Degrading Proteins, Making Medicines MRT-8102 GFORCE-1 Clinical Study Results October 1, 2026 Exhibit 99.2

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Forward-looking statements contained herein include, but are not limited to, statements about our ability to grow our product pipeline and successfully research, develop and, if approved, commercialize our product candidates in current or future indications; statements regarding our progress in developing only-in-class and first-in-class MGD therapeutics; the timing, design, conduct, progress and results of our preclinical and clinical programs; statements regarding the significance, interpretation and potential implications of clinical data for MRT-8102, including safety, tolerability, target engagement, pharmacodynamic, biomarker, genetic and lipid data from GFORCE-1; the potential for MRT-8102 and NEK7 degradation to provide differentiated or clinically meaningful effects across ASCVD, coronary artery disease, gout, hidradenitis suppurativa and other NLRP3/IL-1-driven diseases; the potential relationship between observed biomarker effects and disease biology, clinical outcomes or therapeutic benefit; the potential use of biomarkers, imaging, genetics or pharmacogenomics to identify or enrich for patients who may benefit from treatment, inform dose selection or support more efficient clinical development; statements regarding our planned Phase 2 development program for MRT-8102, including the anticipated timing, design, conduct, endpoints, results and data disclosures for GFORCE-2, GEMINI-1 and GALAXY-1; the potential for such studies to demonstrate proof of concept, safety, efficacy, flare prevention, lesion response, cardiovascular benefit or other clinical outcomes and to inform potential future Phase 3 development; statements regarding the evaluation of additional proof-of-concept studies in further indications; the timing and outcome of regulatory interactions and submissions; statements regarding the potential clinical and commercial opportunities for MRT-8102, including estimates of patient populations, unmet need, market opportunity, competitive positioning and potential differentiation from other therapies, including comparisons to other anti-inflammatory modalities and lipid-modifying agents; statements regarding the effects of MRT-8102 on lipids and lipoproteins, including lipoprotein(a), and the potential clinical significance thereof; statements regarding the expected safety profile of MRT-8102 in patient populations with comorbidities, including chronic kidney disease; statements regarding MRT-9347 and other current or future product candidates, including MRT-2359 and preclinical and discovery-stage programs, their potential applications across immunology and inflammation, oncology, genetic and neurological diseases and other therapeutic areas, their differentiation, strategic value, the timing and results of anticipated clinical data updates, regulatory filings and other development milestones; statements regarding our expectations that our collaborator, Novartis, will advance MRT-6160 and other VAV1-directed MGDs in immune-mediated diseases, including the anticipated timing of additional Phase 2 study initiations; statements regarding our QuEEN™ discovery engine and the potential applications of our platform; the advancement and application of our partnered and wholly owned pipeline, including programs licensed or optioned to Roche and Novartis; our ability to optimize collaborations with industry partners; and our expectations regarding the timing and achievement of development, regulatory and commercial milestones and the success of our programs, among others. 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MRT-8102, a selective first-in-class NEK7 MGD, demonstrated a favorable safety and tolerability profile, sustained NEK7 degradation, and broad normalization of elevated pathogenic drivers of ASCVD Study design: 108 subjects with elevated CVD risk; 8-week study, randomized to MRT-8102 at 5, 20, and 40 mg QD, or placebo for 4 weeks dosing Target engagement: Robust, sustained, and equal NEK7 degradation across all three dose levels Safety: No SAEs; TEAE rate similar to placebo (33% vs. 30%); no increased infection risk Activity on plaque and vessel wall biology and thrombogenic factors demonstrated, supporting broad potential for MRT-8102 to impact ASCVD: Pathogenic drivers of ASCVD, including IL-1b, HMGB1, Calprotectin, S100A12, SAA, and Fibrinogen reduced to healthy-volunteer levels at all doses Opportunity for precision medicine approach: NLRP3 risk-allele carriers show higher baseline levels for DAMPs, suggestive of elevated pathway activity and potential for faster and more severe atherosclerotic remodeling, and identifying a genetically enrichable population for potential future development GFORCE-1: A Phase 1 Study of MRT-8102 in Subjects with Elevated CVD Risk

