Damora Therapeutics, Inc. · NASDAQ:DMRA
Damora Therapeutics — Investor Presentation (May 2026)
22 slides from Damora Therapeutics's investor presentation, May 2026
Slide 1: Redefining care for people with blood disorders
Redefining care for people with blood disorders Company Overview May 2026
Slide 2: Disclaimers
Disclaimers The information contained in this presentation has been prepared by Damora Therapeutics Inc. and its affiliates (“Damora” or the “Company”) and contains information pertaining to the business and operations of the Company. Forward-Looking Statements and Other Information Certain informat
Slide 3: Damora Therapeutics: an emerging leader in blood disorders
Damora Therapeutics: an emerging leader in blood disorders Founded by Fairmount Funds Management with a mission to fundamentally redefine care for patients with blood disorders Portfolio of mutCALR-targeted therapies with best-in- class potential for myeloproliferative neoplasms (MPNs), including es
Slide 4: Rapidly advancing portfolio uniquely positioned to address the spectrum of mutCALR-driven MPNs
Rapidly advancing portfolio uniquely positioned to address the spectrum of patients across mutCALR-driven MPNs DMR-001 DMR-003 Fc-null, extended half-life T-cell engager Blocks mutCALR-driven oncogenic signaling, mutCALR x CD3 bi-specific recruits and directs without engaging immune effector functio
Slide 5: MPNs represent a spectrum of highly debilitating diseases
MPNs represent a spectrum of highly debilitating diseases Essential Thrombocythemia (ET) Myelofibrosis (MF) • High platelet counts increase thrombosis and hemorrhage risk • Bone marrow fibrosis leads to poor survival and high risk of transformation to acute myeloid leukemia • Severe headaches, fatig
Slide 6: INCA'989 provided POC, with significant room for improvement
INCA’989 provided POC, with significant room for improvement Less potent on Type 2 CALR mutations Frequent, high-volume IV doses 100% 100% Intravenous administration 100 Estimated Best Overall Complete Frequent dosing every two weeks Response (CR, %) 80 frequency of CALR in ET patients 69% mutation
Slide 7: DMR-001 has two ways to win: maximize efficacy and improve patient experience
DMR-001 has two ways to win: maximize efficacy and meaningfully improve the patient experience Superior potency and exposure Improve patient experience Next-generation therapy engineered to maximize efficacy across Differentiation through a patient-centric design, maximizing the all CALR mutations t
Slide 8: Clinical development strategy is designed to generate rapid POC
Clinical development strategy is designed to generate rapid POC Stage Program MoA Discovery IND-enabling Clinical Anti-mutCALR mAb Two POC readouts DMR-001 (Fc-null, half-life extended) beginning mid-2027 First regulatory Anti-mutCALR mAb DMR-002 (Fc-enhanced, half-life extended) submission expected
Slide 9: Commercial opportunity
Commercial opportunity Multi- blockbuster potential in mutCALR-driven MPNs
Slide 10: Current MPN treatments leave significant unmet need, with no disease-modifying therapeutics
Current MPN treatments leave significant unmet need, with no disease-modifying therapeutics ET patients are at increased risk for thrombosis, MF leads to poor survival and significant risk hemorrhage, and conversion to MF1 of leukemia, yet SOC largely addresses symptoms5 60-70% of ET patients requir
Slide 11: Estimate >$5B total addressable market for mutCALR-driven MPNs in the US alone
Estimate >$5B total addressable market for mutCALR-driven MPNs in the US alone Essential thrombocythemia Myelofibrosis ~140,000 prevalent patients in the US ~20,000 prevalent patients in the US ~25% have CALR driver mutations ~35% have CALR driver mutations Estimate ~42,000 patients with mutCALR-dri
Slide 12: Significant initial opportunity plus high growth potential with expansion into lower-risk populations
