# EDGAR Filing Document

**Accession Number:** 0001528115
**File Stem:** 0001193125-23-004050
**Filing Date:** 2023-1
**Character Count:** 72064
**Document Hash:** 40e93f340af584109df1094b23ba41d9
**Contains OCR:** False
**Source Format:** 

## Filing Content

## Filing Summary
**0001193125-23-004050.hdr.sgml**: 20230109

**ACCESSION NUMBER**: 0001193125-23-004050

**CONFORMED SUBMISSION TYPE**: 8-K

**PUBLIC DOCUMENT COUNT**: 83

**CONFORMED PERIOD OF REPORT**: 20230108

**ITEM INFORMATION**: Regulation FD Disclosure

**ITEM INFORMATION**: Other Events

**ITEM INFORMATION**: Financial Statements and Exhibits

**FILED AS OF DATE**: 20230109

**DATE AS OF CHANGE**: 20230109

**FILER**: 

**COMPANY DATA:**
- **COMPANY CONFORMED NAME:** Annexon, Inc.
- **CENTRAL INDEX KEY:** 0001528115
- **STANDARD INDUSTRIAL CLASSIFICATION:** PHARMACEUTICAL PREPARATIONS [2834]
- **IRS NUMBER:** 275414423
- **STATE OF INCORPORATION:** DE
- **FISCAL YEAR END:** 1231

**FILING VALUES:**
- **FORM TYPE:** 8-K
- **SEC ACT:** 1934 Act
- **SEC FILE NUMBER:** 001-39402
- **FILM NUMBER:** 23516416

**BUSINESS ADDRESS:**
- **STREET 1:** 1400 SIERRA POINT PARKWAY
- **STREET 2:** BLDG C, SUITE 200
- **CITY:** BRISBANE
- **STATE:** CA
- **ZIP:** 94005
- **BUSINESS PHONE:** (650)-822-5500

**MAIL ADDRESS:**
- **STREET 1:** 1400 SIERRA POINT PARKWAY
- **STREET 2:** BLDG C, SUITE 200
- **CITY:** BRISBANE
- **STATE:** CA
- **ZIP:** 94005

?xml version="1.0" encoding="utf-8" ? 8-K

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### UNITED STATES

### SECURITIES AND EXCHANGE COMMISSION

#### Washington, D.C. 20549

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### FORM 8-K

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#### CURRENT REPORT

#### Pursuant to Section 13 OR 15(d)

#### of the Securities Exchange Act of 1934

#### Date of Report (Date of earliest event reported): January 8, 2023

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## ANNEXON, INC.

#### (Exact name of registrant as specified in its charter)

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| | | |
|:---|:---|:---|
| **Delaware** | **001-39402** | **27-5414423** |
| **(State or other jurisdiction** | **(Commission** | **(IRS Employer** |
| **of incorporation)** | **File Number)** | **Identification No.)** |

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#### 1400 Sierra Point Parkway, Bldg C, Suite 200

#### Brisbane, California 94005

#### (Address of principal executive offices) (Zip Code)

#### Registrant's telephone number, including area code: (650) 822-5500

#### Not Applicable

#### (Former name or former address, if changed since last report)

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Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

☐ Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

☐ Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

☐ Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

☐ Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:

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| | | |
|:---|:---|:---|
| **Title of each class** | **Trading<br>Symbol(s)** | **Name of each exchange**<br> **on which registered** |
| Common Stock, par value $0.001 per share | ANNX | The Nasdaq Stock Market |

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Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§ 230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§ 240.12b-2 of this chapter).

Emerging growth company ☐

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ☐

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| | |
|:---|:---|
| **Item 7.01** | **Regulation FD Disclosure.**  |

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Attached as Exhibit 99.1 is an investor presentation that Annexon, Inc. (the "Company") plans to present during the 41st Annual J.P. Morgan Healthcare Conference commencing on January 9, 2023.

The information in this Item 7.01 of this Current Report on Form 8-K and Exhibit 99.1 attached hereto shall not be deemed to be "filed" for purposes of Section 18 of the Securities Exchange Act of 1934, as amended, or otherwise subject to the liabilities of that Section 11 and 12(a)(2) of the Securities Act of 1933, as amended. The information contained herein and in the accompanying exhibit shall not be incorporated by reference into any filing with the Securities and Exchange Commission made by the Company, whether made before or after the date hereof, regardless of any general incorporation language in such filing.

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| | |
|:---|:---|
| **Item 8.01** | **Other Events.**  |

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On January 8, 2023, the Company provided a corporate update. A copy of the press release, titled "Annexon Highlights Strategic Focus to Advance Four Flagship Complement Programs through Late-Stage Development and Progress Across Three Therapeutic Franchises," is filed as Exhibit 99.2 hereto and is incorporated by reference herein.

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| | |
|:---|:---|
| **Item 9.01** | **Financial Statements and Exhibits.**  |

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(d) Exhibits.

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| | |
|:---|:---|
| **Exhibit No.** | **Description** |
| 99.1 | [Company Presentation, dated January 2023.](d422908dex991.htm) |
| 99.2 | [Press Release, dated January 8, 2023, titled "Annexon Highlights Strategic Focus to Advance Four Flagship Complement Programs through Late-Stage Development and Progress Across Three Therapeutic Franchises."](d422908dex992.htm) |
| 104.1 | Cover Page Interactive Data File, formatted in inline XBRL. |

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#### SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the Registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

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| | | |
|:---|:---|:---|
| Dated: January 9, 2023 |  | **Annexon, Inc.** |
|  | By: | /s/ Jennifer Lew |
|  |  | Jennifer Lew |
|  |  | Executive Vice President and Chief Financial Officer |

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## Exhibit 99.1

![](g422908ex99_1p1g1.jpg)

Exhibit 99.1 GAME-CHANGING MEDICINES FOR COMPLEMENT- MEDIATED DISEASES JANUARY 2023 Nasdaq: ANNX 1

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![](g422908ex99_1p2g1.jpg)

Forward-Looking Statements This presentation contains "forward-looking" statements about Annexon, Inc. the outcomes of any future collaboration agreements; and our ability to and our industry that involve substantial risks and uncertainties. All adequately maintain intellectual property rights for our product candidates. statements other than statements of historical facts, including statements These and other risks are described in greater detail under the section titled regarding our clinical and preclinical programs, timing and commencement of "Risk Factors" contained in our Quarterly Report on Form 10-Q filed with the future nonclinical studies and clinical trials and research and development Securities Exchange Commission (SEC) on November 3, 2022 and our other programs, timing of clinical results, strategic plans for our business and filings with the SEC from time to time. All forward-looking statements in this product candidates, including additional indications which we may pursue, our presentation speak only as of the date of this presentation. Except as required financial position, runway and anticipated milestones, are forward-looking by law, we undertake no obligation to publicly update any forward-looking statements. In some cases, you can identify forward-looking statements by statements, whether as a result of new information, future events or terminology such as "aim," "anticipate," "assume," "believe," "contemplate," otherwise. "continue," "could," "design," "due," "estimate," "expect," "focus," "goal," This presentation concerns drug candidates that are under clinical "intend," "may," "objective," "plan," "positioned," "potential," "predict," "seek," investigation, and which have not yet been approved for marketing by the U.S. "should," "target," "will," "would" and other similar expressions that are Food and Drug Administration (FDA). These are currently limited by federal predictions of or indicate future events and future trends, or the negative of law to investigational use, and no representation is made as to their safety or these terms or other comparable terminology. effectiveness for the purposes for which they are being investigated. Forward-looking statements are not guarantees of future performance and are This presentation also contains estimates and other statistical data made by subject to risks and uncertainties that could cause actual results and events independent parties and by us relating to market size and growth and other to differ materially from those anticipated, including, but not limited to, risks data about our industry. This data involves a number of assumptions and and uncertainties related to: our history of net operating losses; our ability to limitations, and you are cautioned not to give undue weight to such estimates obtain necessary capital to fund our clinical programs; the early stages of or statistical data. Neither we nor any other person makes any representation clinical development of our product candidates; the effects of COVID-19 or as to the accuracy or completeness of such data or undertakes any obligation other public health crises on our clinical programs and business operations; to update such data after the date of this presentation. 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; 2

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![](g422908ex99_1p3g1.jpg)

A bold mission to free the body, brain and eye from complement- mediated disease 3

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![](g422908ex99_1p4g1.jpg)

