Virtual R&D Day |

Guillain-Barr Syndrome: A Focus on its Serious Unmet Need and

Annexon's Novel Therapeutic Approach Douglas Love, President & CEO Annexon Biosciences 2

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preclinical programs, timing and commencement of future nonclinical studies and clinical trials and research and development programs, timing of clinical results, strategic plans for our business and product candidates, including additional

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our history of net operating losses; our ability to obtain necessary capital to fund our clinical programs; the early stages of clinical development of our product candidates; the effects of COVID-19 or other public health crises on our clinical

programs and business operations; our ability to obtain regulatory approval of and successfully commercialize our product candidates; any undesirable side effects or other properties of our product candidates; our reliance on third-party suppliers

and manufacturers; the outcomes of any future collaboration agreements; and our ability to adequately maintain intellectual property rights for our product candidates. These and other risks are described in greater detail under the section titled

"Risk Factors" contained in our Quarterly Report on Form 10-Q filed with the Securities Exchange Commission (SEC) on November 13, 2023 and our other filings with the SEC from time to time. All forward-looking statements in this

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Agenda TOPIC PRESENTER TIME (ET) Douglas Love Annexon: Overview and

Commitment to GBS 10:00-10:05am President & CEO Lisa Butler GBS Patient Voice 10:05-10:15am Executive Director, GBS | CIDP Foundation Intl. Hugh J. Willison, MBBS, PhD GBS Disease Overview and Treatment Landscape 10:15-10:35am Professor Emeritus

of Neurology, University of Glasgow, Scotland David Cornblath, MD 10:35-10:50am Annexon GBS Clinical Program Overview Professor Emeritus of Neurology, Johns Hopkins University School of Medicine Michael Overdorf 10:50-11:00am GBS Market Opportunity

and Annexon's Commercial Approach CBO Douglas Love 11:00-11:05am Closing Remarks President & CEO Q&A Session 11:05-11:30am 4

ANNEXON: Late-stage Clinical Platform for Classical Complement- mediated

Neuroinflammatory Diseases of the Body, Brain and Eye Large market opportunities supported by clinical proof-of-concept First-in-kind approach, data in multiple indications wholly owned pipeline Near-term registrational 2Q 2024 - Pivotal data

in disease of high unmet medical need and no FDA-approved therapy data in GBS Mid to 2H 2024 - Initiation of two pivotal Phase 3 trials in GA (Global ARCHER II Diverse GA registrational sham trial | ARROW head-to-head trial vs. SYFOVRE )

and program & oral POC program 2H 2024 - ANX1502 oral candidate proof of concept in autoimmune disease Runway through multiple mid- and late-stage clinical catalysts Well-capitalized into mid 2026 5 GBS: Guillain-Barr Syndrome; GA:

Only Complement-Pipeline for Diseases of the Body, Brain & Eye

Potential to treat >8 MILLION patients worldwide Preclinical Phase 1 Phase 2 Phase 3 Next Milestone Worldwide Rights FLAGSHIP PROGRAMS Phase 3 data ANX005 Autoimmune Guillain-Barr Syndrome (GBS) 2Q 2024 Phase 3 Ophthalmology ANX007

Geographic Atrophy (GA) initiation Mid 2H 2024 POC data Autoimmune ANX1502 Autoimmune Indications 2H 2024 NEXT WAVE PROGRAMS Huntington's Disease Neurodegenerative ANX005 Amyotrophic Lateral Sclerosis (ALS) Autoimmune ANX009 Lupus Nephritis

POC: Proof-of-Concept 6 Annexon GBS Phase 1b data presented at American Academy of Neurology 2020 and Peripheral Nerve Society Annual Meetings 2021-2022.

Annexon Has a Deep-Rooted History and Commitment to GBS Aligned With Our

Mission Strong Scientific Rationale High Unmet Need to treat diseases driven by classical ANX005 is designed for rapid Well-characterized, underserved complement activation inhibition with a single dose disease afflicting thousands globally ANNEXON

HAS KEY CLINICAL EXPERTISE AND RELATIONSHIPS IN GBS Conducted 3 clinical trials including: Large ongoing Phase 3 Supported 2,000 patient registry 1st placebo-controlled trial in ~40 yrs placebo-controlled trial at IGOS to inform clinical

program Monotherapy and combination trials 7

ANX005: Potential to be First FDA-approved Therapy for GBS Pursuing a

monotherapy label in GBS Demonstrated POC across several clinically-meaningful measures Granted US FDA Fast Track & Orphan Drug Designations Granted EMA Orphan Drug Designation based on potential for benefit over available therapies Phase 3 data

on track for 2Q 2024; Real World Evidence comparability data 1H 2025 in support of BLA submission 8

