Marea TherapeuticsTransformative cardioendocrine therapies Confidential

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Transaction Summary Transaction Structure Proposed sign-and-close merger whereby Lisata Therapeutics would acquire 100% of the outstanding equity interests of Marea Therapeutics in exchange for a combination of common stock and Series C non-voting convertible preferred stock of Lisata, as well as Lisata options exercisable for Series C non-voting convertible preferred stock. Financing Concurrent with the acquisition of Marea, Lisata executed a definitive agreement for an oversubscribed private placement of approximately $225 million in gross proceeds. The financing included participation from RA Capital Management, Forbion, Third Rock Ventures, Alpha Wave Global, Perceptive Advisors, Sofinnova Investments, Omega Funds, Surveyor Capital (a Citadel company), Columbia Threadneedle Investments, Nantahala Capital, Affinity Asset Advisors, LLC, venBio, Rock Springs Capital and other institutional investors. Management and BOD Continuing leadership includes Josh Lehrer, newly appointed President and Chief Operating Officer of Lisata Therapeutics and Chief Executive Officer of Marea. Use of Proceeds The net proceeds from the private placement are primarily to advance MAR001/005 and MAR002 through key clinical milestones, including completion of an ongoing Phase 2b trial in patients with severe hypertriglyceridemia and a Phase 2 trial in patients with acromegaly. Both studies are expected to report topline data in the fourth quarter of 2027. Remaining proceeds will be used for general corporate purposes. Confidential

Capitalization Lisata issued shares of common stock and Series C non-voting convertible preferred stock to Marea security holders and options exercisable for Series C non-voting convertible preferred stock to Marea option holders, in exchange for all of Marea’s outstanding equity interest. Shares of Series C non-voting convertible preferred stock are issuable to investors upon the closing of the $225 million private placement. Shares of Series C non-voting convertible preferred stock will automatically convert into 1,000 shares of common stock, subject to certain beneficial ownership limitations set by each holder and approval by Lisata’s stockholders. Please refer to Lisata’s SEC filings for additional information. 1. Includes 178,673 restricted stock awards. 2. Calculated using the treasury stock method. 3. Common stock consideration is capped at 19.9% of pre-acquisition Lisata common stock outstanding and reflects certificate-level rounding. 4. Represents shares of Series C non-voting convertible preferred stock issuable upon exercise of Lisata Options issued in exchange for outstanding Marea options. Included on a fully diluted basis and equivalent to 22,801,406 shares of Lisata common stock on an as-converted basis. 5. Represents shares of Series C non-voting convertible preferred stock issuable upon the closing of the concurrent financing. 6. Calculated on an as-converted-to-common-stock basis. 7. Represents Lisata’s pre-acquisition common stock outstanding and equity awards, parent common stock and Series C non-voting preferred stock issued to Marea security holders, Series C non-voting preferred stock underlying Lisata options issued in exchange for outstanding Marea options, and Series C non-voting preferred stock issued in the concurrent financing, calculated on an as-converted basis. 8. Market Cap at Deal Price calculated using treasury stock method equals to $580,734,913. Confidential 8

Rapid Path to Value Creation 1. Christian JB, et al., Am J Cardiol. 2011;107(6):891–897; 2. Zafrir B, et al. J Clin Lipidol 2018;12(4):928-936; 3. Marea data on file; 4. Burton T et al. Pituitary 2016;19(3):262-267; 5. EvaluatePharma, ClearView market research, company press releases Abbreviations: GHR: growth hormone receptor; sHTG: Severe Hypertriglyceridemia; SRL: somatostatin receptor ligand *MAR001 is parent antibody; MAR005 formerly known as MAR001-HLE Two potentially first-in-class assets with best-in-disease potential in large addressable markets Confidential Severe Hypertriglyceridemia Potent sHTG candidate with a clean metabolic profile >3M US patients¹ At risk of acute pancreatitis; APOC3 drugs worsen diabetes / liver fat ~70% TG reduction3 Phase 2b sHTG POC (subgroup with baseline TG>500, n=7) TG lowering in Phase 2 similar to approved APOC3s >$10B market opportunity5 First choice for >1.8M2 diabetics with sHTG Clean metabolic profile No HbA1c increase or liver-fat penalty to date – potentially differentiated from approved APOCs MAR002 Acromegaly First long-acting GHR antagonist candidate for acromegaly ~30K US patients4 Highly morbid; >70% uncontrolled Potential Best-in-class anti-GHR mAb Target profile: Best-in-class efficacy, safety and biweekly dosing Phase 1 proof of mechanism Promising IGF-1 suppression (approvable endpoint) >$1B in SRL sales5 Potential to address 3x more patients than SRLs

