Anaptysbio, Inc. · NASDAQ:ANAB
Anaptysbio — Investor Presentation (March 2026)
66 slides from Anaptysbio's investor presentation, Mar 3, 2026
Slide 1: Corporate Overview March 2026
OUR VISIC Transform patient health t Innovative immunology therap s Corporate Overview March 2026
Slide 2: Safe harbor statement
Safe harbor statement Vv 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
Slide 3: Intention to separate into two independent, publicly traded companies
Intention to separate into two independent, publicly traded \o companies to unlock and maximize value as early as Q2 2026 ‘4 First Tracks Biotherapeutics (Biopharma Co) Pib in Celiac Disease ANBO33 (CD122 antagonist) P1b in Eosinophilic Esophagitis Rosnilimab P2b completed in (Pathogenic Rheumatoid
Slide 4: First Tracks Biotherapeutics would retain a leading pipeline
First Tracks Biotherapeutics would retain a leading pipeline t\Y deliver breakthroughs for patients with autoimmune diseases ‘4 yp 2 S 2 a Fi 3 ° = o 1s) o fs a € = a Antibody Program Rosnilimab (Pathogenic Therapeutic Indication Rheumatoid IND Enabling Development Stage and Anticipated Milestones P
Slide 5: Pipeline: Jemperli and imsidolimab programs
V Antibody IND Phase 3 / . Program Indication Enabling Phase 1 Phase 2 Registrational Commercial aL Approved in US Endometrial Cancer and ex-US? AL MMR Deficient DOMENICA Endometrial Cancer Est. primary comp. {(chemo-free regimen) Q2 2026* 2L dMMR/MSI-H Approved in US . Endometrial Cancer and ex-US
Slide 6: AnaptysBio (Royalty Management Co)
AnaptysBio (Royalty Management Co) Jemperli™ (dostarlimab, PD-1 antagonist) Imsidolimab (IL-36R antagonist)
Slide 7: Royalty Management Co would protect and return value of Jemperli and imsidolimab royalties
Royalty Management Co would protect and return value of Jemperli and imsidolimab royalties to shareholders Jemperli: GSK Financial Collaboration + 2025 sales of >$1.1 billion + Exited 2025 with ~$1.4 billion annualized run rate + Q4 2025 sales: $343 million (>13% QoQ growth rate) + Significant royal
Slide 8: Potential royalties to Anaptys from GSK immuno-oncology financial collaboration
Potential royalties to Anaptys from GSK immuno- \f oncology financial collaboration 7 Royalty rate 8% - $0 to $1 billion Jemperii: \ 12% - $1.0 to $1.5 billion (PD-1 antagonist) (annual WW 20% - $1.5 to $2.5 billion net sales) 25% - >$2.5 billion @ Sagard Jemperli capped non-recourse monetization +
Slide 9: Jemperli on a steep growth trajectory with GSK guiding to peak sales
Jemperli on a steep growth trajectory with GSK guiding to \y greater than £2 billion ($2.7 billion) peak monotherapy sales 4 Jemperli Revenue Forecasts Actuals $2,500 4 Sagard paydown expected between I _ . I Q2 2027 (~10% QoQ growth) I Jan '26: GSK sell sid sansensus 1 or Q1 2028 (WS consensus as o
Slide 10: GSK immuno-oncology financial collaboration
GSK immuno-oncology financial collaboration VW Jemperli lw (PD-1 antagonist) (dostarlimab-2xly) ren stom Endometrial cancer (approved indications) + 1L endometrial cancer: Approved in US and EU for primary advanced or recurrent EC in combination with chemo + 2L endometrial cancer: Approved (monother
Slide 11: Imsidolimab out-licensed to Vanda
Imsidolimab (IL-36R antagonist) out-licensed to Vanda VY Key financial terms to Anaptys Exclusive global license to Vanda announced February 2025 $35 million future milestones2 $5 million - FDA approval in GPP $5 million - EMA approval in GPP $25 million - Achievement of $100 million WW annual net s
Slide 12: First Tracks Biotherapeutics (Biopharma Assets)
First Tracks Biotherapeutics (Biopharma Assets) ANBO33 (CD122 antagonist) Rosnilimab (Pathogenic T cell depleter) ANB101 (BDCA2 modulator)
