Slides
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June 2025 Jefferies Global Healthcare Conference
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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, including rosnilimab’s Phase 2b clinical trial in rheumatoid arthritis at Week 38 and initial data for rosnilimab’s Phase 2 clinical trial in ulcerative colitis; whether current trends in rosnilimab's data in the rheumatoid arthritis Phase 2b clinical trial will be maintained once complete Week 38 data become available; whether positive clinical trial results in rosnilimab's Phase 2b clinical trial in rheumatoid arthritis increases the likelihood of getting positive results from rosnilimab's Phase 2 clinical trial in ulcerative colitis; whether any of the Company’s product candidates will be best in class or optimized; the potential to receive any additional milestones or royalties from the GSK collaboration; the Company’s ability to find a licensing partner for etokimab and the timing of any such transaction; and the Company’s projected cash runway. Statements including words such as “plan,” “continue,” “expect,” or “ongoing” and statements in the future tense are forward-looking statements. These forward-looking statements involve risks and uncertainties, as well as assumptions, which, if they do not fully materialize or prove incorrect, could cause its results to differ materially from those expressed or implied by such forward-looking statements. Forward-looking statements are subject to risks and uncertainties that may cause the company’s actual activities or results to differ significantly from those expressed in any forward-looking statement, including risks and uncertainties related to the company’s ability to advance its product candidates, obtain regulatory approval of and ultimately commercialize its product candidates, the timing and results of preclinical and clinical trials, the company’s ability to fund development activities and achieve development goals, the company’s ability to protect intellectual property and other risks and uncertainties described under the heading “Risk Factors” in documents the company files from time to time with the Securities and Exchange Commission. These forward-looking statements speak only as of the date of this presentation, and the company undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date hereof. Certain information contained in this presentation may be derived from information provided by industry sources. The Company believes such information is accurate and that the sources from which it has been obtained are reliable. However, the Company cannot guarantee the accuracy of, and has not independently verified, such information. The trademarks included herein are the property of the owners thereof and are used for reference purposes only. Such use should not be construed as an endorsement of such products. 2 Safe harbor statement
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Immune Cell Modulators ANB033 (CD122 antagonist) P1 in Healthy Volunteers Rosnilimab (PD-1 depleter and agonist) P2b in Rheumatoid Arthritis P2 in Ulcerative Colitis Autoimmune and inflammatory diseases including dermatology, gastroenterology and rheumatology ANB101 (BDCA2 modulator) P1 in Healthy Volunteers Research and Capital Strong capital position Research-driven • Q1 2025 cash: ~$383MM o Expected cash runway: YE 2027 • Excludes significant royalty potential: o GSK royalty and milestone potential for Jemperli and cobolimab o GSK $75MM milestone for Jemperli $1B annual WW sales o Vanda royalty and milestone potential for imsidolimab • Preclinical pipeline of immunology targets Royalty income Best-in-class immune cell modulating antibodies 3
