Anaptysbio, Inc. · NASDAQ:ANAB
Anaptysbio — Investor Presentation (October 2025)
72 slides from Anaptysbio's investor presentation, Oct 14, 2025
Slide 1: October 2025 Corporate Overview
October 2025 Corporate Overview
Slide 2: Forward-looking statements
This presentation and any accompanying oral presentation contains forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995, including, but not limited to: the timing of the release of data from the Company’s clinical trials
Slide 3: Intention to separate into two independent, publicly traded companies
Biopharma Co ANB033 (CD122 antagonist) P1b in Celiac Disease (CeD) Rosnilimab (Pathogenic T cell depleter) P2b complete in Rheumatoid Arthritis P2 in Ulcerative Colitis Focus on developing and potentially commercializing therapeutics for autoimmune diseases ANB101 (BDCA2 modulator) P1 in Healthy Vol
Slide 4: Biopharma Co pipeline and anticipated milestones
Antibody Program Therapeutic Indication Development Stage and Anticipated Milestones IND Enabling Phase 1 Phase 2 Phase 3 Rosnilimab (Pathogenic T cell depleter) Rheumatoid Arthritis Ulcerative Colitis ANB033 (CD122 antagonist) Celiac Disease Inflammatory Disease ANB101 (BDCA2 modulator) Inflammator
Slide 5: Royalty-Bearing Assets
JemperliTM (dostarlimab, PD-1 Antagonist) Imsidolimab (IL-36R antagonist) Royalty-Bearing Assets
Slide 6: Jemperli GSK and imsidolimab Vanda financial collaborations
6 Jemperli: GSK Financial Collaboration Imsidolimab: Vanda Financial Collaboration • Q2 2025 sales: $262m (>19% US QoQ growth rate) o >$1b annualized run rate1 • Significant royalties on global net sales o 8% ($0 to $1b), 12% ($1 - $1.5b), 20% ($1.5 - $2.5b), and 25% (>$2.5b) • Anticipate Sagard pay
Slide 7: Jemperli Revenue Forecasts
Actuals 1. Actual Jemperli Q1 to Q2’25 QoQ growth was 19%, Forecast assumes constant ~10% QoQ sales growth from Q2’25 through Q2’27 and dMMR rectal approval; 2. GSK analyst consensus as of 9/15/2025 converted from GBP to USD using Q3 2025 average exchange rate (1.35x), GSK Analyst Consensus website;
Slide 8: Jemperli indications and trials
Head & Neck squamous cell carcinoma • LA-HNSCC: P3 JADE registrational trial (monotherapy) sequentially after chemoradiation • Significant U.S. market opportunity with 54,000 eligible diagnoses/year1 immuno-oncology financial collaboration Colorectal cancer and dMMR pan tumors • MSI-H Pan Tumors: Ac
Slide 9: Capped non-recourse monetization with Sagard
“Jemperli – only” capped non-recourse monetization • Jemperli receivables payable to Sagard until cumulative $600MM paydown by Mar. 31, 20311,2 • Anticipate ~$250MM accrued to Sagard by YE 2025 • Projected cumulative $600MM paydown mid-2027 and Q2 20283 Potential royalties and milestones to Anaptys
Slide 10: Imsidolimab out-licensed to Vanda
10 Exclusive global license to Vanda announced February 2025 $15 million upfront payment $10 million upfront and $5 million for existing drug supply 10% royalties on global net sales FDA BLA submission for generalized pustular psoriasis (GPP) expected in 20251 Imsidolimab: two positive global Phase
Slide 11: Rosnilimab (Pathogenic T Cell Depleter)
(Pathogenic T Cell Depleter) Rosnilimab
Slide 12: RA and UC market similarities and opportunity
