Cardiff Oncology, Inc. · NASDAQ:CRDF

Cardiff Oncology — Investor Presentation (May 2020)

41 slides from Cardiff Oncology's investor presentation, May 2020

Slide 1: Turning the Tide on Cancer
Turning the Tide on Cancer May, 2020
Slide 2: Forward-Looking Statements
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 si
Slide 3: Company At-A-Glance
Company At-A-Glance Clinical-stage oncology therapeutics company, developing onvansertib, an oral and highly- selective Polo-like Kinase 1 (PLK1) inhibitor San Diego, CA • Selectively targets PLK1, a proven therapeutic target; overexpressed in most cancers Nasdaq: TROV • Stops division of cancer cel
Slide 4: Investment Highlights
Investment Highlights Ovansertib 1st-in-class, 3rd-generation, safe and well-tolerated, oral PLK1 inhibitor; selectively targets PLK1 and blocks cancer cell division Clinical Efficacy Demonstrated 3 ongoing clinical trials with demonstrated efficacy in patients who have developed resistance to stand
Slide 6: 2020 Key Inflection Points
2020 Key Inflection Points 1H2020 Key Inflection Points Event Timing Colorectal Cancer: Phase 1b Safety and Efficacy Data ASCO-GI January 25th Prostate Cancer: Phase 2 Efficacy Data ASCO-GU February 13th Colorectal Cancer: Phase 1b Safety and Efficacy Data AACR April 27th Colorectal Cancer: Phase 1b
Slide 7: Onvansertib is a Platform for Value Creation
Onvansertib is a Platform for Value Creation ► Clinical Programs Based on Scientific Rationale: supported by preclinical and synergy data, and integration of biomarkers to rapidly assess response to treatment ► Addressing Significant Medical Need for New Treatment Options: – Overcome resistance to s
Slide 8: Onvansertib: Stops Cancer Cell Division and Synergistic in Combination Regimens
Onvansertib: Stops Cancer Cell Division and Synergistic in Combination Regimens Inhibition of PLK1 causes arrest of cell Synergistic in combination with chemotherapies division and subsequent cell death1 and targeted therapeutics2 1Zitouni et al., Nat Rev Mol Cell Biol. 2014 Jul;15(7):433-52 1Zitoun
Slide 10: Second-Line Treatment of KRAS-Mutated Metastatic Colorectal Cancer (mCRC)
Indication: Second-Line Treatment of KRAS- Mutated Metastatic Colorectal Cancer (mCRC) Phase 1b/2 open-label trial of onvansertib + FOLFIRI/bevacizumab Principal Investigator Dr. Heinz-Josef Lenz
Slide 11: Improving Response and Progression-Free Survival
Improving Response and Progression-Free Survival Metastatic Colorectal Cancer (mCRC) Establishing a Successful Path Forward: • Positive results from Phase 1b/2 trial may ► Only a 4% response rate to second-line provide an opportunity for Phase 2b standard-of-care chemotherapy + registrational trial
Slide 12: Clinical Outcomes in Patients Receiving Second-Line Treatment
Clinical Outcomes in Patients Receiving Second- Line Treatment – Chemotherapy + bevacizumab1 Chemo + Bevacizumab Outcome Measure Chemo + Bevacizumab KRAS Mutated CRC Progression-Free Survival 5.7 months 5.5 months Overall Survival 11.2 months 10.4 months Complete Response 1% 1% Partial Response 4% 3
Slide 13: Multiple KRAS Mutation Subtypes Differ in Prevalence Across Cancer Types
Multiple KRAS Mutation Subtypes are Present and Differ in Prevalence Across Cancer Types1 Onvansertib is Agnostic to KRAS Subtype Colorectal Lung 2% 1% 3% 3% 2% G12D G12C 6% 6% G12V 8% 8% 79% G12V 84% 39% G13D 39% G12D G12C 21% 18% G12A G12S 22% G12A 24% G13D Q61H G12S G12R G12R Pancreatic Biliary 3
Slide 14: Rationale for Onvansertib + FOLFIRI/Avastin in KRAS-Mutated Metastatic CRC
Rationale for Onvansertib + FOLFIRI® /Avastin® in KRAS-Mutated Metastatic CRC ► Synthetic Lethality Onvansertib Targets KRAS Mutations Through Downstream Effects on Tumor Cell Division – CRC tumor cells harboring KRAS mutation are more vulnerable to cell death with PLK1 inhibition1 – KRAS-mutated ce
Slide 15: Anti-tumor Activity of Onvansertib as Single Agent and in Combination with Irinotecan
Anti-tumor Activity of Onvansertib as Single Agent and Synergy in Combination with Irinotecan 8 Control Tumor volume (cm3) 6 Onvansertib 4 ► Anti-tumor activity of onvansertib in a KRAS-mutant CRC xenograft model (HCT116) as single agent and in 2 combination with irinotecan1-3 0 10 20 30 40 50 Days
