Damora Therapeutics : Corporate Presentation

Published: 2026-05-12 16:39:41 ET DMRA

Published on 05/12/2026 at 04:39 pm EDT

Redefining care for people with blood disorders

Company Overview

May 2026

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-

including essential thrombocythemia (ET) and myelofibrosis (MF)

NASDAQ: DMRA

Corporate and RCD leadership with a proven track record of clinical and commercial success

Premier investor support, with ~$533 million1 in cash,

and into registrational development

1 Cash and cash equivalents as of March 31, 202c.

Fc-null, extended half-life

Blocks mutCALR-driven oncogenic signaling, without engaging immune effector functions

First regulatory submission: mid-2026

T-cell engager

mutCALR x CD3 bi-specific recruits and directs T-cell-mediated killing of malignant cells

First regulatory submission: 2027

Fc-enhanced, extended half-life

Afucosylation enhances antibody-dependent cellular cytotoxicity and amplifies natural immune killing of malignant cells

First regulatory submission: 2H 2026

Myelofibrosis (MF)

High platelet counts increase thrombosis and hemorrhage risk

Severe headaches, fatigue, mental fogginess, tingling in hands and feet, and other symptoms negatively impact QoL

mutCALR patients are younger with higher risk of transformation

to myelofibrosis

Available therapies do not treat underlying cause of disease

and have significant side effects (e.g., hydroxyurea)

Bone marrow fibrosis leads to poor survival and high risk of

transformation to acute myeloid leukemia

Debilitating symptoms include anemia, severe weakness and fatigue, splenomegaly, night sweats and bone pain

Available therapies do not treat underlying cause of disease

and largely only address symptoms

Significant need for highly effective, safe and convenient disease-modifying treatments

ǪoL, quality of life.

Sources: Tefferi 2025 (JAMA); Tefferi 2020 (Am J Hematol).

Best Overall Complete Response (CR, %)

in ET patients

100

100% 100%

27%

69%

Estimated frequency of CALR mutation types

53% Type 1

47% Non-Type 1*

Intravenous administration Frequent dosing every two weeks High-volume up to 2,500 mg

Different dose levels likely needed for Type 1 and Non-Type 1 patients, with dose escalation embedded in design of Phase 3 trial in ET

Type 1 Non-Type 1

IV 24 - 250 mg

anti-mutCALR Fc-null antibody therapy was well-tolerated

INCA'S8S, INCA033S8S; IV, intravenous.

Sources: Klampfl 2013 (NEJM). Complete response defined as platelet count below 400x10S/L; bar graphs for Type 1 and Non-Type 1 generated based on swim plot. CALR mutation type breakdown representative

of all mutCALR MPN patients.* Non-Type 1 mutations include Type 2 (32%) and Other (15%) CALR mutations. Other includes Type 1-like, Type 2-like and other uncategorized mutations.

Superior potency and exposure

Next-generation therapy engineered to maximize efficacy across all CALR mutations through superior potency and optimized exposure levels

Improve patient experience

POTENTIAL

FIRST TO MARKET

Autoinjector format

INFREQUENT SIMPLE ADMINISTRATION

Quick, low-burden delivery

LONG-TERM ADHERENCE

Designed for chronic use

Potential first-in-class convenient solution for chronic therapy

Differentiation through a patient-centric design, maximizing the experience on multi-year therapy with a potential first-to-market, simple, and quick autoinjector

BROAD COVERAGE

Targets both Type 1 & Type 2 mutations

HIGH POTENCY

Potential best-in-class affinity

OPTIMIZED EXPOSURE

Sustained therapeutic levels

Potential best-in-class disease modification in ET and MF

Program

MoA

Stage

Discovery

IND-enabling

Clinical

DMR-001

DMR-002

DMR-003

Anti-mutCALR mAb

(Fc-null, half-life extended)

Anti-mutCALR mAb

(Fc-enhanced, half-life extended)