Similarities: • Focus on achieving low disease activity or remissions long-term • 1/3 to 1/2 relapse within 1 year following initial response at 3-6 months on induction therapy4 • 2L+ markets with blockbuster opportunity • Minimal differentiation between biologics • Assess combinations to enhance sp
Slide 13: Pathogenic T cells mediate autoimmune pathology
Adapted from Akiyama et al, Ann Rheum Dis, 2023. 13 Pathogenic Teff and Tfh/Tph cells mediate autoimmune pathology Lymphoid tissues Periphery Inflamed tissue 13 B cell Tfh Plasma celllg lg lg Tfh FDC Generation CXCL13 IL-21 Tfh Type I Interferon CXCL13 IL-21 Proliferation & inflammatory cytokine sec
Slide 14: Rosnilimab mechanism restoring immune homeostasis
14 Dendritic cell T cell T cell Activation MHCCD80/86 SHP2 TCRCD28 P PD-1 PD-L1 Rosnilimab Fc Receptor Leverage natural immune regulatory pathway to safely restore immune homeostasis1 Rosnilimab aims to: Achieve durable remission and modify disease Rosnilimab selectively targets pathogenic T cells i
Slide 15: Depleting pathogenic T cells in RA
Adapted from Aletaha and Smolen, JAMA, 2018; 1. Chen et al, Clinical and Translational Immunology, 2024. 15 Depleting pathogenic T cells broadly impacts multiple downstream, clinically validated drivers of RA pathogenesis >80% of T cells in RA synovium are pathogenic • Similar findings are observed
Slide 16: Rosnilimab Phase 2b trial design in RA
16 Screening Period (up to 35 days) Blinded Placebo-Controlled Treatment Period All-Active Follow-Up Period Blinded All-Active Treatment Period Week -5 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 34 38 Visit V1 V2 V3 V4 V5 V6 V7 V8 V9 V10 V11 V12 V13 V14 V15 V16 FUV1 FUV2 FUV3 Dosing ()
Slide 17: Patient disposition
Rosnilimab-treated: n=318 b/tsDMARD-Naïve n=188 rosnilimab treated b/tsDMARD-Experienced n=130 rosnilimab treated 17 ITT population1 N=424 (n=318 rosnilimab; n=106 placebo) b/tsDMARD-Naïve: n=250 (188 on rosnilimab; 62 placebo) b/tsDMARD-Experienced: n=1742 (130 on rosnilimab; 44 placebo) Discontinu
Slide 18: Rosnilimab best-in-disease profile in RA
18 Responses durable after 6 months • Potential for maintenance dosing with extended dosing intervals (e.g. Q8W or Q12W) Best-in-disease profile through 6 months • JAK-like efficacy in both 3-month placebo-controlled portion and through 6 months • Favorable safety and tolerability, particularly when
Slide 19: JAK-like efficacy in naïve patients
64% 60% 48% 53% 54% 35% 38% 42% 23% 42% 46% 23% 0% 10% 20% 30% 40% 50% 60% 70% 80% % o f P a ti e n ts Rosnilimab - Pooled Doses Rinvoq - SELECT-COMPARE Humira - SELECT-COMPARE Kevzara - MONARCH Week 28 Week 24/26 Week 28 Week 24/26 Week 28 Week 24/26 CDAI LDA ACR50 ACR70 1. Non-responder imputated
Slide 20: Efficacy in b/tsDMARD-experienced patients
58% 59% 37% 52% 50% 27% 20% 10% 0% 10% 20% 30% 40% 50% 60% 70% 80% % o f P a ti e n ts Rosnilimab - 100mg Q4W Rosnilimab - 400mg Q4W Rosnilimab - 600mg Q2W Rinvoq - SELECT-CHOICE Orencia - SELECT-CHOICE Orencia - Phase 3 Week 28 Week 24 Week 28 Week 24 Week 28 Week 24 N/R 43% 56% 49% 27% 44% 42% 36%
Slide 21: ACR20 in b/tsDMARD-experienced patients
0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100% % o f P a ti e n ts RinvoqTM (P3 SELECT-CHOICE5) Rinvoq vs. Orencia H2H All-Active ACR20: b/tsDMARD-Experienced1 NRI analysis on ITT population (n=174 total; n=44 placebo, n=130 rosnilimab)2 ACR20 at Week 12 Arm Absolute PBO Adjusted b/tsDMARD-Experienced