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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 speed of induction and/or max remission rates • Substantial unmet need for new classes of safe, effective and durable therapies • Mature, non-growth market • Established biosimilar 1L SoC (e.g. TNF) • 2L access possible, but requires contracting • No new MoA in the last decade • Dynamic, growing market • 1L SoC diversified with growth from branded products (IL-23p19, α4β7) • Minimal payor management of 2L+ therapies ~$10bn U.S. sales in b/tsDMARD- experienced market1 $8bn ➔ >$10bn U.S. sales in advanced therapy by 20303 ~500k U.S. b/tsDMARD patients; 20-25% cycle through all classes of therapy2 ~300k and growing U.S. advanced therapy patients; Cycling ramping up as advanced therapy market becomes established to avoid surgeries3 RA: U.S. Market UC: U.S. Market 1. Expected by 2028 (Evaluate 29 Nov 2022); 2. Market research conducted by Ambit in 2022; 3. Market research conducted by ZS Associates in 2025; 4. Phase 3 registrational data from product labels RA and UC in the U.S. are complementary, large commercial markets with similarly high unmet need Treaters seek to maximize and sustain remission in maintenance phases 4
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5 Responses durable after 6 months • Potential for maintenance dosing with extended dosing intervals (e.g. Q8W) 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 compared to standard of care • Monthly (Q4W) dosing Max response rates have not yet been observed • Strict continuation criteria prevented patients with improvement at 3 months from continuing in this P2b trial • Many patients beyond 3 months achieved, or were trending toward, CDAI LDA and ACR50 1 2 3 Rosnilimab demonstrates best-in-disease profile in RA Rosnilimab, a best-in-class depleter and agonist targeting PD-1+ T cells, is well-positioned for the ~$20 billion U.S. RA market which hasn’t had a new mechanism approved since 2012
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0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%% of Patients 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 Rinvoq’s higher response rate in H2H SELECT-CHOICE P3 study likely due to open-label bias from patients knowing they are on active drug from Week 0 Wk0 Wk2 Wk4 Wk6 Wk8 Wk10 Wk12 Wk14 RinvoqTM (P2b TNF-Experienced Study4) Dark Orange – RinvoqTM 6mg BID Light Orange – Placebo ACR20 response rates are comparable to RinvoqTM Most patients had symptomatic and clinical improvement by 3 months Rosnilimab - 100mg Q4W Rosnilimab - 400mg Q4W Rosnilimab - 600mg Q2W Placebo 1. b/tsDMARD-experienced population included 29% (n=50 of n=174 total experienced patients) with prior JAK experience; 2. Non-responder imputated (NRI) analysis on intent-to-treat (ITT) of all b/tsDMARD-experienced patients randomized; b/tsDMARD-experienced population (n=44 placebo, n=44 100mg Q4W, n=45 400mg Q4W, n=41 600mg Q2W; n=130 total rosnilimab b/tsDMARD-experienced patients); 3. RinvoqTM Phase 2b MTX-IR study; 4. RinvoqTM Phase 2b TNF-experienced study; 6mg BID (equivalent to 15mg QD); 5. SELECT-CHOICE Phase 3 study 6
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-20 -18 -16 -14 -12 -10 -8 -6 -4 -2 0 2 4 Mean Change from Baseline (mg/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 Change in CRP: b/tsDMARD-Experienced1 MMRM Analysis on ITT population (n=174 total; n=44 placebo, n=130 rosnilimab) Rosnilimab - 100mg Q4W Rosnilimab - 400mg Q4W Rosnilimab - 600mg Q2W Placebo 1. b/tsDMARD-experienced population included 29% (n=50 of n=174 total experienced patients) with prior JAK experience; 2. Mixed Model for Repeated Measures (MMRM) analysis on intent-to-treat (ITT) of all b/tsDMARD-experienced patients randomized; b/tsDMARD-experienced population (n=44 placebo, n=44 100mg Q4W, n=45 400mg Q4W, n=41 600mg Q2W); 3. RinvoqTM Phase 2b MTX-IR study; 4. RinvoqTM Phase 2b TNF-experienced study; 6mg BID (equivalent to 15mg QD) 5. SELECT-CHOICE Phase 3 study CRP reductions are comparable to RinvoqTM 7
