Slide 1: ANB033 (CD122 antagonist) Investor Event
Oct. 14, 2025 ANB033 (CD122 antagonist) Investor Event
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: Why target CD122?
4 • Targeting only the IL-15 cytokine addresses inflammation, but may allow pathogenic cell survival through alternative escape mechanisms • CD122 is the shared receptor subunit through which both IL-15 and IL-2 signal • IL-15 and IL-2 are central cytokines in pathogenic inflammation across broad in
Slide 5: ANB033 designed for high potency
ANB033 designed for high potency • Specific binding epitope engineered for high affinity • Inhibit both IL-15 and IL-2 signaling Targets pathogenic cells in inflamed tissue • Subsets of activated T cells o Cytotoxic CD8+ T cells o Memory CD4+ Th1/Th2 T cells o IELs • ILC2s • NK cells Subcutaneous do
Slide 6: Broad therapeutic potential across autoimmune and inflammatory 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 7: ANB033 has pipeline-in-a-product potential
7 ANB033: initiated initial P1b in CeD • Multiple pathogenic drivers of disease • Inflamed cells in CeD respond to both IL-15 and IL-2 • Targeting IL-15 / CD122 is clinically validated Expansion opportunities • GI, dermatology and other therapeutic areas • Assessing potential to treat EoE • >250k di
Slide 8: Agenda: ANB033 (CD122 Antagonist)
TOPIC SPEAKER CD122 biology and preclinical data Martin Dahl, Ph.D., Senior Vice President, Research Phase 1a in healthy volunteers John Kwon, M.D., Ph.D. Vice President, Clinical Development Drug development for CeD Joseph Murray, M.D. Professor of Medicine Mayo Clinic College of Medicine, Rocheste
Slide 9: ANB033 blocks CD122 to inhibit pathogenic immune cells
9 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, inclu
Slide 10: ANB033 epitope sits within IL-15 and IL-2 binding footprint
ANB033 epitope sits squarely within IL-15 and IL-2 binding footprint 10-2 10-1 100 101 102 0 25 50 75 100 125 0 10-2 10-1 100 101 102 0 25 50 75 100 125 0 S T A T 5 R e p o rt e r (% o f S ti m ul at ed ) S T A T 5 R e p o rt e r (% o f S ti m ul at ed ) Antibody (nM) Antibody (nM) ANB033’s optimize
Slide 11: ANB033 survival benefit in aggressive GvHD mouse model
11 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 12: ANB033 reduces key CD122+ target cells in cynomolgus monkeys
% 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 Vehicle ANB033 – 10mg/kg SC ANB033 – 100mg/kg SC Recovery -100
Slide 13: CeD characterized by dense infiltration of CD122+ immune cells
13 Granzyme B umap1 IFNγ u m a p 2 IFNG GZMB Cell Biopsy scRNAseq NK CD8+ T cells CD4+ T cells Structural cells, myeloid cells, and B cells CD122 IL15 CeD is characterized by a dense infiltration of inflammatory CD122+ immune cells Richards et al, Cell Rep. 2025 Jul 21;44(8):116039; UMAP of single-c
Slide 14: ANB033's MOA ideal fit for targeting CeD inflammation
14 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 15: Previous approaches have not addressed multiple pathogenic drivers of CeD
15 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 16: ANB033 improves histology in CeD mouse model
16 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 17: ANB033 prevents reduction of Vh:Cd ratio
17 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 18: ANB033 prevents increase in IELs and inflammatory T cells
18 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 19: ANB033 in CeD patient-derived PBMCs vs competing therapies
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). 19 IFNγ secretion 0 50 100 150 200 Antibody (nM) CD4+ Th1/Th2 T cells 10-3
Slide 20: Assessing ANB033's potential to treat EoE
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 PsA Type 1 Diabetes Solid Organ Transplant Assessing ANB033’s potentia
Slide 21: EoE characterized by dense infiltration of CD122+ immune cells
Dense CD122 expression by infiltrating CD8+ T cells, CD4+ T cells, NK cells • Across both dupilumab-sensitive and insensitive mechanisms Broad IL15 expression by structural cells • Epithelial cells, myeloid cells and lymphocytes CD8+ and NK (dupilumab-insensitive pathway) CD4+ and ILC2 (dupilumab-se
Slide 22: ANB033 targets multiple drivers of EoE biology