Therapeutic Rationale for Degrading NEK7

NEK7 Enables Pathogenic NLRP3 Activation to Drive Disease Biology Multiple metabolic and genetic factors can promote NEK7-mediated NLRP3 inflammasome complex assembly in a kinase-independent manner NEK7/NLRP3 pathway activation causes pyroptotic cell death, leading to release of IL-1α/β, IL-18, and DAMPs (e.g., HMGB1, Calprotectin, S100A12) IL-1β and IL-18 are highly inflammatory cytokines DAMPs further stimulate NEK7/NLRP3 activity and concomitantly promote NLRP3-independent cytokine/chemokine production in neighboring cells DAMPs and IL-1β are responsible for the majority of local pathogenesis and tissue changes characteristic of ASCVD, gout, hidradenitis suppurativa (HS) and other indications Interference with pathway at most upstream point, through NEK7 degradation, has potential to achieve most meaningful efficacy across NEK7/NLRP3-driven indications, including ASCVD, gout and HS DAMPs = damage-associated molecular patterns; HMGB1 = High-mobility group box 1; CRP = C-reactive protein NEK7 NEK7/NLRP3 complex Pyroptosis IL-1b Calprotectin Cytokines DAMPs DAMP-induced amplification of NEK7/NLRP3 pathway activity IL-1b NFkB NEK7/NLRP3 activating stimuli S100A12 DAMPs TLR4/ RAGE HMGB1 IL-1a Pyroptotic release of drivers of disease pathology, e.g. damps and cytokines NEK7 serves as a scaffold to enable NLRP3 inflammasome assembly and activation of NEK7/NLRP3 pathway NEK7/NLRP3 activators directly stimulate pathway or enhance expression Metabolites IL-6 IL-18 IFN-g

Members of the NEK7/NLRP3 Downstream Signaling Cascade are Elevated Across Multiple Indications with High Unmet Need Upregulation of pathogenic cascade downstream of pyroptosis is conserved across the top NEK7/NLRP3-active indications ASCVD, HS and gout have highest pathological NEK7/NLRP3 activity scores HS (skin) ASCVD (plaques) Gout (PBMCs) NLRP3 IL1β S100A8 S100A9 Healthy Disease Healthy Disease Healthy Disease Healthy Disease Hidradenitis Suppurativa ASCVD CAPS Gout Indication 5 Indication 6 Indication 7 Indication 8 Indication 9 Indication 10 Indication 11 Indication 12 Indication 13 Data sources: accessions GSE155176, GSE163154, GSE160170 S100A12 Healthy Disease 0 3 6 Calprotectin subunits Calgranulin C NEK7/NLRP3 activity score Log2(fold change)

The Role of the NEK7/NLRP3 Pathway in ASCVD

The Multifaceted Pathogenic Role of the NEK7/NLRP3 Pathway in Plaque Biology and Atherogenic Progression Endothelial Cell dysfunction enhances adhesion molecules and vascular leakage Increased uptake of oxLDL and retention of oxidized cholesterol in foam cells VSMC proliferation or phenotypic transformation/ de-differentiation Thrombogenic factors from pyroptotic macrophages, VSMC and ECs Plaque formation Plaque growth Vessel wall alterations Thrombosis Cardiovascular events (MI / Ischemic stroke / ACS) NEK7/NLRP3 effectors IL-1β | IL-18 | DAMP release | Oxidative stress DAMPs, crystals, metabolic factors Genetic (NLRP3 SNPs, CHIP mutations)

Clinical Experience Supports Upstream Targeting of NEK7/NLRP3 Pathway as a Superior Approach to Impact MACE Clinical efficacy achieved NLRP3 SNP TET2 ChIP Metabolic Genetic Cholesterol LoDoCo2 COLCOT CANTOS ZEUS NEK7/NLRP3 pathway modulation IL-1β neutralization IL-6 neutralization 5,522 pts with chronic CAD (>6 months post MI) randomized to colchicine or pbo Baseline median CRP unknown Colchicine reduced MACE by 31%; no risk of infection, significant GI AEs 4,745 pts < 30 days post-MI randomized to colchicine or pbo Baseline median CRP 4.28 mg/L Colchicine reduced MACE by 23%; no risk of infection, significant GI AEs 10,061 pts > 30 days post MI randomized to canakinumab (anti-IL-1b) or pbo Mean time since MI 4.57 years Baseline CRP>2mg/L (median 4.1 to 4.2) Canakinumab reduced MACE by 15%; risk of infection increased 6,376 pts with ASCVD and moderate-severe CKD randomized to ziltivekimab (anti-IL-6) or pbo Baseline CRP>2mg/L (median 4.5) No significant effect on MACE; risk of infection increased IL-1b/IL18/ DAMPs/ Thrombogenic factors IL-6 Fibrinogen CRP Thrombosis Results are from separate clinical trials with different agents, populations and study designs and should not be interpreted as head-to-head comparisons

