outcomes. Pain measurements andmobility scores are quite remarkable compared to anything currently
available.” – Onc“It’s great to see that the best overall response numbers
improve over long-term. In fact, this would probably leadme to keep some patients on it longer than I usuallywould.” – Onc

TREATMENT CHOICE“I would give [vimseltinib] to all
my future TGCT patients.” - Onc

Notes: Qualitative market research conducted by Deciphera based on vimseltinib Phase 1/2 data presented at ESMO in Aug 2022 comparing target product profiles of vimseltinib (blinded), pexidartinib, and imatinib based on USPIs andpublished/presented literature for each product’s efficacy and safety in TGCT diagnosed patients (n=20 HCPs). No head-to-head/comparative studies have been conducted. CBR=Clinical Benefit Rate, PROs=Patient Reported Outcomes, AEs=Adverse
Events, TEAEs=Treatment-Emergent Adverse Events. (1) HCP asked to select their preferred (only 1) product to systemically treat TGCT patients based on current clinical profiles.

34

VIMSELTINIBNEW GROWTH OPPORTUNITY IN cGVHD
Chronic GVHD affects
30-50% of allogenic
hematopoietic celltransplant recipients(14,000 U.S. prevalence)As oral agent, vimseltinib
may offer best-in-class
CSF1R option as single agent
or in combination with otheroral cGVHD therapies

Significant unmet medical
need in steroid refractorypatients (~50%); movement
toward combination therapy“Very few of my patients
can’t take pills so I’dprefer oral vs. IV inalmost every case”1

CSF1R inhibition clinicallyvalidated in Phase 3 study
with antibody (axatilimab)

Vimseltinib single-agent
Phase 2 in cGVHD expected
to start 4Q 20241

Notes: cGVHD=chronic graft versus host disease; (1) Deciphera market research; (2) Phase 2 study conditional and subject to FDA approval.

35

VIMSELTINIBSIGNIFICANT GROWTH OPPORTUNITIES IN TGCT AND cGVHD

Successful pivotal Phase 3 MOTION study in TGCT withexpected NDA submission in 2Q 2024 and MAA
submission in 3Q 2024
Potential for 2+ years treatment duration based on
Phase 1/2 data in TGCT
Significant commercial opportunity in TGCT that is highly
synergistic with GIST
Label expansion opportunity in cGVHD

Notes: cGVHD=chronic graft versus host disease; (1) Deciphera market research; (2) Phase 2 study conditional and subject to FDA approval.

36

PROPRIETARY DRUGDISCOVERY ENGINE

37

DECIPHERA’S PROPRIETARY DRUG DISCOVERY PLATFORM

DRIVING INNOVATION THROUGH OUR PROVEN DISCOVERY ENGINE
Fueled by our proprietary drug discovery platform, we intend
to advance multiple drug candidates to treat cancer
DCC-3116 (ULK)

DCC-3084 (RAF)

DCC-3009 (KIT)

Early-Stage Pipeline

Potential first-in-class
ULK inhibitor
Designed to inhibit
cancer autophagy, abroad potential
resistance mechanism

Potential best-in-class
pan-RAF inhibitor
Validated target withsingle agent andcombination
opportunities

Potential best-in-classpan-KIT inhibitor
Designed to inhibit the
spectrum of KITmutations that drive
GIST

DP-9149, a potent andselective activator of
the GCN2 kinase

EXPECTED 2024 MILESTONEEXPECTED 2024 MILESTONEEXPECTED 2024 MILESTONEEXPECTED 2024 MILESTONE

RP2D decision for
expansion cohort(s)Initiate Phase 1 study

File IND and initiate
Phase 1 study

Advance researchstage programs

Notes: ULK=unc-51-like kinase; RAF=rapidly accelerated fibrosarcoma; KIT=KIT proto-oncogene receptor tyrosine kinase; RP2D=recommended Phase 2 dose; FDA=U.S. Food and Drug Administration; IND=Investigational New Drug Application;
GCN2=general control nonderepressible 2; GIST=gastrointestinal stromal tumor

38

DCC-3116 | OVERVIEWULK INHIBITOR TO ADRESS AUTOPHAGY: BROAD RESISTANCE MECHANISMULK: Initiating Factor for Autophagy

ULK1complex

ULK1
Initiation

ATG13

1

Isolation
Membrane

DCC-3116 is a potential first-in-class small
molecule designed to inhibit cancer autophagy
by targeting the ULK kinase

Hydrolytic
enzymes

Lysosome

Autophagy
Pathway
LC3II

LC3II

LC3II

LC3II

LC3II

2

Phagophore

3

Autophagosome

4

Autolysosome

The ULK kinase initiates the autophagy
pathway and provides a potential targeted
approach to selectively inhibit autophagy inthese cancers

