Cardiff Oncology : Investor Presentation - September 25, 2020

Turning the Tide on Cancer

September 2020

Forward-Looking Statements

Certain statements in this presentation are forward-looking within the meaning of the Private Securities Litigation Reform Act of 1995. These statements may be identified by the use of words such as "anticipate," "believe," "forecast," "estimated" and "intend" or other similar terms or expressions that concern our expectations, strategy, plans or intentions. These forward-looking statements are based on our current expectations and actual results could differ materially. There are a number of factors that could cause actual events to differ materially from those indicated by such forward-looking statements. These factors include, but are not limited to, our need for additional financing; our ability to continue as a going concern; clinical trials involve a lengthy and expensive process with an uncertain outcome, and results of earlier studies and trials may not be predictive of future trial results; our clinical trials may be suspended or discontinued due to unexpected side effects or other safety risks that could preclude approval of our product candidates; risks related to business interruptions, including the outbreak of COVID-19 coronavirus, which could seriously harm our financial condition and increase our costs and expenses; uncertainties of government or third party payer reimbursement; dependence on key personnel; limited experience in marketing and sales; substantial competition; uncertainties of patent protection and litigation; dependence upon third parties; our ability to develop tests, kits and systems and the success of those products; regulatory, financial and business risks related to our international expansion and risks related to failure to obtain FDA clearances or approvals and noncompliance with FDA regulations. There are no guarantees that any of our technology or products will be utilized or prove to be commercially successful. Additionally, there are no guarantees that future clinical trials will be completed or successful or that any precision medicine therapeutics will receive regulatory approval for any indication or prove to be commercially successful. Investors should read the risk factors set forth in our Form 10-K for the year ended December 31, 2019, and other periodic reports filed with the Securities and Exchange Commission. While the list of factors presented here is considered representative, no such list should be considered to be a complete statement of all potential risks and uncertainties. Unlisted factors may present significant additional obstacles to the realization of forward-looking statements. Forward-looking statements included herein are made as of the date hereof, and we do not undertake any obligation to update publicly such statements to reflect subsequent events or circumstances.

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Investment Highlights

3rd Generation, 1st-in-class,

Oral PLK1 Inhibitor

Onvansertib overcomes the shortcomings of prior PLK inhibitors:

• Highly selective for PLK1
• Orally administered
• 24-hourhalf-life
• Flexible dose and schedule

Specifically targets a known mechanism of cell division that is required for tumor cell viability

Preliminary clinical data demonstrate the safety, tolerability and efficacy of onvansertib in combination with SOC across multiple indications

Strong Lead Program in KRAS-mutated mCRC

Supported by compelling preliminary clinical data from a Phase 1b/2 trial showing a ten-foldimprovement in ORR compared to SOC

Preclinical data support:

• MOA of synthetic lethality between KRAS mutant mCRC and PLK1 inhibition
• Synergy with irinotecan and 5-FU

First Indication: 2nd line treatment in patients who have failed 1st line treatment with FOLFOX with/without bevacizumab

Integrated Biomarker

Strategy

Circulating Tumor DNA: changes in KRAS mutational burden in blood are predictive of subsequent tumor shrinkage (mCRC)

Circulating Tumor Cells: changes are predictive of overcoming anti- androgen resistance (mCRPC)

Circulating Tumor DNA: changes are predictive of decreases in leukemic bone marrow cells (AML)

Diversified Pipeline Across

Numerous Cancers

Clinical data from ongoing trials support the use of onvansertib in combination regimens across numerous aggressive cancers:

• mCRC Phase 1b/2 trial
• mCRPC Phase 2 trial
• AML Phase 2 trial

Potential expansion opportunities:

• Chronic myelomonocytic leukemia
• Pancreatic cancer
• Triple negative breast cancer
• Lung cancer
• Ovarian cancer

PLK: Polo-like Kinase; SOC: Standard-of-care; ORR: Overall response rate; MOA: Mechanism of action; mCRC: metastatic colorectal cancer;

mCRPC: metastatic castration resistant prostate cancer; AML: Acute myeloid leukemia