Annexon Overview: Pursuing Our Mission & Significant Value Pioneering Classical Complement Platform in Autoimmunity, Neurodegeneration & Ophthalmology ▪ Complement clinically / commercially validated with downstream approaches (C1s, C3, C5) ▪ ANNX building on prior learnings to block both up & downstream complement where it starts - Pursuing indications where (i) C1q localizes on disease tissue to anchor complement activation & (ii) complement activity drives disease progression ▪ Multi-faceted 'beach-head' portfolio with 'informed signal finding' and 'confirming' trials ▪ Clinical POC with lead drug candidate (ANX005) in multiple indications: GBS, HD, CAD, ALS Significant 'Enterprise Value' Potential with multiple drivers over the next 3 years ▪ Targeting both Orphan and large patient population diseases with 4 Flagship Programs -- ~$10B market opportunity ▪ Multiple value driving clinical readouts over 2023 & 2024, including GA & GBS confirming trials ▪ Potential 1st-in-class GBS commercialization & initiation of 1st-in-class anti-complement HD pivotal trial ▪ Potential 1st-in-class oral compound for Autoimmune diseases Well-Capitalized with Additional Opportunities ▪ Runway into 2025 ▪ Robust IP estate ▪ Wholly-owned with specific therapeutic-area partnering opportunities 4

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![](g422908ex99_1p5g1.jpg)

Meaningful Progress Across Our Portfolio of Complement- targeted Therapies in 2022 Positive clinical outcomes with ANX005 in patients with HD, CAD & ALS Favorable safety profile with ANX005 across >200 people treated Enrollment completed early for Phase 2 trial of ANX007 for GA First-in-kind oral small molecule shows target drug levels achieved $130M capital raise to expand and extend runway into 2025 5

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![](g422908ex99_1p6g1.jpg)

Revolutionizing Complement Biology in Pursuit of Our Mission Targeting C1q & classical complement cascade to treat autoimmune and neurodegenerative disease 2007 2014 - 2022 1960-70s Understanding C1q's role in Discovery of C1q's role in Annexon launched & advanced into autoimmune disease brain & eye neurodegeneration mid- and late-stage trials by ANNX founder, Dr. Ben Barres targeting C1q-mediated diseases of the body, brain & eye C1q initiates a powerful inflammatory C1q C1q anchors damaging cascade that can lead to r/s complement activation 1 tissue damage✓ Validated role of C1q in autoimmune & on photoreceptor 2 neurodegenerative disease synapses in GA ✓ Full target engagement with multiple drug Immune cell Immune cell recruitment candidates attack ✓ Clinical POC in multiple diseases ✓ Well-capitalized with runway into 2025 ✓ Talented 'Warrior Spirit' team Membrane damage 3 C1q Drives Removal of Functioning Synapses 1 2 3 McGonigal et al. Acta Neuropathologica Communications (2016) 4:23 ; C1q bound to photoreceptor synapses in aged mice: Annexon data on file; Stevens, et al., 2007, Cell 6

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![](g422908ex99_1p7g1.jpg)

CSF C1q (µg/mL) Mean ± SD Robust Clinical Target Engagement of C1q Demonstrated in the Body, Brain & Eye Full C1q Inhibition in Full C1q Inhibition in Full C1q Inhibition in Serum with ANX005 CSF with ANX005 Aqueous Humor with ANX007 10 CSF Levels ANX005 0.03 1 0.1 0.1 0.002 CSF C1q 0.01 0 6 12 18 24 30 36 Week 7 CSF ANX005 (µg/mL) Mean ± SD

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![](g422908ex99_1p8g1.jpg)

Clinical Proof-of-Concept Demonstrated in Both Autoimmune and Neurodegenerative Indications Guillain-Barré Syndrome (GBS) Huntington's Disease (HD) ANX005 ANX005 28% patients 75% patients ≥3 pt improvement improved Composite Unified Huntington's Disease Rating Scale Amyotrophic Lateral Sclerosis (ALS) Cold Agglutinin Disease (CAD) ANX005 All patients improved or maintained Hemoglobin Levels ANX005 progression rate during treatment Patients showed Both patients that stayed on drug > 2-point improvement continued to improve All patients who went off treatment declined 8

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![](g422908ex99_1p9g1.jpg)

Achieving Our Mission With FOUR FLAGSHIP PROGRAMS Stopping Harmful Inflammation and Tissue Damage in the Body, Brain & Eye Guillain-Barré Huntington's Geographic Orally Administered Syndrome (GBS) Disease (HD) Atrophy (GA) Small Molecule AUTOIMMUNE NEURODEGENERATION OPHTHALMOLOGY AUTOIMMUNE Well-validated MOA Pioneering MOA Well-validated MOA Well-validated MOA Fast path to market in No disease-modifying Localized inhibition in eye Ease and convenience of rare disease treatments available oral dosing st st st st 1 complement inhibition 1 up & downstream 1 oral compound targeting 1 placebo-controlled trial in a brain disorder complement approach classical complement in ~40 years 9

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![](g422908ex99_1p10g1.jpg)

Flagship Programs Advancing in Mid-stage and Pivotal Trials 2023 ANTICIPATED INDICATION CANDIDATE PRECLINICAL PHASE 1 PHASE 2 PHASE 3 MILESTONE Complete Phase 3 Guillain-Barré Syndrome ANX005 enrollment in 2H 2023 Initiate Phase 2/3 trial Huntington's Disease ANX005 2023 Report Phase 2 data Geographic Atrophy ANX007 mid-2023 Complete MAD trial Autoimmune Indications ANX1502 and initiate POC trial in patients 10

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![](g422908ex99_1p11g1.jpg)

ANX005 Summary 11

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![](g422908ex99_1p12g1.jpg)

ANX005 Powerfully Inhibits C1q and Entire Classical Complement Pathway in the Body and Brain Key Attributes ✓ Diverse: Utilized in autoimmune & neurodegenerative trials ✓ Potency: High binding affinity to C1q (<10 pM) ✓ Target Engagement: Full C1q inhibition in blood and CSF ANX005 ✓ Safety: Generally well-tolerated in acute and chronic trials ✓ No drug-related deaths & no serious infections observed IV administered monoclonal antibody ✓ No autoimmune events observed post enhanced ANA screening / monitoring ✓ Clinical: Rapid clinical benefit demonstrated in GBS, HD, CAD & ALS Administered to >200 patients to date 12

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![](g422908ex99_1p13g1.jpg)

ANX005 Generally Well-Tolerated in Several Patient Populations KEY TAKEAWAYS Leveraged learnings to No drug related 6 completed and optimize safety profile deaths & no serious 2 ongoing acute and infections observed chronic autoimmune ▪ Low grade, transient IRRs throughout all studies & neurodegenerative during first infusion: trials managed by infusion rate and pre-medication ▪ >100 patients from completed trials ▪ Single serious event of autoimmunity (SLE/ lupus- ▪ >110 patients in like syndrome): no further ongoing trials events of autoimmunity ▪ Exposure up to 1 year observed post enhanced ANA screening / safety monitoring to date 13

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![](g422908ex99_1p14g1.jpg)

ANX005 Generally Well-Tolerated Across Clinical Trials Safety Population Study Deaths and Serious Adverse Events (N=116\*) Treatment Emergent Adverse All CTCAE CTCAE • No deaths and no serious infections observed Events (TEAE) Grade ≥3 Grades • 3 observed serious adverse events related to ANX005 N (%) N (%) ▪ 1 IRR in NHV prior to dosing optimization Any reported TEAEs, N (%) 116 (100.0) 38 (32.8) Most Common TEAE, N (%)▪ 2 in HD P2a trial (lupus like syndrome and idiopathic pneumonitis) prior to implementation of ANA screening and safety monitoring Infusion Related Reaction (IRR) 38 (32.8) 3 (2.6) plan Most Common TEAEs (non-IRR), N (%) Headache 37 (31.9) 0 (0) Adverse Events of Note Pain in extremity 24 (20.7) 0 (0) • Infusion Related Reactions (IRR) primarily first dose effect Rash\*\* 26 (22.4) 7 (6.0) across indications (~95%) and almost always associated with Pyrexia 18 (15.6) 0 (0) transient rash Lab abnormality - CPK 15 (12.9) 7 (6.0) ▪ Adverse events coded as rash were primarily IRR Constipation 13 (11.2) 0 (0) ▪ No IRR observed after 2nd dose of ANX005 Pruritus 13 (11.2) 0 (0) • Elevated creatine phosphokinase (CPK) seen in placebo and Serious TEAEs, N (%) 14 (12.1) 14 (12.1) ANX005 treated GBS patients – consistent with GBS Related to ANX005 3 (2.6) 3 (2.6) Infections 0 (0) 0 (0) \* All completed and open label studies with ANX005 as per 01/05/2023; Includes: FIH, GBS P1b, GBS DDI, HD P2a, ALS P2a, CAD P2, wAIHA P2 trials \*\* Primarily initial dose IRRs, but coded as rash 14

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![](g422908ex99_1p15g1.jpg)

Flagship Programs • Guillain-Barré Syndrome (GBS) • Huntington's Disease (HD) • Geographic Atrophy (GA) • Oral small molecule 15 15

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![](g422908ex99_1p16g1.jpg)

