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Corporate Presentation January 2026
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BioAge Labs, Inc. (the “Company”) does not (nor their respective affiliates, directors, members, officers, employees or agents) make any representation or warranty, express or implied, as to, and no reliance should be placed on, the fairness, accuracy, completeness or correctness of the information and opinions contained in this Presentation or any other written or oral information made available to any interested party or its advisors and any liability therefor is hereby expressly disclaimed. This Presentation includes certain statements, estimates, targets and projections (including, without limitation, projected revenue, growth and demand expectations and estimated costs) provided by the Company with respect to the anticipated future performance of the assets described herein which reflect significant assumptions and subjective judgments by the Company’s management. The Company believes that it is important to communicate its future assumptions and expectations to current and prospective investors. These assumptions and judgments may or may not prove to be correct, are subject to significant business, economic and competitive uncertainties and contingencies, many of which are beyond the control of the Company, and there can be no assurance that any estimates, targets or projections are attainable or will be realized. The actual results may vary from the projected results and such variations may be material. Any forward-looking statement made by the Company in this Presentation speaks only as of the date on which it was made. The Company, and their respective affiliates, directors, members, officers, employees and agents shall have no liability whatsoever (in negligence or otherwise) for the accuracy or sufficiency of the information contained herein, any errors, omissions or misstatements relating hereto, or any direct, indirect, consequential or other loss howsoever arising from any use of this Presentation or its contents or otherwise arising in connection with this Presentation. The Company undertakes no obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise. Nothing contained within this Presentation is or should be relied upon as a promise or representation as to the future. Interested parties should conduct their own investigation and analysis of the business, data and property described herein and the information contained in this Presentation. Only those representations or warranties that are made to the recipient in a definitive written purchase agreement when, as, and if it is executed, and subject to such limitations and restrictions as may be specified in such agreement, shall have any legal effect. By receiving this document the recipient agrees to be bound by the foregoing limitations. This Presentation shall remain the property of the Company, and is for the exclusive use of the recipient to whom it is addressed. The recipient agrees that, unless and until a definitive written purchase agreement has been executed, the Company will not be under any legal obligation of any kind. The recipient further acknowledges and agrees that the Company reserves the right, in its sole discretion without advance notice, to reject any and all proposals made by the recipient with regard to the project and to terminate discussions and negotiations with the recipient at any time and for any or no reason. Trade names, trademarks and service marks of other companies appearing in this presentation are the property of their respective owners. Solely for convenience, the trademarks and trade names referred to in this presentation appear without the ® and TM symbols, but those references are not intended to indicate, in any way, that we will not assert, to the fullest extent under applicable law, our rights, or the rights of the applicable licensor to these trademarks and tradenames. This presentation concerns products that are under clinical investigation and which have not yet been approved for marketing by the U.S. Food and Drug Administration. It is currently limited by federal law to investigational use, and no representation is made as to its safety or effectiveness for the purposes for which it is being investigated. Disclaimer 2
