Curis, Inc. · NASDAQ:CRIS
Curis — Investor Presentation (July 2025)
31 slides from Curis's investor presentation, July 2025
Slide 1: Corporate Presentation July 2025
Corporate Presentation July 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 Potential first-in-class inhibitor of IRAK4 Well tolerated in monotherapy & combination • Being evaluated in Phase 1/2 clinical studies in NHL, AML, and Solid Tumors Demonstrated synergy • Anticipated 2025 milestones: with BTKi, HMA, BCL2i o Data from 30-35 PCNSL patients (Q4 ‘25) • Expe
Slide 4: Curis Leadership Team
Curis Leadership Team Experienced and Accomplished Mr. Dentzer is Chief Executive Officer and a member of the 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 and was named
Slide 5: Emavusertib Has Potential to Address Multiple Unmet Needs
Emavusertib Has Potential to Address Multiple Unmet Needs In Lymphoma In Leukemia In Lymphoma • NFkB dysregulation in NHL is driven by two pathways: BCR and TLR pathways TLR and FLT3 pathways BCR and TLR1 drive disease drive disease • Existing therapies target BTK (in the BCR Pathway); emavusertib t
Slide 6: Emavusertib in NHL
Emavusertib in NHL fen CUS’
Slide 7: Emavusertib Mechanism in NHL
Emavusertib Mechanism in NHL BCR Pathway TLR Pathway B cell TLR1 TLR2 TLR4 TLR5 receptor TLR6 Dual blockade of the TLR and BCR pathways Endosome TLR7 TLR8 TLR9 maximizes downregulation of NF-ĸB1 ibrutinib (BTKi) BTK Myddosome CARD11 MYD88 MALT1 BCL10 IRAK1 IRAK4 emavusertib NF-κB overactivity NF-ĸB
Slide 8: Mechanism Demonstrated in Preclinical NHL Models
Mechanism Demonstrated in Preclinical NHLModels Monotherapy vs. Combination 1400 in NHL model vehicle 1200 Mean Tumor Volume (mm3) + SEM 1000 ibrutinib (BTKi) 800 emavusertib 600 400 Dual blockade 200 emavusertib + BTKi of the TLR and BCR pathways achieved deeper tumor reduction 0 0 5 10 15 20 25 30
Slide 9: Safety profile in NHL
Safety profile in NHL 100 mg BID 200 mg BID 300 mg BID Grade 3+ Treatment-Related Adverse Total ema +ibr ema +ibr ema +ibr Event Reported in > 1 Patients, n (%) (n=47) (n=13) (n=27) (n=7) • 47 patients treated in NHL # patients having grade 3+ TRAEs 5 (38) 11 (41) 6 (86) 22 (47) • Shown to be well t
Slide 10: Single-agent activity demonstrated in NHL
Single-agent activity demonstrated in NHL Tumor Reduction Sustained up to 3+ Years Case Study in Dose Response (WM patient) 2950 50 mg 2850 2750 100 mg 2650 200 mg Dosing increases 2550 2450 2350 2250 2150 led to deeper response 2050 1950 IgM (mg/dL) 1850 1750 300 mg 1650 1550 1450 1350 1250 Year 1
Slide 11: Clinical Study Design
Clinical Study Design Part A in multiple NHL subtypes – Parts B & C in the PCNSL subtype Parts B & C are currently enrolling COMPLETED Part A Part B Part C Multiple NHL Subtypes PCNSL PCNSL dose escalation in BTKi-experienced patients in BTKi-naïve patients • emavusertib + ibrutinib • emavusertib +
Slide 12: PCNSL Clinical Data
PCNSL Clinical Data Anti-cancer activity observed in BTKi-naïve and BTKi-experienced patients Reduction in Tumor Burden Duration of Treatment → → → → → 18 months 8 months BTKi-naïve patients In BTKi-naïve patients: 26 months Adding emavusertib to ibrutinib achieved higher ORR 15 months 10 months tha
Slide 13: PCNSL Case Study
PCNSL Case Study Patient with R/R PCNSL treated with emavusertib + ibrutinib Male patient, 53 yrs Diagnosis: PCNSL diagnosed on 30 Jun 2020 Baseline: Depression, elevated LFTs, loss of appetite, cerebral edema, mixed IBS, hiatal hernia, GERD, essential hypertension, and obstructive sleep apnea Prior
Slide 14: PCNSL Case Study
PCNSL Case Study Patient with R/R PCNSL who achieved CR on emavusertib + ibrutinib after relapse on ibrutinib monotherapy BASELINE SD CR CR CR CR Jan 2023 Apr 2023 May 2023 Aug 2023 Feb 2024 May 2024 (at screening) (Day 43) (Day 81) (Day 187) (Day 349) (Day 442) Tumor Size Disease Stable Tumor Absen