Molecule Target Indication Disc IND-E Ph1 Ph2 Ph3 Anticipated Near-term Milestones MAR001 (parent mAb) ANGPTL4 sHTG MAR005 (half-life extended MAR001) ANGPTL4 sHTG MAR002 Growth hormone receptor Acromegaly Advancing a Late-Stage Cardioendocrine Pipeline Toward Potential 2026-27 Value Inflections MAR001 Phase 2b TYDAL (mHTG/sHTG) Abbreviations: NHV: normal healthy volunteer; sHTG: Severe Hypertriglyceridemia Q2 2026 Phase 2/2b 12-week data H2 2026 Phase 2/2b 24-week data H2 2027 Phase 2 extension (sHTG) topline data Q1 2026 Phase 1 (NHV) topline data Mid-2026 Initiate Phase 2 study Mid-2027 Interim Phase 2 data Q4 2027 Phase 2 topline data H1 2028 Phase 3 FPI MAR001 Phase 2 Mechanistic Study Endocrine  Cardiometabolic Mid-2027 Phase 3 MAR005 dose selection including additional TG efficacy/PD H2 2027 Phase 3 FPI  MAR001 Phase 2b extension (sHTG)  MAR001 has established POC in Phase 2. MAR005 is our Phase 3 candidate- it is an improved version of MAR001 with half-life extension and improved PK. The FDA agreed to PK bridging to Phase 3. Marea also has developed a SiRNA platform and is developing adipose tissue targeted SiRNAs Confidential

MAR005 for sHTG Potent sHTG candidate with a clean metabolic profile Section IV Confidential

Recurrent Pancreatitis in sHTG: A Life-Altering Condition with Limited Options >3 million Americans; $9B in healthcare costs, no approved prevention therapies until recently The Unmet Need Limited Generic Options The Critical Gap Inadequate TG lowering ~30% reduction leaves most sHTG patients above the AP risk threshold No evidence for AP prevention Poor tolerability 1. Marston, NA, et al., N Engl J Med 2025;394:429-441; 2. Gurevitz, C et al., JACC: Advances 2024;3(5) 3. Lee PJ,. Nat Rev Gastroenterol Hepatol. 2019;16(8):479-496; 4. Lu J, et al., BMC Gastroenterology. 2025;25:374. Abbreviations: SOC: standard-of-care; AP: acute pancreatitis; MI: myocardial infarction; CAD: coronary artery disease. 4. Marea claims data analysis Until Recently: Limited Options >3M Americans with sHTG face recurrent AP attacks Up to 20% mortality per episode4 Cumulative attacks cause irreversible pancreatic destruction, chronic pain, and secondary diabetes 60% T2DM1, 30% CAD1, 70% fatty liver 2 : a high-risk population with >$9B annual cost burden3 30% have poorly controlled T2DM (HbA1c>9%)4 Fibrates Omega-3 Fatty Acids Confidential

