Curis, Inc. · NASDAQ:CRIS
Curis — DAVA Oncology 2023 Bermuda Heme Conference
13 slides from Curis's conference presentation, July 2023
Slide 1: DAVA Oncology – 2023 Bermuda Heme Conference
DAVA Oncology – 2023 Bermuda Heme Conference Emavusertib (IRAK4 inhibitor) in Development for Patients with AML/MDS and PCNSL © 2023 Curis, Inc.
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: Emavusertib in Leukemia (AML/MDS)
Emavusertib in Leukemia (AML/MDS)
Slide 4: Unique Molecular Fingerprint
Unique Molecular Fingerprint The NCI selected emavusertib for Molecular design tailored to be the best-in-class IRAK4 inhibitor NCI-sponsored research and clinical studies of IRAK4 Emavusertib Emavusertib Kinase Interaction Map Binding Affinity FLT3 Target Kd nM IRAK4 IRAK1 12,000 IRAK2 >20,000 IRAK
Slide 5: Mechanism of Action
Mechanism of Action The two primary targets of emavusertib are independent drivers of cancer IRAK4 FLT3 spliceosome mutations drive overexpression of IRAK4-Long, which genetic mutations cause constitutive activation of FLT3 constitutively activates the myddosome, driving NF-ĸB overactivity and downs
Slide 6: Preclinical Data
Preclinical Data Rationale for monotherapy and combination with azacitidine/venetoclax Monotherapy in IRAK4 Monotherapy in FLT3 Combination with Aza/Ven 100% “Concomitant targeting of IRAK1 or IRAK4, alongside FLT3, is the most effective means to overcome the adaptive resistance incurred when target
Slide 7: Initial Clinical Data
Initial Clinical Data Emavusertib is showing clear single agent activity where expected in clinical studies 84 AML Patients 8 AML Patients 7 AML Patients all comers, all dose levels Spliceosome Mutation* with FLT3 Mutation* ** ** ** % Change in Marrow Blast from Baseline % Change in Marrow Blast fro
Slide 8: Clinical Strategy in Leukemia
Clinical Strategy in Leukemia TakeAim Leukemia Strategy for Monotherapy and Combination Potential for fast path to NDA Potential for high value front-line position Monotherapy Combination Enroll 20 Patients (2L/3L) Enroll 20 Patients (1L) in genetically-defined populations all comers o R/R AML with
Slide 9: Emavusertib in Lymphoma (NHL/CLL)
Emavusertib in Lymphoma (NHL/CLL)
Slide 10: Emavusertib in Lymphoma
Emavusertib in Lymphoma Combination therapy provides complimentary inhibition of two pathways that drive NF-κB NFκB Biology: Clinical Strategy: Two Pathways Drive NHL/CLL Block both pathways with Combination Therapy BCR and TLR Pathways independently drive NF-κB overactivity In preclinical testing,
Slide 11: Initial Clinical Data in Lymphoma
Initial Clinical Data in Lymphoma Majority of patients achieved decreases in tumor burden, including complete responses NHL/CLL Change in Tumor Burden Over Time combination with ibrutinib combination with ibrutinib BTK-naïve BTK-experienced Note: Data from ASCO 2022 poster presentation Response eval
Slide 12: Clinical Strategy in Lymphoma
Clinical Strategy in Lymphoma TakeAim Lymphoma Strategy for Combination Potential for front-line position Monotherapy Combination not being pursued in NHL Enroll 20 Patients (2L/3L) because blocking both the TLR and BCR Pathways o R/R PCNSL combination with ibrutinib (with IRAK4i and BTKi, respectiv
Slide 13: End of Presentation
ry CURIS End of Presentation