EX-99.1 2 a991ex092120.htm EX-99.1
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 Cardiff Oncology's expectations, strategy, plans or intentions. These forward-looking statements are based on Cardiff Oncology's 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. While the list of factors presented in the 10-K 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 Cardiff Oncology does not undertake any obligation to update publicly such statements to reflect subsequent events or circumstances. 2020 Corporation Presentation I 2

Cardiff Oncology At-A-Glance Exchange Nasdaq: CRDF Cash & Clinical Trial Funding* $30.5M Common Stock Outstanding** 25.0M Clinical-stage biotech company, • Convertible Preferred 3.5M • Outstanding Options – weighted avg. exercise 1.9M developing onvansertib, an oral, price / share $7.65 highly-selective Polo-like Kinase 1 • Option Pool (available for grant) 0.3M (PLK1) inhibitor, to treat cancers • Outstanding Warrants – weighted avg. exercise 8.7M price / share $4.23 ______ with the greatest medical need for Total Fully Diluted Shares Outstanding 39.4M new effective therapies 1H’2020 – Quarterly Cash Burn $3.8M/qtr. average Headquarters San Diego, CA *As of June 30, 2020; ** As of September 18, 2020 2020 Corporation Presentation I 3

Investment Highlights 3rd Generation, 1st-in-class, Strong Lead Program in Integrated Biomarker Diversified Pipeline Across Oral PLK1 Inhibitor KRAS-mutated mCRC Strategy Numerous Cancers Onvansertib overcomes the Supported by compelling preliminary Circulating Tumor DNA: changes in Clinical data from ongoing trials shortcomings of prior PLK inhibitors: clinical data from a Phase 1b/2 trial KRAS mutational burden in blood are support the use of onvansertib in • Highly selective for PLK1 showing a ten-fold improvement in predictive of subsequent tumor combination regimens across numerous aggressive cancers: • Orally administered ORR compared to SOC shrinkage in mCRC • mCRC Phase 1b/2 trial • 24-hour half-life Preclinical data support: Circulating Tumor Cells: changes are • mCRPC Phase 2 trial • Flexible dose and schedule • MOA of synthetic lethality between predictive of overcoming anti- KRAS mutant mCRC and PLK1 androgen resistance in mCRPC Potential expansion opportunities: Specifically targets a known inhibition mechanism of cell division that is • Synergy with irinotecan and 5-FU Circulating Tumor DNA: changes are • Chronic myelomonocytic leukemia required for tumor cell viability predictive of decreases in leukemic • Pancreatic cancer First Indication: 2nd line treatment in bone marrow cells • Triple negative breast cancer Preliminary clinical data demonstrate patients who have failed 1st line • Lung cancer the safety, tolerability and efficacy of treatment with FOLFOX with/without onvansertib in combination with SOC bevacizumab • Ovarian cancer across multiple indications 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 4

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 5

Pipeline and Upcoming Catalysts Indication Preclinical Phase 1b Phase 2 Next Milestone Onvansertib + FOLFIRI/Avastin® in Second-Line KRAS- Q1 2021 mCRC 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 6

Onvansertib 3rd generation, 1st in class, oral and highly selective Polo-like Kinase 1( 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 Inhibition of PLK1 causes arrest of cell ‐ DNA Damage Response division and subsequent cell death1 1Zitouni et al., Nat Rev Mol Cell Biol. 2014 Jul;15(7):433-52; PLK1: Polo-like kinase 1 2020 Corporation Presentation I 8

Onvansertib has Best-in-class Drug Properties and Synergistically Combines with Standard-of-Care Therapies Synergistic in Combination with Standard-of- Best-in-Class Drug Properties Care Chemo and Targeted Therapies High Selectivity Zytiga® For PLK1 (abiraterone) Taxol® Avastin® (paciltaxel) (bevacizumab) Demonstrated Synergistic in Safety and Combination Tolerability Venclexta® Cytarabine (venetoclax) Predictive Flexible Dosing Camptosar® Doxorubicin Biomarker Onvansertib and Scheduling (irinotecan) Onvansertib 5-FU Cisplatin Oral Ideal Administration Pharmacokinetics Beleodaq® Gemzar® (belinostat) (gemcitabine) 24-hour Velcade® Half-life (bortezomib) PLK1: Polo-like Kinase 1 2020 Corporation Presentation I 9

