Curis, Inc. · NASDAQ:CRIS

Curis — Investor Presentation (September 2024)

37 slides from Curis's investor presentation, September 2024

  1. Slide 1: Corporate Presentation

    Corporate Presentation September 2024

  2. 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

  3. Slide 3: Emavusertib is a potential first-to-market IRAK4 inhibitor

    Emavusertib is a potential first-to-market IRAK 4 inhibitor Demonstrated safety and • Being evaluated in Phase 1/2 clinical single-agent activity studies in NHL, AML, and Solid Tumors • Potential for monotherapy and combination use in NHL, AML Demonstrated synergy and Solid Tumors with BTKi, HMA, BC

  4. Slide 4: Broad Market Opportunity in NHL, AML, and Solid Tumors

    Broad Market Opportunity in NHL, AML, and Solid Tumors Significant market opportunities Additional opportunities in current development programs with NHL expansion PCNSL FLT3m AML WM MCL MZL ABC-DLBCL US Incidence per 100K 0.51 1.32 4.23 0.55 0.56 1.57 2.08 Newly Diagnosed Per Year Newly Diagnosed P

  5. Slide 5: Emavusertib in NHL

    Emavusertib in NHL fen CUS’

  6. Slide 6: Emavusertib's Mechanism in NHL

    Emavusertib’s Mechanism in NHL BCR Pathway TLR Pathway Two pathways drive NF-ĸB B cell receptor TLR1 TLR2 TLR4 TLR5 TLR6 (which drives B-cell lymphomas) combining IRAK4i and BTKi Endosome TLR7 TLR8 TLR9 enables dual blockade of NF-ĸB ibrutinib BTK Myddosome CARD11 MYD88 MALT1 BCL10 IRAK1 IRAK4 emavu

  7. Slide 7: Emavusertib is synergistic with BTKi in NHL

    Emavusertib is synergistic with BTKi in NHL Monotherapy vs. Combination emavusertib + BTKi 1400 in NHL vehicle 1200 blocking both BCR and TLR pathways Mean Tumor Volume (mm3) + SEM has been demonstrated to be more effective 1000 than blocking either one alone 800 ibrutinib emavusertib 600 • IRAK4i s

  8. Slide 8: Strategy in NHL

    Strategy in NHL ❶ Demonstrate safety 19 patients1 treated in TakeAim Lymphoma Ph 1b study, acceptable safety profile established, no overlapping dose-limiting toxicity with ibrutinib ❷ Demonstrate single-agent activity Single-agent activity demonstrated, with patients remaining on study up to 4 year

  9. Slide 9: Emavusertib safety profile in NHL

    Emavusertib safety profile in NHL1 • 19 patients treated with emavusertib in 100 mg 200 mg 300 mg Total Grade 3+ TRAE in BID+IBR BID+IBR BID+IBR combination with ibrutinib in multiple NHL (N=2) (N=10) (N=7) (N=19) >1 Patient subtypes n (%) n (%) n (%) n (%) • Shown to be well tolerated with an accep

  10. Slide 10: Strategy in NHL

    Strategy in NHL ❶ Demonstrate safety 19 patients1 treated in TakeAim Lymphoma Ph 1b study, acceptable safety profile established, no overlapping dose-limiting toxicity with ibrutinib ❷ Demonstrate single-agent activity Single-agent activity demonstrated, with patients remaining on study up to 4 year

  11. Slide 11: Single-agent activity demonstrated in Multiple NHL Subtypes

    Single-agent activity demonstrated in Multiple NHL Subtypes Percent Change in Tumor Burden from Baseline (6 patients treated for ~1 year or longer) Case Study in Dose Response (WM patient) 50 mg 100 mg 2950 2850 2750 200 mg 2650 2550 2450 2350 2250 Tumor reduction 2150 2050 Dosing increases led sust

  12. Slide 12: Strategy in NHL

    Strategy in NHL ❶ Demonstrate safety 19 patients1 treated in TakeAim Lymphoma Ph 1b study, acceptable safety profile established, no overlapping dose-limiting toxicity with ibrutinib ❷ Demonstrate single-agent activity Single-agent activity demonstrated, with patients remaining on study up to 4 year