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We are harnessing the biology of human aging to develop new therapies for metabolic diseases 3 The BioAge discovery platform: from human data to therapeutics for metabolic aging Validated platform: ongoing partnerships with Novartis & Lilly to discover drugs and drug targets >150M molecular data points: one of the world’s largest collections of longitudinal human aging data and functional outcomes BGE-102: oral brain-penetrant NLRP3 inhibitor Potential “pipeline in a product” targeting efficacy in-line with injectable anti-inflammatories CV risk: potential best-in-class profile for hsCRP reduction ● 86% reduction in hsCRP in obese subjects ● 93% of patients achieved normalized hsCRP <2 mg/L Ophthalmology: therapeutic retinal exposure enables oral treatment of diseases including DME, where intravitreal anti-IL-6 has shown benefit Anticipated catalysts: full Ph1 data H1:2026, CV risk POC H2:2026, DME POC mid-2027 APJ agonism: exercise mimetic for obesity Obesity: potential to double weight loss & fully restore body composition when combined with an incretin in preclinical models Anticipated catalysts: IND submission 2026 YE
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70 80 90 100 Age of death A 50+ year natural human experiment 150M+ Molecular data points 25K+ Profiles generated 50+ Years of follow-up ● Grip strength ● Walking speed ● Mobility Detailed healthspan trajectories Physical function ● BMI ● Skinfold thickness ● Waist / hip circumference Metabolism 4 The BioAge Platform: Harnessing human data to uncover molecular pathways and novel drug targets that drive metabolic aging and impact healthspan
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mAb drug discovery collaboration for two novel BioAge targets 5 mAb discovery Novel target discovery collaboration focused on the intersection of exercise & healthy aging Exercise response Longitudinal healthspan outcomes Target discovery Validated platform with two ongoing pharma collaborations to advance novel aging targets
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We are supported by an accomplished team of board members and advisors BOARD MEMBERS Eric Morgen, MD Co-Founder, COO Kristen Fortney, PhD Co-Founder, CEO James Healy, MD, PhD Managing Partner, Sofinnova Investments Patrick Enright, MBA Managing Partner, Longitude Capital Vijay Pande, PhD Managing Partner, VZVC Rekha Hemrajani, MBA Public company CEO / CFO experience Michael Davidson, MD CEO, NewAmsterdam Pharma Jean-Pierre Garnier, PhD Chair Former CEO, GSK 6
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~800 Clinical trials* ~130 INDs* ~95 US regulatory approvals* LEADERSHIP TEAM Kristen Fortney, PhD Co-Founder, CEO Eric Morgen, MD Co-Founder, COO Paul Rubin, MD CMO & EVP Research Ann Neale CDO Dov Goldstein, MD, MBA CFO Peng Leong, PhD, MBA CBO & TA Head, Brain Aging BJ Sullivan, PhD Chief Strategy Officer The BioAge leadership team: diverse professional experience across the biopharma ecosystem and an established track record of success * As of May 31, 2024 7
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8 BGE-102 overview Therapeutic areas NLRP3 Phase 1 update