NLRP3 Activating Variants Increase Signaling and Cardiovascular Risk NLRP3 risk variant shows larger effect on inflammatory cytokines and CRP compared to IL-6(R) variant NLRP3 variant associated with strong risk of CVD; IL-6(R) benefit restricted to CHIP+ subgroup NLRP3 risk variants in all comers IL-6(R) variant benefit in all comers IL-6(R) variant benefit in CHIP- IL-6(R) variant benefit in CHIP+ Odds ratio (log scale) hsCRP IL-1β IL-18 % Change per variant CAD, 916 ptsaCAD, age <60, 3,061 ptsbSevere CAD, age <60, 3,061 ptsb CHD, 126,198 ptscCHD, 187,667 ptsdCAD, 547,261 ptse Incident CVD, 50,000 ptsfIncident CAD, 436,875 ptsg Incident CVD, 50,000 ptsfIncident CAD, 436,875 ptsgCVD, 50,000 ptsh 0.95 (0.93–0.97) 0.97 (0.95–0.98) 0.96 (0.96–0.97) 1.63 (1.08−2.46) 2.04 (1.15−3.61) 2.28 (1.29−4.01) 0.46 (0.29–0.73) 0.83 (0.71–0.96) 0.60 (0.40–0.89) 0.95 (0.89–1.01) 0.97 (0.94–0.99) 0.25 0.5 2 4 1.0 Lower risk Higher risk 1 1 1 2 2 3 IL-6(R) rs7529229 NLRP3 rs10754558 Left: ᵃZhou et al. (2016); ᵇSchunk et al. (2021); ᶜSwerdlow et al. (2012); ᵈSarwar et al. (2012); ᵉRosa et al. (2019); ᶠBick et al. (2019); ᵍVlasschaert et al. (2023); ʰKessler et al. (2022); Right: ¹Wu et al. (2022); ²Zhou et al. (2016); ³Tchuisseu-Kwangoua et al. (2025). % differences: NLRP3 rs10754558 = (GG − CC)/CC; IL-6(R) rs7529229 (proxy rs2228145) = (CC − AA)/AA Not reported Not reported Published relative variant impact

Mediators of NLRP3 Pathway Driven Atherosclerosis/-thrombosis are Established Cumulative Cardiovascular Risk Factors NLRP3, relevant cytokines, and DAMP levels are significantly increased in unstable plaques NEK7/NLRP3 pathway DAMPs & thrombogenic factors Data from PMIDs 24026779, 29957458, 21435605, 25341801, 39322770, 28845751, 28428221, 39178030, 30006491, 19622820, 23034020 Cumulative CV risk associated with NEK7/NLRP3-relevant cytokines, lipids, and DAMPs CV risk per standard deviation increase Harmonized per-SD HR Non-harmonized (per-doubling, acute STEMI) HMGB1 IL-1β S100A12 SAA1 RNA‑seq of stable and unstable section of human atherosclerotic plaques GEO GSE120521 1  1.2   1.5   2   3 Stable Unstable Stable Unstable Stable Unstable Stable Unstable Expression (log2 FPKM) IL-6 Lp(A) Calprotectin subunits NLRP3 IL1B S100A8 S100A9 CASP1 PYCARD S100A12 SAA1 1.75 (1.10-2.80)1.45 (1.23-1.71)1.33 (1.13-1.56)1.30 (1.06-1.59)1.26 (1.13-1.41)1.25 (1.19-1.32)1.13 (1.09-1.18) Calprotectin

Results of GFORCE-1 Study

GFORCE-1 Study: Dose Exploration of MRT-8102 in Subjects with Elevated CVD Risk Double blind period CRP endpoint: absolute reduction and reduction to <2 mg/L CRP measurements: pre-dose, D1, D7, D14, D21, D28, D35 Placebo n ~ 27 MRT-8102 (40 mg) n ~ 27 Randomization Day 56 Day 28 Day 1 Safety follow up Study population Obesity, elevated CRP >3 and <15 mg/L Primary endpoint Safety and tolerability of 28 days dosing with 28 days follow up Secondary endpoints Change in CRP levels PK Additional exploratory PD endpoints NEK7 (target engagement) DAMPs and cytokines to inform ASCVD pathogenic drivers + systemic inflammation Thrombogenic factors Lipids, lipoproteins, and other markers of CV risk (Lp(a), LDL-C) MRT-8102 (20 mg) n ~ 27 MRT-8102 (5 mg) n ~ 27