2020 Corporation Presentation I 3

Experienced Management Team With Drug Development and Biomarker Technology Expertise

	Mark Erlander, PhD			Vicki Kelemen
	Chief Executive Officer			Chief Operating Officer

Brigitte Lindsay

Vice President of Finance

2020 Corporation Presentation I 4

Pipeline and Upcoming Catalysts

Indication	Preclinical	Phase 1b	Phase 2	Next Milestone
mCRC	Onvansertib + FOLFIRI/Avastin® in Second-Line KRAS-		Q1 2021
Mutated Metastatic Colorectal Cancer			ASCO-GI
Onvansertib
Solid Tumor
Programs				Q1 2021
mCRPC	Onvansertib + Zytiga® (abiraterone)/prednisone in Zytiga-Resistant
Castration-Resistant Metastatic Prostate Cancer		ASCO-GU

Onvansertib				Q4 2020
Hematologic	AML	Onvansertib + Decitabine in	Relapsed/Refractory Acute Myeloid Leukemia
ASH
Programs

mCRC: Metastatic colorectal cancer; mCRPC: Metastatic castration resistant prostate cancer; AML: Acute myeloid leukemia

2020 Corporation Presentation I 5

Onvansertib

3rd generation, 1st in class, oral and highly selective PLK1 inhibitor addressing unmet needs across a broad range of cancer indications

PLK1 is a Proven Therapeutic Target that is Overexpressed in Most Cancers

• PLK1 is a serine/threonine kinase and master regulator of cell-cycle progression
• PLK1 controls G2/mitosis (G2/M) checkpoint
• Inhibition of PLK1 causes mitotic arrest and subsequent cell death
• Emerging data demonstrate that PLK1 is also a key regulator of cellular functions beyond mitosis that are essential for tumor growth:
• • Biosynthesis of DNA
  • DNA Damage Response

1Zitouni et al., Nat Rev Mol Cell Biol. 2014 Jul;15(7):433-52; PLK1: Polo-like kinase 1

Inhibition of PLK1 causes mitotic arrest

and subsequent cell death1

2020 Corporation Presentation I 7

Onvansertib has Optimal Drug Properties and Synergistically Combines with Standard-of-Care Therapies

Optimal Drug Properties

Synergistic in Combination with Standard-of-

Care Chemo and Targeted Therapies

Demonstrated

Safety and

Tolerability

Predictive

Biomarker

Oral

Administration

High Selectivity

For PLK1

Onvansertib

24-hourHalf-life

Synergistic in

Combination

Flexible Dosing and Scheduling

Ideal

Pharmacokinetics

Taxol®

(paciltaxel)

Venclexta® (venetoclax)

Camptosar®

(irinotecan)

5-FU

Beleodaq®

(belinostat)

Zytiga®

(abiraterone)

Onvansertib

Velcade®

(bortezomib)

Avastin®

(bevacizumab)

Cytarabine

Doxorubicin

Cisplatin

Gemzar®

(gemcitabine)

2020 Corporation Presentation I 8

Second-Line Treatment of KRAS-Mutated mCRC

Phase 1b/2 open-label trial of onvansertib + FOLFIRI/bevacizumab

Trial Sites: USC Norris Comprehensive Cancer Center; Mayo Clinic Cancer Centers

Principal Investigator: Dr. Heinz-Josef Lenz

New Second-Line Therapies are Needed to Improve Response and Increase Progression-Free Survival

50% of patients with mCRC	Prognosis is poor with a five-	Other drugs currently in development
have a KRAS mutation	year survival rate of 10%	do not address the most prevalent
		KRAS mutations in mCRC

4%

Response
to SOC	Significant limitations to standard-of-care (SOC)

5.5	Current second-linestandard-of-care treatment in KRAS-mutated mCRC has an
Months	overall response rate of 4% and progression-free survival (PFS) of 5.5 months1
PFS

1Kubicka et al, Annals of Oncology 2013; 2342-2349; mCRC: Metastatic colorectal cancer