APOC3 Inhibition: New Treatments Driving a Potential Multi-Billion Dollar Opportunity Sources: Marston, NA, et al., N Engl J Med 2025;394:429-441; Ionis AHA 2025 press release; Arrowhead July 2026 press release; Overall NNT=20; ClearView market research; AP: acute pancreatitis; SOC: standard of care First class of medications to demonstrate acute pancreatitis (AP) event reduction Next-Gen Rx sHTG Opportunity 60-80% TG reduction — dramatically superior to fibrates or omega-3 fish oil 78-85% Reduction in AP events first proven AP reduction in sHTG >80% Patients reaching TG <500 mg/dL vs. 35% placebo — bringing most patients below the AP-risk threshold at 12 months Clinical benefit supports premium list pricing at $40–45k PROJECTED US MARKET >$10B Olezarsen (Ionis): >$3B projected peak sales Plozasiran (Arrowhead): $3–4B projected peak sales “What patients really look for is not going through [AP] again. If you can reduce it to almost zero, that’s what patients care about most.” — Endocrinologist “It’s more effective than 6 or 9 fish oil pills and a fibrate every day, forever … one shot at home, every four weeks. I have no trouble convincing somebody.” — PCP Confidential

HbA1c +0.3 despite Rx; Hyperglycemia AEs were most common Plozasiran AE1,4; Plozasiran excluded HBA1c>9 Population Drug / Study TG Reduction Adverse Effects on Glycemic Control (in T2DM) Source mHTG Plozasiran — MUIR Ph2b, Wk 24 58% (56% pbo corrected) – 25mg +0.36% (25mg) absolute vs. placebo Ballantyne, NEJM 2024 sHTG Plozasiran — SHASTA-2 Ph2b, Wk 24 70% (53% pbo-corrected) - 25mg Worsening glycemic control TEAE 16.4% (25 mg) vs 11.5% pbo Gaudet, JAMA Cardiol 2024 sHTG + mHTG Plozasiran — SHASTA-2 + MUIR OLE, 24 mo −83% (SHASTA-2 OLE) – 25mg −67% (MUIR OLE) – 25mg 9.6% T2DM / 6.7% DM / 4.1% "HbA1c increased" as TEAEs; glycemic terms drove 69% of drug d/c Ballantyne, Am J Prev Cardiol 2026 sHTG Plozasiran — SHASTA-3/4 79-81% (52-54% pbo-corrected*) – 25mg, 12 mo +0.2-0.3% in overall population at 6 months (T2DM subgroup not yet reported); 14% glycemic AEs vs 8.7% pbo despite active protocol- mandated management Watts GF, ESC Congress 2026 sHTG Olezarsen — CORE/CORE2 Ph3 63% (49-63% pbo corrected) – 50mg, 6 mo 68-73% (55-72 pbo corrected) – 80mg, 6 mo +0.34% (50mg) / +0.25% (80mg) pbo-adj. at 12 mo, both p<0.05 Marston, NEJM 2025 sHTG Olezarsen – approved sHTG label As above Hepatic fat in Warnings & Precautions Increase in glucose, worse in diabetics (clinical trial section of label) FDA-approved USPI FCS Plozasiran — PALISADE, 10 mo 80% (59% pbo corrected) – 25mg +0.36% HbA1c (25mg); FPG +9 mg/dL (diabetic+nondiabetic); hyperglycemia 40% (nondiabetic) vs 20% placebo Redemplo USPI, Nov 2025 FCS Olezarsen — approved FCS label 30% (43% pbo corrected) – 80mg Hyperglycemia 52% (nondiabetic) vs 35% placebo Tryngolza USPI Summary: APOC3 class effect; 2 molecules, 3 populations (mHTG, sHTG, FCS); 5+ independent studies and 2 FDA labels all show the same ~0.3–0.4% HbA1c signal despite antidiabetic meds 1. Ballantyne et al., NEJM 2024 & Am J Prev Cardiol 2026; 2. Marston et al., NEJM 2025; 3. Gaudet et al., JAMA Cardiol 2024; 4. Tryngolza & Redemplo USP; 5. Watts GF, et al. SHASTA-3/SHASTA-4. ESC Congress 2026 *Placebo correction calculated by Marea APOC3 Class Comes at a Cost:Deterioration in Glycemia / Exclusion of the 30% Patients with Poorly Controlled T2DM Confidential Cross-trial comparisons are subject to inherent limitations and should be interpreted with caution; no head-to-head studies were conducted