GFORCE-1 Participants Baseline Characteristics Baseline Characteristics Placebo (n=27) MRT-8102 5 mg (n=27) MRT-8102 20 mg (n=27) MRT-8102 40 mg (n=27) Total (n=108) Median age, years (IQR) 45 (30 - 53) 38 (34 - 50) 40 (34 - 55) 41 (37 - 52) 41 (34 - 52) Male, n (%) 12 (44.4) 8 (29.6) 11 (40.7) 13 (48.1) 44 (40.7) Female, n (%) 15 (55.6) 19 (70.4) 16 (59.3) 14 (51.9) 64 (59.3) Race, n (%) White African American American Indian/Alaska Native Native Hawaiian/Pacific Multiple 15 (55.6) 11 (40.7) 0 1 (3.7) 0 16 (59.3) 9 (33.3) 1 (3.7) 0 1 (3.7) 16 (59.3) 10 (37.0) 0 0 1 (3.7) 18 (66.7) 8 (29.6) 1 (3.7) 0 0 65 (60.2) 38 (35.2) 2 (1.9) 1 (0.9) 2 (1.9) Median weight, kg (IQR) 96.0 (88.0 – 107.1) 99.8 (87.7 – 110.5) 94.2 (86.1 – 104.2) 92.8 (88.1 – 100.8) 94.5 (87.9 – 105.8) Median BMI, kg/m2 (IQR) 33.3 (32.3 – 36.1) 34.5 (32.7 – 38.3) 34.8 (32.3 – 37.0) 32.8 (31.0 – 35.5) 33.9 (32.2 – 36.6) Median abdominal circumference, in (IQR) 43.0 (38.9 – 45.0) 43.0 (40.0 – 47.0) 42.0 (38.0 – 45.0) 41.0 (39.0 – 42.9) 42.3 (39.3 – 44.5) Median hsCRP, mg/L (IQR) 4.8 (3.8 – 6.6) 6.4 (5.2 – 8.7) 5.6 (4.4 – 8.9) 6.3 (5.2 – 8.9) 5.7 (4.4 – 8.1)

MRT-8102 Achieved Robust and Sustained NEK7 Degradation Robust and sustained degradation of NEK7 noted in peripheral blood T cells (~80 - 90%) across all dose levels at week 4, consistent with preclinical findings Data are medians (IQR). SAD (n=48); MAD (n=40); GFORCE-1 (n=101) SAD MAD GFORCE-1

Safety data were collected over 8 weeks for 108 participants (MRT-8102, n=81; placebo, n=27) No SAEs were reported Frequency of treatment-emergent AEs (TEAEs) was similar between MRT-8102 (33% participants) and placebo (30% participants) Most (86%) of MRT-8102 TEAEs were grade 1* The most frequent TEAEs were Headaches in 4% of participants on MRT-8102 and 11% of participants on placebo Arthralgia in 5% of participants on MRT-8102 and 4% of participants on placebo There were no serious infections; frequency of minor infections was similar in participants on MRT-8102 (7% participants) and placebo (7% participants) GFORCE-1: Summary of Unblinded Safety Data *There was one episode of grade 3 elevation of liver enzymes in a patient with incidental finding of asymptomatic hepatitis A, and one episode of grade 3 shoulder pain in a patient with accidental shoulder dislocation

MRT-8102 Demonstrated a Favorable Safety and Tolerability Profile Over the Period of 8 Weeks Treatment-Emergent Adverse Events (AE) Placebo (n=27) MRT-8102 5 mg (n=27) MRT-8102 20 mg (n=27) MRT-8102 40 mg (n=27) Participants with any AE, n (%) 8 (30) 7 (26) 8 (30) 12 (44) Participants with any AE leading to treatment discontinuation, n (%)a 0 (0) 0 (0) 3 (11) 5 (19) Participants with any Grade 3 AE, n (%)b 0 (0) 0 (0) 0 (0) 2 (7) Participants with any Serious AE, n (%) 0 (0) 0 (0) 0 (0) 0 (0) Infection or Infestation AE, n (%) 2 (7) 2 (7) 2 (7) 2 (7) Serious Infection or Infestation AE, n (%) 0 (0) 0 (0) 0 (0) 0 (0) Neutropenia AE, n (%) 0 (0) 0 (0) 0 (0) 0 (0) Thrombocytopenia AE, n (%) 0 (0) 0 (0) 0 (0) 0 (0) aMRT-8102: 20 mg: grade 2 atopic skin reaction (n=1), grade 1 rash (n=2); 40 mg: asymptomatic, non-QTc related, grade 1 electrocardiogram change (n=3); grade 2 allergic reaction and pruritus (n=1); grade 3 elevation of liver enzymes (n=1) in a patient with incidental finding of asymptomatic hepatitis A bIn addition to the grade 3 liver enzyme elevation in the subject diagnosed with HepA, one episode of grade 3 shoulder pain in a patient with accidental shoulder dislocation was recorded

Clinical Activity of MRT-8102 on Key Pathogenic Drivers of ASCVD

GFORCE-1 enrolled a population at risk of CVD and a biomarker profile that is informative of established ASCVD Population: Obese subjects at elevated CVD risk, reflecting a population with a high ratio of silent atherosclerosis; established ASCVD diagnosis not required Based on REACT study, prevalence of silent atherosclerosis in general population ages 40-49 estimated to be up to 70%1, presumably further enriched in GFORCE-1 by focus on obese subjects with high CRP2. Translational relevance: Baseline levels of key local ASCVD drivers and systemic biomarkers were elevated and closely tracked patterns reported in diagnosed ASCVD patients; degree of elevation for some markers may not equal that in established ASCVD patients Reference arm: A separate healthy-volunteer cohort from the SAD/MAD arm of the trial (not risk-enriched) provided a real-world normal-range comparator for all analyses of key molecular drivers of ASCVD and systemic biomarkers Genetic stratification: NLRP3 SNP genotyping in a subset of participants enabled correlation of baseline elevation of key ASCVD drivers with validated NLRP3 risk alleles: risk-allele carriers show higher levels of key ASCVD pathogenic drivers GFORCE-1 Population: Probing ASCVD Pathogenic Drivers in CVD Risk Subjects 1Bundgaard et al., 2026 NEJM “Prevalence of Silent Atherosclerosis Across Adult Life”; 2Yang et al., 2013 International Journal of Cardiology .