Slide 16: Demonstrating Clinical Benefit in KRAS-Mutated CRC as New Second-Line Option
Demonstrating Clinical Benefit in KRAS-Mutated CRC as New Second-Line Treatment Option Trial Design: Phase 1b/2, multi-center, open label trial in KRAS-mutated mCRC Efficacy Endpoints: Primary: overall response in patients who receive ≥1 cycle (2 courses) of treatment Correlative Biomarker: decrease
Slide 17: Onvansertib Effectively Targets Multiple KRAS Mutation Subtypes in CRC
Clinical Data Shows Onvansertib Effectively Targets Multiple KRAS Mutation Subtypes in CRC Colorectal 2% 1% G12D 6% 6% G12V 79% 8% 39% G13D G12C 18% G12S 22% G12A Q61H G12R ► To date, tumor shrinkage observed in KRAS mutations G12A, G12V, G12D, G13D which make up 85% of KRAS subtypes in CRC1 ► Other
Slide 18: PLK1 Inhibition Induces Arrest and Death of Tumor Cells in KRAS-Mutated CRC
PLK1 Inhibition Induces Profound Arrest and Death of Tumor Cells in KRAS-Mutated CRC ► PLK1 is overexpressed in CRC and its high expression is associated with lower overall survival and poorer clinical parameters1 ► PLK1 inhibition has been identified to have synthetic lethality with KRAS mutant in
Slide 19: Response to Onvansertib Correlates with Decreases in KRAS Mutations in Plasma
Response to Onvansertib Correlates with Decreases in KRAS Mutations to Undetectable Levels in Plasma ► Decreases in plasma KRAS mutation level has been demonstrated to be an early marker for therapeutic response1 ► 7 of the 8 patients had a KRAS mutation detected by ctDNA analysis at baseline (ddPCR
Slide 20: Response to Treatment Confirmed by Radiographic Scan and PFS
Response to Treatment Confirmed by Radiographic Scan and Progression-Free Survival Radiographic Response ► 7 patients were evaluable for efficacy: – 6 of 7 (86%) had clinical benefit of partial response (PR) + stable disease (SD) – 3 of 7 (42%) achieved a PR; 1 patient (02-005) went on to have succe
Slide 21: Onvansertib is Showing Promise as a New Option for KRAS-Mutated mCRC
Onvansertib is Showing Promise as a New Therapeutic Option for KRAS-Mutated mCRC ► The 1st two dose levels (onvansertib 12 mg/m2 and 15 mg/m2) were cleared for safety; the 3rd dose level (onvansertib 18 mg/m2) is enrolling ► Clinical benefit (SD + PR) was observed in 7 (88%) of the 8 evaluable patie
Slide 22: Other Drugs in Development Do Not Address Prevalent KRAS Mutations in CRC
Other Drugs Currently in Development Do Not Address the Prevalent KRAS Mutations in CRC Company and Drug KRAS Program(s) and KRAS Coverage Available Data and Status Candidate Development Stage Trovagene Oncology • Pan-KRAS mutations • Phase 1b/2 trial in KRAS • Preclinical activity in CRC tumors wit
Slide 23: Indication: metastatic Castration-Resistant Prostate Cancer (mCRPC)
Indication: metastatic Castration-Resistant Prostate Cancer (mCRPC) Principal Investigator Dr. David Einstein
Slide 24: Overcoming Resistance and Extending Efficacy
Overcoming Resistance and Extending Efficacy Metastatic Castrate-Resistant Prostate Cancer (mCRPC) 1 Establishing a Successful Path Forward: • Positive results from Phase 2 trial may provide an opportunity for a Phase 2b registrational trial ► Resistance develops to standard-of- care therapy, Zytiga
Slide 25: Mechanism of Action for Onvansertib + Zytiga in CRPC
Underlying Mechanism of Action (MOA) for Onvansertib + Zytiga® in CRPC Onvansertib Mechanism of Action Onvansertib + Zytiga® (abiraterone) demonstrates synergy in mCRPC model (C4-2)1 Inhibits tumor cell division (mitosis) by inducing G2/M arrest Onvansertib + Zytiga® (abiraterone) significantly incr
Slide 26: PLK1 Inhibition + Abiraterone Efficacy in mCRPC Model
PLK1 Inhibition + Abiraterone Efficacy in mCRPC Model PLK1 Inhibition Enhances the Efficacy of Androgen Signaling Blockade in Castration-Resistant Prostate Cancer ► The combination of PLK1 inhibition + abiraterone decreases tumor growth and demonstrates a decrease in PSA within an AR-V7 model 1Zhang
Slide 27: Phase 2 Clinical Trial in mCRPC
Phase 2 Clinical Trial in mCRPC Disease Control Assessed by PSA Stabilization Trial Design: Phase 2 multi-center, open label trial in mCRPC Dosing Schedule Duration Efficacy Endpoint Cohort 1 Onvansertib 24mg/m2 Days 1-5 Disease Control 4 Cycles = 12 Weeks n=32 (21-day cycle) + Zytiga® PSA Stabiliza
