Curis, Inc. · NASDAQ:CRIS
Curis — Investor Presentation (September 2025)
31 slides from Curis's investor presentation, September 2025
Slide 1: Corporate Presentation
Corporate Presentation September 2025
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 Proof-of-Concept
2 Proof-of Concept PCNSL (n=34) Data Sets EMAVUSERTIB 27% ORR vs. n/a1 (pts who progressed on BTKi) 63% ORR vs. 39% for ibrutinib2 (BTKi-naïve) Novel IRAK4 - FLT3 inhibitor $0.6B market3 mFLT3 AML (n=21) 38% CR/CRh vs. 21% for gilteritinib5 $0.5B market4 PCNSL data validate scientific thesis: dual b
Slide 4: Curis Leadership Team
Curis Leadership Team Experienced and Accomplished 2025 Mr. Dentzer is Chief Executive Officer and a member of the Addition Dr. Hamdy is Chief Medical Officer of Curis. Prior to joining Board of Directors of Curis. Mr. Dentzer joined Curis in 2016 Curis, he served as CEO and Chairman of the board of
Slide 5: Emavusertib's mechanism targets key signaling pathways
Emavusertib’s mechanism targets key signaling pathways these 2 pathways these 2 pathways drive CLL & NHL drive AML TLR Pathway In Lymphoma • CLL and NHL are driven by NFkB dysregulation, which is in BCR Toll-like receptor FLT3 turn driven by two pathways: BCR and TLR1 Pathway Pathway • Current stand
Slide 6: Emavusertib in CLL and NHL
Emavusertib in CLL and NHL fen CUS’
Slide 7: Adding emavusertib to BTKi provides deeper responses
Adding emavusertib to BTKi provides deeper responses Mechanism of Action Preclinical Evidence these 2 pathways Monotherapy vs. Combination drive CLL & NHL in NHL model (OCI-Ly10) 1400 vehicle 1200 Mean Tumor Volume (mm ) + SEM 1000 3 800 ibrutinib (BTKi) emavusertib 600 400 emavusertib + BTKi 200 0
Slide 8: The goal in CLL and NHL is fixed duration, oral therapy
The goal in CLL and NHL is fixed duration, oral therapy Emavusertib offers potential to achieve the “one and done” fixed duration benefit of CAR-T, but with an all oral therapy Current Unmet Need / Limitation1 emavusertib + BTKi Therapies Binds to IRAK4 and BTK, 2024 • Bleeding, bruising, headaches,
Slide 9: Clinical Study in NHL
Clinical Study in NHL Three-part design select NHL subtype for pursuing fastest path to 1st label COMPLETED CURRENTLY ENROLLING CURRENTLY ENROLLING Part A Part B Part C multiple NHL subtypes PCNSL PCNSL dose escalation in BTKi-experienced patients in BTKi-naïve patients A1: monotherapy • emavusertib
Slide 10: Part A: early evidence of monotherapy and combination activity in multiple NHL subtypes
Part A: early evidence of monotherapy and combination activity in multiple NHL subtypes dose escalation (50-400mg) combination in CLL, WM, MCL, PCNSL Part A1: monotherapy Part A2: emavusertib + ibrutinib 0% 50 Single Patient 300mg/420mg CLL PR 20 months 50 mg 40 3000 Dose Response 2900 2800 (WM pati
Slide 11: Parts B & C: ongoing pivotal study in PCNSL
Parts B & C: ongoing pivotal study in PCNSL demonstrates that adding emavusertib to ibrutinib provides deep and durable responses Reduction in Tumor Burden Time on Treatment → → → → → 18 months BTKi-naïve progressed on prior BTKi 8 months BTKi-naïve patients 63% ORR (5 of8) BTKi-naïve (n=8) Benchmar
Slide 12: Well tolerated safety profile with duration > 1-2 years
Well tolerated safety profile with duration > 1-2 years emavusertib monotherapy emavusertib + ibrutinib Grade 3+ TRAEs 50-100 mg 50-100 mg 200 mg 300 mg 400 mg Grade 3+ TRAEs 100 mg 200 mg 300 mg Total Total Reported in > 1 Patient QD BID BID BID BID Reported in > 1 Patient BID BID BID (N=34) (n=47)
Slide 13: Expanding beyond PCNSL into larger NHL indications, starting with CLL
Expanding beyond PCNSL into larger NHL indications, starting with CLL Published Studies Support IRAK4 in CLL • Dual inhibition of IRAK and BTK is NHL significantly more potent in patient CLL Subtype Incidence in U.S. Key Targets of Interest Key Therapies Used cells than either drug alone1 CLL/SLL 4.