Slide 13: ANB033 (CD122 antagonist)
ANBO33 (CD122 antagonist)
Slide 14: ANB033 blocks CD122 to inhibit pathogenic immune cells
ANBO33 blocks CD122 to inhibit pathogenic immune cells Y CD122 is the beta subunit (IL-2RB) 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 surviv
Slide 15: Broad therapeutic potential across autoimmune and inflammatory diseases
Broad therapeutic potential across autoimmune and \Y inflammatory diseases ‘4 Gastroenterology Dermatology Other Areas Celiac Disease (CeD) Atopic Dermatitis Asthma/COPD Eosinophilic Esophagitis (EoE) Alopecia Areata Multiple Sclerosis Crohn’s Disease Hidradenitis Suppurativa Psoriatic Arthritis Ulc
Slide 16: ANB033 survival benefit in aggressive GVHD mouse model
ANBO33 shows strong survival benefit and reduced cytolytic \f gene expression in aggressive GVHD mouse model 7 Survival Body weight loss (carried) 10 [LL ¢ End of dosing $ End of dosing t “@ Ans033 = Forte anti-cD122 + Belatacept eK © KKK “@- Isotype Control 40 20 30 40 50 60 o Time (Days) 10 20 30
Slide 17: ANB033 Phase 1a trial ongoing in healthy volunteers
ANBO33 Phase 1a trial ongoing in healthy volunteers VW + Safety and tolerability + Evaluate PK and immunogenicity All healthy volunteers have been dosed o ANBO33: 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* *
Slide 18: ANB033 favorable safety, tolerability and PK profile in Phase 1a
ANBO33 demonstrated favorable safety, tolerability and \y PK profile in Phase 1a ‘4 Phase 1a results to date v Safe and well tolerated vy No unexpected findings v PK and PD support SC dosing Favorable safety and tolerability Rapid and sustained PK profile + No safety concerns at any dose + Favorable
Slide 19: ANB033 reduces CeD relevant CD8+ T cells and NK cells
NK cells after single dose ANBO33 significantly reduces CeD relevant CD8+ T cells and \Y Effect of ANBO33 is limited to CD122 expressing cells 4 CD122+ CD8+ T cell impact CD122+ NK cell impact 20% % 20% 2 0% £ 3 0% G 0% i 5 | S -20% E -20% £ 6 -21% © -40% £ -40% © o & -60% 2 -60% 5 z § 80% -69% 74%
Slide 20: Anti-IL-15 and CD122 therapies show sustained NK cell reduction
Anti-IL-15 and CD122 therapies have demonstrated sustained\Y reduction in CD122+ NK cells with no observed safety issues 4 ANBO33 effect on total NK cells 75% @ Placebo -e-IV Dose =SC Dose ® = 50% TEV-53408 Effect on Total NK Cells (Pooled)+ 3 (through Day 554) 8 e-Picebo e-1-10mg SC -9-50-150mg SC
Slide 21: ANB033 MOA fit for targeting CeD inflammation
ANBO33’s MOA is an ideal fit for targeting CeD inflammation \Y CeD marked by excessive IL-15 and IL-2 production which perpetuates disease Gliadin from re a 1 Inhi Loss of barrier integrity I re ion of IL-15 signaling IL-15 induces proliferation of IELs o Majority of IELs are CD122+ T cells Inhibiti
Slide 22: Previous approaches have not addressed multiple pathogenic drivers of CeD
Previous approaches have not addressed the multiple Y pathogenic drivers of CeD However, a CD122 antagonist targets both key pathogenic drivers of CeD Gliadin from gluten Loss of barrier integrity IL-15 antagonists: Clinical PoC teva Wwnovartis AMGEN he 2 ongoing Pib PoC Lacked potency (— Non-immune
Slide 23: ANB033 prevents gluten-induced villous atrophy
ANBO33 prevents the key CeD histologic manifestation of \y gluten-induced villous atrophy ‘4 Sham Gluten + Gluten + Isotype Control ANBO33 ANBO33 treatment shows improved histology: preserves villus height and crypt depth (Vh:Cd) in CeD mouse model Note: HuDQ8-D‘~villin-IL-15tg mice on a gluten-free
Slide 24: ANB033 prevents reduction of Vh:Cd ratio