2020 Corporation Presentation I 10

KRAS is a Pivotal Diagnostic Biomarker in the CRC Treatment Paradigm

• KRAS-mutatedpatients do not benefit from anti-EGFR agents:
• • No increase in OS, PFS and ORR was observed in KRAS mutant patients treated with EGFR inhibitors vs control arm1,2
  • The use of anti-EGFRs is therefore limited to KRAS wild-type patients
• Mutations in KRAS represent also the most frequent mechanism of resistance to anti-EGFRs (i.e. cetuximab)

KRAS Mutant	KRAS Wild-type	Treatment Paradigm
			mCRC
		KRAS	KRAS
		Mutant	Wild Type
		Chemotherapy ±	Chemotherapy +
		bevacizumab	EGFR inhibitor

1Karapetis et al., NEJM 2008;359:1757-1765;2Amado et al., JCO 2008, 26:1626-1634

2020 Corporation Presentation I 11

Second-line Treatment: Real World Utilization in the US

Flatiron Health Data

255

Cancer clinics representing

1.7 million active cancer patients

14,315

Colorectal cancer patients

7,034

Colorectal cancer patients who

receive second line therapy

Denotes combination with bevacizumab Denotes combination with other antiangiogenics

Source: Hess, L. International Journal of Colorectal Disease; 2019. Data is limited to limited to second-line regimens used in >1% of the cohort. FOLFOX:	2020 Corporation Presentation I 12
fluoropyrimidine, leucovorin, oxaliplatin. FOLFIRI: fluoropyrimidine, leucovorin, irinotecan, FOLFOXIRI: fluoropyrimidine, leucovorin, irinotecan, oxaliplatin

New Second-line mCRC Treatment is an Unmet Need

Outcomes for patients in the 2nd line setting is poor

• Efficacy of FOLFIRI: 4% ORR and 2.5 months PFS1
• Addition of bevacizumab to FOLFIRI improves outcomes2
• However while KRAS WT patients benefit from the addition of bevacizumab, there was no statistically significant improvement in OS for KRAS-mutant patients3

KRAS	Treatment	ORR	PFS	HR and significance	OS	HR and significance of
(months)	of PFS	(months)	OS
	FOLFIRI	5%	4.5	HR=0.61	11.1	HR=0.61
KRAS WT				(95 % CI 0.49-077)		(95 % CI 0.53-0.90)
FOLFIRI + Bev	7%	6.4	15.4
	P <0.0001	P=0.0052
KRAS	FOLFIRI	3%	4.1	HR=0.70	10	HR=0.92
			(95 % CI 0.56-0.89)		(95 % CI 0.71-1.18)
MUTANT	FOLFIRI + Bev	4%	5.5	10.4
P = 0.0027	P=0.4969

1Tournigand et al., JCO 2004;22(2):229-3;2Bennouna et al., Lancet Oncol. 2013; 14(1):29-37;3Kubicka, S, Annals of Oncology 2013, 24:2342-2349; CI:	2020 Corporation Presentation I 13
confidence interval, HR: hazard ration, ORR: objective response rate, PFS: progression-free survival, OS: overall survival, WT: wild-type, MUT: mutant

Magnitude of Response with Other Antiangiogenic Therapy

The anti-angiogenic agents aflibercept and ramucirumab have been approved in combination with chemotherapy in 2nd-line treatment, yet they are used to a much lesser extent than bevacizumab

Trial	Agent/ARM	Patients	ORR	95% CI of ORR (%)
VELOUR Sub-group1	FOLFIRI +	643 (325 FOLFIRI
(received first line therapy	11.8%	6.7 - 16.9
aflibercept	+aflibercept)
and bevacizumab)
RAISE2	FOLFIRI +	1361	13.4%*	10.7-16.6
ramucirumab
* 20% of patients were Asian, which has higher response rate

1Van Cutsem et al., Target Oncology 2016, 11:383-4002Tabernero et al., Lancet Oncology 2015;16:499-508

2020 Corporation Presentation I 14

Synthetic Lethality: Cells with KRAS Mutations are Hypersensitive to Inhibition of PLK1

The output of the RAS-mutated pathway activates PLK1, which is inhibited by onvansertib