First-In-Class Treatment for GBS Acute, antibody-mediated autoimmune disease driven by aberrant C1q activation GBS Overview Role of C1q ANX005 Rapid onset of ✓ Fast Track & Orphan Drug C1q binds autoantibodies on nerve neuromuscular weakness Designations components, anchoring complement and paralysis activation, inflammation & tissue damage ✓ Pursuing monotherapy label 12,000 patients ANX005 blocks all inflammatory / diagnosed/year in North damaging components of classical pathway ✓ Phase 3 pivotal trial ongoing America & Europe for rapid recovery ✓ Productive engagement with FDA No FDA-approved therapies C1q targeting the on the statistical analysis plan for neuromuscular the ongoing pivotal trial junction C1q 16 16

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![](g422908ex99_1p17g1.jpg)

ANX005 Demonstrated Clinical POC in GBS Placebo-Controlled Trial Early improvement in muscle strength and reduction in neuronal damage preceding gain of function Impact on Muscle Strength Impact on Key Neuronal Biomarker Impact on Clinical Function Statistically significant early NfL Patients achieving ≥3 point Rapid increase in muscle strength within first week of treatment reduction (weeks 2-4) improvement in 8 weeks 90 Change in MRC ANX005 30 30 28% patients with 25 ANX005 ≥ 3 point gain 20 0 20 15 Placebo -30 10 10 Placebo 0% -60 5 P<0.05 0 0 -90 ANX005 Placebo 0 2 4 6 8 ANX005 Placebo Weeks (18-75 mg/kg) Guillain-Barré Mean Change in MRC Score from Baseline 6-Point Disability Scale All graphs: ANX005 n=18, Placebo, n=8 17 MRC (Change from Baseline) % Change in NfL % Patients

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![](g422908ex99_1p18g1.jpg)

ANX005 GBS Phase 3 Pivotal Trial Underway On track to complete expanded enrollment in 2H23 with Phase 3 data in 1H24 Trial Design Specifications • Randomized, double-blind trial (N~220) • Recently diagnosed severe patients (3 or higher on GBS-DS) Placebo (n=~75) • Primary endpoint: GBS Disability Scale at week 8 ANX005 30 mg/kg (n=~75) • Patients stratified for baseline muscle strength and time from symptom onset ANX005 75 mg/kg (n=~75) • Productive engagement with FDA on the statistical analysis plan for the ongoing pivotal trial Day 1: 6-month Off-treatment Follow-up • Increased study population by ~40 patients Single Dose 18

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![](g422908ex99_1p19g1.jpg)

First-In-Class Treatment for HD Progressive neurodegenerative disease involving excessive synapse loss and neuronal damage HD Overview Role of C1q ANX005 Progressive, inherited C1q triggers synapse damage, synapse ✓ Phase 2 results demonstrated 2,3 neurodegenerative removal and neuroinflammation benefit in clinical outcomes disorder ANX005 blocks classical complement ✓ Orphan Drug Designation 80K people affected activation to protect synapses, reduce 1 globally; ~300K at-risk neuroinflammation and improve clinical ✓ Productive engagement with FDA outcomes No approved treatments that reverse or slow ✓ Pivotal trial design aimed at C1q Targeting the C1q targeting disease progression slowing rate of disease Neuromuscular synapses on Junction progression striatal neurons of 3 HD patient ✓ Phase 2/3 trial expected to initiate in 2023 1 2 3 1GlobalData and market research reports, Wilton 2021 doi.org/10.1101/2021.12.03.471180; Hong 2016 Science doi 10.1126/science.aad8373; Stevens 2007 Cell doi 10.1016/j.cell.2007.10.036; Fonseca, 2004, J Neurosci; Dejanovic, 2018, Neuron; Vukojicic, 2019, Cell Reports; Howell, 2011, J Clin Inves; Williams, 2016, Mol Neurodegen; Jiao, 2018, Mol Neurodeg; Lui, 2016, Cell 165:921; Krukowski, 19 19 2018, Int.JMol Sci; Holden, 2021, Science; Annexon NfL reduction in SOD1 model, unpublished; Absinta, Nature, 2021

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![](g422908ex99_1p20g1.jpg)

ANX005 Improved Clinical Outcomes in HD Phase 2 Trial Reduced Downstream Complement Reduced Neuroinflammation Improved Clinical Function HD inflammation marker (YKL-40\*) CSF C3 levels decreased in all patients Benefit at all time points in high reduced in patients with high baseline during on and off treatment period complement group (cUHDRS) complement activity (C4a/C4) CSF YKL-40 c cUHDRS UHDRS CSF C3 CSF YKL-40 C4aH.L AM 01.03.23 CSF YKL-40 Impvr.NonImpvr AM 01.03.23 10 10 2 C4a/C4 Low (n=11) Non-improver (n=10) Off Off Off 1.00 treatment treatment treatment C4a/C4 High (n=12) Improver (n=13) 5 5 1 0.75 0 0 0 0.50 -5 -5 -1 0.25 0.00 -10 -2 -10 0 6 12 18 24 30 36 0 6 12 18 24 30 36 0 6 12 18 24 30 36 0 6 12 18 24 30 36 CSF YKL-40 Impvr.NonImpvr AM 01.03.23 Weeks CSF YKL-40 C4aH.L AM 01.03.23 CSF YKL-40 C4aH.L AM 01.03.23 CSF YKL-40 Impvr.NonImpvr AM 01.03.23 Weeks Time (weeks) Time (weeks) 10 10 10 10 C4a/C4 Low (n=11) Non-improver (n=10) C4a/C4 Low (n=11) Non-improver (n=10) C4a/C4 High (n=12) Improver (n=13) C4a/C4 High (n=12) Improver (n=13) 5 5 5 5 0 0 0 0 \*Produced by activated glia - Elevated in HD and other neurological diseases -5 -5 -5 -5 20 -10 -10 -10 -10 0 6 12 18 24 30 36 0 6 12 18 24 30 36 0 6 12 18 24 30 36 0 6 12 18 24 30 36 Time (weeks) Time (weeks) Time (weeks) Time (weeks) CSF C3 levels (Fold change from baselin % Change (Median +/- QR) % Change (Median +/- QR) % Change (Median +/- QR) % Change (Median +/- QR) cUHDRS Change from Baseline % Change (Median +/- QR) % Change (Median +/- QR)

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![](g422908ex99_1p21g1.jpg)

Initiating Pivotal Phase 2/3 Trial of ANX005 in HD Trial Design Key Objectives • Randomized, double-blind, placebo-controlled • Disease progression measured by cUHDRS and TFC • Leveraging precision medicine approach for patients with elevated baseline complement levels • Confirm observations with rapid drug impact on high complement baseline patients • Patient motor, cognition, behavior, functional capacity and quality of life assessments Patient Population • Safety and tolerability of ANX005 • Patients with manifest and pre-manifest HD • CAP score > 400 • UHDRS independence score ≥ 80 EXPECT TO INITIATE IN 2023 21

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![](g422908ex99_1p22g1.jpg)

First-In-Class for Early Complement Inhibition in GA Progressive neurodegenerative retinal disease involving C1q-driven synapse and photoreceptor loss GA Overview Role of C1q ANX007 Leading cause of C1q drives tissue damage in the retina by ✓ Targeting up and blindness in the elderly anchoring complement activation on drusen, downstream complement photoreceptor cells and synapses activation 1M people diagnosed in US; 5M people globally ANX007 has potential to provide more ✓ Aim to slow rate of lesion complete protection by shutting down all growth Current approaches target classical pathway components downstream complement ✓ Fast Track Designation C1q Microglial cell C1q Targeting the Neuromuscular ✓ Administered to 200 Junction patients to date C1q directing synapse ✓ Phase 2 data anticipated engulfment by 1 mid-2023 microglial cells 1 22 22 Annexon data on file

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![](g422908ex99_1p23g1.jpg)

ANX007 Provides Powerful Inhibition of C1q & Classical Pathway in All Layers of the Retina Key Attributes ✓ Potency: <10 pM Fab antibody formulated for intravitreal administration ✓ Target Engagement: Complete C1q inhibition in the eye for at least 4 weeks ✓ Safety: Generally well-tolerated in Phase 1b trial ANX007 ✓ Efficacy: Preclinical data demonstrating protection of photoreceptor cells IVT administered and retinal function antigen-binding fragment (Fab) ✓ Dosing: Pharmacokinetics in patient aqueous humor supports monthly/every other month dosing; optimizing formulation for less frequent dosing Administered to 200 patients to date 23

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![](g422908ex99_1p24g1.jpg)

Targeting C1q's Dual Role in Vision Loss in GA C1q drives inflammation in retina and specific mechanism of synapse loss on photoreceptor neurons C1q Well Positioned to Drive Retinal Damage C1q's Unique Role in Neurodegeneration C1q tags photoreceptor synapses to drive C1q localized on drusen (hallmark pathology of GA) inflammation and neuronal damage Activated microglial cells C1q C1q anchors classical engulf synapses complement activation on drusen C1q C1q guides microglial cells to target Synapses synapses in GA Drusen Modified Image from Jiao, 2018 C1q initiates & propagates neuroinflammation in the retina Retina specimens from GA patients were procured from the San Diego Eye Bank; Annexon data on file; Tassoni et al, IOVS 2022 (ARVO Abstract) 24 24