Biology and Genetics Support Inhibition of ANGPTL4 as Potential Best-in-Disease Profile The first physiologic sink for excess triglycerides Genetics predict differentiated impact on glycemic control* APOC3 Inhibition (Olezarsen/Plozasiran) ANGPTL4 Inhibition (MAR001/5) Abbreviations: LPL: lipoprotein lipase; HFF: hepatic fat fraction;* https://academic.oup.com/ehjopen/article/4/3/oeae035/7659859; https://doi. org/10.1186/s12933-026-03209-w; https://doi.org/10.1038/s41467-018-04611-z A potential mechanism with no observed metabolic penalty Forced hepatic TG clearance HbA1c increases in patients with T2DM HFF increases Physiological adipose TG clearance No hepatic fat loading TG lowering scales with disease severity APOC3 ANGPTL4 T2DM risk Glucose Confidential

TYDAL-TIMI 78 Phase 2b: Establishing a Potential Best in Disease Profile >60% T2DM/pre-DM informs metabolic safety profile; sHTG subgroup informs clinical activity Pre-read 1. Participants are randomized 3:1 MAR001 to placebo (~59 participants per arm); TG: triglycerides; RC: remnant cholesterol; TD2M: Type-2 diabetes mellitus; https://timi.org/tydal-timi-78; 2. 12-week efficacy data available for 23 patients; efficacy numbers are median change to 12 weeks Day 1 Randomization Week 12: Primary Endpoint 300 mg 450 mg 900 mg Placebo MAR001 Active Treatment Arms (Q4W) Week 24 Confidential Study Population (N=235) Key Inclusion Criteria: TG ≥ 150 to < 880 mg/dL Baseline characteristics ~61% pre-DM/T2DM ≥400 mg/dL subgroup (n=252): baseline TG = 495 mg/dL ≥500 mg/dL subgroup (n=12): baseline TG = 606 mg/dL Key Endpoints: Primary (at 12 weeks): % Reduction in TG % Reduction in RC Other secondary and exploratory endpoints HbA1c Lipids at Week 12 and 24 Key 12-week Topline Data Approx 40% TG lowering overall TG lowering scales with baseline TG >65% in TG≥400 mg/dL group (n=15; MAR001 pooled) ~70% in TG≥500 mg/dL group (n=7; MAR001 pooled) Consistent effects at 24 weeks Safety profile consistent with placebo (overall TEAES < pbo) No increase in HbA1c (numeric reduction) No liver enzyme elevation signal (numeric reductions) Injection site reactions similar to placebo PK/PD supports go-forward MAR005 dose of 300mg monthly for Phase 3

MAR001: Emerging Clinical Data Supports Potential Best-in-Disease Profile 1. Marston, NA, et al. N Engl J Med 2025;394:429-441; 2. Gaudet D, et al. JAMA Cardiol. 2024;9(7):620-630; 3. Cummings, B, et al. The Lancet. 2025;405(10493):1923-1934; 4. Ballantyne C, et al. N Engl J Med 2024;391(10):899-912; (the SHASTA-2 study did not report HbA1c in T2DM, this data is from the MUIR study of Plozasiran in mixed dyslipidemia); 5. Marea data on file from MAR-102 and MAR-104; 6. Lepor N, et al. WCIRDC 2025; Poster #0034; 7. Watts GF, et al. SHASTA-3/SHASTA-4. ESC Congress 2026 Confidential MAR001/005 Olezarsen1 Plozasiran2,4,6, 7 TG Lowering HbA1c Hepatic Fat Dosing -70% + Phase 2b, pooled 450/900 mg dose; >500 mg/dL subgroup; median TG 606 mg/dL at baseline -63 to -73% Phase 3 efficacy; median TG 793 mg/dL at baseline -79 to -81% -27% pbo Phase 3 efficacy; median TG 677 mg/dL at baseline -0.2% Decrease in Phase 2b vs. pbo (prelim. & not significant) +0.25 to +0.34% Increase in T2D subgroup in Phase 3 vs. pbo +0.36% Increase in T2D subgroup in Phase 2b vs. pbo; up to 20% diabetes AEs 0% No hepatic fat increase3, 5 +2 to +4% Absolute increase in hepatic fat fraction +1.5% Absolute increase in hepatic fat fraction vs pbo in Phase 3 (NS, p=0.70) Q4W–Q12W SC dosing with MAR005 Q4W SC dosing Q12W SC dosing Cross-trial comparisons are subject to inherent limitations and should be interpreted with caution; no head-to-head studies were conducted

