Curis, Inc. · NASDAQ:CRIS
Curis — Investor Presentation (April 2023)
27 slides from Curis's investor presentation, April 2023
Slide 1: Corporate Presentation
Corporate Presentation NASDAQ: CRIS
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,”
Slide 3: Corporate Overview
Corporate Overview Summary Investment Curis develops novel cancer therapeutics in areas of significant unmet patient need Thesis Cash runway into 2025 – $85.6M as of December 31, 2022 Emavusertib is positioned to become the cornerstone agent in heme malignancies Lead • IRAK4-L is the most prevalent
Slide 4: Pipeline
Pipeline Curis develops first-in-class cancer therapeutics PRE-CLINICAL CLINICAL MARKETED Dose Clinical Indication Proof of Principle Safety Pivotal Commercial Optimization Activity Heme Malignancies Lead Program emavusertib* IRAK4-driven Leukemia • Potential best-in-class, as the only IRAK4 inhibit
Slide 5: Emavusertib: Clinical Data Update at 2022 ASH
Emavusertib: Clinical Data Update at 2022 ASH
Slide 6: Emavusertib Current Data
Emavusertib Current Data ASH 2022 Update Reflects Significant Progress in AML/MDS • New data roughly doubles the dataset for targeted patient population (FLT3 or Spliceosome mutation) • Data continue to show deep and durable responses • Data continue to show competitive profile vs. currently availab
Slide 7: IRAK4 Biology and Mechanism of Action
IRAK4 Biology and Mechanism of Action
Slide 8: Emavusertib Mechanism of Action
Emavusertib Mechanism of Action IRAK4 is a novel and important target across multiple heme malignancies IRAK4 in AML/MDS IRAK4 in NHL/CLL Spliceosome mutation drives overexpression of IRAK4-L TLR Pathway is dependent upon IRAK4 for function (which causes constitutive activation of the myddosome) (2n
Slide 9: Emavusertib Unique Molecular Fingerprint
Emavusertib Unique Molecular Fingerprint The NCI has selected emavusertib Targeted design specifically engineered to hit key oncogenic targets for both clinical and non-clinical studies of IRAK4 inhibition Emavusertib Emavusertib in oncology Kinase Interaction Map Binding Affinity Target Kd nM NCI S
Slide 10: Additional Competitive Advantage in FLT3 AML
Additional Competitive Advantage in FLT3 AML Dual targeting of IRAK4 and FLT3 specifically designed to provide efficacy advantage in AML “Concomitant targeting of IRAK1 or IRAK4, alongside FLT3, is the most effective means to overcome the adaptive resistance incurred when targeting FLT3” IRAK activi
Slide 11: Emavusertib Preclinical Data
Emavusertib Preclinical Data Clear anti-cancer activity suggests broad potential across heme malignancies AML/MDS AML/MDS NHL/CLL Monotherapy Combination Therapy CA-4948 + Ibrutinib Combination Therapy 100% Tumor Growth in OCI-Ly10 Model 1400 Dosing: QDx p<0.05 vehicle Vehicle Vehicle 1200 SEM Relat
Slide 12: Emavusertib PK/PD
Emavusertib PK/PD Attractive PK profile supports BID dosing and high target suppression Trough Dose Attractive PK Profile Exposure (BID) Inhibition High Target Suppression half-life of ~6 hours supports BID dosing 2.5μM 200mg 97% exposure at 300mg BID correlates with 98% inhibition 4.1μM 300mg 98% 5
Slide 13: Genomic data provide clear rationale for monotherapy & combination
Emavusertib in AML/MDS Genomic data provide clear rationale for monotherapy & combination Rationale for Rationale for Monotherapy Combination IRAK4-L is the most prevalent disease driver IRAK4-L is heavily expressed in IRAK4-L is expressed at some level 1,2 800 > 50% of all AML/MDS patients in nearl
Slide 14: Emavusertib Core Development Strategy
Emavusertib Core Development Strategy Strategic Priorities Leukemia Lymphoma Monotherapy Combination Possibility for rapid development in a genetically-defined Possibility to gain first lymphoma approval with a defined study population (patients with FLT3, U2AF1, or SF3B1 mutation) in a small patien