Anti-mutCALR x CD3 bsAb

(T-cell engager)

Two POC readouts beginning mid-2027

First regulatory submission expected 2H26

First regulatory submission expected 2027

Large market opportunity, with ~25-35% of essential thrombocythemia C myelofibrosis driven by mutCALR

Assets designed by Paragon Therapeutics,

with expertise in developing best-in-class biologics

ET patients are at increased risk for thrombosis,

hemorrhage, and conversion to MF1

60-70%

of ET patients require cytoreductive

therapy to reduce risk of thrombosis

20-30%

of patients receiving SOC cytoreductive therapies are resistant or intolerant3

>17%

of mutCALR ET patients transform to MF4

MF leads to poor survival and significant risk

of leukemia, yet SOC largely addresses symptoms5

There is need for highly safe, convenient, and targeted disease-modifying therapies

mutCALR targeted therapy presents an opportunity for much-needed disease modification that eradicates neoplasms

Notes: SOC: standard of care.

Sources: Internal KOL calls; 1Campbell 2005 (Lancet); 2Loscocco 2024 (Blood); 3Hernandez-Boluda 2010 (Brit J Hem); 4Tefferi 2025 (JAMA); 5Gangat 2023 (Blood Cancer J).

Essential thrombocythemia

Myelofibrosis

~140,000 prevalent patients in the US

~25% have CALR driver mutations

~20,000 prevalent patients in the US

~35% have CALR driver mutations

Estimate ~42,000 patients with mutCALR-driven MPNs in the US,

with majority indicated for cytoreductive / targeted treatment

Sources: Klampfl 2013 (NEJM); prevalence based on range from Mehta 2013 (Leukemia & Lymphoma), Shalis 2021 (Hematol Oncol Clin N Am), and Masarova 2025 (ASCO); Incyte 2025 Ǫ2 report.

Incyte estimates a >$7B US addressable market for anti-mutCALR therapy.

~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

20% - 30% resistant or intolerant to SOC

~10.5K - 14K not indicated for cytoreductive Tx

~4.8K - 5.5K with intermediate-to-high-risk MF

~1.4K - 2.1K with low-risk MF

~:1.4B ruxolitinib US revenue attributable to MF alone in 2025

Notes: ET and MF sub-group breakdowns are mutCALR patients based on preliminary internal estimates. Ruxolitinib revenue in MF based on sellside estimates; Incyte does not report revenue by indication.

INCA'989 formatted for in-clinic Q2W intravenous

dosing, with on-body injector in early development

Annual doses of anti-mutCALR

INCA'G8G

IV Ǫ2W

INCA'G8G

OBI

DMR-001

SC Ǫ4W+

KOLs view SC dosing as required for wider adoption,

particularly in ET patients

"50% of patients would not accept IV treatment, whereas

20% would reject SC treatment. Every four weeks is

meaningful for my patients."

- US KOL

"I would prescribe INCA033G8G to all ET patients requiring cytoreduction if it was administered SC and half as many

patients if IV." - US KOL

"IV administration might be a barrier for [expansion into] low-risk ET patients."

- US KOL

DMR-001 is expected to be conveniently administered SC Q4W+ using an autoinjector

Notes: OBI: on-body injector. Annual dose figures reflect dosing frequency projected to match INCA'S8S 2500mg Ǫ2W IV on Ctrough and assume 2x improvement in Type 2 in vivo potency.

mutCALR constitutively activates

JAK/STAT signaling

Wild-type JAK/STAT signaling is driven by TPO binding to MPL

MutCALR activates MPL signaling independent of TPO

mutCALR drives uncontrolled proliferation

and clonal advantage in the bone marrow

Essential thrombocythemia

Post-ET myelofibrosis

Leukemic transformation

Rapid expansion of leukemic clone

Additional leukemic mutation(s)

Clonal expansion

Inflammatory & fibrotic

signaling

Additional mutations

(CALR, JAK2, MPL)

modification

(ex: TP53)

Sources: Imai 2017 (Int J of Hem); Grabek 2020 (Cells).