Significant initial opportunity plus high growth potential with expansion into lower-risk populations Essential Thrombocythemia Myelofibrosis ~35K patients with mutCALR-driven ET in the US ~7K patients with mutCALR-driven MF in the US ~21K – 24.5K indicated for cytoreductive Tx ~4.8K – 5.5K with int
Slide 13: DMR-001 is competitively positioned to achieve significant market share on convenience alone
DMR-001 is competitively positioned to achieve significant market share on convenience alone INCA’989 formatted for in-clinic Q2W intravenous KOLs view SC dosing as required for wider adoption, dosing, with on-body injector in early development particularly in ET patients Annual doses of anti-mutCAL
Slide 14: DMR-001
DMR-001 anti-mutCALR Fc-null antibody lead program
Slide 15: CALR mutations drive constitutive JAK/STAT signaling and uncontrolled proliferation in MPNs
CALR mutations drive constitutive JAK/STAT signaling and uncontrolled proliferation of myeloid progenitors in MPNs mutCALR constitutively activates mutCALR drives uncontrolled proliferation JAK/STAT signaling and clonal advantage in the bone marrow Wild-type JAK/STAT signaling is MutCALR activates M
Slide 16: INCA'989 demonstrated clinical POC in mutCALR-driven ET and MF
INCA'989 demonstrated clinical POC in mutCALR-driven ET and MF Essential Thrombocythemia Myelofibrosis 83.3% of patients achieved CHR at doses ≥ 400mg, At week 24, 42% of patients achieved with 46.6% durable ≥12 weeks SVR25 and 33% achieved SVR35 Best change in spleen volume 2000 INCA033989 dose (mg
Slide 17: DMR-001 is a potentially best-in-class anti-mutCALR mAb
DMR-001 is a potentially best-in-class anti-mutCALR mAb Inhibits mutCALR-mediated proliferation with better in vitro potency than INCA’989 • Demonstrated POC for mechanism of action • Superior potency on Type 2 mutCALR • Similar or better potency on Type 1 mutCALR • Predicted equivalent safety – doe
Slide 18: DMR-001 shows higher binding affinity and ~3x potency improvement on Type 1 mutCALR
DMR-001 demonstrates higher binding affinity and ~3x potency improvement on Type 1 mutCALR compared to reference mAb DMR-001 shows more potent inhibition of Type 1 DMR-001 shows higher binding to Type 1 mutCALR-dependent cell proliferation Notes: MFI: mean fluorescence intensity. mutCALR-dependent c
Slide 19: DMR-001 shows higher binding affinity and ~10x potency improvement on Type 2 mutCALR
DMR-001 demonstrates higher binding affinity and ~10x potency improvement on Type 2 mutCALR compared to reference mAb DMR-001 shows more potent inhibition of Type 2 DMR-001 shows higher binding to Type 2 mutCALR-dependent cell proliferation Notes: MFI: mean fluorescence intensity. mutCALR-dependent
Slide 20: DMR-001 expected to deliver efficacious exposure with convenient, infrequent SC dosing
DMR-001 expected to deliver highly efficacious exposure with convenient, infrequent SC dosing using conservative modeling ~5x longer half-life achieved for DMR-001 versus Dose required to match INCA'989 2500mg IV Q2W reference mutCALR mAb in NHPs on Ctrough would enable Q4W+ SC dosing for DMR-001 Pl
Slide 21: Phase 1/1b trial designed to rapidly identify recommended dose and initiate expansion cohorts
Phase 1/1b trial designed to rapidly identify recommended dose and initiate expansion cohorts First regulatory submission for DMR-001 planned in mid-2026 to enable initiation of global Phase 1/1b trial Phase 1 dose escalation • Dose escalation in combined ET and MF population • Starting dose near an
Slide 22: Exceptional financial position to accelerate development through proof-of-concept and toward registration
Exceptional financial position to accelerate development through proof-of-concept and toward registration 2026 2027 DMR-001 Two POC readouts Mid–year: first regulatory submission (Fc-null anti-mutCALR mAb) beginning mid-2027 DMR-002 2H: first regulatory submission (Fc-enhanced anti-mutCALR mAb) DMR-
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