GBS Patient Voice Lisa Butler Executive Director of the GBS|CIDP

In The Voice of GBS Patients "I was terrified, there was so much

chaos around me as I "Went to ER, turned away for fatigue, dehydration was put in the ICU and told my body was paralyzed by and stress. The next day could not stand, legs this disease I had never heard of and that I would likely buckled, back

to ER, unable to move my entire require a respirator to help me breathe." body, put on respirator that same day." "I have learned that I was put in a medically induced coma." "They told me they would give me something

called IVIG to help stop this, but I had no idea what they were talking about." "They said I would recover to a "new normal", what was that?" "I did PT, OT and speech. I eventually stood up "At one point, I

could only communicate by blinking my eyes. with assistance after 8 weeks, I took my first I had so many questions that I couldn't ask. independent steps at 16 weeks." 12

The Foundation 1980 2024 1980: First Meeting 30,000

patients in database 8 people 20 members of Global Medical Advisory Board 1 Doctor, 2 residents 57 Global Centers of Excellence 0 employees, 2 volunteers in Pennsylvania 200 volunteers in 47 countries

18 FTE, 13 Members of Board of Directors From day one we have never lost our focus on the patient! We exist so that no one takes this journey alone! 13

SUPPORT AND EDUCATION Support: Approximately 100 patient

inquiries monthly Chapter support group meetings 357 registered community members Coffee Chats 681 registered community members Speaker Series 2,218 registered community members Education: 17

symposiums and 7,000+ attendees Website 108,000+ visitors on GBS page in 2023 676K+ views on overall website in 2023 Global Medical Advisors One-on-One Consultation 14

Global Medical Advisory Board GMAB Members: Doctor-to-Doctor

Consultations: Centers of Excellence: United States: 12 2023 United States: 38 COEs Barcelona: 1 2 CIDP consultations International: 22 COEs Denmark: 1 1 IVIG Dosage consultation United Kingdom: 1

Brussels: 1 Netherlands: 1 Australia: 1 Japan: 1 Netherlands: 2 Germany: 1 15

Research $8M total, $50k-$300k Elevation Grant,

Discover Grant, 3-year Benson Fellowship Consortium based Funding support for IGOS coordinating center's research NIH State of Science meeting: 2020 virtual meeting between NINDS and NIAID on state of GBS research

Advocacy Dept of Defense Peer-Reviewed Medical Research Program

(PRMRP): $6 million between 6 researchers since 2017 Congressional Champion: John Garamendi 2019: GBS patient listening session with FDA to increase awareness of the unmet need in GBS despite the current SoC 2024: Hosting FDA

Patient-Focused Drug Development Meeting (PFDD) on GBS to address the continuing unmet need of patients with GBS for novel therapies to Get Better Sooner 17

Getting better slowly Getting better sooner 18

GBS Disease Overview and Treatment Landscape Hugh J. Willison, MBBS,

PhD Professor Emeritus of Neurology, University of Glasgow, Scotland 19

GBS: Neuro-Emergency Needing Urgent and Effective Intervention Most

common cause of acute paralytic inflammatory disease of the peripheral nervous system, known for its severity and rapid progression Frequently follows an infection that generates complement activating auto- antibodies that attack peripheral nerve

tissue leading to nerve conduction failure and nerve fiber death Global annual incidence ~150,000, lifetime likelihood of 1 in 1,000 PERIPHERAL NERVE DAMAGE LEADS TO: Severe weakness Respiratory failure requiring mechanical

ventilation in 25% Mortality rates of 3-17% Irreversible nerve damage preventing patients from resuming a normal life Currently no treatment specifically and immediately targets complement mediated nerve damage IVIg has an

ill-defined mechanism of action and requires Weaned from mechanical ventilation 5-day course to complete therapy 1) van Doorn, 2013; Willison et al., 2016 2(van den Berg et al., 2014) 3 Walgaard et al (2021) Lancet Neurology 20(4):275, 4AAN

Guidelines "Immunotherapy for GBS", 4Hund EF et al (1993) Crit Care Med 20 21:433, 454Fletcher D, et al. (2000) Neurology 27;54(12), 46, 5Van den Berg B, et al (2014) Nat Rev Neurol Aug;10(8), 6Stephan et al (2012) Neuroscience 35:369,

7Lansita et al (2017) Int. J. Toxicol. 36:449

GBS is a Neurological Emergency Requiring Urgent Intervention There is

a limited time window in the acute illness phase to achieve a therapeutic effect PROGRESSION PLATEAU RECOVERY PROGRESSIVE PARALYTIC PHASE: rapidly progressive bilateral muscle weakness peaking by 1 week in most cases (ideal Antibody and NfL Levels

treatment window) and lasting up to 4 weeks maximum Complement Activation Nadir determines risk for mechanical ventilation or death and prognosis Preceding infection PLATEAU PHASE: lasts weeks to months post-treatment Complete/ partial

recovery of muscle window, with duration linked to severity at presentation strength Includes extended periods of ventilation in ICU, and intensive supportive care in the ward Nadir MRC RECOVERY PHASE: gradual muscle strength and functional