5

Degradation

DCC-3116 Phase 1 combination escalation
studies with sotorasib and QINLOCK are
underway, goal to select RP2D for expansion in
2024

Notes: ULK=unc-51-like kinase; ATG13= Autophagy-related protein 13; LC3-II=LC3-phosphatidylethanolamine conjugate; RP2D=recommended Phase 2 dose39

DCC-3116 | PRECLINICAL DATA

DCC-3116 INHIBITS RAS PATHWAY INHIBITOR-INDUCED ULK ACTIVITY
DCC-3116 Reverses KRASG12C
Inhibitor-Induced ULK Activation

-7

-6

-5

inhibitor] (LogM)

-4

200

100

% of DMSO control% of DMSO control

300

IC50
IC50
Adagrasib + DCC-3116 50 nM
Adagrasib + DCC-3116 50 nM
Sotorosib + DCC-3116 59 nM
Sotorosib + DCC-3116 59 nM

300

0
-10

200

100

0
-10
-9

DMSO

-9
-8

-8
-7

-7
-6

-6
-5

[DCC-3116] (LogM)[DCC-3116] (LogM)-5-4

NSCLC: H358 Tumor Growth
DCC-3116 + Sotorasib 1mg/kg

DCC-3116 combo with 1mg/kg Sotorasib

pATG13 ELISA
pATG13 ELISA

Adagrasib
SotorosibDMSO

NSCLC: H358 Tumor Growth
Tumor Growth
DCC-3116H358+ Sotorasib
1mg/kg

DCC-3116 Inhibits KRAS
H358ULK Activity
Inhibitor-Induced
H358

DMSO

-4

End of Dosing
2500

Tumor Burden (mg)

NSCLC: H358 pATG13 ELISA

H358
KRASG12C Inhibitors Induce ULK Activity
G13 ELISA

DCC-3116 inhibitsG12C
KRASG12C- inhibitor
DCC-3116 inhibits
KRAS-activity
inhibitor
inducedULK
NSCLC:
H358
pATG13
ELISA
induced
ULK
activity
G12C
Mean Tumor Burden (mg) +/- SE

ors induce ULK activity

DCC-3116 Demonstrated Deeper and Longer Regressions in
Combination with Sotorasib

2000
1500
1000
500

Sotorasib 1mg/kg

1000

Sotorasib 1mg/kg + DCC-3116
50mg/kg

800
600
400
200
0

0
0

10

20

30

Study Dayp = 0.0002

1200

Vehiclep = 0.0002
Sotorasib 1mg/kg
DCC-3116 50mg/kg
Sotorasib 1mg/kg + DCC-3116
50mg/kg

40

0

10

20

30

Study Day

Notes: Data presented at AACR 2022; G12C=single point mutation with a glycine-to-cysteine substitution at codon 12; pATG13=phospho-ATG13; ULK=unc-51-like autophagy-activating kinase.

40

DCC-3116 | PRECLINICAL DATA

DCC-3116 SHOWS 100% TUMOR REGRESSIONS IN COMBINATION WITH
RIPRETINIB IN KIT EXON 11 MUTATED GIST XENOGRAFT MODEL

Mean Tumor Burden (mg) +/- SEM

GIST-T1: Tumor Volume

400-8% TGI, 0% reg

300
400

200

-8% TGI, 0% reg

300

200

100

96% TGI, 20% reg

100

96% TGI, 20% reg

138% TGI, 100% reg

0
0

10

10

15

15

138% TGI, 100% reg
20

20

25

25

Vehicle Control
Vehicle Control
Ripretinib Chow 25mg/kg
Chow
Ripretinib
DCC-3116
50mg/kg
BID 25mg/kg
Ripretinib
25mg/kg
Chow+ DCC-3116
BID 50mg/kg
DCC-3116 50mg/kg

400-8% TGI, 0% reg

300

200

100

96% TGI, 20% reg
138% TGI, 100% reg

0
10

15

20

25

Days Post Tumor Implant

Days
Days
PostPost
TumorTumor
Implant Implant400

olume mm3

Mean Tumor Burden (mg) +/- SEM

Mean Tumor Burden (mg) +/- SEM

GIST-T1: Tumor Growth Inhibition

Ripretinib
Chow 25mg/kg
VehicleControl
Ripretinib
Chow 25mg/kg+ 25mg/kg
Ripretinib
Chow
DCC-3116 50mg/kg BID

DCC-3116 50mg/kg BID
Ripretinib 25mg/kg Chow + DCC-3116 50mg/kg
25mg/kg Chow + DCC-3116 50mg/kg
Ripretinib
300
Notes: Data presented at the AACR Annual Meeting 2023; % reg is the percent of mice that had regressions; %TGI and %Reg were calculated at the last day of dosing; BID=twice daily; GIST=gastrointestinal stromal tumor; GIST-T1=Exon 11 del;KIT=KIT proto-oncogene receptor tyrosine kinase; Reg.=regression; TGI=tumor growth inhibition.

