Bioage Labs, Inc. · NASDAQ:BIOA
Bioage Labs — Investor Presentation (September 2026)
61 slides from Bioage Labs's investor presentation, September 2026
Slide 1: Corporate Presentation September 2026
Corporate Presentation September 2026
Slide 2: Forward-looking statements
Forward-looking statements This presentation contains “forward-looking statements” within the meaning of, and made pursuant to the safe harbor provisions of, the Private Securities Litigation Reform Act of 1995. In some cases, you can identify forward-looking statements by terms such as “aim,” “may,
Slide 3: The BioAge discovery platform: from human data to therapeutics for metabolic aging
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 out
Slide 4: The BioAge Platform: Harnessing human data to uncover molecular pathways and novel drug targets
The BioAge Platform: Harnessing human data to uncover molecular pathways and novel drug targets that drive metabolic aging and impact healthspan 70 80 90 100 Age of death A 50+ year natural human experiment Detailed healthspan trajectories Physical function Metabolism 150M+ 25K+ 50+ ● ● Grip strengt
Slide 5: Validated platform with two ongoing pharma collaborations to advance novel aging targets
Validated platform with two ongoing pharma collaborations to advance novel aging targets mAb discovery Target discovery Novel target discovery collaboration mAb drug focused on the intersection of discovery exercise & healthy aging collaboration for two novel Exercise Longitudinal BioAge targets hea
Slide 6: We are supported by an accomplished team of board members and advisors
We are supported by an accomplished team of board members and advisors BOARD MEMBERS Jean-Pierre Garnier, PhD Kristen Fortney, PhD Eric Morgen, MD Michael Davidson, MD Chair Co-Founder, CEO Co-Founder, COO CEO, Former CEO, GSK NewAmsterdam Pharma Patrick Enright, MBA James Healy, MD, PhD Rekha Hemra
Slide 7: The BioAge leadership team
The BioAge leadership team: diverse professional experience across the biopharma ecosystem and an established track record of success LEADERSHIP TEAM ~800 Clinical trials* Kristen Fortney, PhD Co-Founder, CEO Eric Morgen, MD Co-Founder, COO Paul Rubin, MD CMO & EVP Research ~130 INDs* Ann Neale Dov
Slide 8: NLRP3
NLRP3 BGE-102 overview Phase 1 results Therapeutic areas 8
Slide 9: Chronic NLRP3 activity drives disease & predicts poor human longevity
P3 LR N BGE-102 OVERVIEW Chronic NLRP3 activity drives disease & predicts poor human longevity NLRP3 overview NLRP3 in human longevity & disease Relative mortality risk (HR) Reduced NLRP3 Normal NLRP3 Excess ● nutrients Cellular activity is stress function: innate associated with immune response lon
Slide 10: Our lead program, BGE-102, is well positioned to address diseases driven by inflammation
P3 LR N BGE-102 OVERVIEW Our lead program, BGE-102, is well positioned to address diseases driven by inflammation in both the CNS and the periphery Key attributes Potential best-in-class potency based on Phase 1 trial results CNS penetrant 1.8 nM IC90 by human ex-vivo whole blood stimulation ~0.7 Kp
Slide 11: BioAge NLRP3 inhibitors: unique, patented binding site & novel mechanism
P3 LR N BGE-102 OVERVIEW BioAge NLRP3 inhibitors: unique, patented binding site & novel mechanism Unique binding site active inactive Our inhibitors bind both the inactive & active BioAge inflammasome, compounds unlike other NLRP3 inhibitors MCC950 BioAge compounds 11 Collaboration with Matthias Gey
Slide 12: NLRP3
NLRP3 BGE-102 overview Phase 1 results Therapeutic areas 12
Slide 13: Phase 1 clinical trial design
