Annexon, Inc. · NASDAQ:ANNX
Annexon — Investor Presentation (January 2023)
68 slides from Annexon's investor presentation, Jan 9, 2023
Slide 1: Game-Changing Medicines for Complement-Mediated Diseases
Exhibit 99.1 GAME-CHANGING MEDICINES FOR COMPLEMENT- MEDIATED DISEASES JANUARY 2023 Nasdaq: ANNX 1
Slide 2: Forward-Looking Statements
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 o
Slide 3: A bold mission to free the body, brain and eye from complement-mediated disease
A bold mission to free the body, brain and eye from complement- mediated disease 3
Slide 4: Annexon Overview: Pursuing Our Mission & Significant Value
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 & downs
Slide 5: Meaningful Progress Across Our Portfolio in 2022
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 sm
Slide 6: Revolutionizing Complement Biology in Pursuit of Our Mission
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
Slide 7: Robust Clinical Target Engagement of C1q Demonstrated in Body, Brain & Eye
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 2
Slide 8: Clinical Proof-of-Concept Demonstrated in Autoimmune and Neurodegenerative Indications
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 (AL
Slide 9: Achieving Our Mission With Four Flagship Programs
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-val
Slide 10: Flagship Programs Advancing in Mid-stage and Pivotal Trials
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 Geograph
Slide 11: ANX005 Summary
ANX005 Summary “ANNEXON biosciences
Slide 12: ANX005 Powerfully Inhibits C1q and Classical Complement Pathway
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: General
Slide 13: ANX005 Generally Well-Tolerated in Several Patient Populations
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 & neurodegener
Slide 14: ANX005 Generally Well-Tolerated Across Clinical Trials
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 (%
Slide 15: Flagship Programs
Flagship Programs • Guillain-Barré Syndrome (GBS) • Huntington’s Disease (HD) • Geographic Atrophy (GA) • Oral small molecule 15 15
Slide 16: First-In-Class Treatment for GBS
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 paralysi
Slide 17: ANX005 Demonstrated Clinical POC in GBS
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 achiev
Slide 18: ANX005 GBS Phase 3 Pivotal Trial Underway
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 Sc
Slide 19: First-In-Class Treatment for HD
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 ben
Slide 20: ANX005 Improved Clinical Outcomes in HD Phase 2 Trial
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 of
Slide 21: Initiating Pivotal Phase 2/3 Trial of ANX005 in HD
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 ra
Slide 22: First-In-Class for Early Complement Inhibition in GA
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 compl
Slide 23: ANX007 Provides Powerful Inhibition of C1q in All Layers of the Retina
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
Slide 24: Targeting C1q's Dual Role in Vision Loss in GA
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 (hallma
Slide 25: Broader Overview of C1q's Role in GA Progression
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
Slide 26: ANX007 Inhibits C1q Throughout the Retina
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
Slide 27: Blocking C1q Protects Photoreceptor Structure and Function
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 Contro
Slide 28: Ongoing ANX007 Phase 2 GA Trial with Data in mid-2023
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)
Slide 29: ANX1502: First Oral, Small Molecule for Complement-Mediated Autoimmune Diseases
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 disease
Slide 30: ANX1502 Inhibits Activated C1s
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 Ant
Slide 31: ANX1502: Structure-Based Screening and Design
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, stabi
Slide 32: ANX1502: Highly Potent and Selective Inhibitor of C1s
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
Slide 33: ANX1502 Well-Tolerated in Ongoing Phase 1 SAD Trial
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
Slide 34: ANX1502 Pharmacokinetic Profile Supports Twice Daily Dosing
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
Slide 35: ANX1502 Advancing Into Multiple Clinical Trials
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/P
Slide 36: MMN: Progressive Disability Despite Standard Therapy
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 ▪ ~12
Slide 37: Strong Rationale for C1 Inhibition as Therapy for MMN
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:
Slide 38: Early Plans for MMN Study With ANX1502
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 usi
Slide 39: Additional Near-Term Opportunities
Additional Near- Term Opportunities 39 39
Slide 40: Numerous Opportunities with Next Wave Programs
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 A
Slide 41: First-In-Class Treatment for ALS
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 neuro
Slide 42: ANX005 Preliminary ALS Phase 2a 12-Week Data
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
Slide 43: Ongoing ANX005 Phase 2a Signal-Finding Study in ALS
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
Slide 44: ANX005 in Two Types of Autoimmune Hemolytic Anemia
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 hemoly
Slide 45: Summary of AIHA Phase 2a Results
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 o
Slide 46: CAD and wAIHA: Autoantibody-Mediated Diseases
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 – I
Slide 47: ANX005: Full Target Engagement in CAD and wAIHA
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
Slide 48: Considerable Heterogeneity in wAIHA Patients
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 level
Slide 49: ANX005 in CAD: Rapid Inhibition of Hemolysis
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 nor
Slide 50: ANX005 in wAIHA: Mixed Effects on Hemolysis and Hemoglobin
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 de
Slide 51: ANX009 Selectively Inhibits Complement Activation in Vascular Space
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 sustai
Slide 52: Ongoing First-In-Class Approach for Lupus Nephritis
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
Slide 53: Preclinical and Phase 1 Support for ANX009 in Lupus Nephritis
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
Slide 54: Progressing ANX009 in Signal-Finding Study for Lupus Nephritis
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 • Safe
Slide 55: ANX105 Next Generation Inhibitor of C1q
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 neur
Slide 56: Advancing Robust Portfolio of Anti-C1 Clinical Candidates
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 admi
Slide 57: A Mission to Enable People to Live Freely from Complement-mediated Diseases
A Mission to Enable People to Live Freely from Complement- mediated Diseases 57 57
Slide 58: Game-Changing Opportunity for C1q-directed Complement Therapies
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, br
Slide 59: 2023 Clinical Milestones Primed to Unlock Significant Value
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 da
Slide 60: Committed to Serving Patients, Families and Communities
WARRIOR SPIRIT SOUND JUDGEMENT PASSION ALL-FOR-ONE THRIVE! Committed to Serving Patients, Families and Communities through Game-changing Medicines 60
Slide 61: Appendix
ANNEXON biosciences APPENDIX
Slide 62: Loss of Functioning Synapses Results in Neurodegeneration
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 re
Slide 63: Reduced Downstream Complement Activation & Neuroinflammation Through 9 Months
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 neuroi
Slide 64: Clinical Disease Progression Stable in Overall Patient Population
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
Slide 65: Complement Activation Correlates with Disease and Functional Decline in HD
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
Slide 66: Rapid Benefit Maintained in Patients with High Baseline Complement Activity
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
Slide 67: 75% of Patients with High Baseline Complement Showed Improvement at Week 24
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%
Slide 68: YKL-40 Decreased in ANX005-treated Patients Exhibiting Clinical Improvement
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., 2