200

41

DCC-3084 | OVERVIEW

DCC-3084 IS A POTENT AND SELECTIVE PAN-RAF INHIBITOR

DCC-3084 is a potential best-in-class pan-RAF inhibitor
engineered using Deciphera’s proprietary switch-control platform
Potent and selective inhibitor of BRAF and CRAF kinases,
shown preclinically to target all relevant aberrant signalingmechanisms (monomers, homodimers, heterodimers)
High permeability, CNS penetration, and solubility at gastric
pH to facilitate tumor accessLong on-target residency time, low efflux, and transporter
inhibition to enable durable efficacy
Strong pre-clinical data supports single agent use in RAF and RAS
mutant cancers, and deeper responses in combination with MEK
inhibitors

Notes: BRAF=proto-oncogene b-RAF; CNS=central nervous system; CRAF=proto-oncogene c-RAF; MEK=mitogen-activated extracellular signal-regulated kinase; RAF=rapidly accelerated fibrosarcoma serine/threonine protein kinase; RAS=rat sarcoma
gene.

42

DCC-3084 | OVERVIEWPOTENTIAL BEST-IN-CLASS BRAF/BRAF HOMODIMER AND BRAF/CRAF
HETERODIMER INHIBITOR
Monomer Signaling

BRAF
Class I

Pan-RAF
Inhibitor

BRAF

Homodimer Signaling

BRAF
Class II

BRAF

BRAF

BRAF
FusionBRAF

BRAF

Heterodimer Signaling

BRAF
Class III

RAS

Mutations

RAS
GTP

RAS
GTP
BRAF

CRAF

BRAF

CRAF

MEK

MEK
Inhibitor
Tumor Growth andSignaling
Notes: BRAF=proto-oncogene b-RAF; CRAF=proto-oncogene c-RAF; GTP=guanosine triphosphate; MEK=mitogen-activated extracellular signal-regulated kinase; RAS=rat sarcoma gene.

43

DCC-3084 | PRECLINICAL DATA

DCC-3084 EXHIBITS OVERALL BEST-IN-CLASS INHIBITION OF CLASS I, II, AND III
BRAF-MUTANTS AND RAF FUSION CELL LINESClass IClass II

FusionClass III + NRAS

Inhibitor

A375

HT-29

BxPC-3

H2405

WM3928

WM3629

DCC-3084

54

13

61

74

42

3

tovorafenib

3,000

5,270

1,100

603

669

305

naporafenib

438

228

19

465

90

3

belvarafenib

144

128

59

149

14

2

exarafenib

170

101

254

549

98

17

JZP815

141

47

200

47

133

2

IC50 (nM)

Notes: Data presented at the AACR Annual Meeting 2023; BRAF=proto-oncogene b-RAF; NRAS=neuroblastoma RAS viral oncogene homolog; RAF=rapidly accelerated fibrosarcoma serine/threonine protein kinase.

44

DCC-3009 | OVERVIEW

DCC-3009 IS A POTENT AND SELECTIVE NEXT-GENERATION KIT INHIBITOR

DCC-3009 is a potential best-in-class pan-KIT inhibitor
engineered using Deciphera’s proprietary switch-control platform

Unmet medical need remains for a pan-KIT inhibitor that canbroadly and potently inhibit the spectrum of KIT mutations thatdrive GIST
Potent inhibitor of primary KIT mutations in exons 9 and 11 andsecondary mutations across exons 13, 14, 17, and 18

Highly selective for KIT with optimized pharmaceutical and
ADME properties
Strong pre-clinical efficacy data in xenograft models driven by
drug resistant KIT mutations

Notes: ADME=absorption, distribution, metabolism, and excretion; GIST=gastrointestinal stromal tumor; KIT=KIT proto-oncogene receptor tyrosine kinase.

45

DCC-3009 | PRECLINICAL DATA

DCC-3009 POTENTLY INHIBITS THE SPECTRUM OF KNOWN PRIMARY AND
SECONDARY DRUG-RESISTANT MUTATIONS IN GIST
Imatinib

Imatinib

Sunitinib

Regorafenib Ripretinib

DCC-3009

IC50 (nM)
500

KITKIT
exon
919
exon

Sunitinib Regorafenib Ripretinib

DCC-3009

IC50 (nM)

Exon 9Exon 9/13 (V654A)
Exon 9/17 (D816G)

2
KITKIT
exon
1111
exon

400

Exon 11 (GIST-T1)
Exon 11/13 (V654A)

KIT
KITexonexon13
13

Exon 11/13 (V654A)

300
KIT
KITexonexon1414
KIT
KITexonexon17
17

Exon 11/14 (T670I)
Exon 11/14 (T670I)

200

Exon 11/17 (D816H)
Exon 11/17 (D820A)
Exon 11/17 (N822K)

KIT
KITexonexon1818
PDGFRAPDGFRAD842V
D842V

100

Exon 11/17 (Y823D)
Exon 11/17 (Y823D)
Exon 11/18 A829P)
PDGFRA (D842V)

Notes: GIST=gastrointestinal stromal tumor; GIST-T1=exon 11 del; (1) exon 9 primary is A502/Y503 duplication; (2) exon 11 primary mutations include deletions or the V560D point mutation.

