Slide 1: Corporate Presentation
Corporate Presentation October 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
EMAVUSERTIB 2 Proof-of Concept datasets Novel IRAK4 - FLT3 inhibitor demonstrate mechanism (n=34) (n=21) PCNSL mFLT3 AML BTKi-experienced 27% ORR (SOC is n/a)1 38% CR/CRh (SOC is 21%)5 BTK-naïve 63% ORR (SOC is 39%)2 $0.5B market4 $0.6B market3 PRE-CLINICAL CLINICAL Validation Dose Proof of Mechanis
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: Early evidence of monotherapy and combination activity in multiple NHL subtypes
Early evidence of monotherapy and combination activity in dose escalation study with multiple NHL subtypes dose escalation (50-400mg) dose escalation in CLL, WM, MCL, PCNSL (100-300mg) monotherapy emavusertib + ibrutinib 0% 50 Single Patient 300mg/420mg CLL PR 20 months 50 mg 40 3000 Dose Response 2
Slide 10: Registrational study design in PCNSL
Registrational study design in PCNSL ongoing study ongoing study supports Full Approval supports Accelerated Approval 1st Line Relapsed/Refractory Salvage Line chemotherapy no standard + BTKi methotrexate ibrutinib treatment ORR1 ORR2 ORR3 80% 39% n/a Goal for BTKi + ema: Goal for BTKi + ema: Enroll
Slide 11: Ongoing registrational study in PCNSL shows deep and durable responses
Ongoing registrational 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 of 8 ITT) BTKi-naïve (n=8) Benchmark
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: Preclinical evidence for IRAK4 in CLL
Preclinical evidence for IRAK4 in CLL • Inhibition of IRAK4 blocks survival and proliferation of CLL cells1 • Dual inhibition of IRAK4 and BTK is significantly more potent in patient CLL cells than either drug alone2 • Differences in TLR function represent an independent and earlier event than acqui
Slide 14: CLL landscape with design for Ph2 study
CLL landscape with design for Ph2 study Sequence of Therapies 1L 2L 3L+ Retreatment Proposed Ph2 Study in CLL cBTKi ncBTKi BCL2i + α-CD20 Fixed Duration BCL2i + α-CD20 Retreatment ncBTKi Study Design: single-arm BCL2i + α-CD20 cBTKi ncBTKi Retreatment Dosing & Admin: 200 mg BID, orally in combinatio
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 • Initiating Phase 2 in larger subtypes, starting with CLL o Early data in CLL, WM, and MCL sho
Slide 17: Emavusertib in AML
Emavusertib in AML fen CUS’
Slide 18: Emavusertib hits two important targets in AML
Emavusertib hits two important targets in AML Emavusertib Emavusertib Kinase Interaction Map Binding Affinity Target Kd nM FLT3 IRAK1 12,000 IRAK4 IRAK2 >20,000 TLR and FLT3 pathways IRAK3 8,500 IRAK4 23 drive disease in AML DYRK1A 25 CLK FLT3 WT 31 1, 2, 4 FLT3 (D835H) FLT3 (D835V) 5 44 blocking bo
Slide 19: 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 20: Dual blockade of IRAK4 and FLT3 could 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 21: 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 22: Emavusertib could 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% emavusertib Best response: CRi CR 7.5 months 38% CR 60% MLFS CR 7.
Slide 23: 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 24: 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 25: 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 26: Solid Tumors
Solid Tumors fen CUS’
Slide 27: 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 28: Other Information
Other Information fen CUS’
Slide 29: 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 30: End of Presentation
End of Presentation fen CUS’