  13. Slide 13: Initial combination study in multiple NHL subtypes

    Initial combination study in multiple NHL subtypes data presented at ASH 2023 All patients (n=19), multiple NHL subtypes No Prior BTKi Failed Prior BTKi 0% • Heavily pre-treated patients MZL sCNS CLL MCL MCL WM WM MZL-N pCNS FL MZL-N pCNS pCNS pCNS pCNS -10% (1-10 prior lines) -20% Best % Change in

  14. Slide 14: Emavusertib combination in PCNSL

    Emavusertib combination in PCNSL TakeAim Lymphoma Study Salvage Line emavusertib adding emavusertib to BTKI + BTKi re-sensitizes patients to BTKi therapy Initial Therapy 2nd Line (ibrutinib) and enables dual-blockade of NFĸB HD-MTX, BTKi Radiation, (ibrutinib) Chemo Salvage Line BTKi (ibrutinib) re-

  15. Slide 15: Strategy in NHL

    Strategy in NHL ❶ Demonstrate safety 19 patients1 treated in TakeAim Lymphoma Ph 1b study, acceptable safety profile established, no overlapping dose-limiting toxicity with ibrutinib ❷ Demonstrate single-agent activity Single-agent activity demonstrated, with patients remaining on study up to 4 year

  16. Slide 16: Additional NHL indications of interest

    Additional NHL indications of interest CLL Waldenström's Macroglobulinemia • TLR signaling is highly activated in lymph node–resident CLL cells1 • MYD88 and CXCR4 mutations activate NF-ĸB through the TLR pathway TLR signature Lymph Node Peripheral Blood maximal inhibition only • Recurring mutations

  17. Slide 17: Summary in NHL

    Summary in NHL Lymphoma • Emavusertib continues to demonstrate clear anti-cancer activity in R/R PCNSL • Work with FDA to clarify registrational path and prepare for potential amendment of the current Ph 1/2 study into a study that would support an NDA filing for accelerated approval • Prioritize ad

  18. Slide 18: Emavusertib in AML

    Emavusertib in AML fen CUS’

  19. Slide 19: Emavusertib binds to IRAK4 and FLT3, blocking both the TLR and FLT3 pathways

    Emavusertib binds to IRAK4 and FLT3, blocking both the TLR and FLT3 pathways 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 Haspin FLT3 (D835H) FLT3 (D835V

  20. Slide 20: IRAK4-L is an independent and powerful driver of disease in AML

    IRAK4-L is an independent and powerful driver of disease in AML IRAK4-L is expressed in nearly all AML patients IRAK4-L is oncogenic in AML 800 Knocking out IRAK4 IRAK4-L stops leukemic activity IRAK4-S (similar findings using CRISPR/CAS9) 600 Sum of IRAK4 variants Control 400 200 Smith Nat Cell Bio

  21. Slide 21: Strategy in AML

    Strategy in AML ❶ Demonstrate safety 123 patients1 treated in TakeAim AML Ph 1/2 study, acceptable safety profile established ❷ Demonstrate single-agent activity Single-agent activity observed; next step is to confirm these initial findings in a larger number of patients ❸ Pursue fastest path to 1st

  22. Slide 22: Safety Profile of Emavusertib as Monotherapy in AML

    Safety Profile of Emavusertib as Monotherapy in AML1 200 mg BID 300 mg BID 400 mg BID 500 mg BID Total Grade 3+ TRAE > 1 patients (n = 27) (n = 78) (n = 15) (n = 3) (n=123) • 123 patients treated with emavusertib n (%) n (%) n (%) n (%) n (%) in TakeAim Leukemia Study Number of patients having 4 (14

  23. Slide 23: Strategy in AML

    Strategy in AML ❶ Demonstrate safety 123 patients1 treated in TakeAim AML Ph 1/2 study, acceptable safety profile established ❷ Demonstrate single-agent activity Single-agent activity observed; next step is to confirm these initial findings in a larger number of patients ❸ Pursue fastest path to 1st

  24. Slide 24: Single-agent activity demonstrated in AML

    Single-agent activity demonstrated in AML Patients treated at 300mg BID All Patients, All Dose Levels who also have FLT3 mutation 100% 100% 80% 80% 60% Before optimizing 60% 6 of 11 evaluable patients for Dose & FLT3m achieved objective response 40% 40% 20% 20% Enrich for 0% Dose & FLT3m 0% -20% -20