Slide 22: Mean change in CRP
-20 -18 -16 -14 -12 -10 -8 -6 -4 -2 0 2 4 M e a n C h a n g e f ro m B a se li n e (m g / L) Wk0 Wk2 Wk4 Wk6 Wk8 Wk10 Wk12 Wk14 RinvoqTM (P3 SELECT-CHOICE5) RinvoqTM vs. Orencia H2H All-Active RinvoqTM (Phase 2b TNF-Experienced Study4) Dark Orange – RinvoqTM 6mg BID Light Orange – Placebo Mean Chang
Slide 23: Sustained reduction of pathogenic T cells
Wk0 Wk6 Wk12 Wk28 Wk38 (12-wk off-drug) -100% -75% -50% -25% 0% 25% 50% 75% 100% C el l C o u n t (% C h a n g e fr o m B a se li n e) Rosnilimab 400mg Q4W T Cell Impact Rosnilimab Tph Impact – Pooled Doses Rosnilimab 600mg Q2W T Cell Impact Rosnilimab 100mg Q4W T Cell Impact -100% -75% -50% -25% 0%
Slide 24: Synovial biopsies show ~90% reduction of pathogenic T cells
Rosnilimab 400mg Q4W Rosnilimab 600mg Q2W T cell markers CD3 PD-1 CXCR5 400mg/600mg doses ~90% reduction 100mg dose Inconclusive reduction Placebo Increased Impact on Tph and Teff cells Baseline Week 6 APC markers PD-L1 Synovial biopsies show ~90% reduction of pathogenic T cells in the target issue
Slide 25: T and B cell activation reduction in synovium
Fold decrease: 4.03, p=1.09e-24 T Cell Activation Fold decrease: 4.06, p=1.77e-18 B Cell Activation G e n e e x p re ss io n ( Z -s co re ) G e n e e x p re ss io n ( Z -s co re ) 5.5 2.9 2.0 0 2 4 6 8 6.1 3.9 1.0 0 2 4 6 8 M a g n it u d e o f re d u ct io n Magnitude of reduction: 4.03, p=1.09e-24
Slide 26: Downstream pathways including TNF and IL-6
IL-6 Production G e n e e x p re ss io n ( Z -s co re ) G e n e e x p re ss io n ( Z -s co re ) Significantly downregulated (p<0.05) genes of interest in RA: Baseline TNF Production Magnitude of reduction: 3.38, p=4.39e-15 Magnitude of reduction: 5.63, p=2.61e-21 T cell activation: IL2RA, TNFSF14 (L
Slide 27: CDAI disease activity framework
27 C D A I S co re 0 2. 8 10 22 38 Remission (CDAI < 2.8) Low Disease Activity (LDA) (CDAI ≤ 10) Moderate Disease Activity (CDAI 10 - 22) High Disease Activity (CDAI >22) Trial baseline: median CDAI-= 36 mean CDAI = 38 Disease Activity ACR20 Initial signal of efficacy; typically plateaus at 3 months
Slide 28: Median change from baseline in CDAI
0 10 20 30 40 50 60 M e d ia n C D A I Wk 0 Wk 2 Wk 4 Wk 6 Wk 8 Wk 10 Wk 12 Wk 14 Wk 16 Wk 18 Wk 20 Wk 22 Wk 24 Wk 26 Wk 28 Wk 30 Wk 34 Wk 38 High Disease Activity (CDAI >22) Low Disease Activity (LDA) (CDAI ≤ 10) Last dose for Week 14 CDAI >10 participants given at Week 12 for Q4W doses and Week 14
Slide 29: CDAI remission in experienced patients
0% 5% 10% 15% 20% % o f P a ti e n ts CDAI Remission: b/tsDMARD-Experienced NRI+W18 analysis* on ITT population (n=130 rosnilimab patients)1 Wk 12 Wk 28 Wk 12 Wk 28 Wk 12 Wk 28 100mg Q4W 400mg Q4W 600mg Q2W 7% 9% 12% CDAI Remission at Week 28 Arm NRI NRI+W18 b/tsDMARD-Experienced Population (as grap
Slide 30: Pain VAS and CRP responses
-37.3 -42.6 -42.8 -47.0 -49.9 -52.4 -60 -50 -40 -30 -20 -10 0 M e a n C h a n g e P a in V A S Pain VAS: Overall MMRM analysis on CDAI Responder Population (n=220)1 Wk 12 Wk 28 Rosnilimab - 100mg Q4W Rosnilimab - 400mg Q4W Rosnilimab - 600mg Q2W 1. Mixed Model for Repeated Measures (MMRM) analysis o
Slide 31: Durable responses off-drug at Week 34
81% 90% 83% 0% 20% 40% 60% 80% 100% % o f P a ti e n ts CDAI LDA: b/tsDMARD-Naïve Week 34 completer analysis (n=101)1 CDAI LDA: b/tsDMARD-Experienced Week 34 completer analysis (n=38)1 Wk34 Wk34 Wk34 88% 87% 73% 0% 20% 40% 60% 80% 100% % o f P a ti e n ts Wk34 Wk34 Wk34 n=29/36 n=27/30 n=29/35 n=7/8