+0.3 HbA1c difference could be clinically meaningful Even small, sustained HbA1c increases carry independent cardiovascular risk1 +0.3 HbA1c increase is estimated to lead to ~6% higher risk of diabetes-related death and ~11% higher risk of microvascular complications2 HbA1c drives physician choice in sHTG HbA1c stabilization #1 physician weighted attribute for new sHTG drugs in T2DM patients3 Potential for 1/3 or more of a $10B market Driven by uptake in the 1.8 M patients with sHTG+T2DM where at least 50% have uncontrolled glucose4 and where competitors excluded poorly controlled T2DM (30% of sHTG patients) “Any new starts would probably go to the ANGPTL4 inhibitor … a much cleaner profile without the hepatic-fat increase, and you don’t see an A1C increase.” — Endocrinologist “The main difference is in the safety category, which I put at the top … there’s no hepatic-fat issue, there’s no A1C issue.” — Cardiologist 1. Luo S, et al. Diabetologia 2021;64(11):2502–2510; 2. Stratton IM, et al. BMJ 2000;321(7258):405–412. Data above are an illustrative linear scaling of this relationship to a 0.3-point change and are not a direct finding from APOC3 clinical trials. 3. Market research conducted by ClearView Healthcare Partners (Q1 2026): quantitative physician survey (N=151: 75 endocrinologists, 70 cardiologists, 6 lipidologists) plus N=15 in-depth qualitative interviews incorporating a blinded discrete-choice/conjoint exercise to isolate the relative importance of individual product attributes (efficacy, safety, dosing) on treatment share; 4. "Trends in Diabetes Treatment and Control in U.S. Adults, 1999–2018," N Engl J Med 2021;384:2219–2228 “I would target the use of [MAR005] for patients who have diabetes or prediabetes, or I think are at high risk for developing diabetes” -Cardiologist Confidential MAR001/5 Profile: Highly Differentiated; Compelling to Physicians; Represents Large Potential Opportunity

As Predicted by Biology: ANGPTL4 Inhibition Overperforms in sHTG vs. mHTG TG lowering scales with baseline TGs: MAR001 is competitive with APOC3 inhibitors in severe patients Notes: Clinical Data from MAR001 and APOC3 Programs; data extrapolation and curve fitting are based on the following: Olezarsen data are from four trials (BRIDGE-TIMI 73a, ESSENCE-TIMI 73b, CORE-TIMI 72a, CORE2-TIMI 72b) at both the 50mg and 80mg Q4W doses, with overall trial populations at Month 6. Plozasiran data are from the MUIR trial (25mg Q12W, overall population, Week 24) and the SHASTA-2 trial (25mg Q12W, overall population, Week 24). Phase 3 plozasiran data pending MAR001 data are from three studies: the Phase 1 single-dose study (450mg, overall populations from Parts IA, IB, and IC at Day 15), the Phase 1b/2a multidose study (MAR-102; 450mg Q2W, overall population, Week 12), and TYDAL-TIMI 78 (MAR-103; 900mg Q4W, overall population and baseline TG subgroups ≥300, ≥400, and ≥500 mg/dL, Week 12). Confidential APOC3: (Olezarsen, Plozasiran) MAR001 Cross-trial comparisons are subject to inherent limitations and should be interpreted with caution; no head-to-head studies were conducted