Slide 15: Emavusertib in Leukemia (AML/MDS)
Emavusertib in Leukemia (AML/MDS)
Slide 16: Emavusertib Initial Clinical Data
Emavusertib Initial Clinical Data Potential for clear regulatory path in two target populations: AML FLT3 and AML Spliceosome CR/CRh Rate FLT3 AML 2/7 (29%) Best Percent Change in Bone Marrow Blast from Baseline Spliceosome AML 2/9 (22%) • All patients were R/R, most patients received prior HMA 1 o
Slide 17: Emavusertib Initial Clinical Data: R/R hrMDS
Emavusertib Initial Clinical Data Clear unmet need in R/R hrMDS – there are no approved therapies ORR Spliceosome MDS 5/11 (45%) • All patients on study were R/R, most patients received prior HMA 1 o Prognosis for this population is very poor; mOS is 4-6 months o There are no approved therapies for
Slide 18: Emavusertib in AML/MDS
Emavusertib in AML/MDS Clinical data support strategy for monotherapy & combination Initial Clinical Data in AML/MDS (patients treated with monotherapy, grouped by mutation status) In patients with a targeted mutation: o Enhanced monotherapy efficacy in a genetically-defined population suggests pote
Slide 19: Emavusertib in Leukemia (AML/MDS)
Emavusertib in Leukemia (AML/MDS) The ideal candidate to address the two largest genetically-defined populations in AML/MDS Emavusertib addresses the two largest genetically-defined populations in AML/MDS: 1 1) IRAK4-L (>50% of population) Next Steps 2 2) FLT3 (>25% of population) TakeAim Leukemia S
Slide 20: Emavusertib in Lymphoma (NHL/CLL)
Emavusertib in Lymphoma (NHL/CLL)
Slide 21: Emavusertib in B Cell Cancers
Emavusertib in B Cell Cancers Combination therapy provides complimentary inhibition of two pathways that drive NF-κB NFκB Biology: Two Pathways Drive B Cell Cancers Clinical Strategy: Use Combination Therapy BCR and TLR Pathways independently drive NF-κB overactivity In preclinical testing, blocking
Slide 22: Emavusertib Initial Clinical Data in Lymphoma – Monotherapy
Emavusertib Initial Clinical Data in Lymphoma – Monotherapy Proof-of-Concept demonstrated with monotherapy Monotherapy Ph1 proof-of-concept study demonstrated durable tumor reduction in monotherapy Change in Tumor Burden (emavusertib monotherapy at 300mg BID) > 50% 25% Best Response 0% -25% -50% < -
Slide 23: Emavusertib Initial Clinical Data in Lymphoma – Combination
Emavusertib Initial Clinical Data in Lymphoma – Combination Majority of patients achieved decreases in tumor burden, including complete responses NHL/CLL combination with ibrutinib Change in Tumor Burden Over Time 100% 80% % Change in Tumor Burden from Baseline 60% 40% BTK-naïve 20% BTK-experienced
Slide 24: Emavusertib in Lymphoma
Emavusertib in Lymphoma 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: Next Steps 1) BCR Pathway: addressed by blocking BTK TakeAim Lymphoma Study 2) TLR Pathway: addre
Slide 25: Corporate Overview
Corporate Overview Summary Investment Curis develops novel cancer therapeutics in areas of significant unmet patient need Thesis Cash runway into 2025 – $85.6M as of December 31, 2022 Emavusertib is positioned to become the cornerstone agent in heme malignancies Lead • IRAK4-L is the most prevalent
Slide 26: End of Corporate Presentation
End of Corporate Presentation NASDAQ: CRIS
Slide 27: Emavusertib Overview
Emavusertib Overview Initial clinical data support development strategy for novel IRAK4 inhibitor with targeted mutations all comers Monotherapy Patients, Grouped by Mutation Status Monotherapy Combination 24 patients 34 patients with targeted mutation without targeted mutation BTK-naïve BTK-experie