Macrophage / neutrophil activation Plaque destabilization / vessel wall alterations Plaque rupture & thrombus formation Acute phase response EC / SMC dysfunction Vulnerable plaque Immune cell recruitment Plaque initiation Ruptured plaque Fibrinogen CRP + Lp(a) Key ASCVD Pathogenic Drivers and Markers of Systemic Inflammation Assessed in GFORCE-1 NEK7/NLRP3 pathway activation in plaque Cytokines and DAMPs IL-1b, calprotectin, HMGB1, S100A12, SAA Localized effects Systemic effects

IL-1β, DAMPs, and thrombogenic factors NEK7/NLRP3 Pathway Related Cytokines, DAMPs and Thrombotic Markers were Elevated at Baseline in GFORCE-1 Subjects Calprotectin (ng/mL) HMGB1 (ng/mL) IL-6 (pg/mL) hsCRP (mg/L) SAA (mg/L) IL-1β (fg/mL) (n=67) (n=101) (n=64) (n=101) (n=66) (n=101) (n=40) (n=101) (n=88) (n=101) (n=88) (n=101) Data are Tukey box-and-whisker plots; GFORCE-1: placebo + MRT-8102 treated; HV: SAD and/or MAD part Systemic acute phase response Fibrinogen (mg/dL) (n=32) (n=101) Baseline levels of key pathogenic drivers of ASCVD and systemic inflammatory biomarkers were elevated in GFORCE-1 relative to the levels observed in healthy volunteers Concentration

NLRP3 Risk Alleles Correlate to Baseline Increase of ASCVD Drivers Two high-priority NLRP3 risk SNPs, rs10754555 and rs10754558, have been linked to increased NLRP3 pathway activation and cardiovascular risk. In line with published data, nearly 1 in 3 subjects (29%) carry a highest-risk genotype (GG at either locus); over half of subjects (57%) carry moderate NLRP3 genetic risk. Significant increases in baseline levels of ASCVD drivers were identified, in particular for DAMPs and cytokines, in carriers of NLRP3 risk (GG) alleles, suggesting elevated pathway activity and potential for faster and more severe atherosclerotic and thrombotic remodeling. S100A12 HMGB1 Calprotectin SAA IL-1β IL-6 CRP Fibrinogen 0 25 50 75 Percent (%) median protein levels above CC allele in GG carriers at rs10754555 or rs10754558 +54 +66 +50 +11 +54 +24 +3 +28 Elevated levels in NLRP3 risk allele carriers

Modulation of Molecular Drivers of Plaque and Vascular Biology

DAMPs, Including Calprotectin, Potently Activate NEK7/NLRP3 in Neighboring Cells to Amplify Plaque Burden and Instability Calprotectin levels correlate with plaque burden, inflammation and instability Croce et al., Circulation, 2009. Data from Peng et al., Cardiovasc Diabetol, 2011, Cheng et al., Front Med, 2022, Cotoi et al. 2014, Demir et al., Medicina, 2026, and GSE163154. Simulated data (n = 300) calibrated to the meta-analytic pooled r = 0.290 (REML, 5 estimates, N = 1,133), median-split into burden groups, and compared by Mann–Whitney U test. Circulating calprotectin levels significantly associate with increased plaque burden, enhanced plaque inflammation, and plaque instability Calprotectin Low High Low High Low High Plaque burden Plaque inflammation Plaque instability Plaque burden Plaque Formation and growth Foam cell Neutrophil Cytokines DAMPs CD68 (macrophage) Instability score S100A9 S100A9

MRT-8102 Potently Inhibits Pyroptosis and Release of DAMPs and IL-1β Pro-IL-1a Pro-IL-1b Pyroptosis Cytokine release Anti-IL-1/IL-6 biologics Pyroptotic Cell Intact Cell NLRP3 NEK7 IL-1a IL-18 IL-1b NEK7 MRT-8102 DAMP release calprotectin NEK7 MGD IL-1/IL-6 blocking biologics Do not inhibit pyroptosis and only neutralize IL-1 or IL-6 IL-6 NEK7 MGDs Inhibit pyroptosis and block release of cytokines and DAMPs extracellular ATP cytokines DAMPs Pyroptosis IL-1β Extracellular ATP Calprotectin DAMP = damage-associated molecular pattern; Data generated using LPS + Nigericin stimulation in human monocyte-derived macrophages (hMDM)