Onvansertib Addresses KRAS Mutation		Cell Viability in Onvansertib-Treated KRAS Mutant
Subtypes in mCRC		and Wild Type Isogenic CRC Cells

		2%	1%
	6%	6%
8%				39%

18%

22%

G12D

G12V

G13D

G12C

G12S

G12A

Q61H

G12R

PLK1: Polo-like Kinase 1; mCRC: Metastatic colorectal cancer

2020 Corporation Presentation I 15

Synergy: Onvansertib in Combination with SOC Irinotecan and 5-FU

Onvansertib works synergistically in combination with standard-of-care FOLFIRI (irinotecan and 5-FU)

Synergy in Combination with Irinotecan		Synergy in Combination with 5-FU

2020 Corporation Presentation I 16

Phase 1b/2 Open Label Trial of Onvansertib + FOLFIRI/bevacizumab

Trial Design

					1 CYCLE = 28 Days
		Treatment Course = 14 Days				Treatment Course = 14 Days
1	2	3	4	5	6 - 14	1	2	3	4	5	6 - 14
Onvansertib					Onvansertib
FOLFIRI + bevacizumab				FOLFIRI + bevacizumab

Efficacy Endpoints

• Overall response in patients who receive ≥1 cycle (2 courses) of treatment
• Progression-freesurvival (PFS)
• Decreases in KRAS mutation burden and response to treatment

What is Clinical Trial Success

• ≥ 5 of 26 (~20%) patients achieve clinical response confirmed by radiographic scan
• Achieve median progression-free survival of ≥ 6 months

2020 Corporation Presentation I 17

Response to Treatment Confirmed by Radiographic Scan

Compelling Preliminary Efficacy Data

• 10 of 11 (91%) patients had clinical benefit:
• • 5 (45%) patients achieved a partial response (PR)
  • 4 patients had a confirmed PR (≥ 30% tumor shrinkage) with 1 patient going on to curative surgery
  • 1 patient with an initial PR went off study prior to confirmatory scan due to non- treatment related event

Best Radiographic Response

2020 Corporation Presentation I 18

Response to Treatment Confirmed by Progression-Free Survival

Response Appears Durable

• 8 (73%) patients had durable responses of >6 months (range 6 to >12 months); 4 patients remain on treatment; median PFS has not yet been reached
• Only 1 patient progressed in <6 months while on treatment

12

15

18

Durability of Response

s

s

s

s

s

ks

k

k

k

eek

k

w

e

wee

e

w

e

w

we

w

ee

e

2

32

e

8

16

40

4

4

8

01-006

01-007

01-003

02-004

02-005

01-010

01-011

02-008

02-012

01-013

01-014

0	8	6	4	2		0	68	96		4		2	80	8		6		4	92
	2	5	8	11	4	2	5	30	3	6
				1		1	1	2		2		2	3		3		3

Days of treatment

ASCO data

ASCO to present

Treatment ongoing

Received bevacizumab in 1st line

Treatment was discontinued due to treatment-unrelated AE*

Reason for discontinuation

Curative surgery

Patient decision

Radiographic assessment

Partial Response (PR)

Stable Disease (SD)

Progressive Disease (PD)

PFS: Progression-free survival

2020 Corporation Presentation I 19

Serial Monitoring of KRAS is Predictive of Radiographic Scan Response

Monitoring KRAS mutations in plasma ctDNA may enable rapid predictions of therapeutic response

• KRAS mutant allelic frequency (MAF) was measured by digital droplet PCR (ddPCR) at baseline and at the end of Cycle 1
• • 9 of 11 patients had a KRAS variant detected by ddPCR at baseline*
  • All patients showed a decrease in KRAS MAF after the 1st cycle of treatment
• The greatest changes in KRAS were observed in patients achieving a PR (ranging from -78% to -100%)
• The patient with disease progression had only a 55% decrease in KRAS mutant allelic frequency

% KRAS MAF Changes After Cycle 1

												PR													SD					PD
	0
% change in KRAS MAF at	-50
																													75% Decrease
-100
baselinefromdaycycle12
					4			0			5			7			3					2			1			6					8
				0			1			0			0			1				1			1			0				0
			0			0			0			0			0				0			0			0				0
		-			-			-			-			-				-			-			-				-
	2			1			2			1			1				2			1			1				2
	0			0			0			0			0					0			0			0					0