Slide 32: Competitive Landscape
32 Competitive Landscape Fc receptor binding affinity Tissue (RA Synovium) Depletion Peripheral (Blood) Depletion Membrane- proximal epitope S tr u ct u ra l ch a ra ct e ri st ic s C li n ic a l/ tr a n sl a ti o n a l o u tp u ts 1 Rosnilimab is a best-in-class pathogenic T cell depleter Competito
Slide 33: Rosnilimab versus peresolimab
0% 10% 20% 30% 40% 50% 60% 70% 80% % o f P a ti en ts 100mg Q4W 400mg Q4W 600mg Q2W Wk 12 Wk 14 Wk 28 0% 10% 20% 30% 40% 50% 60% 70% 80% % o f P a ti en ts 300mg Q4W 700mg Q4W Wk 12 Wk 14 Wk 24 Wk 0 Wk 0 (12-wk off-drug) Wk 383 (12-14 wk off-drug) Wk 36 Rosnilimab P2b: CDAI LDA NRI analysis on ITT p
Slide 34: Black box warnings and RA comorbidities
Black box warnings for increasing SAE incidence of commercial products have not impeded blockbuster sales Black box warning ~30% infection rate vs. 28% placebo5 ~0.7% MACE rate vs. 0.4% placebo5 ~54% infection rate vs. 48% placebo5 ~0.2% MACE rate vs. 0.5% placebo5 Black box warning ~20% infection r
Slide 35: Safety summary
35 Study Period Week 0 through Week 12 (N=424) Week 0 through Week 28 (N=424) Participants with Adverse Events, n (%) Participants with Adverse Events, n (per 100 PY)* Placebo (n=106) 100mg Q4W (n=106) 400mg Q4W (n=107) 600mg Q2W (n=105) Placebo (n=106) 100mg Q4W (n=106) 400mg Q4W (n=107) 600mg Q2W
Slide 36: Pathogenic T cells in UC pathogenesis
Adapted from Gastroenterology & Hepatology Volume 18, Issue 8 August 2022. 1. Chen et al, Clinical and Translational Immunology, 2024. 36 >40% of T cells in lamina propria in UC are pathogenic 2x increase of pathogenic T cells observed in blood vs. healthy controls1 B cells IL-23 antagonists αEβ7 Ly
Slide 37: Depletion of pathogenic T cells reduces cytokines
Reduction of Tfh/Tph cytokine 0 25 50 75 100 0 0.1 1 10 100 Antibody (nM) CX CL 13 & IL -2 1 (% Is ot yp e C on tro l) IL-21 CXCL13 Clinical range Reduction of inflammatory cytokine Depletion of Pathogenic T Cells Parmley et. al. UEGW 2024. October 2024; Anti-CD3+ anti-CD28 stimulation of UC patient
Slide 38: Pathogenic T cells in RA and UC
Pathogenic T cells are prevalent in inflamed tissue and periphery in RA and UC Therapeutic dosing of rosnilimab demonstrated efficacy in a murine model of colitis Tph cells are reduced with remission in UC1,2,4 Tph impact seen in RA Phase 2b trial relevant to UC biology and correlates to reduction o
Slide 39: Milestones in UC treatment
3 Months 6 Months Fast relief needed in most severe patients (<10%) to continue therapy (e.g. JAKs or IV TNF) Symptomatic improvement (e.g. ∆pMMS) needed to continue on therapy; potentially without being re-scoped Clinical Remission or Endoscopic Remission targeted to reduce symptomatic relapse rate
Slide 40: Rosnilimab Phase 2 trial in UC
Rosnilimab Phase 2 in moderate-to-severe UC Enrollment completed; On track for top-line data through Week 12 in Nov/Dec 2025 Blinded Placebo-controlled Treatment Extension Period (TEP) (26 weeks) Screening Period (up to 35 days) Follow-Up Period (10 weeks) Week -5 0 12 24 Rosnilimab SC Dose 1 Q2W Ro
Slide 41: Rosnilimab summary and next steps
