
Exhibit 99.2 Atrium Therapeutics 2 November 2026 RNA L I S T E D
www.atriumtherapeutics.com NASDAQ 1

Forward-Looking Statements Forward - Looking Statements FORWARD LOOKING
STATEMENTS AND OTHER INFORMATION: Certain statements in this Presentation may constitute “forward -looking statem ents” for purposes of the federal securities laws. Our forward -looking statements include, but are not limited to,
statements regarding our future results of operations and financial position, including our exp ected cash runway; business strategies and plans; research and development plans, including the anticipated timing of initiating IND -enabling studies
and of nominating additional development candidates; the anticipated timin g, costs, design, dosing, enrollment, number and location of trial sites and conduct of our ongoing and planned preclinical studies and clinical trials for our product
candidates; the timing of the reporting of data from our clin ical trials, the timing and likelihood of regulatory filings and approvals for our product candidates, the timing and likelihood of success of our research and development programs, plans
and objectives of management for future operations and future results of anticipated product development efforts; the design, capability and scalability of our AOC platform, including its ability to efficiently deliver to cardiac tissue and to
directly target pathogenic RNA across mul tiple genetically defined cardiomyopathies; the therapeutic potential of our product candidates, including their potential to modify disease progression and the potential of ATR 1072 to address PRKAG2
Syndrome; the extent to which results observed in our nonclinical studies, including studies using surrogate molecules in nonclinical models, may be predictive of results in humans; the potential for modulating calcium cycling to improve diastolic
function in cardiom yop athies; our ability to expand into additional indications; our estimates of disease prevalence and market opportunity and identification of higher disease prevalence; and the potential receipt of milestone payments under our
collab orations. The forward -looking statements contained in this Presentation are based on our current expectations and beliefs concerning future developments and their potential effects on us. There can be no assurance that fut ure developments
affecting us will be those that we have anticipated. These forward -looking statements involve a number of risks, uncertainties (some of which are beyond our control) or other assumptions that may cause actual re sults or performance to be
materially different from those expressed or implied by these forward -looking statements including, but not limited to: the initiation, timing, progress, potential registrational quality, and results of our research and development programs, pre
clinical studies, any clinical trials, Investigational New Drug Application, and other regulatory submissions; our ability to identify and nominate additional development candidates on our anticipated t imeline or at all; the beneficial
characteristics, including potential safety, efficacy and therapeutic effects of our product candidates and the potential advantages of our product candidates compared to alternative therapies; the potentia l for clinical trial results to
differ from the results of our nonclinical studies, including data from animal models and from studies using surrogate molecules; the limitations of nonclinical models, which may not fully replicate human disease; the success and capabilities of the
RNA delivery platform, including its ability to efficiently deliver to cardiac tissue; the prevalence of certain diseases and conditions we intend to treat and our estimates of the potential ma rket opportunity for our product candidates;
the number of patients that we will enroll in our clinical trials and the number and location of trial sites; the timing of and costs involved in obtaining and maintaining regulatory approval of our current product candidates and any future
product candidates that we may identify or develop; our ability to meet future regulatory standards with respect to our product candidates, if approved; our plans relating to the further de velopment and manufacturing of our product
candidates, including for additional indications that we may pursue; the rate and degree of market acceptance and therapeutic benefits of our product candidates, if approved; our ability to develop or partner and progress our current and
future product candidates; the implementation of our strategic plans for our business, product candidates, research programs and technologies; the scope of protection we are able to establish and maintain for intellectual property rights
covering our product candidates; anticipated developments related to our competitors and our industry; our competitive position and the success of competing therapies tha t are or may become available; our ability to maintain our
current license agreements and collaborations and identify and enter into future license agreements and collaborations; the expected potential benefits of strategic collab orations with third parties and our ability to attract collaborators
with development, regulatory, manufacturing or commercialization expertise; our reliance on third parties to conduct preclinical studies and clinical trials of our produ ct candidates; our ability to efficiently and cost -effectively
conduct our current and future clinical trials; our reliance on third parties for the manufacture of our product candidates; our plans relating to sales strategy, manufacturing and commercializing our product candidates, if approved;
anticipated regulatory developments in the United States and foreign countries in which we may seek regulatory approval for our product candidates in the future; the timing an d likelihood of the achievement of milestones pursuant to our
existing collaboration agreements; our ability to attract and retain key scientific and management personnel; the costs of operating as a public company; the accuracy of ou r estimates regarding future expenses, future revenue,
capital requirements and the need for additional financing; the period over which we estimate our existing cash and cash equivalents will be sufficient to fund our future ope rating expenses and capital expenditure requirements; our
ability to obtain funding for our operations necessary to complete further development and commercialization of our current and future product candidates; our anticipated use of our existing resources, estimates of our expenses, capital
requirements and needs for additional financing; general economic, political and market conditions, including inflationary pressures, interest rates, and changes in trade pol icy; and other factors specified in the Company's Registration Statement
on Form 10, initially publicly filed by the Company with the Securities and Exchange Commission (the SEC ) on December 10, 2025 and in other filin gs and furnishings made by the Company with the SEC from time to time. Should one or more of these
risks or uncertainties materialize, or should any of our assumptions prove incorrect, actual results may vary in material res pec ts from those projected in these forward -looking statements. We undertake no obligation to update or revise any
forward -looking statements, whether as a result of new information, future events or otherwise, except as may be required under applicable securities laws. TRADEMARKS: This Presentation contains references to trademarks and service marks belonging
to other entities. Solely for convenience, trademarks and trade names re ferred to in this Presentation may appear without the ® or TM symbols, but such references are not intended to indicate, in any way, that the applicable licensor will not
assert, to the f ullest extent under applicable law, its rights to these trademarks and trade names. We do not intend our use or display of other companies’ trade names, trademarks or service marks to imply a relationship with, or endorsement
or sponsors hip of us by, any other companies. PUBLIC DATA SOURCES: Certain facts, forecasts and other statistics in this Presentation have been derived from various public data sources. We believe that the sources of the information are appropriate
sources for such information, and we have taken reasonable care in extracting and reproducing such information. However, such information has not been independently verified by us, our directors, officers, or representatives. Furthermore, any facts,
forecasts, and other statistics from such sources may not be prepared on a comparable basis or may not be consistent w ith other sources. In addition, certain facts, forecasts and other statistics have been taken from public official sources or
statements. Neither we nor any of our directors, officers or representatives are responsible for the accu racy, reliability or completeness of the information from such public data sources. For these reasons, you should not place undue reliance on
such information. You should carefully consider the importance placed on such information or statistics. MARKET AND INDUSTRY DATA: This Presentation also contains information regarding our market and our industry that is derived f rom third-party
research and publications. That information may rely upon a number of assumptions and limitations, and we have not independently verified its accuracy or completeness. This data is subject to change. No repr ese ntation is made as to the
reasonableness of the assumptions made within or the accuracy or completeness of any projections or modeling or any other information contained herein. Any data based on past performance or modeling contained herein is not an indication as to future
performance. 2

