51 slides from First Tracks Biotherapeutics's investor presentation, Oct 13, 2026
Slide 1: Corporate Presentation
Corporate Presentation October 2026 NASDAQ: TRAX First Tracks — BIOTHERAPEUTIC
Slide 2: Safe harbor statement
Safe harbor statement This presentation and any accompanying oral presentation contain forward-looking statements within the meaning of the “safe harbor’ provisions of the Private Securities Litigation Reform Act of 1995, including statements regarding the potential benefits, efficacy and safety pro
Slide 3: Developing differentiated antibody therapeutics in autoimmune and inflammatory diseases
Developing differentiated antibody therapeutics in autoimmune and inflammatory diseases Focused strategy to efficiently advance high-value immunology portfolio + Data-driven development approach prioritizing differentiation, speed and capital efficiency + Global clinical development strategy + Deep
Slide 4: Leading pipeline designed to deliver meaningful advances for patients with autoimmune diseases
Leading pipeline designed to deliver meaningful advances for patients with autoimmune diseases Development Stage and Anticipated Antibody Therapeutic IND ponent Seeeon enabling Phasela Phase Ib Phase 2 Phase 3 line Plb Cohort 2 data in Q1.2027 fe late-stage trial in 2027 Celiac 1 Disease 1 ro ot oct
Slide 5: ANB033
ANBO33
Slide 6: ANB033 blocks CD122 to inhibit pathogenic immune cells
ANBO33 blocks CD122 to inhibit pathogeni: immune cells CD122 is the beta subunit (IL-2R8) of the receptor for IL-15 and IL-2 - Expressed on subsets of CD8+ and CD4+ T cells and NK cells CDI122 antagonism reduces these immune cell subsets * Dependent on IL-15 and/or IL-2 for proliferation and surviva
Slide 7: Broad therapeutic potential across autoimmune and inflammatory diseases
Broad therapeutic potential across autoimmune and inflammatory diseases 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 Ulcerati
Slide 8: ANB033 shows strong survival benefit in aggressive GVHD mouse model
ANBO33 shows strong survival benefit and reduced cytolytic gene expression in aggressive GVHD mouse model survival Body weight loss (carried) 4100. * pa ? End of dosing ¢ End of dosing wo i | 10 ° | “@- Ansoss 2° s | AF aRcx anti-cow2 Eo we BB 2 ~O% Bolatacept +e 2 3. SQ =@ Isotype Control X20 “ 10
Slide 9: Phase 1a demonstrated favorable safety, tolerability and PK profile
Phase la demonstrated favorable safety, tolerability and PK profile with clear impact on immune cells driving CeD ANBO33 Phase 1a results! D122+ CD8+T cell impact Rapid and sustained PK profile g 20% on + Up to 3-week half-life with IV and SQ 3 (0% dosing -20x + Full receptor occupancy (RO) within 2
Slide 10: Anti-IL-15 and CD122 therapies have demonstrated sustained reduction of NK cells
Anti-IL-15 and CD122 therapies have demonstrated sustained reduc CDI122+ NK cells with no observed safety issues ANBO33 effect on total NK cells 78% @-Placebo =@=IVDose | =@=SC Dose 50% ‘TEV-52408 Effect on Total NK Calls (Pooled)! Tevougn coy) 28% 758 ey 2 28% ‘% Change from baseline 50% —— | -78%
Slide 11: ANB033's MOA is an ideal fit for targeting CeD inflammation
ANBO33’s MOA is an ideal fit for targeting CeD inflammation CeD marked by excessive IL-2 and IL-1I5 production which perpetuates disease {+ Inhibition of IL-2 signaling toss of rar intgity ~ IL-2 stimulates = CD4 effector memory T cell activation and proliferation = IFNy production leading to IL-15
Slide 12: Previous approaches have not addressed the multiple pathogenic drivers of CeD
