Vera Therapeutics, Inc. · NASDAQ:VERA

Vera Therapeutics — Investor Presentation (September 2026)

32 slides from Vera Therapeutics's investor presentation, September 2026

  1. Slide 1: Corporate Presentation

    Corporate Presentation September 2026 © 2026 Vera Therapeutics, Inc. Corporate Presentation

  2. Slide 2: Forward-looking statements

    Forward-looking statements Disclaimer This material has been made available to you with the consent of Vera Therapeutics, Inc. ("we", "us", "our", or the "Company"). Statements in this presentation that are not statements of historical fact are "forward-looking statements" within the meaning of the

  3. Slide 3: VERA is a San Francisco-based biotechnology company

    • VERA (Nasdaq) is a San Francisco-based biotechnology company with world-class development and commercialization leadership • First commercial product: TRUTAKNA™ (atacicept-vymj), a first-in-class BAFF and APRIL inhibitor that could transform treatment of autoimmune disease • FDA granted accelerate

  4. Slide 4: Vera pipeline

    Vera pipeline Research & Discovery Preclinical Clinical Marketed IgAN TRUTAKNA pMN, FSGS, MCD Phase 2 Potential future autoimmune indications MAU868 BK virus Phase 2 Potential future VT-109 autoimmune indications Vera holds worldwide, exclusive rights to develop and commercialize TRUTAKNA, VT-109, a

  5. Slide 5: Management team: Successful clinical and commercial track record

    Management team: Successful clinical and commercial track record Marshall Fordyce, MD Nancy Boman, MD, PhD Robert Brenner, MD Lauren Frenz, MBA Founder and CEO Chief Regulatory Officer Chief Medical Officer Chief Business Officer Sean Grant, MBA David Johnson, MBA Matt Skelton Jane Wright-Mitchell C

  6. Slide 6: Strong financial position

    Strong financial position ~$499M ~72.1M Cash, cash equivalents, Shares outstanding (as of 7.29.26) and marketable securities (as of 6.30.26) Additional $425M non-dilutive capital available through Oxford Facility, subject to satisfaction of certain conditions 6 © 2026 Vera Therapeutics, Inc. Corpora

  7. Slide 7: B cell modulation via dual BAFF and APRIL inhibition represents a potential paradigm shift

    B cell modulation via dual BAFF and APRIL inhibition represents a potential paradigm shift in how patients with autoimmunity may be treated Autoimmune disease • Autoantigens and autoantibodies mediate Autoantibodies bind to autoantigens autoimmune disease BAFF • B cells are source of autoantibodies

  8. Slide 8: IgAN: Most common primary glomerular disease worldwide

    IgAN: Most common primary glomerular disease worldwide Estimated worldwide incidence of 2.5/100,000 cases per year in adults1 Predominantly diagnosed in young adults, with most patients presenting with demonstrable CKD at time of diagnosis2-5 At least 50% of patients progress to kidney failure or de

  9. Slide 9: Inhibition of immune complex formation may avoid end-stage kidney disease

    Inhibition of immune complex formation in IgAN may offer the potential to avoid end-stage kidney disease during a patient’s lifetime 80 71 5-Year % Mortality in US1,2 60 59 ESKD 5-year mortality comparable to cancer 40 35 20 8 0 Lung ESKD Colorectal Breast Cancer Cancer Cancer ESKD, end stage kidney

  10. Slide 10: IgAN is a disease of B cell origin with kidney pathology

    IgAN is a disease of B cell origin with kidney pathology B cell activation Formation of circulating immune complexes Immune complex deposition leading to glomerulonephritis and kidney damage BAFF TACI Autoantigen (Gd-IgA1) B cell Autoantibody (anti-Gd-IgA1) Glomerulus APRIL 1 2 3 4 5 BAFF and APRIL

  11. Slide 11: TRUTAKNA: Rationally designed fusion protein conceived in the era of modern biotechnology

    TRUTAKNA: Rationally designed fusion protein conceived in the era of modern biotechnology B cell activation Formation of circulating immune complexes Immune complex deposition leading to glomerulonephritis and kidney damage BAFF TACI Autoantigen (Gd-IgA1) B cell Autoantibody (anti-Gd-IgA1) Glomerulu