MAR-104 Study: Potential Best-in-Class Suppression of Postprandial TGs MAR001 flattens the post-prandial TG surge, the key driver of AP risk Participants are randomized 2:1 MAR001 to placebo (~21 participants in MAR001 arm and 10 patients in placebo arm) TG: triglycerides; AP; acute pancreatitis, iAUC is AUC corrected for baseline fasting TGs Kraaijenhof JM et al. "Plasma reduction of apolipoprotein C-III with olezarsen leads to significant reductions in postprandial triglyceride levels: results from a randomized trial." Eur J Prev Cardiol 2025; Estimate from figure 1D Post-prandial TG suppression similar to or greater than results with Olezarsan (↓50% AUC, 28% iAUC)2 Study Population (N=31) Key Inclusion Criteria TG ≥ 175 to < 500 mg/dL HbA1c: 5.5 to 9% Key Baseline Characteristics % Pts with Pre-DM/T2DM: 87% Mean TG: 261 mg/dL Key Endpoints Post-prandial TG at week 12 and 24 Day 1 Randomization Week 12: Primary Endpoint MAR001 900 mg Q4W Placebo Q4W Week 24 Key 12-week topline data 42% reduction in TG AUC at 12 weeks for MAR001 vs. Pbo 40% reduction in TG iAUC at 12 weeks vs pbo Confidential mixed meal challenge TG (mg/dL) Hours Post-Meal

MAR002 for Acromegaly First long-acting GHR antagonist candidate for acromegaly Section IV Confidential

Acromegaly: Serious Disease with Inadequate Options for Medical Therapy ~30K patients US caused by excess GH production from benign pituitary adenoma. Early Mortality and High Morbidity Bone/organ overgrowth, cardiovascular & metabolic disease. Median lifespan shortened by ~10 years without effective therapy. Medical Therapy Goals: Decrease tumor volume (some patients) Normalize IGF-1 levels (all patients) >70% of patients are addressable: Approx 9K US patients need a better GH antagonist to achieve IGF-1 normalization Efficient Development Path: IGF-1 is an established clinical and regulatory endpoint. Abbreviations: GH: Growth Hormone; GHR; Growth Hormone Receptor; SRL: Somatostatin Receptor Ligand Sources: UpToDate; Holdaway et al., Eur J Endo, 2008; Moustaki et al, Endocrine, 2023; van der Lely et al., Lancet, 2001 The Burden & Opportunity Pituitary Gland Liver Body Tissue Excess IGF-1 Somatic Growth & Metabolic Dysfunction Inhibit Secretion (e.g., SRLs) Acts on pituitary to reduce GH release Can also shrink tumor 1 x Block Action (e.g., Somavert) Blocks GH receptor signaling. 2 Two Approaches to Medical Therapy Confidential

Medical Therapy Treatment Guidelines: Direct Growth Hormone Antagonists Critical for >70% of Patients IGF-1 > ULN after surgery T2DM, unfavorable tumor histology lower IGF-1, favorable tumor histology, tumor mass concerns Direct GHRA (somavert) SRL or Dopamine Agonists IGF-1 uncontrolled add GHRA IGF-1 and glucose uncontrolled, no tumor mass concerns switch to GHRA IGF-1 uncontrolled + tumor mass concerns ~80% ~10-20% >70% SRLs often initiated first for tumor volume control Role for first line GHRA in ~10-20% of patients 70% of patients prescribed SRLs require second-line GHRA First Line Second Line Sources: Melmed & Giustina, Nat Rev Endocrinol, 2025; Fleseriu et al., J Endocr Soc, 2023; Moustaki et al., Endocrine, 2023; Carmichael et al., J Clin Endocrinol Metab, 2014; Colao et al., J Clin Endocrinol Metab, 2014. Abbreviations: GHRA: growth hormone receptor antagonist; SRL: somatostatin receptor ligand. Confidential

