Curis, Inc. · NASDAQ:CRIS

Curis — Investor Presentation (January 2020)

25 slides from Curis's investor presentation, January 2020

  1. Slide 1: Corporate Presentation

    Corporate Presentation NASDAQ: CRIS

  2. Slide 2: Cautionary Note Regarding Forward Looking Statements

    Cautionary Note Regarding Forward Looking Statements This presentation contains certain forward-looking statements about Curis, Inc. (“we,” “us,” or the “Company”) within the meaning of the Private Securities Litigation Reform Act of 1995, as amended. Words such as “expect(s),” “believe(s),” “will,”

  3. Slide 3: Curis Mission & Strategy

    Curis Mission & Strategy Developing the New Generation of Targeted Cancer Drugs Innovation Execution Mission Strategy Work relentlessly to develop Select the right targets innovative and differentiated Design the right drugs therapeutics that improve the lives Study the right patients of cancer pati

  4. Slide 4: Company Overview

    Company Overview Investment Curis seeks to develop novel, first-in-class, cancer therapeutics Thesis that we believe have significant potential in areas of unmet patient need Fimepinostat: first-in-class suppressor of MYC There are no drugs currently approved for MYC inhibition Robust CA-4948: first

  5. Slide 5: Evolution of Curis

    Evolution of Curis Progressing through Clinical Studies on the Path to Potential Registration 2018 2019 2020 Regulatory Planning Dose Escalation Expansion • Report efficacy data for combination study ✓ Work with investigators and FDA to ✓ Report safety/tolerability data for of fimepinostat w/ veneto

  6. Slide 6: Pipeline of Oncology Drug Candidates

    Pipeline Of Oncology Drug Candidates PRE-CLINICAL CLINICAL MARKETED Dose Clinical Indication Proof of Principle Safety Pivotal Commercial Optimization Activity Heme Malignancies Fimepinostat MYC-altered HDAC/PI3K Cancers FDA Fast Track Designation CA-4948* MYD88/TLR-altered IRAK4 NHL CA-4948* IL-1R/

  7. Slide 7: Targeted Programs in Heme Malignancies: Fimepinostat

    Targeted Programs in Heme Malignancies Fimepinostat: In development for treatment of MYC-altered cancers 7

  8. Slide 8: Fimepinostat Overview

    Fimepinostat Overview In Development for Patients with MYC-Altered Cancers PI3Ki Profile Mechanism #1 HDACi Mechanism #2 The HDAC component The PI3K component Suppresses Enhances • First-in-class drug candidate with demonstrated anti-cancer activity as a MYC transcription2 MYC destruction2 Value Pro

  9. Slide 9: Fimepinostat Clinical Data Provides Strong Rationale in MYC-Altered Lymphoma

    Fimepinostat Clinical Data Provides Strong Rationale For Development in MYC-Altered Lymphoma Deep Responses in MYC-altered subset of patients (49 evaluable patients; 60 ITT patients) Monotherapy Anti-Cancer Activity CR/PR Deep responses SD/PD • 8 complete responses (CR); 6 partial responses (PR) MY

  10. Slide 10: Fimepinostat + Venetoclax Appear Highly Synergistic in Preclinical Models

    Fimepinostat + Venetoclax Appear Highly Synergistic in Preclinical Models Fimepinostat + Venetoclax Fimepinostat + Venetoclax As Combination Therapy Partners Appear Highly Synergistic in Preclinical Models (DH DOHH-2 DLBCL model)4 Both drugs are active as single-agents in DLBCL Fimepinostat = 23% OR

  11. Slide 11: Fimepinostat Phase 1 Combination Study Designed to Demonstrate Safety

    Fimepinostat Phase 1 Combination Study Designed to Demonstrate Safety of Combination Patient Population Expansion • Patients with R/R DLBCL, including DH/DE Lymphoma n = 30-60 • 8 Study Sites (US only) Fim: full dose Ven: full dose Treatment Dose Level 2 Fimepinostat: Oral daily (5 days on, 2-days o

  12. Slide 12: Targeted Programs in Heme Malignancies: CA-4948

    Targeted Programs in Heme Malignancies CA-4948: In development for treatment of TLR-altered cancers 12

  13. Slide 13: CA-4948 Overview

    CA-4948 Overview In Development for Patients with MYD88/TLR-Altered Disease Profile Affinity Kinase Kd (nM) • First-in-class IRAK4 inhibitor in cancer Designed to be best-in-class IRAK4 23 • Specific malignancies have overactivity of the myddosome/TLR pathway IRAK4 inhibitor1 Value Proposition IRAK1