*A KRAS mutation was detected by NGS for all 11 patients; ctDNA: Circulating tumor DNAPR: Partial response; SD: Stable disease;

PD: Progressive disease

2020 Corporation Presentation I 20

KRAS-Mutated mCRC Expanded Access Program (EAP)

• Program initiated in June 2020 for a total of 20 patients
• 11 sites participating across the US
• Eligibility criteria includes:
• • Patients not meeting clinical trial inclusion criteria
  • Patients who have received 2 or more lines of prior treatment
  • Patients who have previously been treated with FOLFIRI (with or without bevacizumab)
• All 11 patients treated to-date were progressing on treatment with FOLFIRI/bevacizumab prior to enrolling
• Changes in KRAS mutational burden is being analyzed pre-dose and at the start of each cycle of treatment

# of Sites	# of Patients Treated To-Date	# of Patients Pending Treatment
11	11	9

2020 Corporation Presentation I 21

Catalysts and Milestones: KRAS-Mutated mCRC

Positive Phase 1b/2 results may provide an opportunity for a Phase 2b registrational trial

May 2020: Fast Track	September 2020: ESMO	January 2021: ASCO-GI	Q1 2021: FDA meeting to
Designation	presentation	data presentation (planned)	discuss regulatory path

mCRC: Metastatic colorectal cancer

2020 Corporation Presentation I 22

Metastatic Castration-Resistant Prostate Cancer

Phase 2 open-label trial of onvansertib + abiraterone

Trial Sites: Beth Israel Deaconess, Dana Farber, Mass General

Principal Investigator: Dr. David Einstein

New Therapeutic Options are Needed to Overcome Resistance to SOC Androgen Receptor Signaling Inhibitors (ARSi)

Resistance develops to treatment with standard	ARSi's offer a median overall survival	No effective treatment options are
of care ARSi's within 9-15 months1	(mOS) benefit of only ~4 months1	available for the up to 40% of mCRPC
		patients with an AR-V7 mutation2

9-15

Months until

ARSi resistance

	Limited options for patients once resistant to abiraterone
~4	New treatment options are needed to extend the duration of response

Month mOS

benefit

to ARSi's and increase overall survival

1Antonarakis, Emmannel - Current Understanding of Resistance to Abiraterone and Enzalutamide in Advanced Prostate Cancer; Clinical Advances in Hematology & Oncology - May 2016 - Volume 14, Issue 5; 2Armstrong et al., 2019, JCO 37: 1120-1129; SOC: Standard-of-care; mCRPC: Metastatic castration resistant prostate cancer

2020 Corporation Presentation I 24

Onvansertib Extends the Response to Androgen Receptor Signaling Inhibitors

Onvansertib works synergistically in combination with abiraterone (Zytiga®) and significantly increases mitotic arrest

Onvansertib + Abiraterone (Zytiga®) Demonstrate

Synergy in mCRPC model (C4-2)1

Onvansertib + Abiraterone (Zytiga®) Significantly

Increase Mitotic Arrest1

1Patterson & Yaffe, 2019, MIT; mCRPC: Metastatic castration resistant prostate cancer

2020 Corporation Presentation I 25

Phase 2 Open Label Trial in of Onvansertib + Abiraterone

Disease Control Assessed by PSA Stabilization

Trial Design:

	Dosing Schedule		Duration	Efficacy Endpoint
Cohort 1 (n = 24)	Onvansertib 24mg/m2	Days 1-5(21-day	4 Cycles = 12 Weeks	Disease Control
cycle) + Zytiga® (Abiraterone)	(PSA Stabilization or Decline)
Cohort 2 (n = 32)	Onvansertib 18mg/m2	Days 1-5(14-day	6 Cycles = 12 Weeks	Disease Control
cycle) + Zytiga® (Abiraterone)	(PSA Stabilization or Decline)
Cohort 3 (n = 32)	Onvansertib 12mg/m2	Days 1-14(21-day	4 Cycles = 12 Weeks	Disease Control
cycle) + Zytiga® (Abiraterone)	(PSA Stabilization or Decline)