Calprotectin is elevated in subjects with elevated CVD risk Treatment reduced Calprotectin to levels associated with low risk of future CV events (week 4) MRT-8102 Reduced Plasma Calprotectin to Healthy Volunteer Levels Median reduction of 56% in plasma calprotectin to levels comparable to those observed in healthy volunteers after 4 weeks of dosing -56%* (n=66) (n=101) (n=66) (n=74) (n=74) Data are medians (IQR); GFORCE-1: placebo + MRT-8102 treated; HV: SAD and MAD part; * p<0.0001 compared to predose (MRT-8102 treated); p-value from Wilcoxon test

Plasma Levels of Calprotectin were Equally Reduced Across all Dose Levels in Response to MRT-8102 5mg QD 57% reduction 40mg QD 52% reduction 20mg QD 54% reduction Data are Tukey box-and-whisker plots; HV: SAD and MAD part; * p<0.002 compared to predose (MRT-8102 treated); p-value from Wilcoxon test Calprotectin (ng/mL) (n=66) (n=26) (n=26) (n=66) (n=21) (n=21) (n=66) (n=27) (n=27) -52%* -54%* -57%*

MRT-8102 Reduced Plasma S100A12 and Serum SAA to Healthy Volunteer Levels Median reduction of 46% and 51% in plasma S100A12 and serum SAA, respectively, to levels comparable to those observed in healthy volunteers after 4 weeks of dosing MRT-8102 reduces S100A12 to levels in HVs Data are medians (IQR); GFORCE-1: placebo + MRT-8102 treated; HV: SAD and/or MAD part; * p<0.0001 compared to predose (MRT-8102 treated); p-value from Wilcoxon test -46%* (n=66) (n=101) (n=66) (n=74) (n=74) MRT-8102 reduces SAA to levels in HVs (n=40) (n=101) (n=40) (n=74) (n=74) -51%*

Biological crosstalk between HMGB1 and IL-1β influences multiple aspects of vessel and plaque biology HMGB1 and IL-1β baseline levels strongly correlate, reinforcing biological proximity Pathological Crosstalk between HMGB1 and IL-1β Downstream of NEK7/NLRP3 Reinforces Plaque Progression and Instability in ASCVD Plaque Upregulation of adhesion receptors increases immune cell recruitment Plaque destabilization VSMCs transdifferentiate into foam cells MMP induction degrades fibrous cap IL-1β HMGB1 VSMCs Endothelium Fibrous cap Vessel cross section IL-1b HMGB1 r=0.54 p<0.0001  r = Spearman rank correlation coefficient GFORCE-1 (n=101)

MRT-8102 treatment resulted in meaningful HMGB1 reduction in subjects with higher baseline levels MRT-8102 Treatment Reduced HMGB1 and IL-1β Levels (n=64) (n=101) > 4.7 (ng/mL) (n=20) -40%* (n=67) (n=101) (n=17) > 170 (fg/mL) MRT-8102 treatment resulted in meaningful IL-1β reduction in subjects with higher baseline levels HMGB1 and IL-1β were elevated in GFORCE-1 population versus healthy volunteers (baseline) Treatment led to a median reduction of 40% and 37% in HMGB1 and IL-1β levels, respectively, in subjects with elevated baseline levels; no statistically significant decrease in placebo Data are medians (IQR); GFORCE-1: placebo + MRT-8102 treated; HV: SAD and MAD part; * p=0.05 and † p=0.003 compared to predose (MRT-8102 treated); p-value from Wilcoxon test % indicates Change from Predose; The 75th Percentile (Q3) of GFORCE-1 population (N=101, placebo and treatment) was used to define the cut-offs: 4.7 ng/mL for HMGB1 and 170 fg/mL for IL-1β. Analysis on median reduction based on MRT-8102 treated subjects (predose vs treatment at week 4). -37%†

Treatment significantly reduced fibrinogen to normal physiological levels MRT-8102 Treatment Led to Reductions in Fibrinogen Fibrinogen baseline is elevated in GFORCE-1 population Median reduction of 28% in fibrinogen to levels comparable to those observed in healthy volunteers after 4 weeks of dosing (n=32) (n=74) (n=74) -28%* (n=32) (n=101) Data are medians (IQR); GFORCE-1: placebo + MRT-8102 treated; HV: MAD part; * p<0.0001 compared to predose (MRT-8102 treated); p-value from Wilcoxon test