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 23: Mechanisms targeting only downstream signals 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 24: ANB033 reduces Th2 cytokines from CD4+ T cells and ILC2
IL -5 (% o f Is ot yp e C on tr ol ) 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 IL -1 3 (% o f Is ot yp e C on tr ol ) Antibody (nM)Antibody (nM) Unstim Isotype 5 nM 50 nM 500 nM 0 500 1000 1500 2000 IL-5 secretion IL -5 (p
Slide 25: ANB033 reduces Th1 cytokines and cytolytic markers
IFNγ secretion Granzyme B secretion 0.001 0.01 0.1 1 10 100 0 50 100 150 00.001 0.01 0.1 1 10 100 0 50 100 150 0 IF N γ (% o f Is ot yp e C on tr ol ) G ra n zy m e B (% o f Is ot yp e C on tr ol ) Antibody (nM)Antibody (nM) ANB033 Isotype Control ANB033 reduces CD8+ T cell and NK cell derived Th1 c
Slide 26: ANB033 prevents eosinophilia
26 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 27: Agenda: ANB033 (CD122 Antagonist)
TOPIC SPEAKER CD122 biology and preclinical data Martin Dahl, Ph.D., Senior Vice President, Research Phase 1a in healthy volunteers John Kwon, M.D., Ph.D. Vice President, Clinical Development Drug development for CeD Joseph Murray, M.D. Professor of Medicine Mayo Clinic College of Medicine, Rocheste
Slide 28: ANB033 Phase 1a trial in healthy volunteers
28 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 29: Favorable safety, tolerability and PK profile in Phase 1a
29 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 30: ANB033 reduces CD8+ T cells and NK cells after single dose
30 % 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 31: Sustained reduction in CD122+ NK cells 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 31 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 32: Agenda: ANB033 (CD122 Antagonist)
TOPIC SPEAKER CD122 biology and preclinical data Martin Dahl, Ph.D., Senior Vice President, Research Phase 1a in healthy volunteers John Kwon, M.D., Ph.D. Vice President, Clinical Development Drug development for CeD Joseph Murray, M.D. Professor of Medicine Mayo Clinic College of Medicine, Rocheste
Slide 33: KOL discussion: Joseph A. Murray, M.D.
©2025 Mayo Foundation for Medical Education and Research | WF3855367-33 • Co-founder and past president of North American Society for Study of CeD • Contributed to 2013 guidelines and 2019 AGA practice update on diagnosing and monitoring CeD • Published more than 450+ peer- reviewed papers on CeD •
Slide 34: Gluten and Celiac Disease
©2025 Mayo Foundation for Medical Education and Research | WF3855367-34 Gluten and Celiac Disease (CeD) Gluten Gluten exclusion Normal histology (Marsh 0) • Genetic predisposition • Permanent intolerance to gluten • Inflammation • Villi destruction • Crypt hyperplasia • IEL proliferation Note: Marsh
Slide 35: Majority of CeD patients desire new treatment options
©2025 Mayo Foundation for Medical Education and Research | WF3855367-35 Majority of CeD patients desire new treatment options • In 2022, only 12% of participants agreed “a great deal” that a gluten free diet was a sufficient treatment, compared to 27% in 2014 There has been a significant decline in
Slide 36: CeD has a multi-cell pathology
©2025 Mayo Foundation for Medical Education and Research | WF3855367-36 • Immune scarring is present in treated CeD o Epithelial-stromal- immune impacts / interactions • IL-2, produced by CD4 T cells, elevates following gluten ingestion o Starting 2 hrs. after exposure • Stressed epithelial cells ex
Slide 37: Mechanisms that have been tried in CeD
©2025 Mayo Foundation for Medical Education and Research | WF3855367-37 Some mechanisms that have been tried in CeD… Toxic wheatA B C D E F Non-toxic wheat A Enzymes + Gluten peptide fragmentsWheat Protease supplement (IMGX003), Kumamax (TAK-062), and Allergan Probiotics (B. infantis) Permeabili
Slide 38: Rationale in targeting CD8 and CD4 T cells
©2025 Mayo Foundation for Medical Education and Research | WF3855367-38 • Overactive IL-15 and IL-2 signaling drives pathogenic immune cell expansion and inflammation effects • IL-15 is inflammatory cytokine o Expressed by stressed epithelial cells o Supports T cell and NK cell homeostasis and expan
Slide 39: Serum IL-2 elevated in CeD patients
©2025 Mayo Foundation for Medical Education and Research | WF3855367-39 Serum IL-2, produced by CD4 T cells, elevated in CeD patients • Increase in IL-2 seen within two hours of gluten ingestion • Magnitude of IL-2 response correlates with severity of symptoms • IL-2 elevation key marker for central
