Curis, Inc. · NASDAQ:CRIS
Curis — Investor Presentation (June 2026)
31 slides from Curis's investor presentation, June 2026
Slide 1: Corporate Presentation June 2026
Corporate Presentation June 2026
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 Novel IRAK4 - FLT3 inhibitor 2 Proof-of Concept datasets 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 $0.6B market4 $0.5B market3 PRE-CLINICAL CLINICAL Validation Dose Proof of Mechanis
Slide 4: 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 5: Emavusertib in CLL and NHL
Emavusertib in CLL and NHL fen CUS’
Slide 6: Clear Mechanism: BCR and TLR signaling drive NHL
Clear Mechanism: BCR and TLR signaling drive NHL current standard of care blocks BCR only; blocking both pathways provides deeper responses Mechanism of Action Preclinical Data Dual blockade of BCR and TLR pathways can provide deeper responses Dual blockade demonstrated deeper responses in NHL model
Slide 7: Clinical Study Designs
Clinical Study Designs TakeAim Lymphoma • Part A: Dose Escalation Study o 50 mg QD → 400 mg BID o monotherapy and combination o multiple NHL subtypes, including PCNSL, CLL, WM, and MCL • Part B: Single-arm Study to support Accelerated Approval o Salvage line PCNSL – patients whose disease has progre
Slide 8: TakeAim Lymphoma - Part A: dose escalation data
TakeAim Lymphoma - Part A: dose escalation data demonstrated monotherapy and combination activity in 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 BTKi-ex
Slide 9: TakeAim Lymphoma - Parts B & C: registrational design
TakeAim Lymphoma - Parts B & C: registrational design accelerated approval and confirmatory studies in PCNSL Part C Part B supports Full Approval supports Accelerated Approval 1st Line Relapsed/Refractory Salvage Line chemotherapy no standard + BTKi methotrexate ibrutinib treatment Benchmark ORR1 Be
Slide 10: TakeAim Lymphoma - Parts B & C: ongoing registrational study
TakeAim Lymphoma - Parts B & C: ongoing registrational study Adding emavusertib to BTKi provides deeper responses in PCNSL BTKi-naïve Reduction in Tumor Burden Time on Treatment 63% ORR Benchmark: 39%1 → → → → → 18 months BTKi-naïve BTKi-experienced BTKi-naïve 8 months (5 of 8) for BTKi monotherapy
Slide 11: Goal in CLL: time-limited treatment
Goal in CLL: time-limited treatment provide the “one and done” fixed duration benefit of CAR-T, but with an oral therapy Potential to change the treatment paradigm Emavusertib offers the potential to provide time-limited treatment, in CLL with an all-oral therapy Current Unmet Need / Limitation1 The
Slide 12: Well tolerated safety profile
Well tolerated safety profile 81 patients treated in NHL to date, 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 >
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: Current Treatment Paradigm in CLL
Current Treatment Paradigm in CLL 1st Line 2nd Line 3rd Line+ venetoclax venetoclax ncBTKi + αCD20 re-treatment + αCD20 Standard of Care BTKi sometimes BTKi + αCD20 venetoclax re-treatment + ncBTKi venetoclax αCD20 ORR CR + 81% - 93% 0% - 7% αCD20 ncBTKi re-treatment venetoclax + αCD20 CAR-T venetoc
Slide 15: TakeAim CLL - ongoing Ph2 study in CLL
TakeAim CLL - ongoing Ph2 study in CLL Goal: 1400 Preclinical Study Replicate Preclinical Findings in a Ph2 Study vehicle 1200 Mean Tumor Volume (mm ) + SEM CLL Clinical Study Design 1000 3 Study Design: single-arm ibrutinib (BTKi) 800 Dosing & Admin: 200 mg BID, orally in combination with BTKi emav
Slide 16: 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 17: Summary
Summary • Ongoing registrational study in PCNSL demonstrates adding emavusertib to BTKi provides deeper, durable responses in BTK-naïve patients: in Salvage Line patients: 63% ORR vs. 39%1 27% ORR vs. n/a2 for BTKi monotherapy • Expanding with Phase 2 study into larger NHL subtypes, starting with CL
Slide 18: Emavusertib in AML
Emavusertib in AML fen CUS’
Slide 19: 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 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 the 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 Benchmark C
Slide 23: Emavusertib demonstrates the potential to replace gilteritinib as the 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 24: Well tolerated safety profile in 102 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 in AML patients with FLT3 mutation: 38% CCR vs. 21%1 for gilteritinib • Planning a registrational study vs. gilteritinib in 2nd line mFLT3 AML Goal: Repeat experience from Ph 1/2 Replace gilteritinib as standard
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 Mar 31, 2026 Cash and Investments $15.0M Shares Outstanding 40.0M Composition of Matter IP on Pre-Funded Warrants 2.7M emavusertib extends to 2035 Common Stock Warrants 94.6M (before potential extension) Employee awards 2.5M Fully Diluted 139.8M 30
Slide 31: End of Presentation
End of Presentation fen CUS’