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BioAge Labs : R&D Day Presentation
BioAge Labs : R&D Day
About this update from Bioage Labs, Inc.
R&D Update May 8, 2026 Welcome & Introductions Management attendees Kristen Fortney, PhD Co-Founder & CEO Paul Rubin, MD CMO & EVP Research Dov Goldstein, MD, MBA CFO Guest presenters Matthias Geyer, PhD Director, Institute of Structural Biology University of Bonn Michael Davidsofi, MD Clinical Professor of Medicine Director, Lipid Clinic University of Chicago Pritzker School of Medicine Briafi Hafler, MD, PhD Associate Professor Ophthalmology & Visual Science Yale School of Medicine David Boyer, MD Senior Partner Retina-Vitreous Associates Medical Group Ifitroductiofi Kristen Fortney, PhD Co-Founder & CEO BGE-102 Structural biology ifisights Phase 1 results Cardiovascular Ophthalmology Paul Rubin, MD CMO & EVP Research Matthias Geyer, PhD University of Bonn Paul Rubin, MD CMO & EVP Research Michael Davidson, MD University of Chicago Brian Hafler, MD, PhD Yale University David Boyer, MD Retina-Vitreous Associates Closifig remarks Kristen Fortney, PhD Co-Founder & CEO Q&A Management Team Michael Davidson, MD Brian Hafler, MD, PhD Introduction Kristen Fortney, PhD Co-Founder & CEO We are harnessing the biolo gy of human aging to develop new therapies for cardiometabolic diseases The BioAge discovery platform: from humafi data to therapeutics for metabolic agifig 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 braifi-pefietrafit NLRP3 ifihibitor Potential "pipeline in a pill" 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 87-93% of subjects 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: CV risk POC H2:2026, DME POC mid-2027 APJ agofiism: 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 Chronic NLRP3 activity drives disease & predicts poor human longevity NLRP3 overview NLRP3 ifi humafi lofigevity & disease Relative mortality risk (HR) Normal NLRP3 function: innate immune response to danger signals Excess nutrients Cellular stress Reduced NLRP3 activity is associated with longevity In pathology: cellular stress & nutrient excess stimulates chronic activation Resulting chronic inflammation drives a range of diseases NLRP3 activation Cytokine release (IL-1 β , IL-18) IL-6 Chronic inflammation Strofig humafi gefietic evidefice for NLRP3 ifi 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 Our lead program, BGE-102, is well positioned to address diseases driven by inflammation in both the CNS and the periphery Key attributes Potefitial best-ifi-class poteficy based on Phase 1 trial results 1.8 fiM IC 90 by human ex vivo whole blood stimulation 24h IC 90 coverage at 60 mg QD provided 24-hour IL-1 β suppression ≥90% 86% hsCRP reductiofi; 87-93% of subjects achieved fiormalized hsCRP (<2 mg/L)* in line with injectable anti-IL-6 drugs CNS pefietrafit ~0.7 Kp,uu CSF (120 mg MAD, day 14) Attractive safety & tolerability All AEs to date mild / moderate, self-limited, with no dose dependency 50-97x safety margifi for 60 mg dose** based on 3-month GLP tox Strofig IP positiofi 2045 composition of matter & claims for novel NLRP3 binding site Note: * in MAD cohorts - obese subjects with baseline hsCRP > 3 mg/L; ** based on Phase 1 healthy volunteer MAD at Day 14 BioAge NLRP3 inhibitors: unique, patented binding site & novel mechanism Ufiique bifidifig site Our ifihibitors bifid both the active & ifiactive ififlammasome, ufilike other NLRP3 ifihibitors BioAge compounds MCC950 Inactive decamer Active inflammasome Collaboration with Matthias Geyer, PhD, Director, Institute of Structural Biology University of Bonn NLRP3 Structural biology insights Phase 1 results Cardiovascular Ophthalmology Matthias Geyer, PhD Director, Institute of Structural Biology University of Bonn A fiew way to ifihibit NLRP3 BGE-102 targets a different site on NLRP3 than other inhibitors in development BGE-102 targets a different site on NLRP3 than other inhibitors in development BGE-102 targets a different site on NLRP3 than other inhibitors in development BGE-102 targets a different site on NLRP3 than other inhibitors in development BGE-102 inhibits both forms of NLRP3 -the resting state and the active inflammasome BGE-102 inhibits both forms of NLRP3 -the resting state and the active inflammasome BGE-102 is selective for NLRP3 There are 22 human NOD-like receptors Attention : This is an excerpt of the original content. 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