Anaptysbio, Inc. · NASDAQ:ANAB
Anaptysbio — Investor Presentation (January 2026)
65 slides from Anaptysbio's investor presentation, Jan 9, 2026
Slide 1: January 2026 Corporate Overview
January 2026 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 public companies
Biopharma Co ANB033 (CD122 antagonist) Rosnilimab (Pathogenic T cell depleter) ANB101 (BDCA2 modulator) Royalty Management Co Research-driven • R&D capabilities focused on immunology targets Note: YE 2025 cash: ~$310MM, which includes the receipt in Dec. 2025 of a one-time $75MM commercial sales mil
Slide 4: Biopharma Co would retain a leading autoimmune pipeline
4 Biopharma Co would retain a leading pipeline to deliver breakthroughs for patients with autoimmune diseases Antibody Program Therapeutic Indication Development Stage and Anticipated Milestones IND Enabling Phase 1 Phase 2 Phase 3 Rosnilimab (Pathogenic T cell depleter) Rheumatoid Arthritis ANB033
Slide 5: Royalty Management Co assets and upcoming catalysts
Antibody Program Indication Development Stage and Anticipated Milestones IND Enabling Phase 1 Phase 2 Phase 3 / Registrational Commercial Jemperli1 (PD-1 antagonist) 1L Endometrial Cancer 1L MMR Deficient Endometrial Cancer (chemo-free regimen) 2L dMMR/MSI-H Endometrial Cancer dMMR/MSI-H Pan Tumors
Slide 6: Royalty Assets
JemperliTM (dostarlimab, PD-1 antagonist) Imsidolimab (IL-36R antagonist) Royalty Assets
Slide 7: Jemperli GSK and Imsidolimab Vanda financial collaborations
7 Jemperli: GSK Financial Collaboration Imsidolimab: Vanda Financial Collaboration • Q3 2025 sales: $303 million (>16% US QoQ growth rate) o >$1.2b 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) • >$390 millio
Slide 8: Jemperli revenue forecasts on steep growth trajectory
Actuals 1. Actual Jemperli Q2 to Q3’25 QoQ growth was 16%, Forecast assumes illustrative constant ~10% QoQ sales growth from Q3’25 through Q2’27 and dMMR rectal approval; 2. GSK analyst consensus as of 11/26/2025 (solid blue), 9/15/2025 (dark dashed blue), and 11/26/2024 (light dashed blue) converte
Slide 9: Jemperli development in HNSCC, colorectal and pan tumors
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 • Rectal cancer: P2 AZ
Slide 10: Jemperli capped non-recourse monetization
Jemperli capped non-recourse monetization • Jemperli receivables payable to Sagard until cumulative $600MM paydown by Mar. 31, 20311,2 • As of YE 2025, estimate ~$250MM accrued to Sagard • Projected cumulative $600MM paydown between Q2 2027 to Q1 20283 Potential royalties to Anaptys from immuno- onc
Slide 11: Imsidolimab out-licensed to Vanda
11 Exclusive global license to Vanda announced February 2025 10% royalties on global net sales FDA BLA submitted for generalized pustular psoriasis (GPP) in December 20251 Imsidolimab: two positive global Phase 3 studies in GPP Imsidolimab (IL-36R antagonist) out-licensed to Vanda Key financial term
Slide 12: Biopharma Assets
ANB033 (CD122 antagonist) Rosnilimab (Pathogenic T cell depleter) ANB101 (BDCA2 modulator) Biopharma Assets
Slide 13: ANB033 (CD122 antagonist)
(CD122 antagonist) ANB033
Slide 14: CD122 and ANB033 mechanism
14 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 proliferation and survival Overexpressed in select diseases, including CeD gut
Slide 15: Broad therapeutic potential across autoimmune diseases
Gastroenterology Celiac Disease Eosinophilic Esophagitis (EOE) Crohn’s Disease 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 16: ANB033 survival benefit in GvHD mouse model
16 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 Body Wei L (car ied) Study Day W e ig h t (% o f S ta rt ) Cytolytic gene expression (Day 17) Expression (% of isotype) 0 50 100 150 GNLY GZMA GZMB ✱ ✱ ✱ ANB033 Forte anti-CD122 Belatacept Isoty
Slide 17: ANB033 Phase 1a trial in healthy volunteers
17 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 18: Favorable safety, tolerability and PK in Phase 1a
18 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 19: ANB033 reduces CD8+ T cells and NK cells