P3 LR N PHASE 1 RESULTS Phase 1 clinical trial design Single Ascending Dose Multiple Ascending Dose Multiple Ascending Dose HVs & obese HVs - 14 days of dosing Obese - 14-21 days of dosing Objectives Safety & tolerability, pharmacokinetics, pharmacodynamics (IL-1β, hsCRP) HVs (N=36) Obese subjects S
Slide 14: BGE-102 met key trial objectives
P3 LR N PHASE 1 RESULTS BGE-102 met key trial objectives ● Well tolerated with all mild / moderate, self-limited AEs Safety / tolerability ● No dose-limiting toxicities Pharmacokinetics ● Dose-proportional exposure with T1/2 supporting QD dosing After 14 days of dosing at 60 mg QD in healthy volunte
Slide 15: BGE-102 was well tolerated
P3 LR N PHASE 1 RESULTS BGE-102 was well tolerated All BGE-102 All placebo TEAEs (N=82) (N=22) ● Only mild / moderate treatment-emergent AEs (TEAEs); all self-limited with no dose dependency Subjects with 50 (61.0%) 13 (59.1%) at least 1 AE ● No serious AEs ● No TEAEs leading to discontinuation Subj
Slide 16: Obese MAD cohorts: baseline characteristics
P3 LR N PHASE 1 RESULTS Obese MAD cohorts: baseline characteristics 60 mg obese MAD 120 mg obese MAD Obese placebo Baseline characteristic (N=19) (N=14) (N=8) Age, years, mean (SD) 41.7 (9.8) 39.4 (9.8) 38.8 (6.7) Male, n (%) 7 (36.8) 8 (57.1) 2 (25.0) Female, n (%) 12 (63.2) 6 (42.9) 6 (75.0) Race,
Slide 17: Obese MAD cohorts: safety and tolerability
P3 LR N PHASE 1 RESULTS Obese MAD cohorts: safety and tolerability 60 mg obese MAD 120 mg obese MAD Obese placebo TEAEs (N=19) (N=14) (N=8) Subjects with any related TEAE, n (%) 5 (26.3%) 2 (14.3%) 1 (12.5%) Subjects with TEAE leading to discontinuation, n 0 0 0 Subjects with SAE or severe TEAE, n 0
Slide 18: NLRP3
NLRP3 BGE-102 overview Phase 1 results Healthy volunteer SAD / MAD Obese MAD Therapeutic areas 18
Slide 19: Plasma PK: Dose-proportionality observed in SAD cohorts
P3 LR N HEALTHY VOLUNTEER SAD / MAD Plasma PK: Dose-proportionality observed in SAD cohorts SAD cohorts: mean plasma PK BGE-102 and active metabolite* free concentration Mean free plasma concentration Dose (ng/mL) 10 mg 30 mg 60 mg 120 mg Time (h) 19 Note: * combined concentration of BGE-102 and its
Slide 20: Plasma PK: MAD cohorts showed accumulation out to 14 days
P3 LR N 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 MAD cohorts: mean plasma PK at trough (pre-dose) Mean free plasma concentration BGE-102 and active metabolite free concentration Dose
Slide 21: CSF PK: doses exceeded human IC90 at near steady state
P3 LR N HEALTHY VOLUNTEER SAD / MAD CSF PK: doses of 60 mg and above exceeded human IC90 at near steady state MAD cohorts: Day 14 CSF PK Mean CSF concentration BGE-102 and active metabolite, 11-13 hours post-dose (ng/mL) IL-1β IC90 Human ex vivo whole blood 60 mg 120 mg 21
Slide 22: PK / PD: 90-98% suppression of IL-1β at trough in MAD cohorts
P3 LR N HEALTHY VOLUNTEER SAD / MAD PK / PD: 90-98% suppression of IL-1β at BGE-102 trough in MAD cohorts MAD cohorts: Mean IL-1β with ex vivo stimulation at trough Ex vivo whole blood stimulation baseline vs Day 14 Blood from Inflammatory participant stimulus 98% 90% IL-1β 60 mg 120 mg 22
Slide 23: PK / PD: 24 hours of near maximal suppression of IL-1β by Day 8
P3 LR N HEALTHY VOLUNTEER SAD / MAD PK / PD: 24 hours of near maximal suppression of IL-1β achieved by Day 8 120 mg MAD Day 1 Day 8 Day 14 23
Slide 24: NLRP3
NLRP3 BGE-102 overview Phase 1 results Healthy volunteer SAD / MAD Obese MAD Therapeutic areas 24
Slide 25: The Phase 1 trial included 2 obese MAD cohorts
P3 LR N OBESE MAD The Phase 1 trial included 2 obese MAD cohorts, enabling evaluation of biomarkers including hsCRP Eligibility ● Age 18+ Primary endpoints Placebo ● PK, safety / tolerability ● BMI 32-42 R Exploratory endpoints ● hsCRP > 3 mg/L BGE-102 Dose levels: 60 mg | 120 mg ● Inflammatory and
Slide 26: 60 mg & 120 mg doses of BGE-102 resulted in 86% reductions in hsCRP