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![](g422908ex99_1p25g1.jpg)

Broader Overview of C1q's Role in GA Progression C1q accumulates in all layers of the outer retina and positioned as key driver of complement activation GA Retinal Tissue 1 C1q-expressing microglial cell • Drusen contain activating C1q substrates C1q on photoreceptor C1q / Synapse 1 • C1q activation / inflammation contributes to synapses retinal damage • Microglia/macrophages infiltrate the retina, expressing more C1q C4, downstream of C1q, on photoreceptor cells at leading • C1q directly recognizes components of 2 edge of pathology photoreceptor neurons → cell damage C1q • C1q tags photoreceptor synapses on stressed 3 C1q on and around drusen neurons → synapse pruning / degeneration 1 2 3 Annexon data on file; Katschke, 2018; Jiao, 2018 25 25

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![](g422908ex99_1p26g1.jpg)

ANX007 Inhibits C1q Throughout the Retina C1q Occupancy by ANX007 Following C1q Occupancy by ANX007 In Patient Aqueous Intravitreal Administration in Primates Supports Monthly/Every Other Month Dosing Choroid Retina Vitreous Aqueous Sham 2.5 mg 5 mg 150 150 150 125 100 100 100 75 50 50 50 25 \* 0 0 0 Control D30 Control D30 Control D30 Control D30 D1 D29 D1 D29 D1 D29 nd D30 = Day 30 (30 days post-2 ANX007 dose) D1 = Day 1 (before ANX007 dosing) st D29 = Day 29 (post-1 dose) Two doses of 5 mg ANX007 administered by IVT 28 days apart in cynomolgus monkeys \*Within resolution limits of assay Grover et al, IOVS (in press); Sun et al, AAO Annual Meeting 2020; Annexon Data on File 26 26 Free C1q (% of Control) C1q in Aqueous Humor (% Pre-dose levels)

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![](g422908ex99_1p27g1.jpg)

Blocking C1q Protects Photoreceptor Structure and Function in Mouse Light Damage Model Protection of Retinal Layer Thickness / Cell Number Protection of Photoreceptor Cell Function Anti-C1q Protects Photoreceptor Cells / Retinal Protects Retinal Function Thickness \* \* 6 200 150 4 100 2 50 0 0 Control Anti-C1q Control Anti-C1q \* p < 0.05 \* p < 0.05 Jiao, 2018 27 Rows of photoreceptor nuclei in ONL Amplitude (uV) a-wave

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![](g422908ex99_1p28g1.jpg)

Ongoing ANX007 Phase 2 GA Trial with Data in mid-2023 Specifications ARCHER Trial Design • Randomized, double-masked, sham-controlled trial ANX007 5.0 mg/eye once monthly (n=~90) • Patients stratified based on lesion size and location (>45% patients with non-foveal lesions) Sham once monthly (n=~45) • Primary endpoint: Rate of change (slope) in GA lesion area assessed by fundus autofluorescence ANX007 5.0 mg/eye every 2 months(n=~90) (FAF) • >50% of patients through 12-month treatment Sham every 2 months (n=~45) period with >90% adherence with office follow-ups 12-month Treatment Period 6-month Off-treatment Follow-up PHASE 2 DATA EXPECTED MID-2023 28

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![](g422908ex99_1p29g1.jpg)

ANX1502: First Oral, Small Molecule for Classical Complement-Mediated Autoimmune Diseases Opportunity Role of C1s ANX1502 Targeting active form of C1s responsible Autoimmune indications ✓ Orally administer for chronic for classical pathway activation with strong scientific therapy in several diseases rationale, including: Potent and selective inhibitor of C1s ✓ Achieved target drug levels in (serine protease): selective over related on-going Phase 1 SAD trial • Multifocal motor proteases (200 – 50,000-fold) neuropathy (MMN) ✓ Conducting MAD in healthy Highly specific for classical pathway volunteers • Lupus Nephritis C1q ✓ Initiating POC in 2023 ANX1502 • Myasthenia gravis • Cold agglutinin disease C1s (CAD) 29 29

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Following C1q Binding to a Surface, ANX1502 Inhibits Activated C1s Structure of C1-complex bound to IgM-antigen on a surface Structure of unbound C1-complex ANX1502 blocks ANX1502 this step C1-complex C1r cleaves C1s C1s cleaves C4 IgM C1r C4 activates C4a IG binds to antigen IG binds to antigen Antigens C4b ANX1502 binds to C1s Anti-C1q (e.g., ANX005) Modified from Sharp et al, PNAS, 2019 catalytic site to inhibit binds to globular heads enzymatic activity to block C1q binding (MW ~300 D) (MW ~150,000 D) C1 Complex Is Comprised of C1r, C1s and C1q Sharp et al, PNAS, 2019 Mortensen et al, PNAS, 2017 30

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ANX1502: Structure-Based Screening and Design ANX1502 Discovery From HTS To CTA Submission 2017 2018 2019 2021 2022 HTS Hit to Lead Lead Optimization Candidate Selection HTS: identification of Structure-driven Optimized potency, Introduction of initial inhibitors drug design leads selectivity, stability, prodrug increases to high potency oral availability, stability and Obtained crystal structure and selectivity etc. improves with early hits to identify bioavailability C1s binding mode LEAD ANX1502 Initiate Tops HITs based on Active Moiety Phase 1 structure with C1s • IC ~1 nM • Improved oral • IC ~1 nM 50 50 bioavailability • IC ~1 μM • Highly Selective 50 • Functional Activity • Marginal Stability • Marginal Stability • Highly Selective • Low in vivo clearance • Moderate oral bioavailability 31

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ANX1502: Highly Potent and Selective Inhibitor of C1s Potent for In Vitro Hemolysis in Human Serum • High affinity C1s: 0.6 nM (Biacore) • Potent inhibitor: 1 nM purified 3 enzymatic assay ANX005 2 • Selective over related serine proteases ANX1502 70 nM (200 – 50,000-fold) 5 nM 1 Sutimlimab • Robust functional inhibition of classical pathway (comparable to sutimlimab) 0 0.01 0.1 1.0 10 100 1000 10,000 ▪ In vitro hemolysis assay (IC = 5 nM) 50 Drug (nM) ▪ Clinical target concentration =100 nM IC =100 nM 90 Clinical Target Concentration 32 Hemolysis

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ANX1502 Well-Tolerated in Ongoing Phase 1 SAD Trial; Supports Further Dose Escalation and Multiple Dosing 25 mg 150 mg 450 mg • ANX1502 generally well-tolerated dose Subjects with TEAEs dose dose (N=8) (N=8) (N=8) • Maximum tolerated dose not yet reached • All treatment-emergent adverse events Dose 25 mg 150 mg 450 mg (TEAEs) mild or moderate Subjects with any TEAE 4 (50.0) 3 (37.5) 5 (62.5) • TEAEs included nausea, emesis and headache Subjects with any Serious TEAE 0 0 0 • No serious adverse events (SAEs) • No significant clinical/lab findings Subjects with at least one Grade 1 3 (37.5) 3 (37.5) 4 (50.0) (e.g., liver enzymes, serum chemistry, Drug-related TEAE hematology) Subjects with any ≥ Grade 2 TEAE 0 0 0 33

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ANX1502 Pharmacokinetic Profile Supports Twice Daily Dosing Plasma levels after single dose\* • Single dose of 450 mg achieves target drug levels (100 nM) consistent with twice daily dosing 600 450 mg – 450 mg dose achieved >100 nM for 12 hours 500 150 mg 25 mg T = 9-10 hours 1/2 • SAD dosing to MTD on-going 400 300 • MAD cohorts initiating 1H23 200 Target drug levels 100 0 0 6 12 18 24 30 36 42 48 Time (hr) \*Cohorts where ANX1502 was administered with consistent dosing protocol 34 Concentration (nM)

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ANX1502 Advancing Into Multiple Clinical Trials for Development in Autoimmune Indications ANX1502 Development Plan • Complete Phase 1 SAD / MAD study in healthy volunteers Phase 1 data 2023 ▪ Establish dose for patient studies • Establish rapid POC in CAD Initiate POC trial 2023 ▪ Validate 1502 PK/PD in a short duration trial with objective readout • Expand autoimmune franchise into multifocal motor neuropathy (MMN) Initiate P2 trial 2024 ▪ Strong scientific rationale; supporting data from mechanistically-related GBS indication Next Steps for Program Expansion Expansion 2H23 • Additional franchise expansion informed by emerging data 2H23 ▪ Ph 1b LN data expected in 1H23; informs late-stage trial related diseases ▪ Ongoing assessment of Myasthenia gravis (MG) and other indications 35