Our vision: To pioneer precision RNA medicines for the heart and
profoundly improve the lives of people impacted by cardiac diseases Our vision: To pioneer precision RNA medicines for the heart and profoundly improve the lives of people impacted by cardiac diseases 3

Atrium has made solid progress since our launch in February 2026 KEY
MILESTONES • ATR 1072 cleared for trials in the U.S. and Canada • First patient dosed in Phase 1/2 clinical trial – Corventis PRKAG2 syndrome patient identification: 1 Build bottom-up view of full patient population ATR 1072 &
ATR 1086: 2 Expand into additional cardiomyopathies with shared pathways Next development candidate: 3 Build the pipeline in rare cardiomyopathy 4

Atrium is at the forefront of genetic cardiomyopathy treatment, and
we're moving fast Patients and physicians are looking for more effective treatment options for genetic cardiomyopathies, and the market is primed for precision therapies Rare Cardiac Proven Ability Targeted Disease with High to Execute Platform,
Unmet Need with Urgency Focused Pipeline Serious, genetically driven Atrium has dosed its first patient in A targeted RNA delivery platform cardiomyopathies with significant Corventis , the first interventional powering two lead programs - ATR unmet
need - no approved disease - clinical trial for people living with 1072 (PRKAG2 syndrome) and ATR 1 modifying therapies exist today PRKAG2 syndrome (Ph 1/2) 1086 (PLN cardiomyopathy) – and two undisclosed precision cardiology targets 1 Hutt,
E, et al, “Medical Treatment Strategies for Hypertrophic Cardiomyopathy.” American Journal of Cardiology vol 212, S33 -41 5