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Strong human genetic evidence for NLRP3 in cardiometabolic disease Mendelian randomization: NLRP3 levels strongly predictive of heart failure (↑ 1 SD expression = up to ↑ 70% risk) GoF mutations ↓ lean mass & body composition ↑ atherosclerosis ● Normal NLRP3 function: innate immune response to danger signals ● In pathology: cellular stress & nutrient excess stimulates chronic activation ● Resulting chronic inflammation drives a range of diseases, including obesity NLRP3 9 Reduced NLRP3 activity is associated with longevity NLRP3 overview NLRP3 in human longevity & disease Relative mortality risk (HR) Cellular stress NLRP3 activation Cytokine release (IL-1β, IL-18) Excess nutrients Chronic inflammation SAD / MAD UPDATE Chronic NLRP3 activity drives disease & predicts poor human longevity IL-6
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NLRP3 10 Note: as of January 12, 2026 Attractive safety & tolerability All AEs to date mild / moderate, self-limited, with no dose dependency CNS penetrant ~0.7 Kp,uuCSF (120 mg MAD, day 14) 42-90x safety margin for 60 mg dose NOAEL = highest doses tested in 28 day GLP tox Key attributes Potential best-in-class potency based on ongoing Phase 1 trial 1.8 nM IC90 by human ex-vivo whole blood stimulation 24h IC90 coverage at 60 mg QD provided 24 hour IL-1β suppression ≥90% 93% of subjects normalized CRP (<2 mg/L) – obese inflamed MAD in line with injectable IL-6 drugs Strong IP position 2045 composition of matter & claims for novel NLRP3 binding site BGE-102 OVERVIEW Our lead program, BGE-102, is well positioned to address diseases driven by inflammation in both the CNS and the periphery
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11 MCC950 BAL-1558 Collaboration with Matthias Geyer, PhD, Director, Institute of Structural Biology University of Bonn Novel mechanismUnique binding site Unlike other NLRP3 inhibitors, our compounds have not demonstrated ATPase inhibition MCC950 0.001 0.1 10 Luminescence 150000 120000 90000 60000 0 30000 Cpd conc (𝜇M) 0.001 0.1 10 Luminescence 150000 120000 90000 60000 0 30000 Cpd conc (𝜇M) BAL-0028 representative experiment NLRP3 BGE-102 OVERVIEW BioAge NLRP3 inhibitors: unique, patented binding site & novel mechanism
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12 Phase 1 update Therapeutic areas NLRP3 BGE-102 overview
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Single Ascending Dose HVs & obese 13 NLRP3 Note: HVs = healthy volunteers active placebo For post-baseline visits, window +/- 1 day Multiple Ascending Dose HVs - 14 days of dosing Multiple Ascending Dose Obese - 14-21 days of dosing Objectives Participants Design 5 cohorts x 10 mg | 30 mg | 60 mg (fed & fasted) | 120 mg Safety & tolerability, pharmacokinetics, pharmacodynamics (IL-1β, hsCRP) HVs (N=36) & obese participants (N=9) HVs (N=18) 2 cohorts x 60 mg | 120 mg Status completed completed Obese participants with hsCRP > 3 mg/L (N=54) 120 mg | 2 additional doses <100 mg ongoing - data H1:2026 3 cohorts x PHASE 1 UPDATE Phase 1 clinical trial - full data anticipated H1:2026
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After 14 days of dosing at 60 mg QD in healthy volunteers: ● ≥90% suppression of IL-1β for 24 hours ● Drug levels in CSF > IC90 NLRP3 ● Well tolerated with all mild / moderate, self-limited AEs ● No dose-limiting toxicities 14 Safety / tolerability ● Dose-proportional exposure with T1/2 supporting QD dosingPharmacokinetics Pharmacodynamics After 14 days of dosing at 120 mg QD in obese participants: ● 86% reduction in hsCRP ● 93% of patients achieved normalized hsCRP (<2 mg/L) Efficacy PHASE 1 UPDATE BGE-102 has met key objectives to date
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15 Phase 1 update Therapeutic areas NLRP3 BGE-102 overview Healthy volunteer SAD / MAD Obese MAD
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16 NLRP3 10mg 30mg 60mg 120mg 30 mg 10 mg 120 mg 60 mg Cohort SAD cohorts: mean plasma PK BGE-102 and active metabolite* free concentration Note: * combined concentration of BGE-102 and its sole active metabolite M1, which acts as an NLRP3 inhibitor of comparable potency. M1 has been previously shown to have a large safety margin in rat & dog toxicology studies. Time (h) Mean free plasma concentration (ng/mL) 10mg 30mg 60mg 120mg HEALTHY VOLUNTEER SAD / MAD Plasma PK: Dose-proportionality observed in SAD cohorts