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8 CDAI Score 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 ACR70 Correlates with remission; not expected until 6 months CDAI = 11 Patient would not continue on rosnilimab after 14 weeks CDAI = 10 Patient would continue on rosnilimab through 6 months Illustrative relative improvement 76 Treaters target a well-controlled disease state (e.g., LDA) by 6 months; however, look for an initial signal of response (e.g., ACR20) by 3 months ACR50 Indicates good response to treatment; typically not expected until 4-5 months LDA requirement at 14 weeks to continue on rosnilimab was a high bar for patients with baseline high disease activity 95% of trial participants had high disease activity (CDAI > 22) at baseline
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0 10 20 30 40 50 60Median CDAI 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 for 600 Q2W Median Change from Baseline in CDAI NRI analysis on ITT population (n=318 rosnilimab patients) 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 Week 12 (n=137)1CDAI LDA Responders Week 14 (n=86) Week 18 (n=9)1 9 Max response was not achieved in this Phase 2b trial On average, patients with higher disease activity take longer to achieve CDAI LDA 1. Green line includes 3 patients that achieved CDAI LDA at Week 12, were not CDAI LDA at Week 14, but returned to CDAI LDA at Week 18. These same 3 patients were excluded from the light blue line. In total 12 patients achieved CDAI LDA at Week 18. Time to achieve LDA correlated with baseline disease activity ✓ 69% (220/318) achieved LDA at Week 14 (NRI) ✓ Median CDAI scores for LDA responders consistent through 6 months and, to date, maintained in 12-14 week off-drug period ✓ 73% (232/318, an additional 12 patients) achieved LDA at Week 18 (NRI + W18) • These additional patients were not eligible to enter the All-active Treatment Period ✓ Additional patients trending toward LDA beyond 3 months • ~50% patients achieved ACR20 at Week 14, but were ineligible to enter all-active treatment period
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10 64% 60% 48% 53% 54% 35% 38% 42% 23% 42% 46% 23% 0% 10% 20% 30% 40% 50% 60% 70% 80%% of Patients 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 (NRI) analysis on intent-to-treat (ITT) of all b/tsDMARD-naïve patients randomized; b/tsDMARD-naïve population (n=62 100mg Q4W, n=62 400mg Q4W, n=64 600mg Q2W; n=188 total rosnilimab b/tsDMARD-naïve patients); 2. SELECT-COMPARE Phase 3 study; 3. Kevzara Phase 3 study; NRI data; CDAI = Clinical Diseases Activity Index; LDA = Low Disease Activity; N/R = Not Reported b/tsDMARD-Naïve NRI analysis on ITT population (n=188 rosnilimab patients)1 Legend 2 3 2 Rosnilimab shows JAK-like efficacy in naïve patients Compares favorably despite most conservative analysis and capped trial design TM TM TM
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11 34% 27% 23% 56% 44% 36% 49% 42% 29% 58% 59% 37% 52% 50% 27% 20% 10% 0% 10% 20% 30% 40% 50% 60% 70% 80%% of Patients 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 CDAI LDA ACR50 ACR70 b/tsDMARD-Experienced NRI analysis on ITT population (n=130 rosnilimab patients)1 N/R 2 2 3 Rosnilimab surpassed TPP in experienced patients and comparable at mid/high dose to JAKs in all-active H2H study* Includes 29% with prior JAK experience Excludes 12 CDAI LDA responders that were not in active period but achieved LDA at Week 18 Excludes 7 patients who discontinued in the all-active treatment period while in CDAI LDA Legend TM TM TM 1. Non-responder imputated (NRI) analysis on intent-to-treat (ITT) of all b/tsDMARD-experienced patients randomized; b/tsDMARD-experienced population (n=44 100mg Q4W, n=45 400mg Q4W, n=41 600mg Q2W; n=130 total rosnilimab b/tsDMARD-experienced patients); 2. SELECT-CHOICE Phase 3 study; 3. Orencia Phase 3 study; NRI data; 4. Anaptys Jan. 2025 Target Product Profile (TPP); CDAI = Clinical Diseases Activity Index; LDA = Low Disease Activity; N/R = Not Reported 6 Month TPP4 *In H2H comparator studies, patients know they are on an active drug, resulting in upwards bias on response rates vs. placebo-controlled studies