A precision RNA platform primed for genetic cardiomyopathies Monoclonal
Oligonucleotide Antibody Oligonucleotide Antibodies Therapies Conjugate (AOC) OLIGO mAb mAb OLIGO Targeted Delivery Genetic Precision Scalable Platform ✓ RNA delivery technology designed ✓ Designed to directly target ✓ AOCs
applicable across multiple to efficiently reach heart tissue pathogenic RNA genetically -defined cardiomyopathies ✓ Built on technology developed ✓ Potential to modify disease ✓ Efficient expansion potential to at Avidity
including same antibody progression additional indications and linker 6

Leadership team expertise in rare disease and RNA Leadership team
expertise in rare disease and RNA Rocio Martin | Chief Strategy Officer Kath Gallagher | Chief Executive Officer and Board Member 20+ years in various senior strategy, management and commercial roles in 20+ years in the biopharmaceutical industry
leading portfolio strategy, clinical and commercial organizations program management, investor relations and corporate affairs in preclinical to commercial stage companies AVIDITY, KRONOS, AUDENTES, ULTRAGENYX, CELGENE AVIDITY, AKCEA, MERRIMACK
Brendan Winslow | Chief Financial Officer Steve Hughes, MD | Chief Medical Officer 15+ years of financial leadership experience in biotech and diversified 25+ years in biopharmaceutical industry contributing to 50+ clinical trials and multiple
product filings and healthcare, including global operations, commercialization and strategic launches in rare disease, cardiovascular and neurology therapy areas transformations AVIDITY, IONIS, BIOGEN, CSL BEHRING, SANOFI AVIDITY, ACADIA, BAXTER
Stephanie Kenney | Chief Corporate Affairs Officer Husam Younis, PhD, PharmD | Chief Scientific Officer 25+ years in biopharmaceutical industry leading corporate affairs, investor 20+ years in drug discovery and development, including rare disease
and relations and marketing at preclinical to commercial stage companies in SVP of development science at Avidity autoimmune, cardiovascular and renal therapy areas AVIDITY, NGM, IONIS, PFIZER AVIDITY, HANSA, ASTRAZENECA Atrium Board Members Troy
Wilson Kath Gallagher Sarah Boyce (Chair) Simona Skerjenac Carsten Boess W. Michael Flanagan, Ph.D. 7

Robust wholly - owned pipeline supported by strong capital position
CLINICAL ANTICIPATED UPCOMING TARGET RESEARCH IND- ENABLING PHASE 1 PHASE 2 PHASE 3 MILESTONES Initial POC data PRKAG2 syndrome PRKAG2 ATR 1072 expected 2H 2027 IND filing PLN PLN cardiomyopathy ATR 1086 in 2027 Development Undisclosed Rare
cardiomyopathy candidate in 2027 Rare cardiomyopathy Undisclosed Research ongoing Strong $1.5B $264M balance sheet potential R&D milestone Cash, cash equivalents, and payments from existing runway through end of 2028, extending 1 investments as
of June 30, 2026 2 collaborations with BMS and LLY beyond initial POC data in 2H 2027 1 Does not include the $15M milestone earned from Bristol Myers Squibb announced on August 13, 2026 or proceeds from the $50M private placement financing announced
on October 8, 2026 8 2 Receipt of such milestone payments are subject to the terms and conditions of the collaboration agreements with BMS and LLY, respectively, assigned to the Company in connection with the Separation and Distribution from
Avidity