Previous approaches have not addressed the multiple pathogenic drivers of CeD However, a CD122 antagonist targets both key pathogenic drivers of CeD ean rom guten IL-15 antagonists: Clinical PoC teva Wnovartis AMGEN P2complete ib Poc lacked potency Non-immune cell targeting Wastellas rao ocd Petco e
Slide 13: ANB033 prevents key CeD histologic manifestation of gluten-induced villous atrophy
ANBO33 prevents key CeD histologic manifestation of gluten-induced villous atrophy Sham Gluten+ Gluten+ Isotype Control ANBO33 ANBO33 treatment shows improved histology: preserves villus height and crypt depth (Vh:Cd) in CeD mouse model ‘, Note: Hu008-De-~viinL-I6tg mice no genre et ore changed wth
Slide 14: ANB033 significantly prevents the reduction of Vh:Cd ratio compared to control
ANBO33 significantly prevents the reduction of Vh:Cd ratio compared to control Vh:Cd ratio ANBO33 impact on Vh:Cd ratio Healthy tissue: * * High villus height, lower crypt depth | es | | ‘eri 3 8 rea Vh:cdRatio ovo} @ Ls % Neteatinlln e CeD tissue: e Reduced villus height, extended crypt 4 . . r dep
Slide 15: ANB033 prevents gluten-induced intestinal inflammation
ANBO33 prevents gluten-induced intestinal inflammation Epithelial layer of small intestine 200000 600000-4 -400000-4 Count of cD8+ IELs 2000-4 Count of cD8+ ranzyme B+ els 3 ‘No increase in CDB+ IELs 11 Sham Isotype ANB033. +eluten +Gluten No increase in Granzyme B+ kts — -— Sham Isotype ANB033 4» F
Slide 16: ANB033 shows differentiated impact in CeD patient-derived PBMCs
ANBO33 shows differentiated impact in CeD patient-derived PBMCs compared to competing anti-IL-15s and CD122s cytotoxic CD8+ T cells ‘0. ica “anos oo FB ES o 35 0 ge 20. ° 102 102 10% 10" 401 10108 antibody (nM) Granzyme B secretion 150. a @ 100- g gS Ae 55 50 ox ode 4+ Thi/Th2 T cells 120- ‘ciicat a
Slide 17: CeD patients present with range of histologic activity and symptoms
CeD patients present with range of histologic activity and symptoms that are often not directly correlated Histology (vc ratio) 35 Normal 25 2.0 1s Mucosal damage ‘Abnormal Symptoms are intermittent and can vary from none to mild to moderate to severe across histological damage First Tracks no») Glu
Slide 18: Phase 1b trial in CeD
ANBO33 Phase 1b trial in CeD Anticipate top-line Cohort 2 data in QI! 2027 Screening Randomized 11 28: + United states Prevention of Mucosal Damage Follow-Up Period eam (6 weeks) ‘N8033 SC Dose G2 vn:ed ‘Giten BED Placebo Sc Dose @2W KK aso IK Woor’6 endo. Baseline Endoscopy Week 6 Endoscopy Mucosal
Slide 19: Cohort 1 (gluten challenge) to assess prevention of mucosal damage and symptoms
Cohort 1 (gluten challenge) to assess prevention of mucosal damage and symptoms Prevention of Mucosal Damage Follow-Up Period weeks) Cohort! G I Screening >| ‘an8083 Dose a2W Vn:ca 20 Placebo SC Dose Q2W Bk caoee ie umary cnt Baseline Endoscopy Week 6 Endoscopy a T T T T T T T Wook 0 2 4 6 8 % 2 30
Slide 20: Cohort 2 (Vh:Cd < 2.5) assesses ability to heal mucosal damage
Cohort 2 (Vh:Cd < 2.5) assesses ability to heal mucosal damage in patients with a broad range of histologic and symptom severity Mucosal Heating Follow-UpPeriod Cohort 2 (n=40) screen st6033 SC bose caw (uptoazdcys) >| vn:ed S25 PcebosC dose a2w weeny ety jasoline Endoscopy HK Weoki2 Endoscopy T T T
Slide 21: ANB033 top-line Phase 1b cohort 1 gluten challenge results summary