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81% 90% 83% 0% 20% 40% 60% 80% 100%% of Patients 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%% of Patients Wk34 Wk34 Wk34 n=29/36 n=27/30 n=29/35 n=7/8 n=13/15 n=11/15 12 Only 23 of 139 (17%) patients of Week 28 CDAI LDA responders were not CDAI LDA (≤10) at Week 34: • 25% (6/23) were CDAI <11 • Median CDAI = 13 • 91% (21/23) were CDAI <22 (e.g. remained CDAI moderate disease activity) Most patients who did not sustain CDAI LDA remained near the cutoff of CDAI=10 100mg Q4W 400mg Q4W 600mg Q2W 100mg Q4W 400mg Q4W 600mg Q2W Durable responses for at least 2-months off-drug 83% of Week 28 CDAI LDA responders were still in response at Week 34 1. ~75% of patients who completed Week 28 (n=212) had reached Week 34 as of the March 11, 2025 data cutoff; this responder analysis represents patients who were in CDAI LDA, as of Week 28, relative to their CDAI status as of Week 34
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0% 10% 20% 30% 40% 50% 60% 70% 80% % of Patients 100mg Q4W 400mg Q4W 600mg Q2W Wk 12 Wk 14 Wk 28 0% 10% 20% 30% 40% 50% 60% 70% 80%% of Patients 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 population (n=318 rosnilimab patients)1,2 Peresolimab P2a: CDAI LDA NRI analysis on ITT population (n=74)4 -100% -90% -80% -70% -60% -50% -40% -30% -20% -10% 0% Cell Count (% Change from Baseline) 100mg Q4W 400mg Q4W 600mg Q2W Wk0 Wk6 Wk12 Wk28 -100% -90% -80% -70% -60% -50% -40% -30% -20% -10% 0% Cell Count (% Change from Baseline) Wk 0 2 4 Wk 12 Wk 8 Wk38 (12-14 wk off-drug) Rosnilimab P2b: PD-1high T Cell Impact NRI analysis on ITT population (n=318 rosnilimab patients) Peresolimab P2a: PD-1high T Cell Impact NRI analysis on ITT population – Pooled doses4 At 12-14 weeks off-drug, all rosnilimab doses continue to show greater depletion vs. peresolimab’s max of 57% on-drug 13 LDA response rates and durability for rosnilimab are differentiated from Lilly’s peresolimab 1. Non-responder imputated (NRI) analysis on intent-to-treat (ITT) of all 318 rosnilimab patients randomized; 2. At Week 28, 53% (100mg Q4W), 54% (400mg Q4W), and 63% (600mg Q2W) rosnilimab patients were in CDAI LDA (57% pooled); 3. Off-drug follow-up period ongoing; 4. Tuttle et. al, NEJM, May 2023, Supplemental Appendix, At Week 28, 36% (300mg Q4W) and 37% (700mg Q4W) peresolimab patients were in CDAI LDA
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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 PD-1+ T cells (Tph and Teff) Baseline Week 6 APC markers PD-L1 Synovial biopsies show ~90% reduction of PD-1+ T cells in the target issue Note: Synovial biopsies of the most impacted joint taken at baseline and 6 weeks on study. Immunofluorescence performed to identify PD-1 positive cells. Tph cells (PD-1+CD3+CD4+CXCR5-) 14
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Fold decrease: 4.03, p=1.09e-24 T Cell Activation Fold decrease: 4.06, p=1.77e-18 B Cell Activation Gene expression (Z-score) Gene expression (Z-score) 5.5 2.9 2.0 0 2 4 6 8 6.1 3.9 1.0 0 2 4 6 8 Magnitude of reduction Magnitude of reduction: 4.03, p=1.09e-24 Magnitude of reduction: 4.06, p=1.77e-18 Rosnilimab Wk12 CDAI Responders Rosnilimab Wk12 CDAI Non-responders Placebo Rosnilimab Wk12 CDAI Responders Rosnilimab Wk12 CDAI Non-responders Placebo Week 6 *** *** *** *** *** *** Magnitude of reduction Week 6BaselineBaseline Significant reduction of T and B cell activation demonstrate on target pharmacology within the synovium Note: Gene ontology (GO) pathway analysis performed on samples with evidence of inflammation at baseline (all rosnilimab doses pooled, n=19 paired biopsies) and with myosin normalization. Rows reflect genes with p<0.05 between Weeks 6 and 0. Magnitude of reduction defined as fold enrichment score. Rosnilimab responders achieved CDAI LDA in 3 months. ***p<0.001 for difference in fold change between baseline and Week 6 between groups. 15