About Genetic Cardiomyopathies 9

Millions of people with genetic cardiomyopathies lack disease -
modifying treatments 1 Approximately 1% of patients with genetically driven cardiomyopathies are getting genetic testing ~2 Million 2 50% diagnosed in the US have underlying genetic Most managed through 3,4 5 driver of disease symptom control
Limited targeted or etiology -specific 6 therapies today Opportunity for RNA - based precision therapies 1 Longoni, M. et al, “Real -world Utilization of Guideline -Directed Genetic Testing in Inherited Cardiovascular Diseases.” Front. C
ardiovasc. Med 10:1272433 (2023) 2 Kramer ,C. Et al, Hypertrophic Cardiomyopathy Registry: The rationale and design of an international, observational study of hypert rophic cardiomyopathy. Am Heart J. 2015 Aug;170(2):223 -30 and Ababio, Yaa et al,
Prevalence and Clinical Burden of Idiopathic Dilated Cardiomyopathy in the United States . Am J of Medicine Open Volume 10, 2023. 3 Ho, CY. “Genotype and lifetime burden of disease in hyptertrophic cardiomyopathy 4 Cheng , Z,. et al,
“Hypertrophic Cardiomyopathy: From Phenotype and Pathogenesis to Treatment”. Frontiers in Cardiovascular Medicine vol. 8 (2021) . DOI=10.3389/fcvm.2021.722340 5 Hutt, E, et al, “Medical Treatment Strategies for Hypertrophic
Cardiomyopathy.” American Journal of Cardiology vol 212, S33 -41 10 6 Aro, A. et al, Population Burden of Sudden Death Associated With Hypertrophic Cardiomyopathy”. Circulation vol 136 (2017)

Three phenotypes across the genetic cardiomyopathy spectrum Changes in
cardiac structure and function can present independently and in combination Hypertrophic Dilated Arrhythmogenic Cardiomyopathy Cardiomyopathy Cardiomyopathy (ACM) (HCM) (DCM) Dyspnea, chest pain, Fatigue, exertional dyspnea, fluid retention,
Palpitations, syncope, palpitations, syncope arrhythmias, thromboembolic events ventricular arrhythmias 11

ATR 1072 PRKAG2 Syndrome 12

PRKAG2 s yndrome A rare, progressive disease that can lead to sudden
cardiac death • Autosomal dominant disease caused by gene mutations 0 in PRKAG2 that leads to AMPK overactivity resulting in Approved glycogen accumulation in heart muscle therapies • Contributes to cardiomyopathy due to thickened heart
muscles, electrical conduction problems and arrhythmias 1,000 - 2,000 • Causes heart failure and sudden cardiac death People with PRKAG2 2 • Current treatment limited to symptom management for in the U.S. arrhythmias and myocardial
hypertrophy • No therapy targeting root cause of disease ~100% • Typically emerges during adolescence and early of people inheriting a pathogenic 1 adulthood 3 mutation will develop symptoms 1 van der Steld , L et al. “PRKAG2
syndrome, a rare hypertrophic cardiomyopathy: a Brazilian long -term follow-up with extracardiac disorders.” Einstein (Sao Paulo, Brazil) vol. 22 eAO0549. 26 Jul. 2024, doi:10.31744/ einstein_journal/2024AO0549 2 Murphy, R, et al.
“Adenosine Monophosphate -Activated Protein Kinase Disease Mimicks Hypertrophic Cardiomyopathy and Wolff -Parkinson -White Syndrome.” Journal of the American College of Cardiology vol 45 (2005). d oi:10.1016/j.jacc.2004.11.053 13 3 Hu,
D, et al. “Identification, clinical manifestation and structural mechanisms of mutations in AMPK associated cardiac glyco gen storage disease.” EBioMedicine 54 (2020) 102723

PRKAG2 s yndrome prevalence likely exceeds our initial estimate This
work continues, building towards a confident view of the full population Patient identification strategy is Early findings to uncover the focused in three areas already diagnosed Uncover the already - diagnosed Our initial prevalence estimate of
1,000 - 1 1 Direct, bottom -up engagement with major 2,000 PRKAG2 syndrome patients was genetic -testing labs conservative based on published literature Engage the patient community 2 Early efforts have already uncovered close to Build presence and
advocacy where patients 2,000 individuals with the PRKAG2 mutation already are 2 so far from only a subset of engaged labs Move the field of genetic testing 3 True population likely larger - still unmeasured Partner across stakeholders to widen
testing and recognition 1 Murphy, R, et al. “Adenosine Monophosphate -Activated Protein Kinase Disease Mimics Hypertrophic Cardiomyopathy and Wolff -Parkins on-White Syndrome.” Journal of the American College of Cardiology vol 45 (2005).
doi:10.1016/j.jacc.2004.11.053 14 2 Data on file: Internal sources based on discussions with genetic testing providers