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-line standard-of-care treatment in KRAS-mutated mCRC has an 1 Months overall response rate of 4% and progression-free survival (PFS) of 5.5 months PFS 1Kubicka et al, Annals of Oncology 2013; 2342–2349; mCRC: Metastatic colorectal cancer 2020 Corporation Presentation I 11

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 12

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 SOC: Standard-of-care 2020 Corporation Presentation I 13

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 What is Clinical Trial Success • Overall response in patients who receive ≥1 cycle (2 courses) of treatment • ≥ 5 of 26 (~20%) patients achieve clinical response confirmed by • Progression-free survival (PFS) radiographic scan • Decreases in KRAS mutation burden and response to treatment • Achieve median progression-free survival of ≥ 6 months 2020 Corporation Presentation I 14

Response to Treatment Confirmed by Radiographic Scan Compelling Preliminary Efficacy Data Best Radiographic Response • 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 2020 Corporation Presentation I 15

Response to Treatment Confirmed by Progression-Free Survival Durability of Response Response Appears Durable • 8 (73%) patients had durable responses of >6 months (range 6 12 to >12 months); 4 patients remain on treatment; median PFS has not yet been reached 15 • Only 1 patient progressed in <6 18 months while on treatment 0 2 28 56 84 112 140 168 196 224 252 280 308 336 364 39 PFS: Progression-free survival 2020 Corporation Presentation I 16

Serial Monitoring of KRAS is Predictive of Radiographic Scan Re 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 The greatest changes in KRAS were observed in patients 1st cycle of treatment achieving a PR (ranging from -78% to -100%) • The patient with disease progression had only a 55% decrease in KRAS mutant allelic frequency *A KRAS mutation was detected by NGS for all 11 patients; ctDNA PD: Progressive disease % KRAS MAF Changes After Cycle 1 sponse 0 PR : Circulating tumor DNAPR: Partial response; SD: Stable disease -50 % change in KRAS MAF at cycle 2 day 1 from baseline SD -100 PD 02-004 01-010 02-005 01-007 ; 01-013 75% Decrease 02-012 01-011 01-006 2020 Corporation Presentation 02-008 I 17

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 Patients # of Patients # of Sites Treated To‐Date Pending Treatment 11 11 9 2020 Corporation Presentation I 18

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 19

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 ARSi’s offer a median overall survival No effective treatment options are standard of care androgen receptor signaling (mOS) benefit of only ~4 months1 available for the up to 40% of mCRPC inhibitors (ARSi’s) within 9-15 months1 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 to ARSi’s and increase overall survival Month mOS benefit 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: 2020 Corporation Presentation I 21 Metastatic castration resistant prostate cancer

Onvansertib Extends the Response to Androgen Receptor Signaling Inhibitors Onvansertib works synergistically in combination with abiraterone and significantly increases mitotic arrest Onvansertib + Abiraterone Demonstrate Synergy in Onvansertib + Abiraterone Significantly Increase mCRPC model (C4-2)1 Mitotic Arrest1 1Patterson & Yaffe, 2019, MIT; mCRPC: Metastatic castration resistant prostate cancer 2020 Corporation Presentation I 22