P3 LR N OBESE MAD 60 mg & 120 mg doses of BGE-102 resulted in 86% reductions in hsCRP, consistent with best-in-class efficacy 60 mg MAD 120 mg MAD * Note: median values, error bars show IQR (Q1-Q3); * Day 7 placebo IQR upper limit is 115%; median baseline hsCRP 60 mg cohort 6.30 mg/L for both active
Slide 27: Similar hsCRP trajectories in both obese MAD cohorts
P3 LR N OBESE MAD Similar hsCRP trajectories in both obese MAD cohorts Dose 60 mg 120 mg 27 Note: median values, error bars show IQR (Q1-Q3); median baseline hsCRP for subjects on active treatment 60 mg cohort 6.30 mg/L, 120 mg cohort 4.85 mg/L
Slide 28: 87%-93% of subjects on BGE-102 achieved normal hsCRP levels
P3 LR N OBESE MAD 87%-93% of subjects on BGE-102 achieved normal hsCRP levels (<2 mg/L) 60 mg MAD 120 mg MAD Group / Threshold Placebo ≤ 1 mg/L Placebo <2 mg/L BGE-102 60 mg QD ≤ 1 mg/L BGE-102 60 mg QD <2 mg/L BGE-102 120 mg QD ≤ 1 mg/L BGE-102 120 mg QD <2 mg/L 28 Note: median baseline hsCRP 60 mg
Slide 29: 60 mg & 120 mg doses resulted in comparable IL-6 reductions
P3 LR N OBESE MAD 60 mg & 120 mg doses of BGE-102 resulted in comparable IL-6 reductions 60 mg MAD 120 mg MAD Note: median values, error bars show IQR (Q1-Q3); median baseline IL-6 60 mg cohort 2.2 pg/mL for active treatment and 2.8 pg/mL for placebo, 29 120 mg cohort 2.3 pg/mL for active treatment
Slide 30: BGE-102 reduced CSF IL-6 by 84% in subjects with elevated baseline
P3 LR N OBESE MAD In the 2 subjects with elevated baseline CSF IL-6, BGE-102 reduced levels by 84% in the Day 14 CSF CSF IL-6* Plasma IL-6 Plasma IL-6 (pg/mL) CSF IL-6 (pg/mL) 30 Note: * IL-6 levels >7 pg/mL in the CSF are considered elevated; corresponding decrease in the plasma was 62%; measuremen
Slide 31: Comparable reductions in fibrinogen at 60 mg & 120 mg
P3 LR N OBESE MAD 60 mg & 120 mg doses of BGE-102 resulted in comparable reductions in fibrinogen 60 mg MAD 120 mg MAD 31 Note: median values, error bars show IQR (Q1-Q3); median baseline fibrinogen 60 mg cohort 349 mg/dL for active treatment and 379 mg/dL for placebo, 120 mg cohort 331 mg/dL for co
Slide 32: NLRP3
NLRP3 BGE-102 overview Phase 1 results Therapeutic areas 32
Slide 33: BGE-102 has the potential to broadly address inflammation
3 PP3 LLRR N N THERAPEUTIC AREAS BGE-102 has the potential to broadly address inflammation, in the periphery as well as ocular and CNS compartments 33
Slide 34: NLRP3: Cardiometabolic
NLRP3 BGE-102 overview Phase 1 results Therapeutic areas Cardiometabolic Ophthalmology 34
Slide 35: Targeting IL-1β and the upstream inflammatory cascade can drive a significant MACE benefit in ASCVD
P3 LR N CARDIOMETABOLIC Targeting IL-1β and the upstream inflammatory cascade can drive a significant MACE benefit in ASCVD Inflammatory cascade Upstream Inflammatory mechanisms have shown MACE benefits LoDoCo2 0.69 (0.57–0.83) NLRP3 colchicine 0.5 mg CV death, spontaneous MI, ischemic inflammasome
Slide 36: hsCRP is a PD marker, not the target
P3 LR N CARDIOMETABOLIC hsCRP is a PD marker, not the target: Benefit in ASCVD may require targeting inflammation at its source Inflammatory cascade Upstream NLRP3 inhibition Downstream IL-6 blockade NLRP3 IL-1β, IL-18, pyroptosis ↓ inflammasome sensor Plaque inflammation ↓ IL-1β initiating cytokine
Slide 37: NLRP3 inhibition also has potential benefits beyond IL-1β
P3 LR N CARDIOMETABOLIC NLRP3 inhibition also has potential benefits beyond IL-1β, reducing IL-18 & cell death that may contribute to plaque destabilization NLRP3 drives ASCVD beyond IL-1β Baseline IL-18 is a CVD risk factor in the CANTOS trial NLRP3 inflammasome sensor IL-1β IL-18 Pyroptosis initia
Slide 38: NLRP3 inhibition could address other prevalent cardiometabolic diseases