ANBO33 top-line Phase 1b cohort 1 gluten challenge Results summary Achieved a statistically significant and clinically meaningful protective effect on both gluten-induced intestinal damage and symptoms LS mean change from baseline in Vh:Cd ratio of -0.17 on ANBO33 vs. -0.66 on placebo, a +0.49 place
Slide 22: Cohort 1 baseline characteristics
Cohort 1 baseline characteristics Age (years) aul 443 428 sex(n,%) ‘Male 2 (13.3%) 5 (20.4%) 7 (219%) Female 13 (867%) 12 (70.6%) 25 (78.1%) Baseline mean Vh:Cd ratio 277 274 275 Baseline mean IEL density/100 enterocytes al 2820 22.90 Baseline mean VCIEL -0.004 -0146 0.080 © First Tracks vice = vito
Slide 23: ANB033 demonstrated a statistically significant Vh:Cd histologic benefit vs. placebo
ANBO33 demonstrated a statistically significant Vh:Cd histologic benefit vs. placebo Change in Vh:Cd Ratio at Week 6 0.00 | ANBO33: Vh:Cd Histologic Protection = -o2 <= Prevented a clinically meaningful AA decline below the ~0.25 threshold! 2 £3 £8 = Protected against gluten-induced BS oso Treatment
Slide 24: ANB033 demonstrated statistically significant IEL density and composite VCIEL benefit
ANBO33 demonstrated statistically significant IEL density and composite VCIEL benefit vs. placebo Change in IEL Density at Week 6 Change in VCIEL Composite at Week 6 30.0 0 | | p<0.001 250 20.0 150 5 100 50 Ls mean change from baseline (Week 6 vs. baseline) A LS mean change from baseline (Week 6 vs.
Slide 25: ANB033 is the first therapy to report statistical significance on both histology and symptoms
ANBO33 is the first therapy to report statistical significance on both histology and symptoms Placebo patients experienced a marked increase in symptoms consistent with an intense gluten challenge ANBO33 prevented an increase in symptoms throughout the entire gluten challenge 47% of placebo patients
Slide 26: ANB033 well tolerated with no safety signals observed to date
M> First Tracks | Site! chatange veretneretcre unevouatie or gun cnalangeeicocy ahah ana not underge the secon bopay ck Wes The ANBO33 well tolerated with no safety signals observed to date Treat Participants with any AE 16 (100%) 16 (88.9%) 32 (94.1%) Any SAE 0(ox) 0 (0x) 0 (0x) Any severe AE 1(63%
Slide 27: ANB033 achieved statistically significant and clinically meaningful protective effect
ANBO33 achieved statistically significant and clinically meaningful protective effect on both gluten-induced damage and symptoms Endpoint Targ Resul > . 0.49 Avs. pl be ie oes vhed Protective effect 0.17 change (vheCd «0.25) Below clinically meaningful threshold Histology Soeateen 20.03 Avs. placebo
Slide 28: ANB033 achieved protective effect on both gluten-induced damage and symptoms vs. competitors
ANBO33 achieved statistically significant and clinically meaningful e effect on both gluten-induced damage and symptoms Admin / ‘Symptom ‘Company Guar MOA . Benefit Prevented an increase in symptoms throughout ANBO33 Phase Ib (n=32, 1:1) gaia) GERARD || OEIC? 20.03P804 | _LowercDsD scores vs. p<0.00
Slide 29: Potential blockbuster opportunity for ANB033 in non-responsive CeD
Potential blockbuster opportunity for ANBO33 in non-responsive CeD 4.1 million U.S. adult patients" (Projected prevalence based on ‘serological posttivty rate) 2.1 million U.S. adult patients! (Projected prevalence based on iopsy-confirmation rate) Growing to >50% U.S. gnosis rate? (Actual diagnosed
Slide 30: Similar to CeD, ANB033 targets multiple drivers of EoE biology
Similar to CeD, ANBO33 targets multiple drivers of EoE biology addressing both dupilumab sensitive and insensitive pathways Allergens, irritants, microbes, reflux, ete. Barrier Dysfunction <— cD4+ and Lc2 "| (dupilumab-sensitive) + Reduces CD4+ T cell proliferation + Reduces IL-5/13 from CDI22+ 1LC2