ATR 1072 designed to silence mutant PRKAG2 to normalize AMPK activity
PRKAG2 is the regulatory Mutant PRKAG2 leads to Hypertrophic cardiomyopathy (HCM) characterized Mechanism component of AMPK overactivation of AMPK by glycogen accumulation and arrhythmia of Disease ATR 1072 - mediated degradation Reduced mutant
PRKAG2 leads Attenuates HCM Therapeutic of cardiac PRKAG2 mRNA to normalization of AMPK activity disease progression Approach ATR 1072 15

Targeting PRKAG2 mRNA in the heart led to reversal of glycogen
accumulation as well as improvement in other key 1 features of the disease in nonclinical model Cardiac glycogen accumulation reversed • Encouraging results in measures of 4 weeks after treatment hypertrophy include reduction in heart weight
and left ventricular wall thickness 30 Glycogen • Treatment also led to improvement in p < 0.05 ✱ ECG parameters measuring electrical 20 conduction including PR interval • Further reinforces scientific rationale for 10 ATR 1072
targeting the root cause of PRKAG2 syndrome • Reversibility of downstream parameters 0 | | | consistent with earlier nonclinical data Untreated Disease After Treated Control Untreated features mATR 1072 diseased diseased established treatment
mice mice 1 R302Q Data on file: Mice received PRKAG2 AAV for 3 wk followed by mATR 1072 (single dose 3 mg/kg, siRNA component), a mouse -active surrogate of ATR 1072 . 16 Data presented at 4 wk post mATR 1072; mean ± SD, n=9 -10/grp. *One-Way
ANOVA Glycogen (μg/mg)

ATR 1072 improved measure of cardiac hypertrophy 1 in echocardiogram in
nonclinical model Cardiac wall thickness decreased at 4 weeks after treatment Untreated diseased mice Treated diseased mice LVID LVID LVPW LVPW 1 mm LVID: Left ventricular internal diameter; LVPW: Left ventricular posterior wall thickness 1 Data on
file. This is a representative echocardiogram image. 17

ATR 1072 has a favorable nonclinical safety profile and 1 robust target
knockdown ATR 1072 activity in monkey heart following a ATR 1072 was generally well single dose at 28 days of treatment tolerated in 9 - month, repeat dose chronic toxicity study in PRKAG2 mRNA 150 cynomolgus monkey 125 • No dose limited
toxicity in any organ 100 system at the highest dose tested 75 50 • No effects on cardiac function 25 associated with PRKAG2 mRNA 0 reduction including assessments of PBS ATR 1072 ECG, echocardiogram, histopathology (3 mg/kg) 18 1 Data on
file: Based on preclinical studies PRKAG2 mRNA Relative to PBS (%)

ATR 1072: First trial targeting PRKAG2 syndrome ongoing Initial trial
data demonstrating proof of concept anticipated in 2H 2027 48 - week treatment PART A - Dose Escalation* PART B - Expansion Long - Term Extension Cohort A1 Cohort A2 Cohort A3 Cohort B All participants 40 mg 80 mg 160 mg Recommended Ph 2 dose n = 4
n = 4 n = 4 n = 25 Safety review committee evaluation prior to dose escalation Open label adaptive trial design Primary endpoint: Incidence of treatment -emergent adverse events (TEAEs) ~37 participants enrolled, ~15 sites globally Secondary
endpoints: PRKAG2 mRNA reduction and siRNA tissue concentrations Adults (18-65 yrs) w/ confirmed PRKAG2 mutation and (cardio biopsy in Part A only), plasma PK cardiac phenotype consistent with PRKAG2 syndrome Exploratory endpoints: Echocardiogram,
ECG and Holter parameters, biomarkers, immunogenicity, clinical outcomes, and optional cardiac MRI findings 19 * Dose based on siRNA weight; flat dosing IV Q6W Equivalent to 0.5, 1.0, 2.0 mg/kg