ANBO33 significantly prevents the reduction of Vh:Cd ratio \y compared to control 4 Vh:Cd ratio ANBO33 impact on Vh:Cd ratio Healthy tissue: * bad High villus height, lower crypt depth Uy 1F 1 Healing <> Injury 2 ° 3 e 4 3 8 ® 5? t > Marsh classification e CeD tissue: e Reduced villus height, extend
Slide 25: ANB033 prevents gluten-induced intestinal inflammation
ANBO33 prevents gluten-induced intestinal inflammation VW Epithelial layer of small intestine No increase in CD8+ IELs 4s 8000004 * * Le z + = o 600000: a oO Ss 400000 z 3 2000004 oO oe | = Sham Isotype | ANBO33 +Gluten + Gluten No increase in Granzyme B+ IELs 800005 * * 4 m—,_1r1210O 4 tH oO 4 ay 6
Slide 26: ANB033 differentiated impact in CeD patient-derived PBMCs
ANBO33 shows differentiated impact in CeD patient-derived PBMCs compared to competing anti-IL-15s and CD122s CD4+ Thi/Th2 T cells Cytotoxic CD8+ T cells Clinical 120 Giinical 120. range renge 22 100: 23 100: SS 80 ES 20. a eS gr 6 54 60. 25 £5 ge 40 Se & al 20 20: °. = 0. 102 102 101 10° 101 102 102
Slide 27: Symptomatically controlled CeD patients present with range of histologic activity
Symptomatically controlled CeD patients present with range Y of histologic activity Histology (vn:cd ratio) 3.5 2.5 Normal Symptoms Asymptom 2.0 Mucosal damage Symptom controlled Symptomatically controlled on GF diet Gluten challenge Phase 1 population !, Nearly all P1b/P2a studies only assess abili
Slide 28: ANB033 Phase 1b trial in CeD initiated
ANBO33 Phase 1b trial in CeD initiated \y Anticipate top-line data in Q4 2026 ‘4 Prevention of Mucosal Damage Follow-Up Period Cohort 1 (6 weeks) (n=30) Screening ‘ANBO33 SC Dose Q2W (up to 30 days) Vh:Cd 22.0 Placebo SC Dose Q2W 7 Primary analysis eee SX gests, eeniGlenatener Mucosal Healin, i C2 w
Slide 29: Cohort 1 gluten challenge to assess prevention of mucosal damage
Cohort 1 (Vh:Cd 2 2.0) is a gluten-challenge to assess YY prevention of mucosal damage Prevention of Mucosal Damage Follow-Up Period Cohort 1 Cro) (n=30) Screening ANBO33 SC Dose Q2W (up to 30 days) >| Vh:Cd >2.0 Placebo SC Dose Q2W Primary analysis IK basetine Endoscopy Week 6 Endoscopy a T T T T T
Slide 30: Cohort 2 assesses ability to heal mucosal damage
damage in symptom-controlled patients Cohort 2 (Vh:Cd < 2.0) assesses ability to heal mucosal YY Mucosal Healing Follow-Up Period Cohort 2 (22 weeks) (n=30) Screening ANBO33 SC Dose Q2W (up to 30 days) >| Vh:Cd <2.0 Placebo SC Dose Q2W Primary Analysis KK basetine Endoscopy Week 12 Endoscopy a T T T
Slide 31: Potential blockbuster opportunity for ANB033 in non-responsive CeD
Potential blockbuster opportunity for ANBO33 in \Y non-responsive CeD ‘4 High disease burden + Debilitating symptoms, social isolation U.S. patients? + Disease awareness driving growth (prevalence) + No approved therapies CD122s differentiated from other Tx in development + HCPs favor MOA that targe
Slide 32: New therapies in CeD could grow market
New therapies in CeD could grow market in responsive and \f newly diagnosed patients 4 All-Comers Prevention in newly diagnosed ~1M Subset of Responsive GF diet liberation ~600K Initial Target Population Non-Responsive Mitigate symptoms As the celiac market evolves, more patients, and) camade like t
Slide 33: ANB033 targets multiple drivers of EoE
addressing both dupilumab sensitive and insensitive pathways Similar to CeD, ANBO33 targets multiple drivers of EoE thwave WA Phase 1b trial initiated; Anticipate top-line data in 2027 4 Allergens, irritants, microbes, reflux, etc. Barrier Dysfunction IL. <— CD4+ and ILC2 a ame (dupilumab-sensitive)
Slide 34: Mechanisms targeting only downstream signals have not succeeded in EoE