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MAD cohorts: mean plasma PK at trough (pre-dose) BGE-102 and active metabolite free concentration NLRP3 17 60 mg Dose 120 mg IL-1β IC90 Human ex vivo whole blood Mean free plasma concentration (ng/mL) Study day Note: * IC90 calculated from first 24 hours of treatment of healthy volunteers in SAD & MAD cohorts HEALTHY VOLUNTEER SAD / MAD Plasma PK: MAD cohorts showed accumulation out to 14 days with near steady-state levels above the human IC90 for IL-1β inhibition
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NLRP3 18 MAD cohorts: Day 14 CSF PK BGE-102 and active metabolite, 11-13 hours post-dose Mean CSF concentration (ng/mL) 60 mg 120 mg IL-1β IC90 Human ex vivo whole blood HEALTHY VOLUNTEER SAD / MAD CSF PK: doses of 60 mg and above exceeded human IC90 at near steady state
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NLRP3 MAD cohorts: Mean IL-1β with ex vivo stimulation at trough baseline vs Day 14 19 90.0% reduction 97.7% reduction Baseline Day 14 Baseline Day 14 60 mg 120 mg 90% 98% Ex vivo whole blood stimulation IL-1β Inflammatory stimulus Blood from participant HEALTHY VOLUNTEER SAD / MAD PK / PD: 90-98% suppression of IL-1β at BGE-102 trough in MAD cohorts
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20 NLRP3 Day 14Day 8Day 1 120 mg MAD HEALTHY VOLUNTEER SAD / MAD PK / PD: 24 hours of near maximal suppression of IL-1β achieved by Day 7
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21 Phase 1 update Therapeutic areas NLRP3 BGE-102 overview Healthy volunteer SAD / MAD Obese MAD
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22 NLRP3 Eligibility ● Age 18+ ● BMI 32-42 ● hsCRP > 3 mg/L ● No incretin treatment for 90 days Primary endpoints ● PK, safety / tolerability Exploratory endpoints ● Inflammatory and metabolic biomarkers, including hsCRP Placebo Dosing Day 14-21 end of treatment Screening BGE-102 R Lumbar puncture Lumbar puncture 3 dose levels OBESE MAD The ongoing Phase 1 includes 3 obese MAD cohorts, enabling evaluation of biomarkers including hsCRP
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23 NLRP3 Note: median baseline hsCRP 4.85 mg/L for active treatment and 4.25 mg/L for placebo Placebo <2 mg/L Placebo ≤ 1 mg/L Group/ Threshold BGE-102 120 mg QD <2 mg/L BGE-102 120 mg QD ≤ 1 mg/L 93% 71% 86% 71% 25% OBESE MAD 93% of participants on BGE-102 achieved normal hsCRP levels (<2 mg/L) at Day 14
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Note: median values, error bars show IQR (Q1-Q3); median baseline hsCRP 4.85 mg/L for active treatment and 4.25 mg/L for placebo NLRP3 24 BGE-102 120 mg QD Placebo Treatment-22% -83% -43% -86% N=4 N=14 N=4 N=14 OBESE MAD BGE-102 resulted in an 86% hsCRP reduction at Day 14, consistent with best-in-class efficacy
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25 BGE-102 120 mg QD Placebo Treatment NLRP3 2% 23% -62% -44% Note: median values, error bars show IQR (Q1-Q3); median baseline IL-6 4.2 pg/mL for active treatment and 2.4 pg/mL for placebo OBESE MAD BGE-102 resulted in a 44-62% reduction in IL-6
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26 NLRP3 BGE-102 120 mg QD Placebo Treatment 2% 1% -24% -30% Note: median values, error bars show IQR (Q1-Q3); median baseline fibrinogen 331 mg/dL for active treatment and 290 mg/dL for placebo OBESE MAD BGE-102 resulted in a 30% reduction in fibrinogen at Day 14
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27 NLRP3 CSF IL-6* Plasma IL-6 Note: * IL-6 levels >7 pg/mL in the CSF are considered elevated; corresponding decrease in the plasma was 62%; measurements performed using the Alamar NULISA platform Day 14 OBESE MAD In the 2 participants with elevated baseline CSF IL-6, BGE-102 reduced levels by 84% in the Day 14 CSF CSF IL-6 (pg/mL) Plasma IL-6 (pg/mL)