Markers of Systemic Inflammation

MRT-8102 Induced Rapid and Sustained Reductions in hsCRP and IL-6 Levels Robust decrease of hsCRP after 4 weeks of dosing Data are medians (IQR); * p<0.0001 compared to predose; p-value from Wilcoxon test; HV: SAD and MAD part % Change from predose in hsCRP at week 4 per cohort: 5mg QD -86%, 20mg QD -79%; 40mg QD -85% hsCRP and IL-6 reduced to levels associated with low risk of future CV events Median reduction of 85% in serum hsCRP to levels detected in healthy volunteers; 86% of subjects showed suppression of hsCRP to <2 mg/L Median reduction of 54% in plasma IL-6 to levels associated with low risk of future CV events -85%* -54%* (n=88) (n=74) (n=74) (n=88) (n=74) (n=74)

Update on Development Plans

: A Differentiated Phase 2 Approach Proposed trial design subject to review by FDA Inform an innovative & efficient Phase 3 study design focused on the patient population with the most modifiable disease ASCVD drivers and systemic biomarkers Imaging Genetics DAMPs (calprotectin, S100A12, HMGB1), cytokines (IL-1β, IL-18, IL-6) and thrombogenic factors (tissue factor, SAA, fibrinogen) Assess plaque inflammation using FAI (fat attenuation index) imaging for response and enrichment Confirm genetic basis of NLRP3 activation (activating SNPs) and build correlation to baseline levels of molecular drivers of ASCVD, responses and FAI changes Focus on CAD, where NLRP3 and IL-1 targeting agents have shown success Continue dose exploration and establish long-term safety in a chronic disease setting Allow background medications; no CKD enrichment

: A Phase 2b Study in Patients with Coronary Artery Disease Outcome measures Change in levels of key pathogenic ASCVD drivers including atherogenic, thrombogenic mediators and lipids Change in local cardiac imaging, from baseline to 6 months Exploratory endpoints Cardiac imaging Establish pharmacogenomic evidence base Liver fat/liver inflammation Anemia MRT-8102 5 mg daily MRT-8102 10 mg daily Placebo Enrollment 6-month treatment Population ~160 patients with stable coronary artery disease and residual inflammation R MRT-8102 15 mg daily Study initiation planned for H1 2027 Proposed trial design subject to review by FDA

Ph2 Study in Gout Flare Prevention Following Acute Flare Management Initiation planned Q4 2026 / Q1 2027 Trial ~ 60 pts w/recurrent gout flares 12 weeks Outcome Measures and PoC expectation Reduction in pain VAS by 72 hours Frequency of new flares Ph2 Study in Moderate to Severe Hidradenitis Suppurativa Trial ~ 160 pts w/moderate to severe HS 16 weeks Outcome HiSCR75 after 16 weeks MRT-8102 relative to placebo Initiation planned H1 2027 Planned Phase 2 Studies for Gout and HS Proposed trial design subject to review by FDA GEMINI: Glue Elimination of Monosodium urate-Induced NEK7 Inflammation GALAXY: Glue-mediated Attenuation of Lesions, Abscesses, and eXacerbations in HS therapY

MRT-8102 Opportunities and Pipeline Update

CAD: Large Opportunity to Address Atherosclerotic Risk with a Safe, Oral Treatment Targeting NEK7 MRT-8102 Opportunity Potential to complement existing lipid and metabolic therapies Targeting NEK7/NLRP3 pathway could provide broader suppression of atherogenic and thrombotic pathways Oral administration aligns with SOC and facilitates potential combo approaches Potential for differentiated efficacy and safety profile vs. IL-1 and IL-6 antibodies Upstream mechanism addresses high-risk plaque biology beyond suppression of individual cytokines Ability to provide robust inflammation control without increased infection risk High Unmet Medical Need in CAD CAD Market Overview ~14M Adults suffer from CAD in the U.S. 45-50% Patients have experienced at least 1 prior MI ~1 in 7 CAD patients experience a subsequent MACE event within 5 years despite achieving target LDL-C level >30% CAD patients suffer from residual inflammatory risk despite optimized lipid-lowering therapy ~30-fold Greater risk of cardiac mortality in patients* with high coronary plaque inflammation (determined by FAI score) *Risk of cardiac mortality captures all patients, with and without CAD, from ORFAN study undergoing diagnostic coronary CTA Sources: Su et al. Journal of Vascular Surgery (2024); Alanaeme et al. Am Heart J Plus (2022); Martin et al. Circulation (2025); Chan et al. Lancet (2024); Hassan et al. Front Cardiovasc Med. (2026); Kim et al. Korean Circ J. (2026); Watanabe et al. J Am Heart Assoc. (2026); Virani et al. Circulation (2021); Tsao et al. Circulation (2023); Budoff et al. Eur Heart J. (2023); Peikert et al. Clin Res Cardiol. (2020); Wong et al. J Clin Lipidol. (2019); Sanchez-Bacaicoa et al. Eur J Clin Invest. (2021); Schwartz et al. J Am Coll Cardiol. (2021); O’Donoghue et al. Circulation (2022)