Mechanisms that target only downstream signals of inflammation have not been successful in EoE Allergens, irritants, microbes, reflux, etc. Barrier Dysfunction "other" inflammation (dupilumab-insensitive) “Th2" inflammation (dupilumab-sensitive) igophil recrujser€nt Adapted from Discepolo et. al. Ga
Slide 35: ANB033 prevents eosinophilia by targeting upstream inflammation
ANBO33 prevents eosinophilia by targeting upstream YY inflammation 4 Esophageal eosinophils 2x1044 5x103 4x1034 3x1034 2«1034 Cell Count Cell Count Lung eosinophils gt a a Aspergillus-induced eosinophilia 2105. 1.5*105 1*105 Cell Count g x SG Treatment Unchallenged Isotype control ANBO33 anti-mIL-15
Slide 36: ANB033 prevents cytokine and chemokine secretion driving eosinophils
ANBO33 also prevents cytokine secretion and chemokine \ secretion responsible for eosinophil expansion and recruitment ‘4 Aspergillus-induced eosinophilia Eotaxin 2004 Treatment . Unchallenged 180-7 Isot trol 4 . sotype control & ANBOSS ANBO33 t: e 1% o anti-mIL-15 preven. 50 ¥ i anti-mIL-13 7 é ; ;
Slide 37: ANB033 reduces CD4+ T cell and ILC2 derived Th2 cytokines
ANBO33 reduces CD4+ T cell and ILC2 derived Th2 cytokines, \y proven drivers of EoE pathology 7 IL-5 secretion IL-13 secretion > 77 Clinical 1255 Glinical g 3 = 100 S100 S 8 S 2 we 734 mo 754 oa ae a 8 8 504 4 4 a 3 as ‘S25 = 3 S254 <4 = 4 © 0.001 0 ot tt t00 0 oo tot tt t00 Antibody (nM) Antibody (
Slide 38: EoE is a significant market with increasing prevalence and unmet need
EoE is a significant market with increasing prevalence and VY unmet need 340,000 diagnosed U.S. patients* 170,000 biologic-eligible initial target population ~30,000! Dupixent-treated Significant unmet need with limited approved therapies + «50% PPI or steroid non-responsive or intolerant + Dupixent
Slide 39: Rosnilimab (Pathogenic T Cell Depleter)
Rosnilimab (Pathogenic T Cell Depleter)
Slide 40: Rosnilimab selectively targets pathogenic T cells
Rosnilimab selectively targets pathogenic T cells in periphery \4 and inflamed tissue to restore immune homeostasis 4 Dendritic cell Rosnilimab aims to: Leverage natural immune regulatory pathway to safely restore immune homeostasis EEN HEARS Achieve durable remission and modify disease Illustrative
Slide 41: Pathogenic Teff and Tfh/Tph cells mediate autoimmune pathology
Pathogenic T.,;, and T;,/T,,, cells mediate autoimmune \Y pathology 4 + Secrete CXCL13 and IL-21 which recruit and mature B cells Ty, (follicular helper) into “autoantibody secreting” plasma cells Tpn (peripheral helper) Depletion results in downstream effect on B cells, plasma cell generation and a
Slide 42: Depleting pathogenic T cells impacts multiple drivers of RA
Depleting pathogenic T cells broadly impacts multiple \/ downstream, clinically validated drivers of RA pathogenesis 7 Lymph node are Synovium N, Activated Fibroblast IL-17 «KI IFNy / , -- TNF (ANF inhibitors >) IL-6 (2U6 inhibitors )) 8 B. “ee? I 6 (Bell depleters ) CRP ° Autoantibodies a (e.g., a-
Slide 43: Rosnilimab Phase 2b trial in RA
Rosnilimab Phase 2b trial in RA VW 95% completed 6-month all-active treatment period supporting rosnilimab's favorable efficacy and tolerability profile All-Active Off Drug Follow-Up Blinded All-Active Treatment Blinded Placebo- Screening Controlled Treatment On csDMARD Placebo SC (n=106) Reaithimas
Slide 44: LDA requirement was a high bar for high disease activity patients
LDA requirement at 14 weeks to continue on rosnilimab was \Z a high bar for patients with baseline high disease activity VW 95% of trial participants had high disease activity (CDAI > 22) at baseline Disease Activity 76 Treaters target a well-controlled disease state (e.g., LDA) by 6 months; however