Eligibility Criteria

Initial resistance to Zytiga; 2 consecutive rises in PSA levels

Efficacy Endpoint:

Internationally Recognized Prostate Cancer Working Group

• Primary: disease control evaluated as PSA decline or stabilization (PSA rise <25% over baseline)

What is Clinical Trial Success

• ≥6 of 32 (~20%) patients achieve primary efficacy endpoint of disease control at 12 weeks (PSA stabilization or decrease); confirmed by scan
• Achieve median radiographic PFS of ≥6 months

Note: radiographic assessment by RECIST v1.1 [CR = disappearance of all target lesions, PR = ≥30% decrease, PD = ≥20% increase, SD = does not

meet criteria for PR nor PD]; mCRPC: Metastatic castration resistant prostate cancer; PSA: Prostate specific antigen; PFS: Progression-free survival

2020 Corporation Presentation I 26

Phase 2 Data Demonstrate the Efficacy of Onvansertib in mCRPC

Arm A: 17 patients were evaluable for efficacy

•	5	(29%) patients achieved disease control (DC)
•	9	(53%) had radiographic stable disease (SD) including
	4 with durable SD (range 8 months - 1.7 years)

Treatment Response and Duration

Arm B: 9 patients were evaluable for efficacy

• 3 (33%) patients achieved DC
• 5 (55%) had SD including 4 with durable SD >7 months

Arm C: 3 patient safety lead-in completed

Efficacy demonstrated in patients with AR alterations

• N = 8 [AR-V7 (6), AR T878A (2)]
• 3 (37%) achieved DC
• 4 (50%) had SD; 3 durable (range 7-9 months)

Arm B (5+9)

Arm A (5+16)

01-025

01-026

03-030

01-024

02-041

01-033

03-039

02-042

01-014

03-017

03-037

01-021

02-036

03-013

02-003

03-004

02-007

03-023

03-009

01-019

03-028

02-020

0

s

s

s

r

th

th

th

n

n

n

a

e

o

o

o

y

m

m

m

1

3

6

9

	0		0		0		0
0	0	0	0
1		2		3		4

Days of treatment

					r
				a
			e
			y
.5
1

	0		0
0	0
5		6

Met PSA efficacy endpoint

PD

SD Radiographic assessment

PR

AR-V7+	AR alterations

AR T878A

Ongoing Transitioned to Arm B

2020 Corporation Presentation I 27

Onvansertib-Induced Circulating Tumor Cell Decrease is Associated with Progression-Free Survival

Circulating tumor cell (CTC) count, reported as favorable or unfavorable (<5 versus ≥5 CTC/7.5mL of blood, respectively) is a prognostic factor for survival in CRPC - conversion from unfavorable to favorable is associated with improved survival

• At baseline, 25 (78%) patients had unfavorable CTC count
• 10 patient with unfavorable CTC count were re-analyzed 12 weeks post-treatment
• • 5 (50%) patients had an 80% CTC decrease, including 2 AR-V7+ patients (01-024 and 01-025)
  • 4 (40%) patients converted from unfavorable to favorable CTC level
  • Median time on treatment for patients with CTC decrease (n=5) is 7 months to-date, with 4 patients remaining on treatment
  • Conversely, median time on treatment for patients with CTC increase (n=5) was 5 months

Percent Change in CTC: 12-Weeks vs Baseline in Patients with Unfavorable CTC Level at Baseline

	baseline	2000	Favorable CTC level at 12 weeks
atCTC	100
		1500	Remain on treatment
		1000
change%in	fromweeks12
50
		0
		-50
		-100

	03		0		09		13		21			3			14		24			2		3
0		0	7	0		0		0			0	0		0		0			0	5	0	6
-			-			-			-			-			-			-			-			-			-
02		2		3		03		1		3			1			01		01			02
	0			0				0			0				0

Patients

CRPC: Castration resistant prostate cancer

2020 Corporation Presentation I 28

Catalysts and Milestones: mCRPC

Positive Phase 2 results may provide an opportunity for a Phase 2b registrational trial