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Mean IL-1β with ex vivo stimulation at trough baseline vs Day 14 28 NLRP3 120 mg 93% Baseline Day 14 Ex vivo whole blood stimulation IL-1β Inflammatory stimulus Blood from participant OBESE MAD 93% suppression of IL-1β at BGE-102 trough
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29 NLRP3 Phase 1 update BGE-102 overview Therapeutic areas
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Neuro- inflammation Peripheral inflammation NLRP3 BGE-102 addressable diseases CVD (ASCVD, HF) Insulin resistance Neurodegeneration 30 MASLD / MASH Ocular THERAPEUTIC AREAS BGE-102 has the potential to address a range of cardiometabolic and neuroinflammatory disorders
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31 NLRP3 BGE-102 overview Ophthalmology Phase 1 update Therapeutic areas Cardiovascular
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“In aggregate, the evidence linking inflammation with atherosclerotic CVD is no longer exploratory but is compelling and clinically actionable. The time for taking action has now arrived.” 32 NLRP3 Source: Ridker 2024, Ridker 2018 Inflammation (hsCRP) is more predictive of MACE than LDL or Lp(a) Risk of MACE in 30-year longitudinal data from the Women's Health Study hsCRP LDL-C Lp(a) The NEW ENGLAND JOURNAL of MEDICINE 1.8 1.6 1.4 1.2 1.0 0.8 Quintile (reference) Quintile 2 Quintile 3 Quintile 4 Quintile 5 1.00 1.00 1.00 1.11 1.030.99 1.32 1.37 1.67 1.38 1.24 1.04 1.21 1.08 0.94 CANTOS trial validated the anti-inflammatory strategy 25% reduction in MACE for patients with hsCRP normalization Hazard ratio HR (95% CI) p Placebo 1 (ref) ref On-treatment hsCRP ≥ 2.0 mg/L 0.95 (0.84-1.09) 0.48 On-treatment hsCRP < 2.0 mg/L 0.75 (0.66-0.85) <0.0001 CARDIOVASCULAR DISEASE Normalizing hsCRP (<2 mg/L) can drive a 25% reduction in MACE
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Inflammatory cascade & targeting modalities 33 VTX3232 30 mg QD | CV risk, 12 weeks NLRP3 -50% -25% -100% -75% Maximum % change in hsCRP NT-0796 225 mg BID | CV risk, 28 days Ziltivekimab 15 mg | CKD, 12 weeks Pacibekitug 15 mg | CKD, 30 days NLRP3 IL-1β IL-6 Canakinumab 300 mg | CANTOS, 12 weeks NLRP3 inflammasome hsCRP Fibrinogen IL-1β IL-6 Sources: NodThera, Tourmaline Bio, Ventyx Biosciences, Wada 2023, Ridker 2017 BGE-102 120 mg QD | CV risk, 14 days 0% CARDIOVASCULAR DISEASE NLRP3 inhibitors are a potential “oral IL-6” with comparable reductions in hsCRP
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NLRP3 34 Source: Ridker 2020, Mallat 2001, Zeng 2021 NLRP3 inflammasome IL-1β IL-6 IL-18 Pyroptosis Plaque destabilization NLRP3 drives ASCVD beyond IL-6 Baseline IL-18 is a CVD risk factor in the CANTOS trial CRP Fibrinogen CARDIOVASCULAR DISEASE NLRP3 inhibition also has potential benefits beyond IL-6, reducing IL-18 & cell death that contribute to plaque destabilization
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35 NLRP3 $50B expected global market size of lipid-lowering therapies by 2035 Inflammation is an independent risk factor for CVD >80% of statins are prescribed by PCPs Potential for oral fixed-dose combinations with other CV risk mechanisms (e.g., PCSK9, GLP-1) Orals are highly preferable Lipid-lowering therapies set precedent for large market ~60% of 20M ASCVD patients have elevated hsCRP 12M addressable patients in the US alone Source: Ridker 2002, Zhang 2024, Mazhar 2024, Broker reports, Towards Healthcare <1.0 1.0-3.0 >3.0hsCRP (mg/L) CARDIOVASCULAR DISEASE The CV opportunity
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Note: double-blind and placebo-controlled NLRP3 36 Eligibility ● Age 18+ ● BMI 32-42 ● hsCRP > 3 mg/L ● No incretin treatment for 90 days Primary endpoint ● % change in hsCRP Exploratory endpoints ● Additional CV risk factors (e.g., Lp(a), fibrinogen, IL-6) ● MRI imaging ● Metabolic parameters (e.g., fasting glucose, HbA1c) ● PROs & QoL ● Body weight Placebo Dosing Week 12 end of treatment N=50 Screening Week 16 end of study BGE-102 N=50 Dose to be selected from Phase 1 SAD / MAD R CARDIOVASCULAR DISEASE Planned BGE-102 POC in patients with obesity & CV risk factors