Slide 45: Rosnilimab demonstrates best-in-disease profile in RA
Rosnilimab demonstrates best-in-disease profile in RA VW 5 Late-breaking oral presentation by Professor Paul Emery at ACR Convergence 202 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 more
Slide 46: ACR20 response rates are comparable to Rinvoq
ACR20 response rates are comparable to Rinvoq™ YY Most patients had symptomatic and clinical improvement by 3 months ACR20;btedMaRD Experience oo NRI analysis on ITT population (n=174 total; n=44 placebo, n=130 rosnilimab)? (AREY 23 Mees 12 100% PBO Arm Absolute | adjusted Rinvog's higher response r
Slide 47: CRP reductions are comparable to Rinvoq
CRP reductions are comparable to Rinvoq™ \Z Mean Change in CRP: b/tsDMARD-Experienced! MMRM Analysis on ITT population (n=174 total; n=44 placebo, n=130 rosnilimab) Change in CRP at Week 12 4 f mm “ Baseline PBO | Rinvoa™ (Phase 2b TNF-Experienced Study*) Arm Mean cre | Adjusted 2 AL | Dark Orange ~
Slide 48: Rosnilimab shows JAK-like efficacy in naive patients
Rosnilimab shows JAK-like efficacy in naive patients VY Compares favorably despite most conservative analysis and capped trial design b/tsDMARD-Naive NRL analysis on ITT population (n=188 rosnilimab patients)* 80% ' 1 70% t H BRosnilimab - Pooled Doses 64% mRinvoq’- SELECT-COMPARE™ cox |_ 60% i Humi
Slide 49: Rosnilimab comparable to JAKs in experienced patients
comparable at mid/high dose to JAKs in all-active H2H study Includes 29% with prior JAK experience Excludes 7 patients who discontinued in all-active treatment period while in CDAI LDA Rosnilimab surpassed TPP in experienced patients and ‘Vv b/tsDMARD-Experienced “In H2H comparator studies, patients
Slide 50: JAK-like CDAI remission rates deepened into six months
JAK-like CDAI remission rates which deepened into six months Includes 29% with prior JAK experience Excludes 2 patients who discontinued in the all-active treatment period while in CDAI remission 20% 15% 10% % of Patients 5% 0% CDAI Remission: b/tsDMARD-Experienced * NRI+W18: adds to NRI anal who we
Slide 51: Similar responses regardless of prior therapy type, including JAKs
Similar responses observed across more stringent endpoints \Y regardless of prior therapy type, including JAKs ‘4 Rosnilimab Week 28 Responses Based on Prior Therapeutic Agent NRI analysis on ITT population (n=318 rosnilimab patients, pooled doses) 9 60% x 54% 9 50% 47% 43% 40% 40% 2 9) é 33% 32% Z
Slide 52: Durable responses for 3 months off-drug
Durable responses for 3- months off-drug \4 82% of Week 28 CDAI LDA responders were still in response at Week 38 7 Rosnilimab Week 28 Responders Maintaining Response Off-Drug (Week 38) Week 38 complete analysis 90% om : 80% 2% 80% 79% 78% of " " op 79% 80% 6 77% aS 77% 550, 99% 70% 67% 02% 60% 2 FS
Slide 53: Max response was not achieved in this Phase 2b trial
Max response was not achieved in this Phase 2b trial \Z On average, patients with higher disease activity take longer to achieve CDAI LDA Median Change from Baseline in CDAI NRI analysis on ITT population (n=318 rosnilimab patients) 60 Time to achieve LDA correlated with baseline disease a ¥ 69% (22
Slide 54: Clinically meaningful improvement across multiple PROs and CRP
Highly meaningful clinically and symptomatic improvement \Y across multiple PROs and CRP ‘4 HAQ-DI: Overall Pain VAS: Overall MMRM analysis on CDAI Responder Population (n=220) MMRM analysis on CDAI Responder Population (n=220)4 0.0 0 MCID: -0.22 from baseline? wo MCID: -10 from baseline? $-10 $ -0.
