Damora Therapeutics, Inc. · NASDAQ:DMRA
Damora Therapeutics — Investor Presentation (August 2026)
23 slides from Damora Therapeutics's investor presentation, August 2026
Slide 1: Redefining care for people with blood disorders
Redefining care for people with blood disorders Company Overview August 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 patients across mutCALR-driven MPNs
Rapidly advancing portfolio uniquely positioned to address the spectrum of patients across mutCALR-driven MPNs ✓ Phase 1/1b CLARITY-101 trial initiated 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
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 non-Type 1 CALR mutations Frequent, high-volume IV doses 4 26 6 11 N= N= N= Durable Complete Hematologic 100% Intravenous administration CALR mutation Response (DCHR, %) 81% 80% 70% types in INCA’989 Frequent dosing every tw
Slide 7: DMR-001 has two ways to win: maximize efficacy and meaningfully improve the 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 Status Two clinical POC Anti-mutCALR mAb DMR-001 readouts beginning (Fc-null, half-life extended) mid-2027 Anti-mutCALR mAb First regulatory DMR-002 (Fc-enhanced, half-life submission ex
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 of myeloid progenitors in MPNs
CALR mutations drive constitutive JAK/STAT signaling and uncontrolled proliferation of myeloid progenitors in MPNs Healthy TPO-dependent Ligand-independent Inhibition of mutCALR activation of TPO receptor signaling driven by mutCALR signaling with DMR-001 1 2 TpoR/MPL DMR-001 wtCALR mutCALR 3 STAT p
Slide 16: 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 versus reference mutCALR mAb • Demonstrated POC for mechanism of action • Superior potency on Type 2 mutCALR • Similar or better potency on Type 1 mutCALR • Favorable safety p
Slide 17: DMR-001 shows higher binding affinity and slower off-rate in both Type 1 and Type 2 mutCALR
DMR-001 shows higher binding affinity and slower off-rate in both Type 1 and Type 2 mutCALR compared to reference mutCALR mAb ~26-fold improvement in binding affinity ~30-fold improvement in binding affinity in Type 1 mutCALR in Type 2 mutCALR KD = 0.074 nM KD = 0.31 nM Relative response (RU) Relati
Slide 18: DMR-001 robustly inhibits cellular proliferation in both Type 1 and Type 2 mutCALR
DMR-001 robustly inhibits cellular proliferation in both Type 1 and Type 2 mutCALR compared to reference mutCALR mAb Robust anti-proliferative activity ~26-fold greater anti-proliferative activity in Type 1 mutCALR in Type 2 mutCALR 100 100 75 75 Inhibition Inhibition %Inhibition % Inhibition 26X 50
Slide 19: DMR-001 expected to deliver highly 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 in NHPs Dose required to match INCA'989 2500mg IV Q2W versus reference mutCALR mAb on C would enable Q4W+ SC dosing trough Kwan, EHA 2026. Notes: Reference m
Slide 20: DMR-001 preclinical data supports potential best-in-class profile
DMR-001 preclinical data supports potential best-in-class profile INCA’989 emerging clinical profile DMR-001 preclinical profile ~5x increase in half-life versus reference Dosing 750 mg - 3,500 mg Q2W IV mutCALR mAb supports Q4W SC dosing ET:1 81% durable CHR (21/26; ≥750 mg) Improved binding affini
Slide 21: Phase 1/1b CLARITY-101 trial of DMR-001 initiated in Q3 2026
Phase 1/1b CLARITY-101 trial of DMR-001 initiated in Q3 2026 Global, multi-center, open-label, dose escalation and expansion trial in mutCALR-driven ET and MF Recommended dose ET population Phase 1 dose Phase 1b dose MF population escalation expansion Combination in MF 100 mg Q4W SC starting dose Ad
Slide 22: Financials and future anticipated milestones
Financials and future anticipated milestones
Slide 23: 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 clinical POC readouts ✓ Phase 1/1b CLARITY-101 trial initiated (Fc-null anti-mutCALR mAb) beginning mid-2027 DMR-002 2H: first regulatory submission (Fc-enhanced anti-mutCA
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