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MMN: Progressive Disability Despite Treatment With Standard Therapy Nerve Damage Mediated by Classical Disease Overview Complement in MMN • Clinical features INTACT NERVE GM1 ganglioside ▪ Slowly progressive asymmetrical distal limb weakness to muscle ▪ Muscle wasting over time axon • Patients ▪ ~12K in US / EU ▪ Commonly middle-aged men MMN C1 • Pathophysiology complex Complement activation Axon and myelin damage ▪ Anti-GM1 antibodies IgM ▪ Motor conduction block GM1 ganglioside to muscle • Treatment axon Nerve ▪ Treated with IVIg, but progressive nerve damage continues impulse ▪ Life-long and time-consuming treatment National Organization for Rare Diseases https://rarediseases.org/rare-diseases/multifocal-motor-neuropathy/ Vlam, Lotte et al., Neuroimmunology Neuroinflammation, 2015 36

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Strong Rationale for C1 Inhibition as Therapy for MMN IgM driven disease related to GBS Classical Complement Complement Activation C1 Inhibition Reduces Effect Activation in MMN Correlates with Severity of MMN Antibodies Patient sera: C1q, C4b and C3b Neuronal culture: Anti-C1q blocks Patient sera: In vitro complement deposition on GM1 ganglioside in vitro neurotoxic calcium influx caused by IgM deposition on GM1 ganglioside correlates with anti-GM1 IgM titers GM1antibodies correlates with MMN disease severity MMN serum Control serum 0.4 \* 3 0.3 2 0.2 Damaging calcium influx Serum C1q 1 0.1 C4b MMN serum C3b 0 0 0 Minor Mild Moderate Severe 0 1 2 3 MMN serum +anti-C1q Muscle weakness Anti-GM1 antibody titer (OD) Yuki, et al., J Neurol Neurosurg Psychiatry 2011 Vlam, et al., Neurology 2015 Harschnitz, et al., Annals Neurol 2016 37 Complement deposition (OD) C3b deposition ()OD values)

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Early Plans for MMN Study With ANX1502 Trial Design Key Objectives • Randomized, double-blind trial assessing • Safety and tolerability efficacy of ANX005 vs. IVIg • Confirm first use of oral drug candidate in • IVIg rescue provided MMN patient population • Measures of peripheral muscle strength using MRC sum score and hand-held dynamometry Target Patient • Patient function • Early MMN and documented response to IVIg • Need of IVIg retreatment (run-in period) TIMELINE: INITIATE IN 1H 2024 38

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Additional Near- Term Opportunities 39 39

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Numerous Opportunities with Next Wave Programs 2023 ANTICIPATED INDICATION CANDIDATE PRECLINICAL PHASE 1 PHASE 2 PHASE 3 MILESTONE Amyotrophic Lateral Report Phase 2 data ANX005 in 2023 Sclerosis (ALS) Report Phase 1 data Lupus Nephritis (LN) ANX009 in 1H 2023 Report Phase 1 data Autoimmune/ Neuro ANX105 in 2023 \*warm autoimmune hemolytic anemia (wAIHA) evaluated in Phase 2 trial; wAIHA development deprioritized as company intends to pursue autoimmune diseases with greater market potential. 40

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First-In-Class Treatment for ALS Targeting up & downstream complement activity in both the brain and peripheral nerves ALS Overview Role of C1q ANX005 C1q targets both central and peripheral nerve Rapidly progressing Differentiated, targeting both components – motor neurons (MN) and peripheral neurodegenerative 1, 2, 3 central and peripheral nervous neuromuscular junction (NMJ) disorder (fatal within 3-5 system years from diagnosis) C1q activation drives inflammation and 1,2 neurodegeneration Aim to slow rate of disease Affects ~19,000 people progression ANX005 blocks all downstream components each year in the US of classical cascade to prevent tissue damage Phase 2a trial actively enrolling, data expected 2023 C1q C1q 4 3 C1q on NMJ C1q on central motor neurons 1 2 3 4 41 41 Bahia El Idrissi 2016, Henkel et al 2004, Kawamata et al 1992, Sta et al 2011, Kjaldgaard 2018; Lee, et al. 2018; Data on file

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ANX005 Preliminary ALS Phase 2a 12-Week Data Show Disease Progression Slowed During Treatment, Increased Off-treatment Reduction in Plasma NfL Impact on ALSFRS Rate of Progression Reduction trend in plasma NfL All patients showed improvement or maintenance during treatment period of progression rate during treatment Both patients Increased in that stayed on 10 off-treatment drug continued to 2 improve period 0 0 -10 -2 -20 All patients who -4 -30 went off treatment On treatment Off treatment declined On treatment Off treatment -40 -6 0 6 12 18 24 0 6 12 18 24 Week Week Individual patients 12 wks on drug, 12 wks off Individual patients 24 weeks on drug On-treatment: N=8; Off-treatment: n=6 (all patients who completed 12- N=8 (All patients who completed 12 or 24-week treatment protocol): Data as of 12/6/2022 week treatment protocol): Data as of 12/6/2022 42 NfL %Change from Baseline (median ± IQR ALSFRS-R Change from Previous Visit (Points/Month)

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Ongoing ANX005 Phase 2 Signal-Finding Study in ALS Trial Design Specifications Target patients: • All forms of ALS, onset of weakness within 3 years prior to enrollment, ALSFRS-R ≥ 30 Off-Treatment Open-Label Treatment Period Endpoints: Period 1 3-6 Months 3 months • Primary: Safety, PK, C1q target engagement, and NfL concentrations in serum 1 Protocol amendment extended treatment period from 3 months to 6 months • Secondary: Clinical outcomes (ALSFRS) ENROLLMENT ONGOING WITH DATA EXPECTED IN 2023 43

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ANX005 in Two Types of Autoimmune Hemolytic Anemia ANNX Approach Confirm efficacy in CAD (n=3) with prior validation in anti-complement Endpoints: therapy • Safety, target engagement and complement inhibition Inform patient enrichment strategy in primary wAIHA via natural history • Anemia and hemolysis markers (e.g., hemoglobin and / feeder study (n=60) bilirubin) Test precision medicine approach in wAIHA in subset of patients with • Quality of Life (FACIT fatigue score) CAD-like complement activity (n=6) Cold Agglutinin Disease (CAD) Warm Autoimmune Hemolytic Anemia (wAIHA) Ph2a Study Design (Confirmatory 1-Year Study) AIHA Ph2a Study Design (Signal Finding 1-Month Study) ANX005 2-dose 6-week ANX005 Chronic Treatment Phase 0 9-week Treatment 9-week run-in 4-12 months feeder follow up Day 1 and Day 8 follow up period (n=3) study (n=6) Primary CAD patients with active hemolysis & anemia Primary wAIHA patients with high levels of complement activation (Hgb <10 g/dL) and with active hemolysis & anemia (Hgb < 10 g/dL) 44 44

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Summary of AIHA Phase 2a Results • ANX005 generally well tolerated for up to 1 year in CAD, longest treatment duration of ANX005 to date • ANX005 achieved full target engagement, completely inhibiting C1q and downstream complement components – consistent with ANX005 in other indications • Positive outcomes in all CAD patients (n=3), consistent with other complement-based inhibitors • Mixed outcomes in signal-finding study with wAIHA patients (n=6) ▪ Successfully identified patients with active complement deposition – blocked by anti-C1q ▪ Indication that 2 doses of drug was insufficient (3-6 weeks complement inhibition) • Due to disease heterogeneity / mixed response will not pursue further development of ANX005 in wAIHA 45

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CAD and wAIHA: Autoantibody-Mediated Diseases Different Overlapping Processes of Red Blood Cell Elimination CAD – IgM autoantibodies Driven by 1 process of elimination C1q Complement-receptor dependent 1 extravascular RBC removal by macrophages C4b and intravascular lysis IgM C3b C5b-9 RBC wAIHA – IgG autoantibodies Heterogeneous - driven by 2 processes of elimination Complex interplay Complement-receptor dependent 1 C1q extravascular removal of RBC by macrophages Fc Receptor-dependent C1q 2 C4b and intravascular lysis IgG C4b removal by macrophages C3b C5b-9 RBC Michalak, et al., 2020 Immunity & Aging 17:3; Barcellini and Fattizzo, 2021 Blood 136:1283 46

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Serum ANX005 (ug/mL) Serum ANX005 (ug/mL) ANX005: Full Target Engagement in CAD and wAIHA Patients Results consistent with findings in other ANX005 studies CAD Patient 1 wAIHA Patient 1 50 1000 100 1000 Serum ANX005 Serum ANX005 Serum Free C1q Serum Free C1q 10 100 10 5 100 10 1 1 1 0 10 20 30 40 50 60 0 1 2 3 4 Study Week Study Week Annexon data on file 47 Serum C1q (ug/mL) Serum C1q (ug/mL)