Slide 55: Deep, sustained reduction of pathogenic T cells
Deep, sustained reduction of pathogenic T cells led to favorable T ceil VY composition reflective of immune homeostasis and durable response Rosnilimab 400mg Q4W T Cell Impact 100% 2 75% % 50% = at 25% noe §2 0% ao] $3 -25% a £ -50% a é £ -75% ae -100% = WkO = =Wk6) =~ Wk12 Wk28 Wk38 (12-wk off-drug
Slide 56: Impact on Tph and Teff cells in synovium
: 7 n d I nm n i VW Impact on Tpn and Ter cells ~90% reduction Inconclusive reduction Increased Rosnilimab 600mg Q2wW T cell markers APC markers PD-1 56 Note: Synovial biopsies of the most impacted joint taken at baseline and 6 weeks on study. Immunofluorescence performed to identify PD-1 positive c
Slide 57: On-target pharmacology within the synovium
on target pharmacology within the synovium T Cell Activation Bw B Cell Activation Baseline Week 6 a Baseline Week 6 Significant reduction of T and B cell activation demonstrate Vv i aus Gene expression (Z-score) Gene expression (Z-score) a ! + —__ = = = a 2 eo - me | . = a = = = : —! Magnitude of re
Slide 58: Reduction of downstream pathways including TNF and IL-6
Significant reduction of additional downstream pathways \f including TNF and IL-6 within the synovium ‘4 TNF Production | 4 | IL-6 Production Baseline Week 6 ry Baseline Week 6 z La Gene expression (Z-score) Gene expression (Z-score) 1 | | wi mt in| a . Aes ee 1 hb ] = 5 Magnitude of reduction: 3.38
Slide 59: Rosnilimab is a best-in-class pathogenic T cell depleter
Rosnilimab is a best-in-class pathogenic T cell depleter Vy sii Competitors lack ability to potently deplete pathogenic T cells to restore immune homeosta First Tracks . . i i Lilly NJ Gilead Be eaiteas Peresolimab JNJ-4703 GS-0151 (IgGik) (igG1k) (IoGik) (1961 mut. FC) Membrane- ~ x Y proximal epit
Slide 60: LDA response rates and durability differentiated from peresolimab
LDA response rates and durability for rosnilimab are \Y differentiated from Lilly’s peresolimab ‘4 Rosnilimab P2b: CDAI LDA Peresolimab P2a: CDAI LDA NRI analysis on ITT population (n=318 rosnilimab patients)*? NRI analysis on ITT population (n=74)? 80% 80% 100mg Q4W =emedo0mg Q4W —emGoOmG Q2W 5+ 30
Slide 61: RA patients have significant co-morbidities exacerbated with treatment
RA patients have significant co-morbidities which are further \y exacerbated with treatment ‘4 Increased co-morbidity rate in RA patients vs. general population 2x 2-3x 2x Infection Rate! DVT, PE, and MACE Risk1!/2 Malignancy Rate? Black box warnings for increasing SAE incidence of commercial produc
Slide 62: Low dropout rate due to AEs; well tolerated
<2% dropout rate overall due to AEs through 6 months, with only 1 dropout due to AE (headache-moderate) after 3 months Rosnilimab well tolerated with no safety signals 4 Week 0 through Week 12 Week 0 through Week 38 (N=424) (N=424) Participants with Adverse Events, n (%) Participants with Adverse Ev
Slide 63: RA is substantial opportunity for new class of biologics
RA is substantial opportunity for new Rheumatoid Arthritis US Prevalence ~1.8 Million Treated ~1 Million Treated with biologics and JAKs (b/tsDMARDs) Target Population ~500,000 2L (e.g. TNF-class insufficient responders) class of biologics Y Target population in US generated ~$10 billion in 20212 »
Slide 64: Next steps for rosnilimab
Next steps for rosnilimab To provide an update in Q2 2026 on advancement of rosnilimab in RA Strategic Next Steps in RA + Assessing potential to advance rosnilimab in RA funded by strategic or other sources of capital without diluting our royalties Vv Positive Phase 2b data reported + Best-in-diseas
Slide 65: ANB101 (BDCA2 modulator)
ANB101 (BDCA2 modulator)
Slide 66: ANB101: BDCA2 modulator of pDC function
ANB101: BDCA2 modulator of plasmacytoid dendritic cell WZ (pDC) function Phase 1 trial ongoing in healthy volunteers BDCA2 is a molecule ANB101 will potently inhibit interferon specifically expressed on pDCs secretion and immune activation tase Ah . “tee; . Complex YaSy Activated pDCs bridge innate