Phase 2 Open Label Trial in of Onvansertib + Abiraterone Disease Control Assessed by PSA Stabilization Trial Design: Dosing Schedule Duration Efficacy Endpoint Onvansertib 24mg/m2 Days 1-5 (21-day Disease Control Cohort 1 (n = 24) 4 Cycles = 12 Weeks cycle) + Zytiga® (Abiraterone) (PSA Stabilization or Decline) Onvansertib 18mg/m2 Days 1-5 (14-day Disease Control Cohort 2 (n = 32) 6 Cycles = 12 Weeks cycle) + Zytiga® (Abiraterone) (PSA Stabilization or Decline) Onvansertib 12mg/m2 Days 1-14 (21-day Disease Control Cohort 3 (n = 32) 4 Cycles = 12 Weeks cycle) + Zytiga® (Abiraterone) (PSA Stabilization or Decline) Eligibility Criteria What is Clinical Trial Success Initial resistance to Zytiga; 2 consecutive rises in PSA levels • ≥6 of 32 (~20%) patients achieve primary efficacy endpoint Efficacy Endpoint: of disease control at 12 weeks (PSA stabilization or Internationally Recognized Prostate Cancer Working Group decrease); confirmed by scan • Primary: disease control evaluated as PSA decline or stabilization (PSA rise <25% over baseline) • 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 23

Phase 2 Data Demonstrate the Efficacy of Onvansertib in mCRPC Arm A: 17 patients were evaluable for efficacy Treatment Response and Duration • 5 (29%) patients achieved disease control (DC) • 9 (53%) had radiographic stable disease (SD) including s s s 4 with durable SD (range 8 months – 1.7 years) h h h r ar nt nt nt a e o o o ye y m m m 1 .5 3 6 9 1 Met PSA 01-025 efficacy endpoint 01-026 Arm B: 9 patients were evaluable for efficacy 03-030 01-024 02-041 01-033 PD • 3 (33%) patients achieved DC ArmB (5+9) 03-039 Radiographic 02-042 SD assessment • 5 (55%) had SD including 4 with durable SD >7 months 01-014 03-017 PR 03-037 01-021 02-036 03-013 AR-V7+ AR alterations Arm C: 3 patient safety lead-in completed 02-003 AR T878A 03-004 02-007 Arm A(5+16) 03-023 03-009 Ongoing Efficacy demonstrated in patients with AR alterations 01-019 03-028 Transitioned to Arm B 02-020 • N = 8 [AR-V7 (6), AR T878A (2)] 0 0 0 0 0 0 0 0 0 0 0 0 0 1 2 3 4 5 6 • 3 (37%) achieved DC Days of treatment • 4 (50%) had SD; 3 durable (range 7-9 months) 2020 Corporation Presentation I 24

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 Percent Change in CTC: 12-Weeks vs Baseline in • 10 patient with unfavorable CTC count were re-analyzed 12 Patients with Unfavorable CTC Level at Baseline 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 CRPC: Castration resistant prostate cancer 2020 Corporation Presentation I 25

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 26

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 Activating RAS Pathway Can Be Therapeutically mutations such as NRAS, KRAS, CBL, PTPN11 and NF1, Targeted with PLK1 Inhibitors 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 PLK1 • In-vitro and in-vivo experiments with onvansertib as a single agent have shown a dose-dependent inhibition of CMML cell growth, with improved cell differentiation 2020 Corporation Presentation I 28

Phase 2 Two-Arm Randomized Trial of Onvansertib +/- Decitabine in RAS- Pathway Mutated CMML Determine the safety and overall response rate (ORR) of onvanserib, 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: What is Clinical Trial Success • Newly diagnosed or relapsed/refractory to prior therapy • RAS pathway mutant: NRAS, KRAS, PTPN11, CBL and NFI with • ≥4 of 32 (12.5%) patients with an objective frequency allele of ≥5% response to single agent treatment with Onvansertib in the first 4 or the first 3 cycles Efficacy Endpoint: of treatment (Arm A or B, respectively) • Overall response rate following single agent treatment with onvansertib 2020 Corporation Presentation I 29

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 Mutant KRAS is Essential for PDAC Growth – pancreatic adenocarcinoma, which is present in Activated RAS Proteins Contribute to Tumorigenesis ~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 2020 Corporation Presentation I 30