The Marea Opportunity Most patients are not fully controlled or cannot tolerate current therapies MAR002 (anti-GHR mAb) A Potential Optimal Direct GHRA SRLs: First line, but limited control Somatostatin receptor ligands: <30% disease control SRL class causes GI intolerance and hyperglycemia Often used first-line for tumor mass control A $1B US market despite addressing only 30% of patients The most effective drug class is underused Direct GHRA: 81% disease2 control The only approved GHRA has poor PK, tolerability 1-2 daily painful injections, LFTs Real-world efficacy is only 50% (low compliance) $300M global sales despite severe limitations Strong drive to treat patients to IGF-1 Goal 2.5x mortality rate in patients who do not achieve IGF-1 normalization1 Guidelines mandate medical therapy to control 1. Holdaway IM, et al. Eur J Endocrinol 2008;159(2):89–95; 2. Trainer PJ, et al. N Engl J Med 2000;342(16):1171–1177; 3. Marea data on file; 4. Cross-trial comparisons are subject to inherent limitations and should be interpreted with caution. MAR002: Marea data on file (single 900 mg SC dose, n=8); Pegvisomant (Somavert) comparator estimated from Thorner MO, et al. J Clin Endocrinol Metab 1999;84(6):2098–2103, Fig 6 (single 1.0 mg/kg SC dose, n=6); *SRL projected market opportunity; Abbreviations: GHRA: growth hormone receptor antagonist IGF-1 max suppression3 >60% >10x Longer duration of >45% IGF-1 suppression vs. Somavert in healthy volunteers4 >$1B* Potential to address 3x more patients than SRLs “I loved how I felt on GHR-antagonist therapy, but the daily injections were hard to sustain. Having that same level of clinical control without the daily burden would be life-changing. MAR002 isn’t just a new drug; it’s a chance to get our lives back.” Jill Sisco, President, Acromegaly Community This drug could improve control in most patients, either alone or in combination with an SRL. leading U.S. KOL Confidential

An Optimal Direct GHRA Could Address 3-4x More Patients than the SRL Class A better GHRA than Somavert is needed to address >9K patients Sources: Crinetics, FDA Pegvisomant and Paltusotine labelling; https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/219070s000lbl.pdf; https://labeling.pfizer.com/ShowLabeling.aspx?id=3213 SRLs: <30% Disease Control in Treatment-naïve patients (Paltusotine) GH Antagonist: >90% Disease Control (Somavert) Treatment-naive subgroup (n=22) analysis from Phase 3 Pathfinder-2 Study Safety: mechanism-related hyperglycemia (74% of treated participants developed at least 1 incident) and GI AEs Limitations: daily, painful injections, LFT elevations related to pegylation, poor access IGF > normal (uncontrolled, 2.5x mortality) 77% IGF normal (controlled) Naïve to GHRA treatment 18% 23% 82% Phase 3 The Marea opportunity Mono-and combination with SRLs TAM 3-4x SRL class Confidential

MAR002: Allosteric Mechanism, Potential for greater Efficacy than Somavert Maintains Potent GHR Antagonism at High GH Levels (Preclinical Data) Confidential Somavert: loses efficacy at high GH concentrations MAR002: maintains reduction at high GH concentrations Increasing growth hormone levels Growth hormone signaling No drug: increasing GH leads to increased signaling Source: Kurylo K, et al. Development and characterization of a long-acting allosteric GHRA for acromegaly. Endocrinology 2026

Phase 1 Healthy Volunteer Study Established Potential Best-in-Class Profile Potential best-in-disease suppression; 300 mg Q2W predicted clinical dose 1. Cross-trial comparison, not a head-to-head study. MAR002: Marea data on file (single 900 mg SC dose, n=8); Pegvisomant (Somavert) comparator estimated from Thorner MO, et al. J Clin Endocrinol Metab 1999;84(6):2098–2103, Fig 6 (single 1.0 mg/kg SC dose, n=6); 2. Tiberg F et al. Br J Clin Pharmacol 2015;80(3):460–472. 3. Madan A et al. Pituitary 2022;25(2):328–339; Abbreviations: FIH: first-inhuman; POM: proof-of-mechanism; SAD: single ascending dose; BL: baseline; SC: subcutaneous; all cohorts N = 8 (6:2); All doses of MAR002 were a single dose except for 900mgx3 Confidential Phase 1 Study Design Healthy men (n=45), baseline IGF-1 > 100 ng/ml MAR002 Safety Summary to Date Generally well tolerated No serious AEs All doses tolerated No related signals Somavert (49%)1 SRLs (37-40%)2,3 Somavert (<4 days)