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IL-6 Production Gene expression (Z-score) Gene expression (Z-score) 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 (LIGHT), CD28, CD69, CD40L, ICOS, CD226, ZAP70, TCF7, IRF1 B cell activation: IL7R, CD27, CD79A, BTK, SYK, IL21R TNF and IL-6 production: MYD88, PTPN22, LILRB1, LILRB2, NOD2, CCR2, NLRC3, IRAK3, IL1RAP, IL6R, IL17RA Mediators of RA structural damage: MMP1, MMP3, and RANK-L IBD-related genes: NOD2, TREM1, IL12RB, IFNGR1, S100A8 Pathway changes reflect rosnilimab’s broad MOA Week 6Baseline Week 6Baseline Significant reduction of additional downstream pathways including TNF and IL-6 within the synovium Note: Gene ontology (GO) pathway analysis performed on samples with evidence of inflammation at baseline (all rosnilimab doses pooled, n=19 paired biopsies) and with myosin normalization. Rows reflect genes with p<0.05 between Weeks 6 and 0. Magnitude of reduction defined as fold enrichment score. Gene expression (Z-score) 16
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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 rate vs. 18% placebo5 ~3.4% MACE rate vs. 2.5% placebo5 ~4.2% malignancy rate vs. 2.9% placebo5 Black box warning ~39% infection rate vs. 34% placebo5 ~1.7% MACE rate vs. 1.3% placebo5 Increased co-morbidity rate in RA patients vs. general population 2-3x DVT, PE, and MACE Risk1,2 2x Infection Rate1 2x Malignancy Rate3 $4.5B RA sales4 $3.6B RA sales4 $2.3B RA sales4 ~$1B RA sales RA patients have significant co-morbidities which are further exacerbated with treatment 1. Avina-Zubieta et al., A&R, 2008, 2. Fazal et al., BMC Rheumatology, 2024, 3. Smitten et al., ART, 2008, 4. Evaluate Pharma 2023 WW RA sales, 5. Phase 3 registrational data from product labels. 17
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18 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 (n=105) Any AE 36 (34%) 51 (48%) 48 (45%) 38 (36%) 39 (125.6) 73 (260.9) 66 (206.5) 52 (149.1) Any SAE1 1 (1%) 1 (1%) 1 (1%) 3 (3%) 1 (2.4) 2 (3.8) 2 (3.7) 4 (7.7) Any Drug-Related SAE 1 (1%) 0 (0%) 0 (0%) 0 (0%) 1 (2.4) 0 (0) 0 (0) 0 (0) Severe AE2 2 (2%) 1 (1%) 0 (0%) 4 (4%) 2 (4.8) 4 (7.5) 1 (1.9) 4 (7.8) Drug-Related AE 18 (17%) 13 (12%) 18 (17%) 17 (16%) 18 (48.8) 17 (36.1) 28 (62.0) 19 (41.7) AE Leading to Treatment Discontinuation 1 (1%) 1 (1%) 2 (2%) 2 (2%) 1 (2.4) 1 (1.9) 3 (5.6) 2 (3.8) Infections 14 (13%) 24 (23%) 21 (20%) 12 (11%) 16 (41.5) 41 (98.7) 39 (89.4) 31 (67.6) Serious 1 (1%) 1 (1%) 0 0 1 (2.4) 1 (1.9) 1 (1.9) 1 (1.9) Opportunistic3 2 (1.9%) 0 (0%) 0 (0%) 0 (0%) 2 (4.8) 1 (1.9) 1 (1.8) 1 (1.9) Participants with any AEs > 5% Headache 4 (4%) 7 (7%) 6 (6%) 4 (4%) 4 (9.7) 10 (19.9) 10 (19.4) 5 (9.8) Upper respiratory tract infection 1 (1%) 7 (7%) 2 (2%) 3 (3%) 2 (4.8) 14 (27.8) 7 (13.4) 10 (19.6) Nasopharyngitis 4 (4%) 5 (5%) 5 (5%) 0 4 (9.6) 9 (17.5) 8 (15.4) 1 (1.9) Elevated ALT (alanine aminotransferase)4 1 (1%) 4 (4%) 3 (3%) 3 (3%) 1 (2.4) 8 (15.5) 5 (9.5) 4 (7.8) Rosnilimab well tolerated with no safety signals <2% dropout rate overall due to AEs through 6 months, with only 1 dropout due to AE (headache-moderate) after 3 months * Measured as an exposure adjusted incidence rate (per 100 patient years) 1. SAEs (severe unless otherwise noted): RSV – moderate (600mg Q2W); anaphylaxis from wasp sting (600mg Q2W); ureter stone (600mg Q2W); cholecystitis / pericardial effusion (600mg Q2W); meniscus tear – moderate (400mg Q4W); diverticulitis – moderate (400mg Q4W); embolic ischemic stroke (100mg Q4W); pneumonia – mild (100mg Q4W); cellulitis/diarrhea (placebo) 2. Severe AEs (excluding SAEs): RA flare (600mg Q2W); blood creatine phosphokinase increase (400mg Q4W); endometriosis (100mg Q4W); alanine aminotransferase increased/aspartate aminotransferase increase (100mg Q4W); flu/headache (100mg Q4W); macular degeneration/retinal hemorrhage (placebo) 3. Values shown are for herpes zoster, none were severe and are the only opportunistic infection reported. 4. No patient met the predefined protocol liver function test stopping criteria. Only one ALT elevation was severe, which was at a single time point, and resolved without interruption of therapy. None were serious, all were transient, resolved without interruption of therapy, and had an outcome of recovered/resolved or recovering/resolving.