Slide 40: Gluten exposure induces significant serum IL-2 increase
©2025 Mayo Foundation for Medical Education and Research | WF3855367-40 Gluten exposure induces significant serum IL-2 increase vs. sham Immunotherapy aiming to restore tolerance in CD4+ T cells failed to reduce significant IL-2 induction from gluten challenge Nexvax2 Placebo Gluten Sham Gluten Glut
Slide 41: IL-15 a key driver of IEL expansion
©2025 Mayo Foundation for Medical Education and Research | WF3855367-41 IL-15 a key driver of IEL expansion Left panel: Mouse model over-expressing IL-15Ra in the intestinal epithelial cell Right panel: Mouse models with genetic predisposition to celiac disease (HLA-DQ8) and IL-15 expression driven
Slide 42: Inhibiting CD122+ CD4+ and CD8+ cells and IL-15 and IL-2 signaling
©2025 Mayo Foundation for Medical Education and Research | WF3855367-42 • CD122 shared receptor subunit through which both IL-15 and IL-2 signal • Expressed on range of immune cells: CD8+ and CD4+ T cells, NK cells • Inhibiting IL-15 and IL- 2 signaling inhibits subsets of these cells, reducing infl
Slide 43: Latiglutenase: effective in prevention but not healing
©2025 Mayo Foundation for Medical Education and Research | WF3855367-43 Latiglutenase attenuates mucosal damage by ~80% based on ratio of means for IMGX003 vs. placebo arms Based on means latiglutenase attenuated abdominal pains for 2g gluten per day by 93% This MOA was not predictive for symptomati
Slide 44: Considerations for Phase 1b CeD trial design
©2025 Mayo Foundation for Medical Education and Research | WF3855367-44 • Traditional P1b gluten challenge o Controlled symptoms and limited mucosal damage at baseline • P2b and P3 population targets symptomatic CeD patients with mucosal damage • Drugs whose MOA breaks down gluten (e.g., latiglutena
Slide 45: Perspectives on FDA guidance for CeD
©2025 Mayo Foundation for Medical Education and Research | WF3855367-45 • GREAT Conference* o Significant public engagement at advocacy meetings (Beyond Celiac 2024) • Alignment on P2/P3 target population: symptomatic CeD despite a GFD* • Need to prevent symptoms of gluten exposure in CeD patients a
Slide 46: Agenda: ANB033 (CD122 Antagonist)
TOPIC SPEAKER CD122 biology and preclinical data Martin Dahl, Ph.D., Senior Vice President, Research Phase 1a in healthy volunteers John Kwon, M.D., Ph.D. Vice President, Clinical Development Drug development for CeD Joseph Murray, M.D. Professor of Medicine Mayo Clinic College of Medicine, Rocheste
Slide 47: Symptomatically controlled CeD patients present with range of histologic activity
47 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 48: ANB033 Phase 1b trial in CeD initiated
Primary Analysis ANB033 Phase 1b trial in CeD initiated Anticipate top-line data by year-end 2026 48 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 49: CeD quantitative histology and qualitative symptom assessments
Qualitative evaluation to track changes during treatment or gluten exposure • CeD Symptom Diary (CDSD) monitors symptoms, including o Severity: nausea, abdominal pain, tiredness, and bloating o Frequency: vomiting, diarrhea, and bowel movements Symptom controlled Poorly controlledAsymptomatic Sympto
Slide 50: Cohort 1: gluten challenge to assess 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 51: Cohort 2: ability to heal mucosal damage
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 52: Agenda: ANB033 (CD122 Antagonist)
TOPIC SPEAKER CD122 biology and preclinical data Martin Dahl, Ph.D., Senior Vice President, Research Phase 1a in healthy volunteers John Kwon, M.D., Ph.D. Vice President, Clinical Development Drug development for CeD Joseph Murray, M.D. Professor of Medicine Mayo Clinic College of Medicine, Rocheste
Slide 53: Potential blockbuster opportunity for ANB033 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 54: New therapies in CeD could grow market
54 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 55: Assessing potential to treat EoE: significant market
55 340,000 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 56: Antibody program development stage 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