Large Market Opportunities Supported by Strong Biological Rationale Hidradenitis suppurativa Highest NEK7/NLRP3-pathway activity score of any indication studied, with consistent upregulation of NLRP3, IL-1β, and DAMPs in lesional tissue ~400-450K U.S. addressable population Significant unmet need with ~55% patients poorly managed with SOC IL-1 antibodies provide promising POC for the NEK7/NLRP3 pathway Opportunity to target inflammasome assembly, upstream of IL-1 and DAMP-driven pathogenesis in HS lesions, unlike single-mediator TNF/IL-17 biologics Coronary artery disease Central role of NEK7/NLRP3 in plaque biology and atherogenic progression ~14M U.S. patient population, with 45-50% of patients having experienced at least one prior MI >30% of CAD patients suffer from residual inflammatory risk despite optimized lipid-lowering therapy NEK7 degradation and NEK7/NLRP3 pathway inhibition provide a novel, upstream approach that goes beyond downstream single-cytokine depletion to address residual CVD risk Gout Canonical NEK7/NLRP3-pathway disease: MSU crystals trigger NEK7-mediated NLRP3 assembly, driving IL-1β release and flare pathology ~10M U.S. patient population, with ~30% comorbid with renal disease SOC treatment often insufficient in preventing gout flares, resulting in breakthrough flares, a leading contributor to poor adherence High unmet need for long-term flare prophylaxis: >55% of gout-treating physicians surveyed are not satisfied with current prophylaxis options (>65% for CKD co-morbid patients) Sources: Su et al. Journal of Vascular Surgery (2024); Alanaeme et al. Am Heart J Plus (2022); Peikert et al. Clin Res Cardiol. (2020); Martin et al. Circulation (2025); Virani et al. Circulation (2021); Tsao et al. Circulation (2023); Singh et al. Rheumatology (Oxford) (2019); Cowen Therapeutics Outlook (Oct 2024, Oct 2025); Monte Rosa survey of gout-treating physicians (Nov 2025)

Summary and Next Steps WHAT GFORCE-1 SHOWED Favorable safety profile across all dose levels tested: no SAEs, no infection signal Robust, sustained target engagement: ~80–90% NEK7 degradation at all dose levels Broad normalization of ASCVD pathogenic drivers: markers of local plaque progression, thrombosis, and systemic inflammation reduced to healthy-volunteer levels at all doses A built-in precision-medicine hypothesis: NLRP3 risk-alleles define a genetically enrichable population; plaque imaging could further define disease-modifiable population WHAT'S NEXT Program Study Milestone Timing Gout GEMINI-1 Study initiation Q4 2026/ Q1 2027 CAD GFORCE-2 Study initiation H1 2027 HS GALAXY-1 Study initiation H1 2027 Next-gen MRT-9347 IND Q4 2026 KEY CONSIDERATIONS GFORCE-2 design focused on imaging, levels of key molecular drivers of ASCVD and genetics to inform innovative and efficient Phase 3 study MRT-9347 (next-gen NEK7 degrader) provides strategic optionality across indications MRT-8102’s differentiated safety and translational activity profile de-risk a broad NEK7 franchise opportunity; heading into multiple Phase 2 starts through H1 2027

Monte Rosa Pipeline and Upcoming Milestones GSPT1 Castration-resistant Prostate Cancer NEK7/NLRP3-driven Diseases VAV1 Licensed to Novartis* Sjögren's disease Preclinical Target Indication(s) Ph 1/2 update in 2026; Ph 2 update in 2027 Next Anticipated Milestone Phase 1 Phase 2 Multiple Ph 2 initiations in 2026-27; Gout data update in H2 2027 Additional Ph 2 initiations Multiple Targets Includes those licensed/optioned to Roche and Novartis I&I, Oncology, Genetic and Neurological Diseases Announce additional targets NEK7 Compound MRT-2359 MRT-6160(DDY391) MRT-8102 Discovery IND submission in 2026 Next Generation CCNE1/CDK2 CCNE1 Amplified Tumors ER+ Breast Cancer IND submissions in 2027 Discovery Immunology & Inflammation Oncology Various * Novartis has exclusive worldwide rights to develop, manufacture and commercialize MRT-6160 (DDY391) and other VAV1 MGDs. Monte Rosa is eligible for up to $2.1B in development, regulatory, and sales milestones, beginning upon initiation of Phase 2 studies, and is also eligible for 30% US P&L share and ex-US tiered royalties. Notes: IND = investigational new drug. ER = estrogen receptor. I&I = immunology and inflammation. Phase 3 Coronary artery disease, gout, hidradenitis suppurativa Psoriatic arthritis

Q&A

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