October 2020: Prostate	February 2021: ASCO-GU	April 2021: AACR	Q3 2021: FDA meeting to
Cancer Foundation (PCF)	presentation (planned)	presentation (planned)	discuss regulatory pathway
			(anticipated)

2020 Corporation Presentation I 29

New Clinical Programs Planned

Chronic Myelomonocytic Leukemia (CMML) Pancreatic Ductal Adenocarcinoma (PDAC)

Phase 2 Study to Evaluate the Safety and Efficacy of Onvansertib in RAS-pathway Mutant CMML

Study Rationale

• Proliferative CMML is enriched for activating RAS pathway mutations such as NRAS, KRAS, CBL, PTPN11 and NF1, all of which have been associated with adverse outcomes
• RAS pathway mutations drive proliferative CMML via a novel RAS-KMT2A-PLK1 axis, which can be therapeutically targeted with PLK1 inhibitors
• In-vitroand in-vivo experiments with onvansertib as a single agent have shown a dose-dependent inhibition of CMML cell growth, with improved cell differentiation

Activating RAS Pathway Can Be Therapeutically

Targeted with PLK1 Inhibitors

PLK1

2020 Corporation Presentation I 31

Phase 2 Two-Arm Randomized Trial of Onvansertib +/- Decitabine in RAS- Pathway Mutated CMML

Determine the safety and overall response rate (ORR) of onvansertib, a novel oral PLK1 inhibitor in RAS- pathway mutant chronic myelomonocytic leukemia

Trial Design:

	Dosing Schedule	Duration	Efficacy Endpoint
		4 cycles monotherapy (option to add	Interim analysis of first 18 patients after 4
Arm A (n = 38)	Onvansertib 24 mg/m2 days 1-5(14-day cycle)	decitabine at cycle 5 if lack of efficacy
cycles to evaluate objective response
		with single agent)
		3 cycles monotherapy (option to add	Interim analysis of first 18 patients after 3
Arm B (n = 38)	Onvansertib 12mg/m2 Days 1-14(21-day cycle)	decitabine at cycle 4 if lack of efficacy
cycles to evaluate objective response
		with single agent)

Eligibility Criteria:

• Newly diagnosed or relapsed/refractory to prior therapy
• RAS pathway mutant: NRAS, KRAS, PTPN11, CBL and NFI with frequency allele of ≥5%

Efficacy Endpoint:

• Overall response rate following single agent treatment with onvansertib

What is Clinical Trial Success

• ≥4 of 32 (12.5%) patients with an objective response to single agent treatment with Onvansertib in the first 4 or the first 3 cycles of treatment (Arm A or B, respectively)

2020 Corporation Presentation I 32

Phase 2 Study of Onvansertib in Combination with 5-FU and Nal-IRI for Second Line Treatment of KRAS-Mutated Metastatic Pancreatic Ductal Adenocarcinoma (PDAC)

Study Rationale

• KRAS is the most common oncogene mutated in pancreatic adenocarcinoma, which is present in ~95% of tumors
• Mutant KRAS is essential for PDAC growth, where the constitutive activated RAS proteins contribute to tumorigenesis, treatment resistance and metastases
• No effective RAS inhibitors have been approved for the treatment of KRAS-mutated pancreatic cancer
• Significant need for new effective second line treatment option

Mutant KRAS is Essential for PDAC Growth -

Activated RAS Proteins Contribute to Tumorigenesis

2020 Corporation Presentation I 33

Phase 2 Open Label Trial of Onvansertib + 5-FU and Nanoliposomal Irinotecan in KRAS-Mutated PDAC

Trial Design (35 patients):

1 CYCLE = 14 Days

Treatment Course (Days)

1

2

3

4

5

6 - 14

Onvansertib 18mg/m2

5-FU + Nanoliposomal Irinotecan (nal-IRI)

Eligibility Criteria

• Patient with tumors harboring a confirmed KRAS mutation
• Patient that have not had prior irinotecan or nal-IRI
  Efficacy Endpoints
• Overall response in patients who receive ≥2 cycles of treatment
• Progression-freesurvival at 6 months
• Decreases in KRAS mutation burden and response to treatment

