R&D Day Presentation

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

University of Bonn

University of Chicago Pritzker School of Medicine

Yale School of Medicine

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 biology of human aging

to develop new therapies for cardiometabolic diseases

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

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-1β, 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 IC90 by human ex vivo whole blood stimulation

24h IC90 coverage at 60 mg QD provided 24-hour IL-1β 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,uuCSF

(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

Director, Institute of Structural Biology University of Bonn

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