Slide 31: Mechanisms that target only downstream signals of inflammation have not been successful in EoE
Mechanisms that target only downstream signals of inflammation have not been successful in EoE Allergens, irritants, microbes, reflux, ete. 1-25 (Aarmins) “Th2" inflammation® | (qupiiumab- o~ tee ita Barrier Dysfunction “other” inflammation (duplumat-insensttve) MX First TrACKS rcoptes trom viscepot
Slide 32: ANB033 prevents eosinophilia by targeting upstream inflammation
ANBO33 prevents eosinop inflammation ia by targeting upstream Aspergillus-induced eosinophilia Esophageal eosinophils Eos observed in histology Treatment Isotype Control © Unchallenged @ Isotype control @ =ANBO33 @ = anti-miL-15 @ = anti-miL-13 @ = anti-mTSLP Lung ILC2s ANBO33 2xt0°. ° 7 e108 ° I Se
Slide 33: ANB033 also prevents cytokine and chemokine secretion
ANBO33 also prevents cytokine secretion and chemokine secretion responsible for eosinophil expansion and recruitment Aspergillus-induced eosinop! Eotaxin 2005 Treatment . © Unchallenged 1504 @ Isotype control z ° e ANBO33 ANB033 prevents - rd 1005 x e e © = anti-miL-15, of & PS iibalstiibadied + Cyt
Slide 34: ANB033 reduces CD4+ T cell and ILC2 derived Th2 cytokines
ANBO33 reduces CD4+ T cell and ILC2 derived Th2 cytokines, proven drivers of EoE pathology IL-5 secretion IL-13 secretion ice ‘Clinical Land Clinica g ied e ‘cree = 100% se © 00d a ny 8 5 S 9g % oe 1 a #5 ons 2 oo. 22 50 2 2 2% Parc 0- ~ 0. Antiooy (om) Antibody (nt) IL-5 secretion IL-13 secretion 2
Slide 35: Phase 1b trial in EoE ongoing
ANBO33 Phase Ib trial in EoE ongoing Anticipate top-line data in Q3 2027 screenin Double-blind Treatment Period (uptoa2 days) ones Follow-Up Period N=60 randomized 12 ANBO33 SC Dose Q2W sites: + United states 5 este ey Piaoabo $c Dose qa 1 astata Petar Anette Follow-Up (On-orug) baseline Endoscopy W
Slide 36: EoE is a significant market with increasing prevalence and unmet need
EoE is a significant market with increasing prevalence and unmet need 340,000 gnosed U.S. patients! 170,000 iologic-eligible initial target population ~30,000! Dupixent-treated Significant unmet need with limited approved therapies +» ~50% PPI or steroid non-responsive or intolerant + Dupixent QW ap
Slide 37: Rosnilimab
Slide 38: Rosnilimab selectively targets pathogenic T cells in periphery and inflamed tissue
Rosnilimab selectively targets pathogenic T cells in periphery and inflamed tissue to restore immune homeostasis poate Rosnilimab aims to: (1) Leverage natural immune regulatory pathway to safely restore immune homeostasis (080/86 MHC cox) _ ZF e Achieve durable remission and modity SS — disease r P
Slide 39: Pathogenic Teff and Tfh/Tph cells mediate autoimmune pathology
Pathogenic Teff and Tfh/Tph cells mediate autoimmune pathology ; + Secrete CXCLI3 and IL-21 which recruit and mature B cells into @ Tm (follicular helper) “autoantibody secreting” plasma cells Tpn (peripheral helper) . _ pepletion results in downstream effect on B cells, plasma cell generation and a
Slide 40: Depleting pathogenic T cells broadly impacts multiple drivers of RA pathogenesis
Depleting pathogenic T cells broadly impacts multiple downstream, clinically validated drivers of RA pathogenesis synovium Activated haa , Lymph node Deplete Deplete ‘Autoantibodies roeca eA Rheumatoid factor MX First TRACKS copies tom stare and smcen JAMA 20 1.Chen et ol Cnical and Translational mm