MAR002: Emerging Clinical Data Supports Potential Best-in-Class Profile Confidential MAR002 Somavert Peak IGF-1 Suppression in HV In vitro potency with excess GH IGF-1 Normalization PK/Dosing -64% -49%1 90% suppression 24% suppression2 competitive peptide Expected > Somavert 81% IGF-1 normalization in patients3 (Phase 3) Q2W SC Qday dosing4 Painful injections Vial and syringe Allosteric mAb Tolerability No signals to date Significant LFTs, ISRs4 1. Thorner MO, et al. J Clin Endocrinol Metab 1999;84:2098–2103 (single 1.0 mg/kg SC, day 5, n=6); 2. Kurylo K, et al. Development and characterization of a long-acting allosteric GHRA for acromegaly. Endocrinology 2026; 3. Trainer PJ, et al. N Engl J Med 2000;342:1171–1177 (15 mg/day, week 12, n=112); 4. SOMAVERT (pegvisomant) US Prescribing Information, rev. 7/2023, §§2.1, 5.2, 6.1, 16. Cross-trial comparisons are subject to inherent limitations and should be interpreted with caution; no head-to-head studies were conducted

Efficient Development to POC to Evaluate 1st and 2nd Line Label Phase 2 study population supports 1) first line monotherapy 2) second line combination therapy 3) second line monotherapy Week 10: Primary Endpoint 150 mg Q2W 300 mg Q2W 600 mg Q2W Placebo + Open Label Extension MAR002 Active Treatment Arms Study Population (N~72) All-Comers Untreated Controlled on peg therapy – washout Uncontrolled on stable medical therapy - add on IGF-1 > 1.3x ULN 1st dose: 900 mg loading dose Key week-10 Topline Data Assess the effect on serum insulin-like growth factor 1 (IGF-1) response Explore effects on acromegaly symptoms Assess safety and tolerability Confidential

Molecule Target Indication Disc IND-E Ph1 Ph2 Ph3 Anticipated Near-term Milestones MAR001 (parent mAb) ANGPTL4 sHTG MAR005 (half-life extended MAR001) ANGPTL4 sHTG MAR002 Growth hormone receptor Acromegaly Advancing a Late-Stage Cardioendocrine Pipeline Toward Potential 2026-27 Value Inflections MAR001 Phase 2b TYDAL (mHTG/sHTG) Abbreviations: NHV: normal healthy volunteer; sHTG: Severe Hypertriglyceridemia Q2 2026 Phase 2/2b 12-week data H2 2026 Phase 2/2b 24-week data H2 2027 Phase 2 extension (sHTG) topline data Q1 2026 Phase 1 (NHV) topline data Mid-2026 Initiate Phase 2 study Mid-2027 Interim Phase 2 data Q4 2027 Phase 2 topline data H1 2028 Phase 3 FPI MAR001 Phase 2 Mechanistic Study Endocrine  Cardiometabolic Mid-2027 Phase 3 MAR005 dose selection including additional TG efficacy/PD H2 2027 Phase 3 FPI  MAR001 Phase 2b extension (sHTG)  MAR001 has established POC in Phase 2. MAR005 is our Phase 3 candidate- it is an improved version of MAR001 with half-life extension and improved PK. The FDA agreed to PK bridging to Phase 3. Marea also has developed a SiRNA platform and is developing adipose tissue targeted SiRNAs Confidential

Experienced Team; Strong Investor Base MANAGEMENT TEAM Josh Lehrer, MD CEO Caitlin Murray, Esq Fractional GC Ian Clements, PhD CFO Ethan Weiss, MD CSO, Scientific Founder Shishir Gadam, PhD CTO Max Zeiberg SVP, Corp Dev Rebecca Juliano, PhD CDO SCIENTIFIC FOUNDERS Joshua Rabinowitz, MD, PhD Professor of Chemistry, Princeton University Sir Stephen O’Rahilly, MD, FRS Professor of Clinical Biochemistry & Medicine, University of Cambridge Charles Homcy, MD Founder: Myokardia, GBT, BridgeBio, Portola, Maze, Pliant INVESTORS Confidential