19 % C h a n g e f r o m b a s e li n e % C h a n g e f r o m b a s e li n e % C h a n g e f r o m b a s e li n e % C h a n g e f r o m b a s e 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
Slide 20: Sustained NK cell reduction with no safety issues
% C h a n g e f r o m b a s e 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 20 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)
Slide 21: ANB033 mechanism fit for celiac disease
21 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 22: CD122 antagonist targets both key drivers of celiac disease
22 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 23: ANB033 improves histology in CeD mouse model
23 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 24: ANB033 prevents reduction of Vh:Cd ratio
24 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 25: ANB033 limits IEL and T cell increases in CeD model
25 Sham Isotype ANB033 0 200000 400000 600000 800000 C o u n t o f C D 8 + I E L s * * Sham Isotype ANB033 0 20000 40000 60000 80000 C o u n t o f G ra n z y m e B + I E L s * * Sham Isotype ANB033 0 2000 4000 6000 C o u n t o f C D 4 + I F N -g + c e ll s * Epithelial layer of small intestine C o u
Slide 26: ANB033 differentiated 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), 100nM dose for all arms 26 IFNγ secretion 0 50 100 150 200 Antibody (nM) C
Slide 27: CeD patients present with range of histologic activity
27 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 28: ANB033 Phase 1b trial in CeD design
Primary Analysis ANB033 Phase 1b trial in CeD initiated Anticipate top-line data in Q4 2026 28 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 of Muc
Slide 29: Cohort 1 gluten challenge prevention of mucosal damage
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 30: 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 31: 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 32: New therapies could grow celiac market
32 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 33: 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 34: Downstream-only mechanisms have not succeeded 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 35: Eosinophilic inflammation model results
0 5×105 1×106 1.5×106 2×106 Lung ILC2 0 2×106 4×106 6×106 8×106 1×107 Lung eosinophils C e ll c o u n t 0 1×103 2×103 3×103 4×103 5×103 2×104 Esophageal eosinophils C e ll c o u n t sophageal sinophil ung e sinophils Lung ILC2s Model of eosinophilic inflammation: Balb/c mice were challenged intranas
Slide 36: ANB033 reduces Th2 cytokines driving EoE
I L -5 (% o f Is o ty p e C o n tr o l) IL-13 secretionIL-5 secretion 0.001 0.01 0.1 1 10 100 0 25 50 75 100 125 0 0.001 0.01 0.1 1 10 100 0 25 50 75 100 125 0 I L -1 3 (% o f Is o ty p e C o n tr o l) Antibody (nM)Antibody (nM) Unstim Is oty pe 5 n M 50 n M 500 n M 0 500 1000 1500 2000 IL-5 secreti
Slide 37: EoE significant market with unmet need
37 340,000 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 38: Rosnilimab (Pathogenic T Cell Depleter)
(Pathogenic T Cell Depleter) Rosnilimab
Slide 39: Rosnilimab targets pathogenic T cells
39 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 40: Pathogenic Teff and Tfh/Tph cells mediate autoimmunity
Adapted from Akiyama et al, Ann Rheum Dis, 2023. 40 Pathogenic Teff and Tfh/Tph cells mediate autoimmune pathology Lymphoid tissues Periphery Inflamed tissue 40 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 41: Depleting pathogenic T cells impacts RA drivers
Adapted from Aletaha and Smolen, JAMA, 2018; 1. Chen et al, Clinical and Translational Immunology, 2024. 41 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 42: Rosnilimab Phase 2b trial in RA
42 Screening Placebo SC (n=106) All-Active Off Drug Follow-Up Blinded Placebo- Controlled Treatment Blinded All-Active Treatment Rosnilimab SC 100mg Q4W (n=106) Rosnilimab SC 400mg Q4W (n=107) Rosnilimab SC 600mg Q2W (n=105) Rosnilimab SC 100mg Q4W (n=73) Rosnilimab SC 400mg Q4W (n=73) Rosnilimab SC
Slide 43: RA disease activity measures and continuation criteria