Peak disease improvement occurring over weeks to years as nerve regeneration takes place ~20% unable to walk or dead at 1 year Additional ~20% continue to experience symptoms Course of GBS Infection Antiganglioside antibodies Adapted

from van den Berg, et al. (2014) Nat Rev Neurol 10, 469-482 21

Auto-Antibodies Fix Complement to Peripheral Nerve Myelin & Axons

COMPLEMENT - ACUTE NERVE DAMAGE BIOMARKER ELEVATED MEDIATED NERVE DAMAGE IN ALL GBS NEUROTYPES AIDP AMAN AMSAN Equivocal HC N=58 N=12 N=7 N=14 N=53 Auto-antibody-mediated nerve damage affects both myelin The gold standard

biomarker of axonal damage, and axon, as known antigens are present on both neurofilament light (NfL) is elevated in all types of GBS Autoantibodies fix complement to both myelin and axon NfL levels correlate with disease course,

severity and prognosis, irrespective of GBS neurotype All GBS neurotypes are present worldwide, but the proportion is variable: e.g. AIDP is more common in EU (54%) than in Bangladesh (40%) Mart n-Aguilar et al, J Neurol Neurosurg Psych

(2020) Doets, et al (2018). Brain, 141(10), 2866-2877 22 Log Nfl (pg/ml)

Complement is Pivotal Force in Driving Nerve Damage in GBS C1q binds to

IgG and IgM antibodies on nerve and activates the classical complement pathway leading to neuroinflammation, directs clearance of debris by macrophages (C3b) and inflicts direct membrane damage (C5b-9) causing sudden and prolonged loss of muscle

strength CLASSICAL COMPLEMENT PATHWAY DIRECTS IMMUNE NERVE FROM HUMAN AUTOPSIES CELLS TO SITE OF INFLAMMATION Activated complement Macrophage Activated complement Node of Ranvier Node of Ranvier myelin sheath Macrophage C1q C4b C3b C5b-9 IgG IgM IgM

Neuromuscular Axon and Myelin Nerve conduction impaired junction break down Hafer-Macko C et al., (1996) Ann Neurol 39 & 40 23

ANX005 is a Targeted Immunotherapy Against Complement- Mediated Nerve

Fiber Damage Immediate C1q inhibition with a single dose of ANX005 is designed to block all downstream complement components involved in acute or ongoing inflammation and nerve damage and allow nerve fiber recovery to start 24

Prognostic Factors of Functional Recovery Used in clinical prognostic

tools, critical in clinical trial design, essential to show comparability between populations Baseline factors have been identified from multiple, large, prospective and retrospective studies including IGOS that are highly prognostic for functional

outcome and need for mechanical ventilation 1 MRC sum score (muscle strength ranging from 0-60) 2 GBS-DS (function: ranging from 0-6) 3 Age 4 Time of onset of weakness 5 Preceding diarrhea 6 Serum neurofilament light (NfL) 7 Electrophysiology: ulnar

distal compound muscle action potential (CMAP) 25 Walgaard 2011; Papri 2022, Islam 2019; Hughes et al., 1978; van Koningsveld et al., 2007; Papri 2021; Walgaard 2010; Doets 2022; Mart n-Aguilar et al., 2021; van Tilburg et al., 2022; Cornblath

Characteristics of an Effective Therapy to Combat GBS - Get

Better Sooner Directly targets mechanism driving extensive nerve damage and paralysis 1 Treatment goal is to target complement-mediated acute nerve damage and inflammation to prevent paralysis, severe morbidity, disability and mortality Rapid onset

of action 2 Block acute and ongoing destruction of nerves immediately Provides clinical benefit across entire disease spectrum 3 Effective in all GBS patients, and impacting all aspects of the disease that are important to patients Minimal

side-effects 4 Single infusion with manageable infusion related reactions 26

ANX005 GBS Phase 1b POC Study Randomized, double-blind trial,

placebo-controlled Phase 1 trial; completed 2020 STUDY DESIGN KEY OBJECTIVES Safety / Tolerability / PK KEY RESULTS N=50 Adults with GBS in Bangladesh C1q target engagement SAD: ANX005 3 mg/kg to 100mg/kg No

deaths MAD: 2 x 75mg/kg No treatment-related SAEs Mean time from onset of weakness to treatment: 8.1 days Full C1q inhibition >1 week 18mg/kg 1 Mean GBS-DS at baseline: 4 and above Target

engagement in blood & CSF STUDY SCHEMATIC MTD not established Placebo (N=12) 1 Early Reduction in Nerve Damage ANX005 (N=38) 1 Early Improvement in MRC Day 1 Week 8 1 Consistent shift to better on GBS-DS 1

18-75mg/kg dose cohorts 27

C1q function (% hemolytic activity) ANX005 Phase 1b: Rapid and Complete

Complement Inhibition ANX005 DEMONSTRATED RAPID COMPLEMENT INHIBITION AT DAY 1 Serum PK/PD after Single 75 mg/kg Dose C1q activity not detectable when ANX005 was present in the circulation (Data from 75 mg/kg patient) Single dose of ANX005