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Therapeutic dosing of rosnilimab demonstrated efficacy in a murine model of colitis PD-1high 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 of remission % PD-1high Tph cells Parmley et. al. UEGW 2024. October 2024 1. PD-1high Tph cells defined by CD3+CD4+CD45RA-PD-1+TIGIT+ICOS+CXCR5-. Long et al, Immunology Letters 233 (2021) 2-10.; 2. Rao et al, Nature, 2017. *** p<0.001, * p<0.05; 3. Rosnilimab formatted to mIgG2a to mediate effector function in mice. Suzuki et al., Sci. Immunol. 8, eadd4947 (2023); 4. Reduction of Tfh/Tph cells should impact plasma cell generation and autoantibody levels, including anti-microbial IgG antibodies that are contributing to colonic inflammation and barrier disruption: Uzzan et al, Nature, 2022. 0 20 40 60 Body weight (%) 100 110 120 90 Rosnilimab Isotype 0 p<0.05 Anti IL-12 p40 Colitis Induction (Day 0-21) hPD-1 CD4 T cell transfer biweekly dosing (4 weeks)Day 21 Rosnilimab mIgG2a3 Anti IL-12 p40 Isotype Rosnilimab Tph Impact in RA Phase 2b 0 20 40 60 Cell Count (per μL in Blood) Wk0 Wk12 Wk0 Wk12 Placebo Rosnilimab Wk28 *** *** 19
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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 rates and cancer risk (biologic class are largely undifferentiated) Milestones in UC Treatment 1 year4-6 Weeks UC TPP guidance • 3 months: ∆MMS vs. placebo (primary endpoint) is statistically significant ― Adequate symptomatic improvement to stay on drug to potential remission (by 6+ months) • 6 months: “IL-23-like” clinical remission and endoscopic remission as measured by imputed ITT (not maintenance responder analysis) • 6 – 12 months: Better durability than biologics, where 1/3 to 1/2 relapse within 1 year Clinical Remission or Endoscopic Remission targeted to reduce symptomatic relapse rates and cancer risk (biologic class are largely undifferentiated) Increasingly, differentiation to be driven by 6+ month objective endpoints AbbVie: focus on “extended induction” (~6 months) to maximize clinical response on IL-23p19’s J&J: primary endpoint of DUET TNF + IL-23p19 combo study is clinical remission at Week 48 Treaters target a well controlled disease state (e.g. endoscopic remission) in 6-12 month maintenance phase However, treaters look for a signal of response (e.g., improved clinical symptoms) by 3+ month induction phase 20
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Rosnilimab Phase 2 in moderate-to-severe UC Enrollment ongoing; On track for interim 6-month data in Q4 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 Rosnilimab SC Dose 2 Q4W Placebo SC Rosnilimab SC Dose 1 Q2W Rosnilimab SC Dose 2 Q4W Placebo SC Responders Rosnilimab SC Dose 1 Q2W (3-months treatment) N = 132 randomized 1:1:1 Final Statistical Analysis ClinicalTrials.gov: NCT06127043 Rosnilimab SC Dose 3 Q8W Responders Rosnilimab SC Dose 3 Q8W Responders Placebo SC Q8W Responders Rosnilimab SC Dose 3 Q8W Responders (9-months total treatment) 50 60 Primary Statistical Analysis (Week 12) Blinded Placebo-Controlled Treatment Period (24 weeks) Assess: clinical response at Week 24(2) Assess clinical response at Week 12(1) 6-Month Data 3-Month Off-Drug Data12-Month Data • Primary endpoint: Change in mMS3 (stool frequency + rectal bleeding + endoscopy score) vs. placebo at Week 12 ― Assesses symptomatic and objective clinical improvement at 3 months • “Treat-through” design aligned with clinical practice to give a real-world assessment of remission at 6 months ― Distinctly different from trials with an enriched responder analysis in 6 or 12-month maintenance