Rheumatoid Arthritis Ulcerative Colitis Positive Phase 2b data reported • Best-in-disease profile • Favorable safety and tolerability • JAK-like efficacy through 6 months o Max response rates not yet observed due to trial design • Sustained 12-14 week off-drug responses through 9 months • ACR late-b
Slide 42: ANB033
ANBO33 > ne = is) is) g isd % N N a 1S) =
Slide 43: ANB033 blocks CD122
43 CD122 is the beta subunit (IL-2Rβ) of the receptor for IL-15 and IL-2 • Expressed on subsets of CD8+ and CD4+ T cells and NK cells CD122 antagonism reduces these immune cell subsets • Dependent on IL-15 and/or IL-2 for maintenance, proliferation and survival Overexpressed in select diseases, incl
Slide 44: Broad therapeutic potential across autoimmune diseases
Gastroenterology Celiac Disease Crohn’s Disease Eosinophilic Esophagitis (EOE) Ulcerative Colitis Dermatology Atopic Dermatitis Alopecia Areata Hidradenitis Suppurativa Lichen Planus Vitiligo Other Areas Asthma Multiple Sclerosis Psoriatic Arthritis Type 1 Diabetes Solid Organ Transplant • P1b PoC i
Slide 45: ANB033 in GvHD mouse model
45 Body weight loss (carried) W e ig h t ( % o f S ta rt ) End of dosing 0 10 20 30 40 50 60 -20 -10 0 10 Study Day Cytolytic gene expression (Day 17) Expression (% of isotype) 0 50 100 150 GNLY GZMA GZMB ✱ ✱ ✱ ANB033 Forte anti-CD122 Belatacept Isotype Control ANB033 Isotype Control ****** Survival
Slide 46: ANB033 Phase 1a trial design
46 Objectives • Safety and tolerability • Evaluate PK and immunogenicity Design • All healthy volunteers have been dosed o ANB033: n=60 o Placebo: n=20 • Administered both IV and SC dosing • 10 cohorts: Four SAD IV, three SAD SC and three MAD SC • Follow-up to ~7 months* ANB033 Phase 1a trial ongoin
Slide 47: Favorable safety, tolerability and PK in Phase 1a
47 Favorable safety and tolerability • No safety concerns at any dose o No SAEs, severe AEs, or discontinuations o Any adverse events mild or moderate • No unexpected lab abnormalities • No signs of viral infections • No clinical pharmacology findings of concern Rapid and sustained PK profile • Favo
Slide 48: ANB033 reduces CD8+ T cells and NK cells
48 % C h a n g e f ro m b a se li n e % C h a n g e f ro m b a se li n e % C h a n g e f ro m b a se li n e % C h a n g e f ro m b a se li n e CD122+ CD8+ T cell impact CD122+ NK cell impact Overall CD8+ T cell impact Overall NK cell impact Graphs reflect SAD data and maximum reductions were achieve
Slide 49: NK cell reduction with no safety issues
% C h a n g e f ro m b a se li n e -75% -50% -25% 0% 25% 50% 75% 0 7 13 19 25 31 37 43 49 55 61 67 73 79 85 Placebo IV Dose SC Dose 49 Anti-IL-15 and CD122 therapies have demonstrated sustained reduction in CD122+ NK cells with no observed safety issues ANB033 effect on total NK cells Time (days) No
Slide 50: ANB033 mechanism in celiac disease
50 Activated CD4+ T cell IL-2 TG2 Anti-gliadin Anti-TG2 IEL APC B cell Gliadin Gliadin from gluten ANB033 Deamidated gliadin IFNγ ANB033 HLA Loss of barrier integrity IL-15 CD122+ NK cell Peripheral blood Lamina propria Inhibition of IL-2 signaling • IL-2 stimulates o CD4 effector memory T cell acti
Slide 51: Previous approaches in celiac disease
51 Activated CD4+ T cell IL-2 TG2 Anti-gliadin Anti-TG2 IEL APC B cell Gliadin Gliadin from gluten ANB033 Deamidated gliadin IFNγ ANB033 HLA Loss of barrier integrity IL-15 CD122+ NK cell Peripheral blood Lamina propria OX-40L antagonist P2 ongoing Non-immune cell targeting P1 ongoing HLA-DQ2.5 glut