46

DCC-3009 | PRECLINICAL DATA

DCC-3009 RESULTED IN TUMOR REGRESSIONS IN GIST XENOGRAFTMODELS, INCLUDING KIT EXONS 9, 11, 13 AND 17 MUTATIONS
V654A: BaF3 KIT Exon9
End of dosing
AY dup / Exon 13

0
10

750

500

End of dosing

500

250

15

20

0
Implant20
10 Days Post Tumor
15

Days Post Tumor Implant

VehicleVehicleVehicle25
25

End of dosing
750

VehicleVehicleEnd of dosing
750

VehicleDCC-3009
50 mg/kg
BID
22% regressionDCC-3009
DCC-3009 50
50 mg/kg
mg/kg
BID 22%22% regression
DCC-3009 50
50 mg/kg
mg/kgBID
BID 22% regression
80% regression
DCC-3009
BID
regression
DCC-3009 50 mg/kg BID
22% regression
Sunitinib
20
mg/kg
BID
Sunitinib
mg/kg
6% regression
Sunitinib
2020
mg/kg
BIDBID6%
regression
6% regression Sunitinib 20 mg/kg BID 6% regression
Sunitinib 20 mg/kg BID
6% regression
Ripretinib
100
mg/kg/day
7% tumor growth
inhibition
Ripretinib
100
mg/kg/dayformulated
diet
7%
TGI
Ripretinib 100 mg/kg/day formulated diet
7% 500TGI

ean tumor burden (mg) ± SEM

0Y823D: GIST PDX KIT Exon 11
delWK / Exon 17

750

ean tumor burden (mg) ± SEM

0Mean Tumor Burden (mg) +/- SEM

0

V654A: GIST PDX KITExon 11 delWK / Exon 13

End of dosing
VehicleVehicleDCC-3009 50
50 mg/kg
mg/kgBID
BID 22% regression
99.7% regression
DCC-3009

Sunitinib 20 mg/kg BID 6% regression

500

Notes: Data presented at the AACR Annual Meeting 2023; BID=twice daily; GIST=gastrointestinal stromal tumor; KIT=KIT proto-oncogene receptor tyrosine kinase; PDX=patient-derived xenograft.

250

250

250
47

DECIPHERA

FINANCIAL HIGHLIGHTS AND EXTENDED CASH RUNWAY
As of December 31, 2023

Weighted-Average
SharesOutstanding1

86.7MM
Weighted average shares includes outstanding
common stock and common stock issuable upon
exercise of prefunded warrants

Cash, Cash Equivalents& Marketable Securities$352.9MM

Cash Expected to Fund
Operating Expenses into
Second Half of 20261

Notes: As of December 31, 2023, there were 80.5MM outstanding shares, 6.4MM prefunded warrants, and 9.3MM options outstanding. (1) cash guidance based on current operating plan.

48

DECIPHERAEXPECTED 2024 MILESTONES✓

Continue enrolling INSIGHT pivotal Phase 3 study in 2L KIT exon 11+17/18 GIST patients(2024)
Published in Nature Medicine the INTRIGUE clinical results in 2L KIT exon 11+17/18 GIST
patients (January 2024)
Continue geographic expansion for 4L GIST in European and international markets(2024)

Vimseltinib
Submit NDA (2Q 2024) and MAA (3Q 2024) for TGCT and prepare for commercial
launchPresent additional results from Part 1 of Phase 3 MOTION study in TGCT (2Q 2024)
Present updated data from Phase 1/2 study in TGCT (2H 2024)
Initiate Phase 2 POC study in cGVHD (4Q 2024)

Early-Stage Pipeline
DCC-3116: Select recommended Phase 2 dose for expansion cohort(s) (2024)
DCC-3084: Initiate Phase 1 study (1H 2024)
DCC-3009: Submit IND to FDA (1H 2024) and initiate Phase 1 study (2H 2024)

Notes: 2L=second line; NDA=New Drug Application; LATAM=Latin America; cGVHD=chronic graft versus host disease; FDA=Food and Drug Administration; (1) Phase 2 study conditional and subject to FDA approval.

49

THANK YOU
THANK YOU