Slide 28: Efficacy Demonstrated in Zytiga-Resistant Patients Treated with Onvansertib
Efficacy Demonstrated in Zytiga®-Resistant Patients Treated with Onvansertib ► Overall, 63% (12 of 19) of evaluable patients achieved partial response (PR) or stable disease (SD) following 12 weeks of treatment with onvansertib + abiraterone ► Response to treatment was evaluated based on PSA values
Slide 29: Onvansertib-Induced CTC Decrease is Associated with Progression-Free Survival
Onvansertib-Induced CTC Decrease is Associated with Progression-Free Survival ► CTC count, reported as favorable or unfavorable (<5 versus ≥5 CTC/7.5mL of blood, respectively) is a prognostic factor for survival in CRPC and the conversion from unfavorable to favorable is associated with improved sur
Slide 30: Efficacy Observed in Patients with Abiraterone-Resistant AR Alterations
Efficacy Observed in Patients with Abiraterone-Resistant AR Alterations ► AR mechanisms of resistance to abiraterone include the expression of the constitutively active AR splice variant AR-V7 and the AR gain-of function point mutation T878A6 Best PSA Response in AR-V7 Positive ► Among the 19 patien
Slide 31: Indication: Acute Myeloid Leukemia (AML)
Indication: Acute Myeloid Leukemia (AML) Principal Investigator Dr. Amer Zeidan
Slide 32: Addressing the Need for New Treatment Options
Addressing the Need for New Treatment Options Relapsed Acute Myeloid Leukemia (AML) Establishing a Successful Path Forward: • Positive results from Phase 2 trial and Orphan Drug Designation may provide an ► 5-year survival rate of only 25%1 opportunity for a Phase 2b registrational trial ► Standard-
Slide 33: Providing a New, Safe and Effective Treatment
Providing a New, Safe and Effective Treatment Trial Design: Phase 2 multi-center, open label trial in AML Relapsed or Refractory Onvansertib 60mg/m2 Days 1-5 Onvansertib +Decitabine Patients (n=32) (21-28 Day Cycle) Efficacy Endpoint Primary: safety and preliminary efficacy Correlative Biomarker: As
Slide 34: Phase 1b Completed Trial Efficacy Summary
Phase 1b Completed Trial Efficacy Summary Patients Treated with ≥ 1 Cycle (n=36) ► At the 4 higher dose levels (27 to 90 Onvansertib + Decitabine mg/m2), CR/CRi was observed in: → 12 mg/m2 07-009 07-011 – 5 of 16 (31%) patients in the decitabine 07-013 Arm 40 mg/m2 27 mg/m2 18 mg/m2 01-021 CR ► Medi
Slide 35: Conclusions
Conclusions Phase 1b Study of Onvansertib in AML1 ► Safety: onvansertib treatment was well tolerated – MTD/RP2D was established at 60 mg/m2 in both arms and no DLT was observed through this dose level – Onvansertib-related toxicities were primarily on-target hematological events, in accordance with
Slide 36: Corporate
Corporate A OS Cardiff Oncology
Slide 37: Strong Patent Portfolio
Strong Patent Portfolio ► Core Technology: 3 Issued Patents to 2030 in US, Europe and Asia with extension to 2035 in US – Compound (onvansertib): US 8614220 – Salt forms of onvansertib: US 8648078 – Combinations with anti-neoplastic compounds: US 8927530 ► Evergreening: Combination Therapy – Exclusi
Slide 38: Business Development Strategy
Business Development Strategy Objective: Joint Development and Commercialization Partnerships Co-Research Collaborations ► Financial and clinical support for ► MIT to evaluate combination of Onvansertib company-sponsored and/or investigator with androgen receptor signaling inhibitors; sponsored (IST
Slide 39: Financials
Financials 2019 and Early 2020 Raised Capital & Clinical Research • ~$18.0 million Commitment • Q1’19 = $11.3M Quarter Ending Cash and Cash Equivalents • Q2’19 = $10.8M • Q3’19 = $ 9.0M • Q4’19 = $10.2M Estimated Quarterly Cash Burn • ~$4.0M Copyright © 2020 Cardiff Oncology, Inc. 39
Slide 40: 2020 Key Inflection Points
2020 Key Inflection Points 1H2020 Key Inflection Points Event Timing Colorectal Cancer: Phase 1b Safety and Efficacy Data ASCO-GI January 25th Prostate Cancer: Phase 2 Efficacy Data ASCO-GU February 13th Colorectal Cancer: Phase 1b Safety and Efficacy Data AACR April 27th Colorectal Cancer: Phase 1b