Slide 14: CLL landscape with design for Ph2 study
CLL landscape with design for Ph2 study Sequence of Therapies 1L 2L 3L+ Retreatment cBTKi ncBTKi Proposed Ph2 Study in CLL BCL2i + aCD20 Fixed Duration BCL2i + aCD20 Retreatment ncBTKi Study Design: single-arm BCL2i + aCD20 cBTKi ncBTKi Retreatment Dosing & Admin: 200 mg BID, orally in combination w
Slide 15: MRD emerging as new primary endpoint in CLL
MRD emerging as new primary endpoint in CLL Regulatory Support for MRD Approved Assay for MRD Clinical Trials using MRD in CLL MRD in CLL: some answers, “Assay is key” • Venetoclax-Obinutuzumab +/- Acalabrutinib in R/R CLL Phase3 NCT04560322 • Mosunetuzumab for CLL MRD Clearance Phase 1/2 NCT07052
Slide 16: Summary in CLL and NHL
Summary in CLL and NHL • Adding emavusertib to BTKi provides deep and durable responses in PCNSL in patients who progressed on BTKi: in BTKi-naïve patients: 27% ORR vs. n/a1 63% ORR vs. 39% for ibrutinib2 • Expanding into larger subtypes, starting with CLL o Early data in CLL, WM, and MCL continue p
Slide 17: Emavusertib in AML
Emavusertib in AML fen CUS’
Slide 18: Emavusertib Hits Multiple Targets of Interest in AML
Emavusertib Hits Multiple Targets of Interest in AML IRAK4-L and mFLT3 are important drivers of disease Emavusertib Emavusertib Kinase Interaction Map Binding Affinity FLT3 Target Kd nM IRAK4 IRAK1 12,000 IRAK2 >20,000 IRAK3 8,500 IRAK4 DYRK1A 23 25 Binds tightly to IRAK4 CLK 1, 2, 4 FLT3 WT 31 FLT3
Slide 19: The goal in AML is deeper response, longer survival
The goal in AML is deeper response, longer survival Emavusertib offers potential to replace gilteritinib as the best-in-class FLT3i these 2 pathways drive AML Current Unmet Need / Limitation Therapies emavusertib monotherapy fit (1st Line) Chemo + FLT3i • Low 5yr OS (22%), despite 60-65% composite C
Slide 20: IRAK4-L is a disease driver in nearly all AML patients
IRAK4-L is a disease driver in nearly all AML patients IRAK4-L is expressed IRAK4-L is oncogenic in nearly all AML patients Knocking out IRAK4 800 IRAK4-L stops leukemic activity IRAK4-S 600 Sum of IRAK4 variants Control 400 200 adding back IRAK4-L adding back IRAK4-S restarts activity has no effect
Slide 21: Emavusertib's dual blockade of IRAK4 and FLT3 has potential to outperform approved FLT3 inhibitors
Emavusertib’s dual blockade of IRAK4 and FLT3 has the potential to outperform approved FLT3 inhibitors Because IRAK4 drives adaptive resistance to FLT3i IRAK4 activity IRAK4i + FLT3i IRAK4i + FLT3i increased after treatment with FLT3i were synergistically cytotoxic significantly extended leukemia-fr
Slide 22: Ph 1/2 study design in AML
Ph 1/2 study design in AML 1st Line Goal: Demonstrate dual blockade of IRAK4 and FLT3 can overcome adaptive resistance to FLT3i Chemo + FLT3i Relapsed/Refractory Salvage Line Fit Patients midostaurin quizartinib FLT3i IRAK4 / FLT3i gilteritinib emavusertib HMA Unfit Patients + venetoclax Composite C
Slide 23: Emavusertib demonstrates potential to replace gilteritinib as best-in-class FLT3i
Emavusertib demonstrates the potential to replace gilteritinib as the best-in-class FLT3i Reduction in Tumor Burden Time on Treatment Comparison to Standard of Care 100% (n=21) MLFS CR 10.8 months Composite CR Rate 80% 9.4 months 40% Best response: emavusertib CR CRi CR 7.5 months 38% 60% MLFS CR 7.
Slide 24: Well tolerated safety profile in patients with AML
Well tolerated safety profile in 102 patients with AML Grade 3+ Treatment-Related Adverse 200 mg BID 300 mg BID 400 mg BID 500 mg BID Total Event Reported in > 1 Patients*, n (%) (n=17) (n=75) (n=8) (n=2) (n=102) • 102 patients treated in AML # patients having grade 3+ TRAEs 1 (5.9) 29 (38.7) 3 (37.
Slide 25: Study design for head-to-head vs. gilteritinib
Study design for head-to-head vs. gilteritinib Current Standard of Care Opportunity with additional funding Proposed Pivotal Study Study Design: randomized vs. gilteritinib in 2nd Line Dosing & Admin: 300 mg BID, orally Primary Endpoint: CR Secondary Endpoints: Duration of response (DOR), OS Study P
Slide 26: Summary in AML
Summary in AML • Emavusertib monotherapy has potential to be best-in-class in mFLT3 AML o 38% CR/CRh(i) vs. 21% for gilteritinib1 • Planning a registrational study vs. gilteritinib in 2nd line mFLT3 AML Goal: Repeat experience from Ph 1/2 Replace gilteritinib as standard of care in R/R mFLT3 AML 1 U
Slide 27: Solid Tumors
Solid Tumors fen CUS’
Slide 28: ISTs of emavusertib in Solid Tumors
ISTs of emavusertib in Solid Tumors Tumor Type Institution (Investigator) Emavusertib Combination NCI Pancreatic CRADA* Washington University (Grierson) gemcitabine, nab-paclitaxel NCT05685602 NCI Colorectal CRADA* Oklahoma University (Ulahannan) FOLFOX, bevacizumab NCT06696768 Gastro/Esophageal Was
Slide 29: Other Information
Other Information fen CUS’
Slide 30: Financials and IP
Financials and IP June 30, 2025 $10.1M* Cash and Investments July 2025 Financing 10.7M* Shares Outstanding Additional $7M of gross proceeds raised in July 2025 extended expected cash runway into 2026 27.4M* Fully Diluted Shares 2035 Composition of Matter IP on emavusertib (before potential extension
Slide 31: End of Presentation
End of Presentation fen CUS’