Slide 52: ANB033 preserves villus height in CeD mouse model
52 Sham Gluten + Isotype Control Gluten + ANB033 ANB033 treatment shows improved histology: preserves villus height and crypt depth (Vh:Cd) in CeD mouse model ANB033 prevents key CeD histologic manifestation of gluten-induced villous atrophy Note: HuDQ8-Dd-villin-IL-15tg mice on a gluten-free diet a
Slide 53: Vh:Cd ratio improvement
53 Healthy tissue: High villus height, lower crypt depth CeD tissue: Reduced villus height, extended crypt depth ANB033 impact on Vh:Cd ratio Sham Isotype ANB033 1 2 3 * * V h :C d R a ti o Vh:Cd ratio ANB033 significantly prevents reduction of Vh:Cd ratio compared to control ANB033 treatment shows
Slide 54: ANB033 effect on IELs and T cells
54 Sham Isotype ANB033 0 200000 400000 600000 800000 C ou nt o f C D 8+ IE Ls * * Sham Isotype ANB033 0 20000 40000 60000 80000 C ou nt o f G ra nz ym e B + IE Ls * * Sham Isotype ANB033 0 2000 4000 6000 C ou nt o f C D 4+ IF N -g + ce lls * Epithelial layer of small intestine C o u n t o f C D 8 +
Slide 55: ANB033 in CeD patient-derived PBMCs
Top Panel: PBMC from CeD donors measuring proliferation (Ki67 staining), stimulated for 7 days with IL-15 + IL-2 (N=4 donors). Bottom Panel: PBMC from CeD donors stimulated for 3 days with anti-CD3 and anti-CD28 (N=4 donors). 55 IFNγ secretion 0 50 100 150 200 Antibody (nM) CD4+ Th1/Th2 T cells 10-3
Slide 56: CeD patients present with range of histologic activity
56 Symptomatically controlled on GF diet Symptomatic on GF diet Persistent mucosal damage despite paucity of symptoms Non-responsive (Phase 1b) Added additional cohort to P1b to inform on potential to heal mucosa in patients with existing histologic mucosal damage and further derisk 2b Symptom contr
Slide 57: ANB033 Phase 1b trial in CeD
Primary Analysis ANB033 Phase 1b trial in CeD initiated Anticipate top-line data by year-end 2026 57 Screening (up to 30 days) N=60 randomized 1:1 Sites: • Western EU • Australia • New Zealand Week 0 6 124 302 Dosing () Cohort 1 (n=30) Vh:Cd ≥ 2.0 Week 6 Endoscopy Gluten challenge Prevention
Slide 58: Cohort 1 gluten challenge
Minimal evidence of mucosal damage (Vh:Cd ≥ 2.0) • Symptom-controlled CeD patients • Receive GC after pre-treatment with ANB033 vs. PBO • ANB033 dose at Week 0, 2, 4 (pre-treatment) • Gluten challenge allows for controlled induction of mucosal damage o Beginning Week 4, 6g gluten dose daily (study s
Slide 59: Cohort 2 mucosal healing
Screening (up to 30 days) Week 0 6 124 302 Dosing () 8 10 Cohort 2 (n=30) Vh:Cd < 2.0 Primary Analysis Week 12 Endoscopy Persistent evidence of histologic CeD activity (Vh:Cd < 2.0) • Symptom-controlled CeD patients • Substantial mucosal damage already present (no gluten-challenge) • Proxy: n
Slide 60: Blockbuster opportunity in non-responsive CeD
2.1 million U.S. patients1 (prevalence) ~250,000 Diagnosed Initial target population High disease burden • Debilitating symptoms, social isolation • Disease awareness driving growth • No approved therapies CD122s differentiated from other Tx in development • HCPs favor MOA that targets both symptoms
Slide 61: New therapies could grow CeD market