P3 LR N CARDIOMETABOLIC NLRP3 inhibition has the potential to address a range of other prevalent cardiometabolic diseases Insulin resistance MASLD / MASH Kidney disease 38
Slide 39: Phase 2 to assess cardiometabolic benefits and dose-response
P3 LR N CARDIOMETABOLIC Phase 2 to assess cardiometabolic benefits and evaluate dose-response for peripheral inflammation Primary endpoint Placebo N=40 ● % change in hsCRP Key eligibility criteria Additional endpoints ● Age 18+ BGE-102 30 mg QD N=40 ● % normalization of hsCRP ● BMI 32-42 (<2 mg/L) R
Slide 40: NLRP3: Ophthalmology
NLRP3 BGE-102 overview Phase 1 results Therapeutic areas Cardiometabolic Ophthalmology 40
Slide 41: The retinal opportunity for BGE-102
P3 LR N OPHTHALMOLOGY The retinal opportunity for BGE-102 Greater efficacy Oral treatment to lower with new MOA treatment burden Simultaneous treatment Ocular and systemic of bilateral disease biology addressed BGE-102 has shown therapeutic retinal exposure across species, including primates 41
Slide 42: NLRP3 activation is a central feature of retinal diseases DME & GA
P3 LR N OPHTHALMOLOGY NLRP3 activation is a central feature of retinal diseases DME & GA Diabetic retinopathy / Dry age-related macular degeneration diabetic macular edema (DME) (AMD) / geographic atrophy (GA) Hyperglycemia & oxidative stress Accumulation of cellular debris (drusen, lipofuscin) and
Slide 43: Prevalent retinal diseases with significant unmet needs
P3 LR N OPHTHALMOLOGY Prevalent retinal diseases with significant unmet needs DME GA (late-stage AMD) ● Vision loss due to vascular leakage ● Loss of central vision Description ● Leading cause of vision loss in ● 20% become legally blind within adults <65 1 year of diagnosis Prevalence (US) ● 1M ● 1
Slide 44: Key treatment challenges
P3 LR N OPHTHALMOLOGY Key treatment challenges Limited Systemic High Eyes efficacy of disease injection treated approved drivers not burden individually therapies addressed DME ~45% of patients are ~50% discontinue ~70% develop Insulin resistance is a key risk factor for refractory to anti-VEGFs ant
Slide 45: DME: intravitreal anti-IL-6 has validated the anti-inflammatory approach
P3 LR N OPHTHALMOLOGY DME: intravitreal anti-IL-6 has validated the anti-inflammatory approach in multiple trials of retinal diseases driven by inflammation, including DME Anti-IL-6 in DME Incremental NLRP3 biology beyond IL-6 Rapid improvements in ~1 line: Incremental visual acuity & CST: vision wi
Slide 46: DME: oral BGE-102 preserved retinal vascular integrity in a preclinical model
P3 LR N OPHTHALMOLOGY DME: oral delivery of BGE-102 preserved retinal vascular integrity in a preclinical model of diabetic retinopathy Retinal vascular permeability Blood-retinal barrier integrity measured via fluorescein angiography claudin-5 IHC (endothelial tight junctions) Microvascular degener
Slide 47: DME: BGE-102 improved insulin sensitivity in obese mice
P3 LR N OPHTHALMOLOGY DME: BGE-102 improved insulin sensitivity in obese mice, recapitulating mouse genetics & establishing potential to treat the key disease driver BGE-102 Nlrp3 -/- HOMA-IR Insulin (Day 26) tolerance test (6 weeks) WT Nlrp3-/- Note: BGE-102 was dosed PO QD; semaglutide was dosed S
Slide 48: Phase 2 design: evaluating visual acuity with oral BGE-102
P3 LR N OPHTHALMOLOGY Phase 2 design: evaluating visual acuity with oral BGE-102 Primary endpoint Key eligibility criteria Anti-VEGF + oral placebo N=60 ● Change from baseline in ● Age 18+ best-corrected visual acuity DME with center (BCVA) at Week 12 ● R Anti-VEGF + BGE-102 90 mg QD N=60 involvemen
Slide 49: GA: oral BGE-102 analog preserved RPE integrity in an AβO mouse model