  12. Slide 12: A therapy that comprehensively addresses KDIGO treatment goals would...

    A therapy that comprehensively addresses KDIGO treatment goals would... Reduce immune complexes (Gd-IgA1) Resolve inflammation (hematuria) Reduce proteinuria Stabilize eGFR Figures are illustrative only. 12 © 2026 Vera Therapeutics, Inc. Corporate Presentation

  13. Slide 13: ORIGIN Phase 2b long-term results consistent with disease modification

    ORIGIN Phase 2b long-term results consistent with disease modification 0 Reduction in Gd-IgA1 0 Resolution of hematuria Mean ± SE % Change from BL in % Participants (95% CI) -15 -20 Change from BL in Gd-IgA1 -30 -40 -45 -60 -60 -80 -75% -66% -75 -100 0 12 24 36 48 60 72 96 0 12 24 36 48 60 72 84 96

  14. Slide 14: Phase 3 trial design

    Phase 3 trial design Multinational, randomized, placebo-controlled trial of TRUTAKNA, self-administered at home via weekly 1-mL SC injection Double-Blind Treatment Open-Label Extension Placebo TRUTAKNA 150 mg SC QW TRUTAKNA 150 mg SC QW Week 0 36 52 104 156 1° Endpoint met Final analysis: 2° Endpoin

  15. Slide 15: Interim analysis set

    ORIGIN 3 interim analysis set participant disposition 750 screened 319 failed screening 431 randomized 428 randomized and treated Full analysis set and 214 TRUTAKNA 214 placebo safety analysis set 106 TRUTAKNA Interim analysis set 97 placebo Interim analysis set 7 discontinued treatment 13 discontin

  16. Slide 16: ORIGIN 3 and ORIGIN 2b demographics and baseline characteristics

    ORIGIN 3 and ORIGIN 2b demographics and baseline characteristics ORIGIN 3 Interim Analysis Set ORIGIN 2b TRUTAKNA Placebo Total Total n=106 n=97 n=203 N=116 Age, median (range), years 40 (18, 72) 39 (19, 70) 40 (18, 72) 37 (18, 67) Male sex, n (%) 57 (54) 58 (60) 115 (57) 69 (59) Race, n (%) White 4

  17. Slide 17: Primary endpoint: UPCR reduction

    Primary endpoint: UPCR reduction Δ 42% 95% CI 29, 52 10 10 p<0.0001 Mean (95% CI) % Change from Baseline 0 0 -10 -10 -20 -20 -7% -30 -30 95% CI -19, 8 -40 -40 -50 -50 -60 -60 -46% 0 12 24 36 95% CI -53, -38 n= Week Placebo 97 96 97 95 TRUTAKNA Placebo TRUTAKNA 106 104 104 103 n=103 n=95 Interim Anal

  18. Slide 18: UPCR efficacy consistent across prespecified subgroups

    UPCR efficacy consistent across prespecified subgroups n (%) Mean UPCR % Change at Week 36 Mean UPCR % Reduction TRUTAKNA Placebo TRUTAKNA Placebo Favors Placebo Favors TRUTAKNA vs Placebo (95% CI) Overall 106 97 -46% -7% 42% (29, 52) <40 48 (45) 49 (51) -44% +0.5% 45% (23, 60) Age, years ≥40 58 (55

  19. Slide 19: Gd-IgA1 reduction and hematuria resolution

    Gd-IgA1 reduction and hematuria resolution Gd-IgA1 Reduction Hematuria Resolution 0 Mean (95% CI) % Change from Baseline1 0 Patients with Hematuria (95% CI)2 -3% -21% Change from Baseline in % -20 -15 -40 -30 Δ 67% Odds ratio 19.1 p<0.0001 -60 p<0.0001 -45 -60 -80 -81% -68% -75 -100 0 4 12 24 36 0 2

  20. Slide 20: TRUTAKNA was generally well tolerated in ORIGIN 3 interim analysis

    TRUTAKNA was generally well tolerated in ORIGIN 3 interim analysis TRUTAKNA Placebo Participants, % n=214 n=214 Most common adverse events (≥5%) • Most adverse events were mild or moderate in Infections 32 28 severity and resolved without treatment interruption or discontinuation Upper respiratory t