Slide 15: Next Steps
Next Steps Expand across NHL, to wherever BTKi monotherapy is used NHL Subtype Incidence in U.S. Key Targets of Interest Therapies Used Published Studies Support Potential ABC-DLBCL 2 per 100,000 IRAK4, MYD88, CD79, NF-kB BTKi, R-CHOP in Multiple NHL Subtypes PCNSL 0.5 per 100,000 IRAK4, MYD88, CD79
Slide 16: Summary in NHL
Summary in NHL Lymphoma • Demonstrated anti-cancer activity in PCNSL • Orphan Drug designation received from both FDA and EMA in PCNSL • Next steps: ⁻ Continue enrollment in PCNSL toward potential Conditional Approval and Accelerated Approval ⁻ Work with EMA and FDA on confirmatory trial design in 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 FLT3m 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: 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: FLT3m is a disease driver in ~1/3 of newly diagnosed AML patients
FLT3m is a disease driver in ~1/3 of newly diagnosed AML patients1 IRAK4 inhibition overcomes adaptive resistance to FLT3i IRAK4 activity IRAKi + FLT3i IRAKi + FLT3i increased after treatment with FLT3i were synergistically cytotoxic significantly extended leukemia-free survival 100 – 100 – 0.8 – FL
Slide 21: Safety profile in AML
Safety profile in 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 (37.5) 1 (50.0) 34 (33.3) Blood creati
Slide 22: Single-agent activity demonstrated in AML
Single-agent activity demonstrated in AML Patients with < 3 lines of prior therapy with All Patients, All Dose Levels FLT3m and treated at 300mg BID 100% 100% 80% 80% 60% 60% 40% Before enriching 40% 10 of 19 evaluable patients for Optimal Dose & FLT3m achieved objective response1 20% 20% Enrich for
Slide 23: TakeAim Leukemia Study design
TakeAim Leukemia Study design 1st Line TakeAim Leukemia Study in FLT3m AML Chemo Fit Patients FLT3i Relapsed/Refractory Salvage Line midostaurin quizartinib FLT3i gilteritinib emavusertib HMA Unfit Patients venetoclax Enroll patients after they progress on FLT3i Objective is to demonstrate that by b
Slide 24: Clinical Data in FLT3m AML
Clinical Data in FLT3m AML CR + CRh/i Rate Salvage Line 40% emavusertib is 38% 35% CRh/i 9.5% 81% of patients 30% were previously treated with a FLT3i (n=21) FLT3i-naïve 25% Benchmark is 21% 20% Emavusertib is a potential best-in-class CRh therapy in FLT3m AML 13% of patients 15% 9.4% CR were previo
Slide 25: Clinical Data in FLT3m AML
Clinical Data in FLT3m AML 200 mg BID (n=3) Duration of Treatment MLFS CR CRi CR MLFS CR MLFS MLFS 7 of 10 responders achieved their first response at first assessment CRi Proceeded to stem cell transplant CRh (Cycle 2 Day 1) Patient MLFS CR Proceeded to stem cell transplant CRi CR Indicates time of
Slide 26: Summary in AML
Summary in AML Leukemia • Emavusertib, as monotherapy, has the potential to be the best-in-class therapy in FLT3m AML • With additional funding, next step is a registrational head-to-head study vs. gilteritinib 26
Slide 27: Solid Tumors
Solid Tumors fen CUS’
Slide 28: Ongoing studies (ISTs) of emavusertib in Solid Tumors
Ongoing studies (ISTs) of emavusertib in Solid Tumors Tumor Type Institution (Investigator) Emavusertib Combination Partner Pancreatic CRADA Washington University (Grierson) gemcitabine, nab-paclitaxel Colorectal CRADA Oklahoma University (Ulahannan) FOLFOX, bevacizumab Gastro/Esophageal Washington
Slide 29: Other Information
Other Information fen CUS’
Slide 30: Financials and IP
Financials and IP March 31, 2025 $20.3M Cash 10.5M Common Shares Outstanding 26.0M Fully Diluted Shares Outstanding 2035 Composition of Matter IP on emavusertib (before potential extension) 30
Slide 31: End of Presentation
End of Presentation fen CUS’