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Considerable Heterogeneity in wAIHA Patients Muti-Parameter Analysis of Plasma Samples in wAIHA & CAD Patients Cluster 1 Cluster 2 Cluster 3 Cluster analysis of 17 parameters of disease pathology, including: • Hemolysis markers (e.g., bilirubin) • Anemia markers (e.g., hemoglobin) • Complement levels (e.g., C3, C4) • Complement deposition on RBC (e.g., C1q, C4d, C3d) Best wAIHA responder Key takeaways (63 samples from 60 primary wAIHA and 3 CAD patients) Samples from 60 patients with primary Samples from three CAD patients Samples from five wAIHA patients with low, CAD-like levels of wAIHA revealed significant heterogeneity clustered together (all with with low C4 C4 selected for treatment (N=5) demonstrated significant within multiple subgroups levels, <1.5 lower limit of normal) heterogeneity in multiple baseline parameters; best responder most closely resembled CAD based on all parameters Annexon data on file 48

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ANX005 in CAD: Rapid Inhibition of Hemolysis and Sustained Increases in Hemoglobin Total Bilirubin CAD: Key Data Takeaways CAD Patient #1 CAD Patient #2 4 4 3 3 • ANX005 fully blocked complement deposition on 2 2 Normal Range Normal Range red blood cells in all patients 1 1 • Rapid and sustained normalization of hemolysis 0 0 (bilirubin) 0 20 40 0 5 10 15 Time (weeks) Time (weeks) • Significant and durable improvement in anemia (increase in hemoglobin) Hemoglobin Change From Baseline ▪ Hgb ≥2 g/dL & achieved Hgb > 10 g/dL CAD Patient #1 CAD Patient #2 6 6 • ANX005 generally well tolerated 5 5 for up to 1 year 4 4 3 3 2 2 ▪ Longest treatment duration of ANX005 to date 1 1 Baseline Baseline 0 0 -1 -1 -2 -2 0 20 40 0 5 10 15 Time (weeks) Time (weeks) Annexon data on file 49 Change from Baseline Total Bilirubin (g/dL) (mg/dL)

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ANX005 in wAIHA: Complement Deposition Blocked on RBC, But Mixed Effects on Hemolysis and Hemoglobin Total Bilirubin wAIHA Patient #1 wAIHA Patient #2 Non responder Partial responder 4 4 Off drug wAIHA: Key Data Takeaways 3 3 2 2 1 1 • ANX005 fully blocked complement Normal Range Normal Range 0 0 deposition on red blood cells in all patients 0 1 2 3 4 0 1 2 3 4 Time (weeks) Time (weeks) ▪ Measured by flow cytometry (data not shown) • Mixed responses on bilirubin and Hemoglobin Change From Baseline hemoglobin wAIHA Patient #1 wAIHA Patient #2 Non responder Partial responder 6 6 • ANX005 generally well tolerated 5 5 4 4 Off drug 3 3 2 2 1 1 Baseline 0 0 Baseline -1 -1 -2 -2 0 1 2 3 4 0 1 2 3 4 Time (weeks) Time (weeks) Annexon data on file 50 Change from Baseline Total Bilirubin (g/dL) (mg/dL)

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ANX009 Selectively Inhibits Complement Activation in Vascular Space Key Attributes ✓ Subcutaneous formulation of an antigen-binding fragment (Fab) ✓ Target Engagement: Selectively inhibits C1q in the vascular space ✓ Safety: Well-tolerated in Phase 1 trial, twice weekly dosing provided ANX009 sustained C1q inhibition in the circulation Subcu administered antigen-binding fragment (Fab) ✓ Dosing: Designed to enable chronic dosing for use in future trials of autoimmune indications 51

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Ongoing First-In-Class Approach for Lupus Nephritis; Data 1H23 Endogenous, pathogenic autoantibodies against C1q enhance its activity and uniquely amplify kidney inflammation and damage LN Overview Role of C1q ANX009 ~60,000 US patients/year C1q and PACAs amplify kidney Targeting patients with high baseline inflammation and damage complement activity by increased C4d/C4 Pathogenetic auto- antibodies against C1q ANX009 blocks binding, activation & tissue (PACAs) enhance LN damaging inflammation in LN Well-tolerated in Phase 1 trial, twice disease activity weekly dosing provided sustained C1q inhibition in the circulation C1q Phase 1b signal-finding trial underway, with initial data in 1H23 C1q targeting the renal glomerulus \*Induced by injection of auto-reactive antibodies against kidney glomerular basement membrane antigens Trouw et al. J Clinical Investigation (2004) 114:679 52 52

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Preclinical and Phase 1 Support for ANX009 in Lupus Nephritis Precision Medicine Approach High baseline complement activity correlated with disease activity Selectively Inhibiting C1q to Stop Complement-Mediated Disease Full inhibition of C1q in serum with ANX009 in Phase 1 study 53

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Progressing ANX009 in Signal-Finding Study for Lupus Nephritis Trial Design Specifications Target patients: • Classical complement activity, smoldering disease, proteinuria, stable background therapy ~8-week ANX009 ~3 weeks 11-week Objective endpoints: Run-in treatment (n=~6) follow up Period • Safety and tolerability, complement PD markers, exploratory markers of renal tissue damage and function ENROLLMENT ONGOING WITH DATA EXPECTED IN 1H 2023 54

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ANX105 Next Generation Inhibitor of C1q & Classical Pathway Key Attributes ✓ Full-length mAb for IV administration ✓ Target Engagement: Designed to fully inhibit C1q in blood and CSF ANX105 ✓ Dosing: Designed with potentially improved dosing properties for use in future trials of autoimmune and neurodegenerative indications IV administered monoclonal antibody ✓ Phase 1 SAD study in normal healthy volunteers ongoing 55

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Advancing Robust Portfolio of Anti-C1 Clinical Candidates Protecting against tissue damage, neuroinflammation and cell death to improve patient outcomes ANNX Programs ANX007 ANX005 ANX1502 • Full-length mAb for IV • Subcutaneous formulation of a • Oral, small molecule administration Fab for IVT administration • Inhibition of active form of • Selective inhibition of C1q and • Inhibition of C1q and classical C1s and classical pathway in classical pathway in the eye complement pathway in the the body body & brain ANX009 ANX105 • Subcutaneous formulation of a Fab • Full-length mAb for IV administration • Selective inhibition of C1q and • Fast follower to ANX005 designed to classical pathway in the body offer enhanced dosing administration (vascular space) 56

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A Mission to Enable People to Live Freely from Complement- mediated Diseases 57 57

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Game-Changing Opportunity for C1q-directed Complement Therapies in Current Indications and Beyond Significant Unmet Need Multi-Billion Market Opportunity C1q-directed complement agents on Expansion into additional 0 the market or in late-stage development complement-mediated diseases of the body, brain and eye Disease-modifying treatments available 0 for GBS or HD Treatments that target both up and 0 downstream complement pathway for GA >$10 BILLION Market opportunity in Orally administered, small molecule current pipeline indications 0 complement treatments available Annexon data on file 58

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![](g422908ex99_1p59g1.jpg)

2023 Clinical Milestones Primed to Unlock Significant Value Well capitalized with runway into 2025 ANX005 Complete enrollment in pivotal GBS trial Phase 3 complete enrollment in 2H 2023 ANX005 Initiate pivotal HD trial Phase 2/3 initiates in 2023 ANX007 Demonstrate clinical efficacy in GA Phase 2 data in mid-2023 ANX1502 Initiate clinical POC trial with oral, small molecule Phase 1 MAD data in healthy subjects by end of 2023 Initiate POC trial in CAD patients by end of 2023 ANX005 Ph 2 ALS data in 2023 Demonstrate efficacy signal in "next wave" indications and ANX009 Ph 1 LN data in 1H 2023 target engagement with next generation mAb ANX105 Ph1 data in 2023 59

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WARRIOR SPIRIT SOUND JUDGEMENT PASSION ALL-FOR-ONE THRIVE! Committed to Serving Patients, Families and Communities through Game-changing Medicines 60

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APPENDIX

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Loss of Functioning Synapses Results in Neurodegeneration 2 Blocking C1q protects functioning synapses, prevents loss and decreases disability C1q's Normal Role In Development C1q's Role In Neurodegenerative Disease • C1q recognizes, tags & drives removal of excess • C1q recognizes, tags & drives removal of synapses functioning synapses • Strong synapses remain to form appropriate • Triggers inappropriate synapse damage and loss, circuits and normal brain health neuroinflammation and degeneration Pathway turns off Chronic pathway C1q drives after developmental activation and C1q sculpts synaptic window functional decline inappropriate synapse connects for appropriate damage and loss neuronal network C1q C4b C3b C5b-9 Synapse 1 Wilton 2021 doi.org/10.1101/2021.12.03.471180; Hong 2016 Science 10.1126/science.aad8373; Stevens 2007 Cell DOI 10.1016/j.cell.2007.10.036; Fonseca, 2004, J Neurosci; Dejanovic, 2018, Neuron; Vukojicic, 2019, Cell Reports; Howell, 2011, J Clin Inves; Williams, 2016, Mol Neurodegen; Jiao, 2018, Mol Neurodeg; Lui, 2016, Cell 165:921; Krukowski, 2018, Int.J Mol Sci; Holden, 2021, Science; Annexon NfL reduction in SOD1 model, unpublished; Absinta, Nature, 2021 62