  25. Slide 25: Strategy in AML

    Strategy in AML ❶ Demonstrate safety 123 patients1 treated in TakeAim AML Ph 1/2 study, acceptable safety profile established ❷ Demonstrate single-agent activity Single-agent activity observed; next step is to confirm these initial findings in a larger number of patients ❸ Pursue fastest path to 1st

  26. Slide 26: Emavusertib in FLT3m AML

    Emavusertib in FLT3m AML fen CUS’

  27. Slide 27: Emavusertib's dual-targeting of IRAK4 and FLT3 enables monotherapy opportunity in FLT3m AML

    Emavusertib’s dual-targeting of IRAK4 and FLT3 enables monotherapy opportunity in FLT3m AML IRAKi synergy with FLT3i 100% – 75% – FLT3i Control IRAK4 inhibition overcomes adaptive resistance to FLT3i 50% – IRAKi 25% – Concomitant targeting of IRAK1 or IRAK4, alongside FLT3, is the most effective mea

  28. Slide 28: Emavusertib is a potential best-in-class therapy in FLT3m AML

    Emavusertib is a potential best-in-class therapy in FLT3m AML CR + CRh/CRi Rate 35% Salvage Line Patients 30% treated with emavusertib achieved > 30% CR/CRh rate 25% Benchmark ~1.5X greater than the benchmark in FLT3i-naïve patients is for FLT3i-naïve patients 20% 21% CR/CRh rate 15% 9 of 12 patient

  29. Slide 29: Updated data in FLT3m AML

    Updated data in FLT3m AML presented at ASCO/EHA 2024 Duration on Treatment CR CR MLFS went to SCT CR → went to SCT 6 of 11 evaluable patients ongoing CRh → achieved objective response ongoing MLFS → ongoing → ongoing → Not Evaluable Days on Treatment 0 days 50 100 150 200 250 300 Data include all pa

  30. Slide 30: Strategy in AML

    Strategy in AML ❶ Demonstrate safety 123 patients1 treated in TakeAim AML Ph 1/2 study, acceptable safety profile established ❷ Demonstrate single-agent activity Single-agent activity observed; next step is to confirm these initial findings in a larger number of patients ❸ Pursue fastest path to 1st

  31. Slide 31: Emavusertib in All Comers

    Emavusertib in All Comers fen CUS’

  32. Slide 32: Emavusertib combination with aza/ven targets all comers in frontline AML

    Emavusertib combination with aza/ven targets all comers in frontline AML oncogenic IRAK4-L is expressed emavusertib synergy with aza/ven ema/aza/ven in nearly all AML patients in preclinical studies triplet combination 800 Preclinical Data All Comers Model Relative cell growth in AML cell lines (THP

  33. Slide 33: Summary in AML

    Summary in AML Leukemia • Emavusertib targets both FLT3 and IRAK4 • Emavusertib offers potential for best-in-class therapeutic in FLT3m AML (a genetically-defined population) • Oncogenic IRAK4 is expressed in nearly all AML patients and is not addressed by current standard-of-care (azacitidine and v

  34. Slide 34: Solid Tumors

    Solid Tumors fen CUS’

  35. Slide 35: Ongoing studies (ISTs) of emavusertib in Solid Tumors

    Ongoing studies (ISTs) of emavusertib in Solid Tumors Tumor Type Institution (Investigator) Emavusertib Combination Partner CRADA Washington University (Grierson) Pancreatic gemcitabine, (nab)-paclitaxel Washington University (Lim) CRADA Oklahoma University (Ulahannan) Colorectal FOLFOX + bevacizuma

  36. Slide 36: Other Information

    Other Information fen CUS’

  37. Slide 37: Financials and IP

    Financials and IP We believe cash is sufficient to achieve anticipated As of June 30, 2024 near-term milestones $28.4M Cash and investments1 • Updated PCNSL data 15-20 patients (4Q24/1Q25) ~5.9M Shares Outstanding • AML triplet safety data (4Q24/1Q25) ~7.0M Shares Fully Diluted 2035 Composition of M

Curis — Investor Presentation (September 2024) on 6ix