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37 NLRP3 BGE-102 overview Ophthalmology Phase 1 update Therapeutic areas Cardiovascular
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38 NLRP3 OPHTHALMOLOGY NLRP3 activation is a central feature of retinal diseases DME & GA Diabetic retinopathy / diabetic macular edema (DME) Hyperglycemia & oxidative stress IL-6 Vascular leakage & vision loss VEGF NLRP3 activation (IL-1β, IL-18) RPE cells | microglia Dry age-related macular degeneration (AMD) / geographic atrophy (GA) Accumulation of cellular debris (drusen, lipofuscin) and Alu RNA Photoreceptor collapse & vision loss NLRP3 activation (IL-1β, IL-18) endothelial cells | Müller cells, microglia pyroptosis Source: Zheng 2023 Chronic inflammation pyroptosis
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NLRP3 Description ● Vision loss due to vascular leakage ● Leading cause of vision loss in adults <65 ● Loss of central vision ● 20% become legally blind within 1 year of diagnosis Prevalence (US) ● 1M ● 1.2M Key risk factors ● Hyperglycemia ● Age, inflammation, cardiometabolic disease Approved therapies ● Intravitreal anti-VEGFs, intravitreal steroids, laser ● Intravitreal complement inhibitors (Syfovre, Izervay) Key unmet needs ● Reduced injection burden: real world treatment outcomes are suboptimal given poor compliance ● New MOAs: significant anti-VEGF refractory population ● Disease control: approved therapies offer limited efficacy 39 Prevalent retinal diseases with significant unmet needs OPHTHALMOLOGY Sources: Al Sakini 2024, Lai 2024, Varma 2014, Seddon 2003, CDC, Mayo Clinic, Broker estimates GA (end-stage AMD)DME
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40 High injection burden NLRP3 Key treatment challenges OPHTHALMOLOGY Eyes treated individually Systemic disease drivers not addressed GA Limited efficacy of approved therapies ~90% are not treated given current drugs only slow progression 15-20% ~45% of patients are refractory to anti-VEGFs despite compliance Source: Kulkarni 2021, Kuo 2024, Bressler 2018, AREDs Research Group, Astellas / Apellis company reports, BioAge market research DME (Bi)monthly injections required for approved therapies, often in elderly patients ~50% discontinue anti-VEGFs after an average of 6 months ~65% develop bilateral disease; treatment limited to 1 eye per visit ~70% develop bilateral disease within 1 year of diagnosis Inflammation is both a risk factor & prognostic marker Insulin resistance is a key risk factor for refractory disease
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41 NLRP3 The retinal opportunity for BGE-102 OPHTHALMOLOGY Oral treatment to lower treatment burden Greater efficacy with new MOA Ocular and systemic biology addressed Simultaneous treatment of bilateral disease BGE-102 has shown therapeutic retinal exposure across species, including primates
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42 NLRP3 DME: intravitreal anti-IL-6 has validated the anti-inflammatory approach in multiple trials of retinal diseases driven by inflammation, including DME OPHTHALMOLOGY Rapid improvements in visual acuity & CST: seen within 4-8 weeks in Phase 2 trials ~1 line: Incremental vision with anti-VEGF, sustained through 1 year Broad utility: efficacy in treatment-naïve and actively treated (anti-VEGF) patients Orphan strategy: uveitic macular edema, where steroids are SOC and anti-IL-6 has shown robust efficacy MEERKAT trial: up to 36.9% of patients achieved a ≥15 letter improvement from baseline in BCVA at week 16 Anti-IL-6 in DME Source: Company Presentations (Kodiak, Eyepoint, Roche)