What is Clinical Trial Success

• Achieve ≥10 of 35 (~30%) patients achieve clinical response confirmed by radiographic scan
• Achieve median progression-free survival of ≥ 6 months

2020 Corporation Presentation I 34

Corporate

Strong Patent Portfolio

Core Technology: 3 Issued Patents to 2030 in US, Europe and Asia, with anticipated extension to 2035

Compound (onvansertib): US 8614220

Salt forms of onvansertib: US 8648078

Combinations with anti-neoplastic compounds: US 8927530

Evergreening: Combination Therapy

Exclusive license from MIT for 2 US issued patents with broad method claims for combination of PLK inhibitor + anti- androgen compounds to treat any cancer

US 9566280; US 10155006; Expiration 2035

Evergreening: Biomarkers

Method for assessing PLK1 target phosphorylation status for identifying patients to be treated with PLK1 inhibitors

PCT US1948044, Expiration 2039

Method for treating patient with a PLK inhibitor when there is a PSA rise

Provisional, Expiration 2040

PLK: Polo-like kinase; PSA: Prostate specific antigen

2020 Corporation Presentation I 36

Cardiff Oncology At-A-Glance

Clinical-stage biotech company, developing onvansertib, an oral, highly-selectivePolo-like Kinase 1 (PLK1) inhibitor, to treat cancers with the greatest medical need for

new effective therapies

Exchange	Nasdaq: CRDF
Cash & Clinical Trial Funding*	$30.5M
Common Stock Outstanding**	25.0M
• Convertible Preferred	3.5M
• Outstanding Options - weighted avg. exercise	1.9M
price / share $7.65
• Option Pool (available for grant)	0.3M
• Outstanding Warrants - weighted avg. exercise	8.7M
price / share $4.23	______
Total Fully Diluted Shares Outstanding	39.4M
Quarterly Cash Burn	1H'2020 -
$3.8M/qtr. average
Headquarters	San Diego, CA

*As of June 30, 2020; ** As of September 18, 2020

2020 Corporation Presentation I 37

Investment Highlights

3rd Generation, 1st-in-class,

Oral PLK1 Inhibitor

Onvansertib overcomes the shortcomings of prior PLK inhibitors:

• Highly selective for PLK1
• Orally administered
• 24-hourhalf-life
• Flexible dose and schedule

Specifically targets a known mechanism of cell division that is required for tumor cell viability

Preliminary clinical data demonstrate the safety, tolerability and efficacy of onvansertib in combination with SOC across multiple indications

Strong Lead Program in KRAS-mutated mCRC

Supported by compelling preliminary clinical data from a Phase 1b/2 trial showing a ten-foldimprovement in ORR compared to SOC

Preclinical data support:

• MOA of synthetic lethality between KRAS mutant mCRC and PLK1 inhibition
• Synergy with irinotecan and 5-FU

First Indication: 2nd line treatment in patients who have failed 1st line treatment with FOLFOX with/without bevacizumab

Integrated Biomarker

Strategy

Circulating Tumor DNA: changes in KRAS mutational burden in blood are predictive of subsequent tumor shrinkage in mCRC

Circulating Tumor Cells: changes are predictive of overcoming anti- androgen resistance in mCRPC

Circulating Tumor DNA: changes are predictive of decreases in leukemic bone marrow cells

Diversified Pipeline Across

Numerous Cancers

Clinical data from ongoing trials support the use of onvansertib in combination regimens across numerous aggressive cancers:

• mCRC Phase 1b/2 trial
• mCRPC Phase 2 trial

Potential expansion opportunities:

• Chronic myelomonocytic leukemia
• Pancreatic cancer
• Triple negative breast cancer
• Lung cancer
• Ovarian cancer

PLK: Polo-like Kinase; SOC: Standard-of-care; ORR: Overall response rate; MOA: Mechanism of action; mCRC: metastatic colorectal cancer;

mCRPC: metastatic castration resistant prostate cancer; AML: Acute myeloid leukemia

2020 Corporation Presentation I 38

Thank You

for more information contact: [e-mail]