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Evidence of Reduced Downstream Complement Activation & Neuroinflammation Through Entire 9 Month Study Drug Effects Continue into Off-treatment Period %CSF C4a %CSF C3a Off treatment Baseline levels 4 ANX005 showed: 1.0 ▪ Reduction of downstream complement C3a 3 activation (C3a) ▪ Reduction of neuroinflammation (C3) 0.5 C3 2 ▪ C3 is produced by activated, neurotoxic 1 astrocytes in the brain 1 0.0 0 6 12 18 24 30 36 0 6 12 18 24 30 36 Last Dose Weeks Weeks N = 23 1 Liddelow, Barres, 2017 Nature 541: 481–487 63 C4a Levels (Fold change from baseline) C3a levels (Fold change from baseline)

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Clinical Disease Progression Stable in Overall Patient Population Through Entire 9-month Study cUHDRS Stable Over 9 Months TFC Stable Over 9 Months 2 2 Off treatment Off treatment 1 1 0 0 -1 -1 -2 -2 -2 0 6 12 18 24 36 -2 0 6 12 18 24 36 N = 23 Week Week MMRM; LS means +/- 95% CI 1 Expected decline = interpolated natural history from Schobel 2017 (TRACK-HD) 64 cUHDRS (Mean Change from Baseline) TFC (Mean Change from Baseline)

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Complement Activation Correlates with Disease and Functional Decline in HD Patients with higher baseline complement activity may be more likely to respond to anti-C1q therapy CSF C4a Activation Correlate with HD Functional Decline CSF C4a Elevated and Increase with HD Progression\* CSF C4a Levels CSF C4a Clinical endpoints p-value 40 p=0.011 p=<0.0001 p<0.001 Total functional score (TFC) 0.0333 30 Motor & Total motor score (TMS) 0.0181 20 Function Disease burden score (DBS) 0.1310 10 0 Symbol digit mod. Test (SDMT) 0.0324 Verbal fluency 0.0255 Cognitive Scales Stroop color naming (SCN) 0.0454 Stroop word recall (SWR) 0.0710 Early manifest consistent with patients enrolled in current study \*Higher complement activity in CSF (C4a) of HD Patients associated with disease severity & functional decline Presented at HSG, November 2021; Annexon Collaboration with Ed Wild UCL 65 Control Early Pre. Late Pre. Early HD Moderate HD ng/mL

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Rapid Benefit Maintained in Patients with High Baseline Complement Activity Through Treatment and Follow-up Periods Benefit at All Time Points in High Complement Group (TFC) Benefit at All Time Points in High Complement Group (cUHDRS) 2 2 Off Off treatment treatment 1 1 0 0 -1 -1 C4a/C4 higher (n=12) C4a/C4 higher (n=12) -2 -2 p=0.037\* p=0.293\* C4a/C4 lower (n=11) C4a/C4 lower (n=11) -2 0 6 12 18 24 36 -2 0 6 12 18 24 36 Week Week \*Comparing higher vs lower C4a/C4 groups at week 24 \*Comparing higher vs lower C4a/C4 groups at week 2; MMRM; LS means +/- 95% CI; N=23 1 Expected decline = interpolated natural history from Schobel 2017 (TRACK-HD) 66 cUHDRS (Mean Change from Baseline) TFC (Mean Change from Baseline)

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75% of Patients with High Baseline Complement Levels Showed Improvement at Week 24, Maintained at Week 36r Twice as many patients with high complement improved compared to patients with low complement Week 24 cUHDRS (Change from Baseline) Week 36 cUHDRS (Change from Baseline) Week 24 Week 36 4 4 75% patients with elevated 75% maintained baseline complement during 3-month 2 2 improved (9/12) follow-up period vs. 0 0 36% with lower baseline complement (4/11) -2 -2 \*p=0.134 \*p=0.032 -4 -4 Low High Low High Baseline Complement Activity (C4a/C4) Baseline demographics evenly matched between patients with higher and lower CSF complement activation \*Wilcoxon-Mann-Whitney Test 67 cUHDRS (Mean Change from Baseline) cUHDRS (Mean Change from Baseline)

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Independent Marker of Inflammation in HD (YKL-40\*) Decreased in ANX005-treated Patients Exhibiting Clinical Improvement ANX005-treated Improvers Showed Rapid, Consistent YKL-40 Increased in CSF of HD Patients Decrease of YKL-40 10 Off treatment 5 Non-improver 0 -5 Improver -10 ^ Rodrigues, et al., 2016. Plos One Baseline 6 12 24 36 DOI:10.1371/journal.pone.0163479 Time (weeks) Rodrigues 2016 PLoS One 11 e0163479 Annexon data on file \*Produced by activated glia - Elevated in HD and other neurological diseases 68 % Change (Median +/- QR)

## Exhibit 99.2

**Exhibit 99.2**![LOGO](g422908g0108085738865.jpg)

**Annexon Highlights Strategic Focus to Advance Four Flagship Complement Programs through Late-Stage Development and Progress Across Three Therapeutic Franchises** 

*Mid-stage and Pivotal Trials of ANX005, ANX007 and ANX1502 Poised to Achieve Numerous Catalysts in Multiple Disease Indications* 

*Well-Capitalized with Operating Runway into 2025* 

*Company to Present Pipeline Updates at 41<sup>st</sup> Annual J.P. Morgan Healthcare Conference* 

*on January 11, 2023, at 7:30 a.m. PT* 

**BRISBANE, Calif., Jan. 8, 2023** – <u>Annexon, Inc.</u> (Nasdaq: ANNX), a clinical-stage biopharmaceutical company developing a new class of complement medicines for patients with classical complement-mediated autoimmune, neurodegenerative and ophthalmic disorders, today reported progress across its broad portfolio of complement therapies and outlined its focus on four flagship programs to support its advancement to a late-stage biopharmaceutical company developing first-in-class treatments for complement-mediated diseases of the body, brain and eye.

Annexon has prioritized resources and execution of late-stage development of its four flagship programs: Guillain-Barré syndrome (GBS), Huntington's disease (HD), geographic atrophy (GA) and its first-in-kind oral small molecule, ANX1502. In so doing, Annexon's goal is to create near-term value for patients, physicians and stakeholders with the achievement of the following objectives by the end of 2023:

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Complete expanded enrollment in its ongoing pivotal Phase 3 trial for ANX005 in patients with GBS – the
first placebo-controlled trial in this indication in nearly 40 years

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Initiate a pivotal Phase 2/3 trial for ANX005 in patients with HD – the first complement inhibitor in
development to treat a brain disorder

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Demonstrate clinical efficacy in an ongoing Phase 2 trial for ANX007 in patients with GA – the first up- and downstream complement approach for this indication

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Initiate a clinical proof-of-concept trial with ANX1502 and expand into additional autoimmune indications – the first oral small molecule therapy targeting classical complement

"At Annexon, we envision a world in which every person gets to live out their talents, without being robbed of their physical and cognitive health due to disease. Our mission is to free the body, brain and eye from diseases driven by the classical complement cascade," said Douglas Love, president and CEO of Annexon. "To achieve this, we've purposefully developed a broad pipeline across three therapeutic franchises – autoimmune, neurodegeneration and ophthalmology – allowing us to rigorously evaluate an array of diseases for which the classical pathway drives disease burden. Based on data and learnings generated to-date, we're advancing four flagship programs that each have game-changing potential for patients and their families."

Love continued, "Throughout 2022, we made significant progress across our pipeline and our business, setting up a strong foundation for growth and multiple catalysts on the horizon in 2023 and beyond. We're encouraged by the recent engagements with the FDA on the pivotal trial design for ANX005 in two indications – GBS and HD – and are well-underway with our flagship program for GA, with initial clinical data anticipated mid-year. Across each therapeutic franchise, we've shown that our approach to stopping the classical pathway at its start can have a measurable impact on devastating and difficult-to-treat diseases."