Slide 41: Rosnilimab Phase 2b trial in RA
Rosnilimab Phase 2b trial in RA 95% completed 6-month all-active treatment period supporting rosnilimab's favorable efficacy and tolerability profile Blinded Placebo- Controlled Treatment Blinded All-Active Treatment All-Active Off Drug Follow-Up Screening OncsDMARD Placebo SC (o=08) Rosnilimab SC 1
Slide 42: LDA requirement at weeks to continue on rosnilimab was a high bar
LDA requirement at 14 weeks to continue on rosnilimab was a high bar for patients with baseline high disease activi 95% of trial participants had high disease activity (CDAI > 22) at baseline Disease activity Treaters target a well-controlled disease state (e.g, LDA) by 6 months; however, look for a
Slide 43: Rosnilimab demonstrates best-in-disease profile in RA
Rosnilimab demonstrates best-in-disease profile in RA Late-breaking oral presentation by Professor Paul Emery at ACR Convergence 2025 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 44: Max response was not achieved in this Phase 2b trial
Max response was not achieved in this Phase 2b trial On average, patients with higher disease activity take longer to achieve CDAI LDA Median Change from Baseline in CDAI 60 \NRI analysis on ITT population (n=318 rosnilimab patients) ‘Time to achieve LDA correlated with baseline disease activity 89%
Slide 45: Deep, sustained reduction of pathogenic T cells led to favorable T cell composition
Deep, sustained reduction of pathogenic T cells led to favorable T cell composition reflective of immune homeostasis and durable response Rosnilimab 400mg Q4W T Cell Impact Wika We Wikt2 wee wae (i2-weoffeug) Rosnilimab T,, Impact - Pooled Doses 60 oe cali count (per hin atocd) & Rosnilimab wo WK wa
Slide 46: Synovial biopsies show ~90% reduction of pathogenic T cells in the target tissue
Synovial biopsies show ~90% reduction of pathogenic T cells in the target issue Baseline Week 6 Impact on Tpn ANd Toy cells Rosnilimab 400mg 400mg/600mg doses Qaw ~90% reduction 100mg dose Inconclusive reduction Placebo Increased Rosnilimab 600mg Q2w dentty P| postive coli. Tph cells (PD-1¥CD3+CD4+C
Slide 47: Significant reduction of T and B cell activation within the synovium
Significant reduction of T and B cell activation demonstrate on target pharmacology within the synovium T Cell Activation a a B Cell Activation Baseline Week 6 - ry Baseline Wook 6 = j | (eal = - H 2 Se on a & Le . 5 5 Se a = 3 3 =e B B = 5 g e 3 3 H g = - é é — a Magnitude of reduction 4.03,p=109e-
Slide 48: Rosnilimab well tolerated with no safety signals
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 Week 0 through week 12 (n=a24) artcipants with Adverse Events, (4) Week 0 through Week 38 (v=424) Participants with Adverse Events,
Slide 49: Rosnilimab Phase 2b data reported
e Phase 2b data reported Best-in-disease profile Favorable safety and tolerability JAK-like efficacy through 6 months © Max response rates not yet observed due to trial design Sustained 12-14 week off-drug responses through 9 months Late-breaking data presented at ACR 2025 » Completed End-of-Phase 2
Slide 50: ANB101
Slide 51: ANB101: BDCA2 modulator of plasmacytoid dendritic cell (pDC) function
ANBI01: BDCA2 modulator of plasmacytoid dendritic cell (pDC) function Phase | trial completed in healthy volunteers BDCA2is a molecule specifically expressed on pDCs roe Sy emotes Immune Tolerance Plasmacytoid dendritic cell Ienmune KP rctvation Type tin ANBIO1 potently inhibits interferon secretion