studies 1. Week 12 visit: All patients, regardless of study arm, treat-through to Week 24 and remain blinded to treatment arm. Placebo-treated patients who achieved partial modified Mayo score (pmMS) clinical response or at Week 12 remain on placebo, while placebo-treated patients who are non-responders on pmMS are crossed over to the subcutaneous high-dose rosnilimab treatment arm; 2. Week 24 visit: All patients, regardless of study arm, can opt into the TEP to Week 50 if achieved pmMS clinical response by Week 24. All non-responders proceed to study follow-up; 3. mMS = modified Mayo score 21
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22 CD122 is a shared beta subunit of the receptors for IL-15 and IL-2 CD122 antagonist mAb will potently inhibit IL-15 and IL-2 biology Both IL-15 and IL-2 mediate: • Proliferation and survival of T cell subsets, particularly CD8+ TEMRA, and NK cells • Inflammatory cytokine secretion (IFNγ) during T cell activation ANB033 reduces pathogenic T cells • Preferentially inhibits lower affinity dimeric IL-2 receptor complex • Spare Tregs which express higher affinity trimeric IL-2 receptor complex ANB033 has targeted reduction of CD122 expressing TRM cells • TRM cells require IL-15 for survival • May potentially drive durable response Tregs TEMRA, TRM cells NK cells CD122 CD122 ANB033 ANB033: CD122 high affinity antagonist reduces pathogenic T cells and NK Cells Phase 1 trial ongoing in healthy volunteers; R&D IR event in H2 2025
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Actuals $31 $57 $73 $101 $137 $170 $190 $220 $0 $50 $100 $150 $200 $250 Q2 2023 Q3 2023 Q4 2023 Q1 2024 Q2 2024 Q3 2024 Q4 2024 Q1 2025 Sales (in USD millions) 1. GSK earnings presentation, US dollar conversion 2. GSK analyst consensus as of 3/20/2025 converted to USD (1.3x conversion rate as of March 2025), GSK website - https://www.gsk.com/en-gb/investors/analyst-consensus/ 3. GSK June 2024 Oncology Management IR event converted to USD (1.25x conversion rate as of June 2024). $28 $176 $598 $906 $1,113 $1,258 $1,356 $1,424 $1,482 $1,542 $0 $550 $1,100 $1,650 $2,200 $2,750 2022 2023 2024 2025 2026 2027 2028 2029 2030 2031 Sales (in USD millions) Potential GSK future growth drivers • 1L “all-comers” endometrial: Approved in US mid-’24; in EU Jan. ‘25 • 2L+ NSCLC: Phase 3 COSTAR (Jemperli + cobolimab) OS data in mid-20251 • Locally advanced dMMR/MSI-H rectal cancer: granted FDA Breakthrough Therapy Designation • Substantial investment in additional Jemperli indications and combinations ongoing GSK Peak Revenue Guidance >$2.5 billion3 Anaptys’ strong capital position • $383MM Q1 2025 cash • Cash runway: YE 2027 • Excludes GSK royalty and milestone potential for Jemperli and cobolimab • Excludes GSK $75MM milestone anticipated in 2025/2026 for Jemperli $1B annual WW sales • Excludes Vanda royalty and milestones for imsidolimab Strong capital position with ~$383MM Q1 2025 cash and significant GSK royalty upside potential 23 Jemperli Quarterly Performance1 Jemperli Mar. ‘25 Wall Street Consensus1,2
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Antibody Program Therapeutic Indication Development Stage and Anticipated Milestones IND Enabling Phase 1 Phase 2 Phase 3 Rosnilimab (PD-1 depleter and agonist) Rheumatoid Arthritis Ulcerative Colitis ANB033 (CD122 antagonist) Inflammatory Diseases ANB101 (BDCA2 modulator) Inflammatory Diseases 24 P2b data updated in June 2025 Initial P2 data Q4 2025 P1 initiated R&D event in H2 2025 Immune Cell Modulators P1 initiated Leading pipeline of immune cell modulating antibodies with multiple 2025 catalysts