43 C D A I S c o r e 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 mont
Slide 44: Rosnilimab best-in-disease profile through 6 months
44 Responses durable for at least 3-months off-drug • 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 • Similar responses observed across mo
Slide 45: ACR20 response comparable to Rinvoq
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 46: 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 r o m B a s e 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 C
Slide 47: JAK-like efficacy in naive 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 48: 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 49: JAK-like CDAI remission rates
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 50: Responses by prior therapeutic agent
Rosnilimab Week 28 Responses Based on Prior Therapeutic Agent NRI analysis on ITT population (n=318 rosnilimab patients, pooled doses) 50 Similar responses observed across more stringent endpoints regardless of prior therapy type, including JAKs Graf et. al, “Rosnilimab, a Selective and Potent Deple
Slide 51: Durable responses off-drug at Week 38
Rosnilimab Week 28 Responders Maintaining Response Off-Drug (Week 38) Week 38 complete analysis 51 Durable responses for 3-months off-drug 82% of Week 28 CDAI LDA responders were still in response at Week 38 Graf et. al, “Rosnilimab, a Selective and Potent Depleter of Pathogenic T Cells, Demonstrate
Slide 52: Time to achieve LDA correlated with baseline activity
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 53: Pain VAS and CRP in CDAI responders
-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 54: Deep 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 e ll C o u n t ( % C h a n g e f r o m B a s e 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
Slide 55: Synovial biopsies show ~90% T cell reduction
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 56: Synovial gene expression: T and B cell activation
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 r e s s io n ( Z -s c o r e ) G e n e e x p r e s s io n ( Z -s c o r e ) 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 r e d u c ti o n Magnitude of reduction: 4.03,
Slide 57: Pathway changes reflect broad MOA
IL-6 Production G e n e e x p r e s s io n ( Z -s c o r e ) G e n e e x p r e s s io n ( Z -s c o r e ) 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, TN
Slide 58: Competitive Landscape
58 Competitive Landscape Fc receptor binding affinity Tissue (RA Synovium) Depletion Peripheral (Blood) Depletion Membrane- proximal epitope S tr u c tu r a l c h a r a c te r is ti c s C li n ic a l/ tr a n s la ti o n a l o u tp u ts 1 Rosnilimab is a best-in-class pathogenic T cell depleter Compe
Slide 59: Rosnilimab vs peresolimab: CDAI LDA and T cell impact
0% 10% 20% 30% 40% 50% 60% 70% 80% % o f P a ti e n 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 e n ts 300mg Q4W 700mg Q4W Wk 12 Wk 14 Wk 24 Wk 0 Wk 0 (12-wk off-drug) Wk 38 (12-14 wk off-drug) Wk 36 Rosnilimab P2b: CDAI LDA NRI analysis on ITT
Slide 60: Black box warnings have not impeded blockbuster sales
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 61: Rosnilimab Phase 2b adverse events
61 Study Period Week 0 through Week 12 (N=424) Week 0 through Week 38 (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 62: RA is substantial opportunity for new class of biologics
Target population in US generated ~$10 billion in 20212 • Rituxan/biosimilars (typically salvage therapy) achieves well over $1 billion sales in 3L+ RA despite infection risk Fragmented market with lack of established SOC in 2L+ • No clear treatment of choice after failure of anti-TNFs • No new ther
Slide 63: Next steps for rosnilimab
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 • Late-break
Slide 64: ANB101 (BDCA2 modulator)
(BDCA2 modulator) ANB101
Slide 65: ANB101 BDCA2 modulator of pDC function
ANB101 will potently inhibit interferon secretion and immune activation 65 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