Cardiff Oncology — Investor Presentation (May 2020) on 6ix

Cardiff Oncology — Investor Presentation (May 2020)

Slide 1: Turning the Tide on Cancer

Slide 2: Forward-Looking Statements

Slide 3: Company At-A-Glance

Slide 4: Investment Highlights

Slide 5: Significant Value Creation in 2020

Slide 6: 2020 Key Inflection Points

Slide 7: Onvansertib is a Platform for Value Creation

Slide 8: Onvansertib: Stops Cancer Cell Division and Synergistic in Combination Regimens

Slide 9: Optimal Attributes for a Safe and Effective Drug

Slide 10: Second-Line Treatment of KRAS-Mutated Metastatic Colorectal Cancer (mCRC)

Slide 11: Improving Response and Progression-Free Survival

Slide 12: Clinical Outcomes in Patients Receiving Second-Line Treatment

Slide 13: Multiple KRAS Mutation Subtypes Differ in Prevalence Across Cancer Types

Slide 14: Rationale for Onvansertib + FOLFIRI/Avastin in KRAS-Mutated Metastatic CRC

Slide 15: Anti-tumor Activity of Onvansertib as Single Agent and in Combination with Irinotecan

Slide 16: Demonstrating Clinical Benefit in KRAS-Mutated CRC as New Second-Line Option

Slide 17: Onvansertib Effectively Targets Multiple KRAS Mutation Subtypes in CRC

Slide 18: PLK1 Inhibition Induces Arrest and Death of Tumor Cells in KRAS-Mutated CRC

Slide 19: Response to Onvansertib Correlates with Decreases in KRAS Mutations in Plasma

Slide 20: Response to Treatment Confirmed by Radiographic Scan and PFS

Slide 21: Onvansertib is Showing Promise as a New Option for KRAS-Mutated mCRC

Slide 22: Other Drugs in Development Do Not Address Prevalent KRAS Mutations in CRC

Slide 23: Indication: metastatic Castration-Resistant Prostate Cancer (mCRPC)

Slide 24: Overcoming Resistance and Extending Efficacy

Slide 25: Mechanism of Action for Onvansertib + Zytiga in CRPC

Slide 26: PLK1 Inhibition + Abiraterone Efficacy in mCRPC Model

Slide 27: Phase 2 Clinical Trial in mCRPC

Slide 28: Efficacy Demonstrated in Zytiga-Resistant Patients Treated with Onvansertib

Slide 29: Onvansertib-Induced CTC Decrease is Associated with Progression-Free Survival

Slide 30: Efficacy Observed in Patients with Abiraterone-Resistant AR Alterations

Slide 31: Indication: Acute Myeloid Leukemia (AML)

Slide 32: Addressing the Need for New Treatment Options

Slide 33: Providing a New, Safe and Effective Treatment

Slide 34: Phase 1b Completed Trial Efficacy Summary

Slide 35: Conclusions

Slide 36: Corporate

Slide 37: Strong Patent Portfolio

Slide 38: Business Development Strategy

Slide 39: Financials

Slide 40: 2020 Key Inflection Points

Slide 41: Thank You