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 What is Clinical Trial Success • Patient with tumors harboring a confirmed KRAS mutation • Patient that have not had prior irinotecan or nal-IRI • Achieve ≥10 of 35 (~30%) patients achieve clinical response Efficacy Endpoints confirmed by radiographic scan • Overall response in patients who receive ≥2 cycles of treatment • Achieve median progression-free survival of ≥ 6 months • Progression-free survival at 6 months • Decreases in KRAS mutation burden and response to treatment 2020 Corporation Presentation I 31

Corporate

Strong Patent Portfolio Core Technology: 3 Issued Patents Evergreening: Combination Evergreening: Biomarkers to 2030 in US, Europe and Asia, Therapy with anticipated extension to 2035 Method for assessing PLK1 target Exclusive license from MIT for 2 US issued phosphorylation status for identifying Compound (onvansertib): US 8614220 patents with broad method claims for patients to be treated with PLK1 inhibitors combination of PLK inhibitor + anti- PCT US1948044, Expiration 2039 Salt forms of onvansertib: US 8648078 androgen compounds to treat any cancer Method for treating patient with a PLK Combinations with anti-neoplastic US 9566280; US 10155006; Expiration 2035 inhibitor when there is a PSA rise compounds: US 8927530 Provisional, Expiration 2040 PLK: Polo-like kinase; PSA: Prostate specific antigen 2020 Corporation Presentation I 33

Cardiff Oncology At-A-Glance Exchange Nasdaq: CRDF Cash & Clinical Trial Funding* $30.5M Common Stock Outstanding** 25.0M Clinical-stage biotech company, • Convertible Preferred 3.5M • Outstanding Options – weighted avg. exercise 1.9M developing onvansertib, an oral, price / share $7.65 highly-selective Polo-like Kinase 1 • Option Pool (available for grant) 0.3M (PLK1) inhibitor, to treat cancers • Outstanding Warrants – weighted avg. exercise 8.7M price / share $4.23 ______ with the greatest medical need for Total Fully Diluted Shares Outstanding 39.4M new effective therapies 1H’2020 – Quarterly Cash Burn $3.8M/qtr. average Headquarters San Diego, CA *As of June 30, 2020; ** As of September 18, 2020 2020 Corporation Presentation I 34

Investment Highlights 3rd Generation, 1st-in-class, Strong Lead Program in Integrated Biomarker Diversified Pipeline Across Oral PLK1 Inhibitor KRAS-mutated mCRC Strategy Numerous Cancers Onvansertib overcomes the Supported by compelling preliminary Circulating Tumor DNA: changes in Clinical data from ongoing trials shortcomings of prior PLK inhibitors: clinical data from a Phase 1b/2 trial KRAS mutational burden in blood are support the use of onvansertib in • Highly selective for PLK1 showing a ten-fold improvement in predictive of subsequent tumor combination regimens across numerous aggressive cancers: • Orally administered ORR compared to SOC shrinkage in mCRC • mCRC Phase 1b/2 trial • 24-hour half-life Preclinical data support: Circulating Tumor Cells: changes are • mCRPC Phase 2 trial • Flexible dose and schedule • MOA of synthetic lethality between predictive of overcoming anti- KRAS mutant mCRC and PLK1 androgen resistance in mCRPC Potential expansion opportunities: Specifically targets a known inhibition mechanism of cell division that is • Synergy with irinotecan and 5-FU Circulating Tumor DNA: changes are • Chronic myelomonocytic leukemia required for tumor cell viability predictive of decreases in leukemic • Pancreatic cancer First Indication: 2nd line treatment in bone marrow cells • Triple negative breast cancer Preliminary clinical data demonstrate patients who have failed 1st line • Lung cancer the safety, tolerability and efficacy of treatment with FOLFOX with/without onvansertib in combination with SOC bevacizumab • Ovarian cancer across multiple indications 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 35

Thank You for more information contact: ir@cardiffoncology.com