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43 Healthy control STZ STZ + BGE-102 (20 mpk) STZ + BGE-102 (50 mpk) Retinal vascular permeability measured via fluorescein angiography NLRP3 DME: oral delivery of BGE-102 preserved retinal vascular integrity in a preclinical model of diabetic retinopathy Note: Streptozotocin diabetic mouse model; BGE-102 is more potent in human cells, for example 150–250x higher potency in microglia Source: Wolf 2023 Blood-retina barrier integrity claudin-5 IHC (endothelial tight junctions) OPHTHALMOLOGY Microvascular degeneration
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44 BGE-102 HOMA-IR (Day 26) Nlrp3 -/- Insulin tolerance test (6 weeks) WT Nlrp3-/- Note: BGE-102 was dosed PO QD; semaglutide was dosed SC QD. Source: Vandanmagsar 2011 NLRP3 DME: BGE-102 improved insulin sensitivity in obese mice, recapitulating mouse genetics & establishing potential to treat the key disease driver OPHTHALMOLOGY
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Primary endpoint ● % change in intraocular IL-6 Exploratory ● Additional intraocular biomarkers ● Plasma biomarkers ● BCVA ● CST DME Week 8 End of Treatment DosingScreening VEGF + BGE-102 N= 30R Follow up 45 VEGF + oral placebo N= 30 Sham + BGE-102 N= 30 Planned BGE-102 Phase 1b/2a POC in DME: Goal is to demonstrate PD in the eye NLRP3 OPHTHALMOLOGY Philip Rosenfeld, MD, PhD Professor of Ophthalmology, Bascom Palmer Eye Institute, University of Miami David Boyer, MD Senior Partner, Retina-Vitreous Associates Medical Group Key program advisors
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46 NLRP3 OPHTHALMOLOGY Goals of DME POC: ● Demonstrate PD in the eye with oral delivery of BGE-102 ● Motivate subsequent development in additional ophthalmology indications, including GA
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47 WT Vehicle AβO 100 0Healthy % NLRP3 OPHTHALMOLOGY GA: Nlrp3 knockout rescues integrity of the RPE in mice Vehicle Alu overexpression Vehicle Alu overexpression Nlrp3 -/- Vehicle AβO 100 100 Drusen ( Aβ oligomers) Alu RNA (overexpression) 100 0Healthy % 100 100 Pro-inflammatory hallmarks of GA Source: Narendran 2021, Tarallo 2012
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48 NLRP3 OPHTHALMOLOGY GA: In a natural AMD preclinical model, oral delivery of a BGE-102 analog prevented age-related lipofuscin accumulation, a key disease feature Natural AMD model Lipofuscin punctae accumulate with age in outbred (HET3) mice BAL-1901 prevented lipofuscin accumulation with 3 mo of treatment beginning at 15 mo vehicle BGE-1901 30 months 3 months 0.6 13.4 23.6 39.6
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49 NLRP3 OPHTHALMOLOGY GA: Inflammasome inhibition in humans: promising early signals of potential efficacy Note: * Comparison made to fellow contralateral eye Source: Ambati 2021, Heier 2023, Inflammasome Therapeutics Alu RNA Vehicle Vehicle Fluoxetine Hazard Ratio 0.778 (p<0.001) Fluoxetine exposure Exposed Unexposed Inflammasome inhibitor implant N=10, p=0.03 53% reduction in lesion growth, 3 months* Syfovre (complement inhibitor) Ph3 trials (OAKS + DERBY average) ~15% reduction in lesion growth, 12 mo Decreased incidence of AMD observed with the SSRI fluoxetine, a weak NLRP3 inhibitor (µM potency), in retrospective analysis Pilot study shows potential for greater efficacy Inflammasome inhibitor intravitreal implant, K8, vs. complement inhibition
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50 Apelin / APJ
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APJ Shared biology between apelin & exercise Exercise stimulates release of apelin into circulation Systemic benefits Balance of lean & fat mass Basal metabolic rate Protein synthesis Mitochondrial biogenesis Insulin sensitivity / glucose metabolism Source: Adapted from Bertrand 2015; Ceraudo 2014 Apelin is an exerkine and mimics many benefits of exercise 51