  14. Slide 14: CA-4948 Mechanism of Action

    CA-4948 Mechanism of Action In Development for Patients with MYD88/TLR-Altered Disease Inhibiting either of these two pathways should provide benefit to patients with B cell lymphoma, CA-4948 targets oncogenic activity in the TLR pathway by blocking IRAK4 BTK Pathway TLR Pathway B cell TLR1 TLR2 TLR

  15. Slide 15: CA-4948 Phase 1 Study in R/R Lymphoma

    CA-4948 Phase 1 Study in R/R Lymphoma Preliminary Clinical Data Demonstrate Tolerability, PK, PD, and Anti-Cancer Activity Patient Population • Patients with R/R Lymphoma (incl DLBCL, WM, 50mg BID and patients with MYD88-altered disease) n=3 [+3] 50mg QD 100mg BID 200mg BID 400mg BID Continue dose e

  16. Slide 16: CA-4948 Phase 1 Study: Dose Response Observed

    CA-4948 Phase 1 Study in R/R Lymphoma Dose Response Observed as Study Enrolls at Therapeutic Dose Levels Change in Change in Tumor Tumor Burden Burden Sub-Therapeutic Dose Levels 50mg - 100mg 60% 50mg – 100mg QD & BID (qd & bid) 40% Best Response 20% 14 evaluable patients; 16 ITT patients -20% -40%

  17. Slide 17: CA-4948 Phase 1 Study in R/R Lymphoma

    CA-4948 Phase 1 Study in R/R Lymphoma Dose Response Observed as Study Enrolls at Therapeutic Dose Levels Dose Response Observed Increased tumor reduction observed as patient increased dose 17

  18. Slide 18: Two CA-4948 Ph1 Studies in NHL

    Two CA-4948 Ph1 Studies in NHL Potent Preclinical Anti-Cancer Activity in MYD88-altered DLBCL Anti-cancer activity in MYD88-altered DLBCL1 (OCI-Ly10) Preclinical Anti-Cancer Activity Potent as Single Agent vehicle • Anti-cancer activity demonstrated in MYD88-altered DLBCL • Interim readout in dose e

  19. Slide 19: Additional CA-4948 Ph1 Study in AML/MDS

    Additional CA-4948 Ph1 Study in AML/MDS Potential Path to Accelerated Approval Specific Genetic Mutations Lead to Expression of the Long Isoform of IRAK4 (IRAK4-L) Spliceosome mutations (incl. SF3B1 and U2AF1) drive expression of IRAK4-L in >50% of AML/MDS IRAK4-L is Oncogenic CA-4948 Directly Targe

  20. Slide 20: Monoclonal Antibody Immune Checkpoint Inhibitor CI-8993

    Monoclonal Antibody Immune Checkpoint Inhibitor CI-8993: In development for treatment of VISTA-expressing cancers 20

  21. Slide 21: CI-8993 Overview

    CI-8993 Overview In Development for Patients with VISTA Expressing Cancers Curis is the first to advance an oral small molecule checkpoint inhibitor into the clinic Profile • First-in-class monoclonal antibody antagonist of VISTA Value Proposition • No anti-VISTA antibodies currently in the clinic •

  22. Slide 22: Illustrative Example of VISTA's Role in Immune Suppression

    CI-8993 Illustrative Example of VISTA’s Role in Immune Suppression In Pre-Clinical Testing1, Blocking VISTA Results in: Reduced suppressive mediators and enhanced antigen presentation of MDSCs Altered chemotaxis (reduced traffic of MDSCs into the TME) Immune Suppression Temporary Immune Activation V

  23. Slide 23: Company Summary

    Company Summary Investment Curis seeks to develop novel, first-in-class, cancer therapeutics Thesis that we believe have significant potential in areas of unmet patient need Fimepinostat: first-in-class suppressor of MYC There are no drugs currently approved for MYC inhibition Robust CA-4948: first-

  24. Slide 24: Leadership Team

    Curis Leadership Team Rachel Blasbalg James Dentzer Christine Guertin Robert Martell Head, Human Resources President & CEO Head, Regulatory Head, R&D Mark Noel Reinhard von Roemling Raul Soikes Nancy Soohoo William Steinkrauss Head, Intellectual Property Head, Clinical Development Head, Portfolio Ma

  25. Slide 25: End of Corporate Presentation

    End of Corporate Presentation NASDAQ: CRIS

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