61 New therapies in CeD could grow market in responsive and newly diagnosed patients Increasing # of addressable patients Nearer Term Opportunity Longer Term Opportunity Non-Responsive Mitigate symptoms and damage ~250K GF diet liberation ~600K All-Comers Prevention in newly diagnosed ~1M Initial Ta
Slide 62: ANB033 targets multiple drivers of EoE
CD8+ and NK (dupilumab-insensitive) • Inhibiting IL-15 signaling reduces – o IFNγ o Granzyme B o CD8+ T cell proliferation o NK cells Upstream pathways lead to downstream eosinophilic infiltration into tissue IL-15 Allergens, irritants, microbes, reflux, etc. Eosinophil recruitment IL-15 IgE IL-2 IL
Slide 63: Downstream-only mechanisms unsuccessful in EoE
Ongoing tezepelumab (anti-TSLP) IL-15 Tissue damage Allergens, irritants, microbes, reflux, etc. Eosinophil recruitment IL-15 IgE IL-2 IL-4 IL-5 IL-13 IL-15 ANB033 "Th2" inflammation (dupilumab-sensitive) "other“ inflammation (dupilumab-insensitive) Barrier Dysfunction Tissue destruction IFNγ Downst
Slide 64: ANB033 prevents eosinophilia
64 E o si n o p h il s ( p e r u m 2 ) Saline Isotype Control ANB033 Surrogate 0 1×10-5 2×10-5 3×10-5 4×10-5 Lung eosinophils E o si n o p h il s ( p e r m m 2 ) Saline Isotype Control ANB033 Surrogate 0 2×102 4×102 6×102 8×102 1×103 Esophageal eosinophils ANB033 prevents eosinophilia by targeting u
Slide 65: EoE market and unmet need
65 340,000 diagnosed U.S. patients1 Diagnosed 170,000 biologic-eligible ~30,0001 Dupixent-treated Significant unmet need with limited approved therapies • ~50% PPI or steroid non-responsive or intolerant • Dupixent QW approved in 2022 • 20-30% Dupixent non-responsive Increasing disease recognition w
Slide 66: ANB101 (BDCA2 modulator)
(BDCA2 modulator) ANB101
Slide 67: ANB101 inhibits interferon secretion
ANB101 will potently inhibit interferon secretion and immune activation 67 Activated pDCs bridge innate and adaptive immunity • Secrete Type I IFN (1000x increase over other cell types) • Present antigens to adaptive immune system pDCs enriched in tissue in rheumatology and other inflammatory diseas
Slide 68: Appendix
Appendix
Slide 69: Baseline characteristics
69 Baseline Characteristic Placebo (n=106) 100mg Q4W (n=106) 400mg Q4W (n=107) 600mg Q2W (n=105) Overall (N=424) Age, years, mean (SD) 58 (11) 57 (10) 57 (12) 56 (11) 57 (11) Female, n (%) 83 (78%) 79 (75%) 79 (74%) 80 (76%) 321 (76%) Weight (kg), mean (SD) 78 (17) 78 (19) 81 (19) 77 (16) 78 (18) Ge
Slide 70: Mean change in DAS28-CRP over time
70 -3.0 -2.5 -2.0 -1.5 -1.0 -0.5 0.0 M e a n C h a n g e f ro m B a se li n e ** Week 12 statistical significance • 600mg Q2W: p=0.0062 • 400mg Q4W: p=0.0016 • 100mg Q4W: p=0.0092 ** ** * * Mean Change in DAS28-CRP Over Time MMRM analysis on ITT population (N=424 total; n=106 placebo, n=318 rosnilim
Slide 71: CDAI LDA in experienced patients
71 0% 20% 40% 60% 80% % o f P a ti e n ts 43% 51% 29%34% CDAI LDA: b/tsDMARD-Experienced NRI+W18 analysis* on ITT population (n=130 rosnilimab patients)1 Wk 12 Wk 28 Wk 12 Wk 28 Wk 12 Wk 28 100mg Q4W 400mg Q4W 600mg Q2W Demonstrated JAK-like CDAI LDA rates by 6 months CDAI LDA at Week 28 Arm NRI NRI
Slide 72: ACR50 and ACR70 in experienced patients
0% 10% 20% 30% 40% 50% % o f P a ti e n ts ACR50: b/tsDMARD-Experienced NRI+W18 analysis* on ITT population (n=130 rosnilimab patients)1 ACR70: b/tsDMARD-Experienced NRI+W18 analysis* on ITT population (n=130 rosnilimab patients)1 0% 10% 20% 30% 40% 50% 60% % o f P a ti e n ts Wk 12 Wk 28 Wk 12 Wk 2