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Human insights from the BioAge platform: Apelin signaling impacts muscle & metabolism Human proteomic associations Change in probability of a good outcome Apelin protein levels (percentile) Preservation of grip strength 20 40 60 1.4 1.2 1.0 2.0 1.6 1.8 0 80 100 Relative probability Longevity APJ BioAge aging dataset 52
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Apelin KO ↑ adiposity ↑ insulin resistance Apelin transgenic ↓ weight gain on high fat diet ↑ basal metabolic rate No impact on energy intake Insulin tolerance test APLN ↑APLN High-fat diet Consistent genetic evidence in humans: Genome-wide significant associations for the apelin receptor APJ include BMI, lean mass, and serum lipids P<0.001 Visceral fat Source: Yue 2010, Yue 2011, Yamamoto 2011, Pulit 2019, Sakaue 2021, Pei 2020, Richardson 2020, Wakil 2016 p<0.05 * p<0.01 APJ Apelin genetics reinforce beneficial role in systemic metabolism 53
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54 APJ We previously demonstrated that APJ agonism can restore body weight & body composition to that of lean controls when combined with an incretin Overall weight loss Lean Control Obese Control Azelaprag (0.275g/L) Azelaprag (1.1g/L) Tirzepatide (10nmol/kg) Tirzepatide (10nmol/kg)+ Azelaprag (0.275g/L) Lean Control Obese Control Tirzepatide (10nmol/kg)+ Azelaprag (1.1g/L) Note: Mice in all groups lose both lean mass and fat mass; with azelaprag, lean body composition (% lean mass) is restored. Lean and fat mass were measured with EchoMRI. % Lean Mass Lean Control Obese Control Body composition % Fat Mass Obese Control Lean Control
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In a clinical trial, APJ agonism resulted in significant muscle & metabolic benefits in older subjects on bed rest Ph1b design 10 days of bed rest & dosing Healthy subjects 65+ (N=10 placebo, N=11 azelaprag) Azelaprag (240mg) or placebo via daily IV infusion Double-blind, non-randomized Muscle size Fat infiltration Metabolism Circumference Diameter (thickness) Cross- sectional area Muscle grade (progression) Cumulative protein synthesis p<0.001 p<0.01 p<0.05 p<0.005 p<0.005 Thigh circumference Muscle size (vastus lateralis) Muscle degeneration Muscle protein synthetic rate APJ 55
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6 -0.02 coef 0.00 -log10(p.val) 0.02 4 2 0 Significantly upregulated by APJ agonism p=1.5E-24 Legend: Endurance exercise positive associations Endurance exercise negative associations Source: Robbins 2023 APJ In the trial, APJ agonism shifted the serum proteome consistent with recapitulating the benefits of exercise 56
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APJ agonist activity (cAMP) Collaboration with JiKang Therapeutics 57 APJ ● Composition of matter IP filed on small molecules with picomolar potency ● Scaffold distinct from azelaprag Vehicle ● Exclusive option on APJ agonist nanobodies with potency 10x greater than apelin, the natural ligand Our goal is to advance APJ agonists for both oral and parenteral delivery Apelin-13 APJ nanobody Oral Recent progress on APJ Parenteral APJ Agonist 1 APJ Agonist 2Apelin-13 APJ agonist activity (cAMP) Concentration (M) Concentration (M)
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Strong balance sheet with $295.9M in cash, cash equivalents, and marketable securities as of September 30, 2025 Pipeline overview Leveraging the BioAge platform to address key unmet needs in metabolic aging 58 Full Phase 1 data H1:2026 CV risk Phase 2a results H2:2026 BGE-102 CV risk NLRP3 inhibitor (CNS penetrant) Oral QD APJ Obesity APJ agonist Oral QD Program 1 Cardio- metabolic - various Undisclosed Program 2 Undisclosed Target discovery -Multiple targets - SQ QW Obesity IND submission 2026 YE IND submission 2026 YE Discovery Phase 1IndicationProgram Mechanism of action Target dosing Lead op IND- enabling Anticipated milestonesPhase 2 Diabetic macular edema DME Phase 1b/2a Initiation mid-2026 Results mid-2027