Essential Thrombocythemia Myelofibrosis

83.3% of patients achieved CHR at doses ≥ 400mg, with 46.6% durable ≥12 weeks

2000

Platelet count (x10G/L)

1500

1000

500

At week 24, 42% of patients achieved SVR25 and 33% achieved SVR35

INCA033G8G dose (mg)

*CALR non-Type 1 mutation

(n)

Baseline C1D15 C2D1 C2D15 C3D1 C3D15 C4D1 C4D15 C5D1 C5D15 C6D1 C6D15 C7D1 C7D15 C8D1 C8D15 C9D1 C9D15 C10D1 C10D15 C11D1 C11D15 C12D1

C12D15

Best change in spleen volume from baseline(%)

Visit

30 30 30 29 28 27 27 27 26 24 23 23 20 19 19 17 14 9 10 9 10 7 6 5

Non-Type 1 patients underperform as seen by fewer patients hitting SVR25 and SVR35

Requires Ǫ2W IV infusion with lower efficacy seen in Type 2 patients

SVR35 and SVR25, spleen volume reduction of 35% and 25%, respectively.

Sources: Mascarenhas 2025 (ASH). Notes: Durable complete hematologic response (CHR) defined as platelet count <400x10S/L and leukocytes<10x10S/L for ≥12 weeks.

Inhibits mutCALR-mediated proliferation with better in vitro

potency than INCA'G8G

Demonstrated POC for mechanism of action

Superior potency on Type 2 mutCALR

Similar or better potency on Type 1 mutCALR

Predicted equivalent safety - does not bind to wild-type CALR

Subcutaneous formulation

Targeting lower dose to enable convenient SC autoinjector format

Half-life extension through validated Fc modification

Longer exposure to enhance sustained mutCALR inhibition and reduce dosing frequency

Effector-null human IgG1 Fc

Novel IP(1) for composition of matter into 2040s

DMR-001

(1) Damora has exercised its option to acquire certain intellectual property license rights pursuant to the antibody discovery and option agreement by and among Damora Therapeutics LLC, Paragon Therapeutics, Inc. and Paramora Holding LLC, dated October 7, 2025.

DMR-001 shows higher binding to Type 1

DMR-001 shows more potent inhibition of Type 1

mutCALR-dependent cell proliferation

Notes: MFI: mean fluorescence intensity. mutCALR-dependent cells are Ba/F3 cells expressing TpoR and mutCALR; Reference mutCALR mAb produced recombinantly based on US20230272055A1.

DMR-001 shows higher binding to Type 2

DMR-001 shows more potent inhibition of Type 2

mutCALR-dependent cell proliferation

Notes: MFI: mean fluorescence intensity. mutCALR-dependent cells are Ba/F3 cells expressing TpoR and mutCALR; Reference mutCALR mAb produced recombinantly based on US20230272055A1.

~5x longer half-life achieved for DMR-001 versus reference mutCALR mAb in NHPs

Dose required to match INCA'989 2500mg IV Q2W on Ctrough would enable Q4W+ SC dosing for DMR-001

Plan to pursue convenient SC dose with less frequent administration to maximize convenience

SC, subcutaneous.

Notes: Reference mutCALR mAb produced recombinantly based on US20230272055A1. Day 42 Interim NHP PK Data after a single 30 mg/kg IV dose (n=4 per group). Bar chart reflects projections to match

benchmark mAb 2500mg IV Ǫ2W on Ctrough and conservatively models 2x improvement in Type 2 potency in vivo.

Disclaimer

Damora Therapeutics Inc. published this content on May 12, 2026, and is solely responsible for the information contained herein. Distributed via Public Technologies (PUBT), unedited and unaltered, on May 12, 2026 at 20:35 UTC.