ATR 1086 PLN Cardiomyopathy 20

PLN Cardiomyopathy A rare progressive disease with frequent family
history • PLN -R14del is the most common disease - relevant PLN mutation 0 • Mutant PLN -R14del forms aggregates and impairs Approved cardiomyocyte function therapies • Characterized by dilated, arrhythmogenic or hypertrophic
cardiomyopathy • Notable for frequent family history of premature sudden 2,000 - 4,000 cardiac death and progressive cardiac failure People with pathogenic PLN 2 • High incidence of sudden cardiac death, ventricular variants in the U.S.
arrhythmias and cardiac transplantation 1 • Current treatment focuses on symptom management • No therapy to target root cause of disease 1 Vafiadaki E, et al. “ Phospholamban R14del disease: The past, the present and the
future.” Frontiers in Cardiovascular Medicine vol 10 (2023). doi:10.3389/fcvm.2 02 3.1162205 21 2 Internal sources based on discussions with genetic testing providers

ATR 1086: Designed to silence mutant PLN to prevent 1 protein
aggregates and target root cause of disease Phospholamban (PLN) regulates R14del mutation on PLN causes Dilated and Arrhythmogenic Mechanism Ca2+ handling in cardiomyocytes PLN to form protein aggregates cardiomyopathy (DCM & ACM) of Disease ATR
1086 mediated degradation Reduced mutant PLN prevents Attenuates DCM & ACM Therapeutic of cardiac PLN mRNA protein aggregate formation disease progression Approach ATR 1086 22 1 Data on file: Based on preclinical studies

ATR 1086 demonstrates functional improvement and 1 survival in
preclinical model of disease Reduction of human PLN expression Improved survival (Kaplan - Meier survival curve) and ejection in the heart following treatment with fraction following repeated ATR 1086 treatment (6 mg/kg) in a ATR 1086 (6 mg/kg )
humanized mouse model of hPLNR14/R14 ATR 1086 ATR 1086 ATR 1086 PLN mRNA levels were measured in cardiac tissue in Ejection fraction measured at 6 -weeks of treatment. Dotted lines indicate WT levels. Data are presented as mean ± SEM.
transgenic mice expressing hPLN WT. Student’s t -test, * p < 0.05. 23 1 Data on file: Based on preclinical studies

Expansion Opportunities for ATR 1072 and ATR 1086 A biology -driven
pipeline with multiple indication expansion opportunities 24

ATR 1072 and ATR 1086 have opportunities for indication expansion
beyond a single genetically defined population Central Pathways in Opportunities for Cardiac Function Indication Expansion AMPK dysregulation is implicated Energy sensing across multiple genetic PRKAG2 regulates AMPK AMPK ATR 1072 cardiomyopathies
beyond activity, the key energy sensor in the heart PRKAG2 syndrome Influencing calcium cycling may Calcium handling improve diastolic function in PLN inhibits SERCA2a, an 2+ Ca ATR 1086 multiple cardiomyopathies beyond essential mediator of calcium
cycling PLN cardiomyopathy 25

Atrium is accelerating momentum post - launch, with strong execution
and multiple milestones ahead Achievements Anticipated Upcoming Milestones • GMP manufacturing• Initial proof-of-concept data by 2H 2027 • IND clearance and NOL ATR 1072 • First patient dosed in Corventis Ph 1/2 trial •
Identified lead candidate• IND-enabling studies initiated in 2026 ATR 1086• Preclinical proof -of-concept • IND filing in 2027 • GMP manufacturing Rare • Identified two promising targets• Next development
candidate in 2027 cardiomyopathies 26 26

Atrium has the expertise, leadership and focused pipeline to deliver in
precision cardiology Execution Pipeline Platfor m Strong balance sheet with Focused pipeline with Proprietary RNA delivery experienced leadership indication expansion platform ideal for precision team opportunities cardiology 27 27

IR Contact Stephanie Kenney, Chief Corporate Affairs Officer
investors@atrium -tx.com 28