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![LOGO](g422908g0108085738865.jpg)

**Flagship Program Progress** 

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **ANX005 Pivotal Phase 3 Trial for GBS Underway:** Annexon is evaluating ANX005, a monoclonal antibody (mAb)
designed to *fully* inhibit C1q and the entire classical complement pathway, in a randomized, double-blind, placebo-controlled Phase 3 trial in patients with GBS. GBS is an autoimmune condition with no U.S. Food and Drug Administration
(FDA)-approved therapies, and where maximum suppression of C1q and the classical cascade early in the disease process may act to rapidly prevent nerve damage and irreversible neurological disability. Following a productive engagement with the FDA
regarding the statistical analysis plan for the ongoing pivotal trial, the company increased the study population by approximately 40 patients for a total of 220 patients. Expanded enrollment is expected to be completed in the second half of 2023
with pivotal data anticipated in the first half of 2024.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **Initiation of a Pivotal Trial for ANX005 for HD Planned in 2023:** Annexon successfully completed a Phase 2
clinical trial in 2022 in patients with HD, a slowly progressing, inherited and fatal neurodegenerative disease that leads to excessive synapse loss and neuronal damage. Following Phase 2 trial results demonstrating benefit in clinical outcomes in
HD patients and a productive engagement with the FDA, the company plans to advance ANX005 into a randomized, double-blind, placebo-controlled Phase 2/3 pivotal trial for patients with HD in 2023.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **ANX007 Phase 2 Trial in GA On-track for Initial Data in Mid-2023:** ANX007 is being evaluated in a global Phase 2 clinical trial in patients with GA, the leading cause of blindness resulting from damaged and dying retinal cells. ANX007 is designed to block C1q locally
in the eye, to provide more complete protection against excess classical complement activity, a key driver of disease. Enrollment in the trial is complete and the company anticipates reporting initial data in mid-2023, with additional data to be presented after the conclusion of the six-month off-treatment period by the end of 2023.
Additionally, Annexon is continuing to collaborate with DelSiTech to further optimize ANX007 for an extended-release formulation designed to enable less frequent administration.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **ANX1502 Achieved Target Drug Levels and was Well-Tolerated in Phase 1 Single-Ascending Dose (SAD) Trial Preliminary Data; Advancing into Multiple Clinical Trials in 2023:** Annexon is evaluating ANX1502 in an ongoing Phase 1 SAD trial in healthy volunteers. In the SAD trial, a single dose of ANX1502 has achieved target drug levels in plasma in
patients dosed at 450 mg, consistent with twice daily dosing. Additionally, ANX1502 has been generally well-tolerated with no safety signals observed. The SAD trial is ongoing to identify the maximum tolerated dose, and Annexon is preparing to
initiate a multiple-ascending dose (MAD) study of ANX1502 in the first half of 2023, as well as a proof of concept study in 2023 in patients with cold agglutinin disease (CAD), which is supported by positive data generated by ANX005 in CAD patients.
The company also plans to expand development into additional autoimmune indications with strong scientific rationale, including multifocal motor neuropathy (MMN), in early 2024.

**Continued Progress Across Broad Pipeline of Complement Programs** 

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **Preliminary Phase 2a Data with ANX005 in Amyotrophic Lateral Sclerosis (ALS) Show Slowing of Disease Progression During Treatment; Full Data Expected in 2023:** ANX005 is being evaluated in a Phase 2a signal-finding trial in patients with ALS, a fatal neurodegenerative disorder characterized by loss of central and peripheral motor neurons.
Preliminary data (n=8) showed that treatment with ANX005 has resulted in a reduction in neurofilament light (NfL) and slowing of disease progression, as measured by reductions in revised ALS functional rating scores, during the initial 12-week on-treatment period, followed by an increase in disease progression while off treatment. Enrollment in the trial is ongoing with full data expected in 2023.

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&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **Deprioritizing wAIHA to Focus on Diseases with a Clearly Defined Role for C1q Inhibition:** Annexon
completed its Phase 2 signal-finding trials in two types of autoimmune hemolytic anemia, CAD and warm autoimmune hemolytic anemia (wAIHA). ANX005 achieved full target engagement and blocked complement deposition on red blood cells in both CAD and
wAIHA. ANX005 improved clinical outcomes for the CAD patients (n=3) but demonstrated a mixed effect on hemolysis and anemia in wAIHA patients (n=5). The company's enrichment strategy selected patients with signs of excess complement activation;
however, patients enrolled exhibited heterogeneity in other factors contributing to disease. Following an assessment of the market opportunity in wAIHA and a range of additional autoimmune indications, Annexon has determined not to advance
development in wAIHA. The company intends to evaluate its anti-C1q drug candidates, including ANX1502, in indications where classical complement is an understood driver of disease, such as CAD and MMN.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **Data from Signal-finding Trial of ANX009 for Lupus Nephritis (LN) Expected in the First Half of 2023:** The
company's Phase 1b signal-finding trial of ANX009 using a precision medicine approach for patients with LN who have high baseline complement activity is underway. LN is an autoimmune disease for which pathogenic autoantibodies against
C1q enhance activity and uniquely amplify kidney inflammation and damage. ANX009 is a subcutaneously administered agent designed to selectively inhibit C1q in the vascular space for use as a chronic treatment. Enrollment in the trial is ongoing with
multiple patients dosed and data are expected in the first half of 2023.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **Continued Progress with ANX105 in Phase 1 SAD Study:** Annexon is evaluating ANX105, its next-generation
full-length mAb, in a Phase 1 SAD study in healthy volunteers. Enrollment is ongoing and initial data are expected in 2023.

*More information on Annexon's programs across its autoimmune, neurodegenerative and ophthalmologic franchises can be found in the corporate presentation accessible on the company's website at <u>www.annexonbio.com</u>.* 

"This is a remarkable time in the evolution of Annexon. Since the company was founded, the field of complement therapeutics has advanced dramatically. I am proud of the role Annexon has played in revolutionizing complement biology, carrying on our founders' legacy with ground-breaking discoveries in the brain-body-eye connection," stated Mr. Love. "Today, we have an extensive complement pipeline in development with several late-stage trials underway, and a strong balance sheet and disciplined investment approach that supports our near- and long-term plans for our company. Together with a passionate and talented team, we have an incredible opportunity to achieve something tremendous in the field of medicine, and I am excited and confident in the future ahead for us and most importantly, for patients."

**Cash Position and Updated Operating Runway** 

As of September 30, 2022, Annexon had $269.5 million in cash, cash equivalents and short-term investments. Annexon is updating its runway guidance to into 2025 from into the second half of 2025. The update is based on the company's plan to initiate a pivotal trial of ANX005 in HD in 2023, which it has now incorporated into its financial forecast.

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**J.P. Morgan Healthcare Conference** 

Mr. Love will present Annexon's pipeline updates at the 41st Annual J.P. Morgan Healthcare Conference on Wednesday, January 11, 2023, at 7:30 a.m. PT in San Francisco. A live webcast of the event can be accessed under the 'Events & Presentations' section on the Investors page at www.annexonbio.com. A replay of the webcast will be archived on the Annexon website for 30 days following the presentation.

**About Annexon** 

Annexon (Nasdaq: ANNX) is a clinical-stage biopharmaceutical company seeking to bring game-changing medicines to patients with classical complement-mediated diseases of the body, brain and eye. The classical complement cascade is a seminal pathway within the immune system that anchors and drives a host of autoimmune, neurodegenerative and ophthalmic diseases. Annexon is advancing a new class of complement medicines targeting the early classical cascade and all downstream pathway components that contribute to disease, while selectively preserving the beneficial immune functions of other complement pathways. Annexon is rigorously developing a pipeline of diversified product candidates across multiple mid- to late-stage clinical trials, with clinical data anticipated throughout 2023 and beyond.

**Forward Looking Statements** 

This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. In some cases, you can identify forward-looking statements by terminology such as "aim," "anticipate," "assume," "believe," "contemplate," "continue," "could," "design," "due," "estimate," "expect," "goal," "intend," "may," "objective," "plan," "positioned," "potential," "predict," "seek," "should," "suggest," "target," "on track," "will," "would" and other similar expressions that are predictions of or indicate future events and future trends, or the negative of these terms or other comparable terminology. All statements other than statements of historical facts contained in this press release are forward-looking statements. These forward-looking statements include, but are not limited to, statements about: anticipated milestones; cash operating runway; engagement with regulators; the potential benefits from treatment with anti-C1q therapy; timing of data reports; and continuing advancement of the company's innovative portfolio. Forward-looking statements are not guarantees of future performance and are subject to risks and uncertainties that could cause actual results and events to differ materially from those anticipated, including, but not limited to, risks and uncertainties related to: the company's history of net operating losses; the company's ability to obtain necessary capital to fund its clinical programs; the early stages of clinical development of the company's product candidates; the effects of COVID-19 or other public health crises on the company's clinical programs and business operations; the company's ability to obtain regulatory approval of and successfully commercialize its product candidates; any undesirable side effects or other properties of the company's product candidates; the company's reliance on third-party suppliers and manufacturers; the outcomes of any future collaboration agreements; and the company's ability to adequately maintain intellectual property rights for its product candidates. These and other risks are described in greater detail under the section titled "Risk Factors" contained in the company's Annual Report on Form 10-K and Quarterly Reports on Form 10-Q and the company's other filings with the SEC. Any forward-looking statements that the company makes in this press release are made pursuant to the Private Securities Litigation Reform Act of 1995, as amended, and speak only as of the date of this press release. Except as required by law, the company undertakes no obligation to publicly update any forward-looking statements, whether as a result of new information, future events or otherwise.

The contents of the company's website at <u>www.annexonbio.com</u> and the presentation accessible through the company's website are not incorporated by reference into this press release.

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**Investor Contact:** 

Chelcie Lister

THRUST Strategic Communications

<u>chelcie@thrustsc.com</u> 

**Media Contact:** 

Sheryl Seapy

Real Chemistry

949-903-4750

<u>sseapy@realchemistry.com</u>