P3 LR N OPHTHALMOLOGY GA: oral delivery of BGE-102 analog preserved RPE integrity in an AβO mouse model, consistent with Nlrp3 knockout GA model: subretinal injection of amyloid β oligomers (AβOs) AβOs are a major drusen component in dry AMD/GA and drive RPE degeneration Oral treatment with BAL-1901
Slide 50: GA: BGE-102 analog prevented age-related lipofuscin accumulation
P3 LR N 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 BAL-1901 prevented lipofuscin accumulation Lipofuscin punctae accumulate with age in outbred (HET3) mice with 3 mo of
Slide 51: GA: Inflammasome inhibition in humans: promising early signals
P3 LR N OPHTHALMOLOGY GA: Inflammasome inhibition in humans: promising early signals of potential efficacy Trial shows potential for greater efficacy Decreased incidence of AMD Inflammasome inhibitor intravitreal implant, K8, observed with the SSRI fluoxetine (µM NLRP3 inhibitor) vs. complement inhi
Slide 52: Apelin / APJ
Apelin / APJ 52
Slide 53: Apelin is an exerkine and mimics many benefits of exercise
PJ A Apelin is an exerkine and mimics many benefits of exercise 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 m
Slide 54: Human insights from the BioAge platform: Apelin signaling impacts muscle & metabolism
PJ A Human insights from the BioAge platform: Apelin signaling impacts muscle & metabolism BioAge aging dataset Human proteomic associations Change in probability 2.0 of a good outcome Relative probability 1.8 Longevity 1.6 1.4 1.2 Preservation of grip strength 1.0 0 20 40 60 80 100 Apelin protein l
Slide 55: Apelin genetics reinforce beneficial role in systemic metabolism
PJ A Apelin genetics reinforce beneficial role in systemic metabolism Visceral fat Insulin tolerance test p<0.05 Apelin KO * ↑ adiposity APLN ↑ insulin resistance p<0.01 Apelin transgenic High-fat diet ↓ weight gain on high fat diet ↑APLN ↑ basal metabolic P<0.001 rate No impact on energy intake Con
Slide 56: APJ agonism can restore body weight & body composition when combined with an incretin
PJ A We previously demonstrated that APJ agonism can restore body weight & body composition to that of lean controls when combined with an incretin Body composition Overall weight loss % Lean Mass % Fat Mass Lean Control Obese Control Obese Control Obese Control Lean Lean Control Control Lean Contro
Slide 57: APJ agonism resulted in muscle & metabolic benefits in older subjects on bed rest
PJ A In a clinical trial, APJ agonism resulted in significant muscle & metabolic benefits in older subjects on bed rest Ph1b design Muscle size Fat infiltration Metabolism Thigh Muscle size Muscle Muscle protein circumference (vastus lateralis) degeneration synthetic rate 10 days of bed rest & dosin
Slide 58: APJ agonism shifted the serum proteome consistent with exercise benefits
PJ A In the trial, APJ agonism shifted the serum proteome consistent with recapitulating the benefits of exercise 6 Significantly upregulated by APJ agonism Legend: 4 Endurance exercise positive associations p=1.5E-24 Endurance exercise negative associations -log10(p.val) 2 0 -0.02 0.00 0.02 coef 58
Slide 59: Our goal is to advance APJ agonists for both oral and parenteral delivery
PJ A Our goal is to advance APJ agonists for both oral and parenteral delivery Recent progress on APJ Oral Parenteral ● Composition of matter IP filed on small molecules with ● Exclusive option on APJ agonist nanobodies with potency picomolar potency 10x greater than apelin, the natural ligand ● Sca
Slide 60: Pipeline overview
Pipeline overview Leveraging the BioAge platform to address key unmet needs in metabolic aging Mechanism Target IND- Program of action dosing Indication Discovery Lead op enabling Phase 1 Phase 2 Anticipated milestones Chronic QUELL CV inflammation Results H2:2026 NLRP3 inhibitor BGE-102 (CNS penetr
Slide 61: BioAge
BIOAGE