Slide 1: Corporate Presentation January 2024
Corporate Presentation January 2024
Slide 2: Cautionary Note Regarding Forward Looking Statements and Disclaimers
Cautionary Note Regarding Forward Looking Statements and Disclaimers 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),” “beli
Slide 3: Investment Overview
Investment Overview Emavusertib is a novel, highly-active IRAK4 inhibitor with potential cornerstone utility in heme and solid tumors Full development program underway in front-line and end-stage AML/MDS; BTKi combination PoC study in PCNSL Single agent and combination study results near-term (2024)
Slide 4: IRAK4 is a Novel Anti-Cancer Target
IRAK4 is a Novel Anti-Cancer Target Oncogenic IRAK4 activity promotes inflammation and impairs T cell function slide 4 Koziczak-Holbro M 2008 • Upregulation of IRAK4 in tumors leads to activation of NF-κB, JNK, and MAPK1,2 • IRAK-4 upregulation is associated with increased phenotypically exhausted T
Slide 5: Emavusertib Has A Unique Molecular Fingerprint
Haspin Emavusertib Has A Unique Molecular Fingerprint Targeted design is specifically engineered to be best-in-class Emavusertib Kinase Interaction Map % Inhibition at 0.1 nM Illustration reproduced courtesy of Cell Signaling Technology Target Kd nM IRAK1 12,000 IRAK2 >20,000 IRAK3 8,500 IRAK4 23 DY
Slide 6: Emavusertib in Leukemia
Emavusertib in Leukemia
Slide 7: Emavusertib Has a Unique Mechanism of Action
Emavusertib Has a Unique Mechanism of Action The two primary targets of emavusertib are independent drivers of cancer 1) Guillamot et al. Nat Cell Biol 2019; 2) Smith et al. Nat Cell Biol 2019; 3) American Cancer Society, Cancer Facts & Figures 2020; 4) Leukemia & Lymphoma Society, Facts and Statist
Slide 8: Preclinical Data: Rationale for monotherapy and combination with azacitidine/venetoclax
0% p<0.05 p<0.05 50% 100% -50% Preclinical Data Rationale for monotherapy and combination with azacitidine/venetoclax 1) Choudhary et al. AACR 2017; 2) Melgar, Sci Transl Med. 2019; 3) Curis AML MDS poster, EHA 2021 Control Re la tiv e Ce ll G ro w th Aza Aza + emavusertib Aza/Ven emavusertib demons
Slide 9: Emavusertib Compelling Initial Clinical Data
mCR mCR mCR CR mCR mCR mCR CR CR CRh MLFS -100% -80% -60% -40% -20% 0% 20% 40% 60% 80% 100% Emavusertib Compelling Initial Clinical Data Showing clear single agent activity where expected in AML/MDS clinical studies Note: 84 total AML/MDS patients enrolled in monotherapy as of Feb 9, 2023 with data
Slide 10: Emavusertib in Leukemia (AML/MDS)
Emavusertib in Leukemia (AML/MDS) The ideal candidate to address the two largest genetically-defined populations in AML/MDS Next Steps TakeAim Leukemia Study • Monotherapy: R/R AML with FLT3 R/R AML with Spliceosome • Combination: AML/MDS in combination with azacitidine/venetoclax Emavusertib addres
Slide 11: Emavusertib in Lymphoma
Emavusertib in Lymphoma
Slide 12: Emavusertib in Lymphoma
Emavusertib in Lymphoma Combination therapy provides complimentary inhibition of two pathways that drive NF-κB NFκB Biology: Two Pathways Drive NHL/CLL BCR and TLR Pathways independently drive NF-κB overactivity (and NF-κB drives NHL/CLL) Clinical Strategy: Block both pathways with Combination Thera
Slide 13: ASH 2023 Clinical Data in Lymphoma
ASH 2023 Clinical Data in Lymphoma All patients achieved decreases in tumor burden, including multiple complete responses slide 13 • 19 treated patients, 11 of whom had received prior BTKi treatment, demonstrated anti-cancer activity • Median treatment duration was 96 days (range 21-613 days), sugge
Slide 14: ASH 2023 Clinical Data in PCNSL
ASH 2023 Clinical Data in PCNSL All patients achieved decreases in tumor burden, including multiple complete responses slide 14 -100% -80% -60% -40% -20% 0% % C ha ng e fr om B as el in e PCNSL combination with ibrutinib BTK-experienced CRCRCR 5 evaluable PCNSL patients previously treated with BTKi
Slide 15: Clinical Strategy in Lymphoma
Clinical Strategy in Lymphoma Emavusertib is the ideal candidate to combine with BTKi to maximize downregulation of NF-κB • Patients are currently treated with BTKi because it downregulates NF-κB • Two pathways drive NF-κB: 1) BCR Pathway: addressed by blocking BTK 2) TLR Pathway: addressed by block
Slide 16: Investment Overview
Investment Overview Emavusertib is a novel, highly-active IRAK4 inhibitor with potential cornerstone utility in heme and solid tumors Full development program underway in front-line and end-stage AML/MDS; BTKi combination PoC study in PCNSL Single agent and combination study results near-term (2024)
Slide 17: End of Presentation
End of Corporate Presentation NASDAQ: CRIS