  21. Slide 21: Vera Announces Alignment with FDA on Earlier ORIGIN Phase 3 Analysis

    Vera Therapeutics Announces Alignment with U.S. FDA on Earlier ORIGIN Phase 3 Analysis to Support Potential Full Approval for Atacicept in Adults with IgA Nephropathy • Revised ORIGIN 3 eGFR analysis now planned for Q3 2026, pulled forward from 2027 • Pending positive eGFR analysis, plans to submit

  22. Slide 22: ORIGIN 3 final efficacy analysis: demographics and baseline characteristics

    ORIGIN 3 final efficacy analysis: demographics and baseline characteristics TRUTAKNA Placebo Total n=214 n=214 n=428 Age, median (range), years 41 (18, 74) 41 (18, 70) 41 (18, 74) Male sex, n (%) 122 (57) 132 (62) 254 (59) Race, n (%) Asian 117 (55) 114 (53) 231 (54) White 94 (44) 95 (44) 189 (44) O

  23. Slide 23: TRUTAKNA stabilized eGFR compared to placebo through 104 weeks

    TRUTAKNA stabilized eGFR compared to placebo through 104 weeks 2 Mean change Annualized Mean (95% CI) eGFR change from baseline, 0 from baseline eGFR slope at 52 weeks1 at 104 weeks2 -2 Placebo- adjusted Δ 5.6 Δ 5.0 -4 difference (3.7, 7.5) (3.6, 6.5) mL/min/1.73m2 p<0.0001 p<0.0001 -6 TRUTAKNA -0.1

  24. Slide 24: TRUTAKNA achieved unprecedented kidney protection with a 76% risk reduction

    TRUTAKNA achieved unprecedented kidney protection with a 76% risk reduction in the composite kidney endpoint • The hazard ratio for composite kidney disease Kidney disease progression events progression was 0.24 (95% CI 0.12, 0.48; 40 38 p<0.0001), resulting in a 76% risk reduction 18% through 104 w

  25. Slide 25: TRUTAKNA was well tolerated with a favorable safety profile

    TRUTAKNA was well tolerated with a favorable safety profile, and generally comparable to placebo TRUTAKNA Placebo Participants, n (%) n=214 n=214 Adverse events 160 (75) 167 (78) • Most adverse events were mild or moderate in severity and resolved without treatment Serious adverse events1 15 (7) 33

  26. Slide 26: ORIGIN 3 final efficacy analysis summary

    ORIGIN 3 final efficacy analysis summary • TRUTAKNA has demonstrated that upstream inhibition of BAFF and APRIL achieves results that reflect the potential for comprehensive disease modification in IgAN • Met all predefined endpoints, including unprecedented placebo-adjusted eGFR and composite kidne

  27. Slide 27: Estimated IgAN epidemiology in 2032

    Estimated IgAN epidemiology in 2032 US IgAN Prevalence: ~0.04% of US Population (360.5M)1 + ~40K ~160K Low Risk (~24% of patients)2 + ~30K Moderate Risk (~20% of patients)2 ~90K High Risk (~56% of patients)2 Phase 3 population Phase 2 study ongoing BAFF & APRIL inhibition Patient counts rounded to n

  28. Slide 28: Clinical practice guidelines encourage proactive treatment of IgAN

    Clinical practice guidelines encourage proactive treatment of IgAN to minimize nephron loss Treatment guidelines1 TRUTAKNA may hit the mark Biopsy and treatment initiation threshold of ≥0.5g/day proteinuria ü Potentially disease-modifying, dual-inhibition MoA • Prevention of IgA-IC formation ü 68% G

  29. Slide 29: IgAN market and TRUTAKNA have many hallmarks of an attractive commercial opportunity

    IgAN market and TRUTAKNA have many hallmarks of an attractive commercial opportunity IgAN Market TRUTAKNA • We believe the nephrology market is ripe for • Potentially differentiating product attributes disruption due to limited adoption of • Phase 2b eGFR data highly valued with approved therapies e

  30. Slide 30: Potential $10B+ U.S. market opportunity in IgAN and pipeline autoimmune diseases

    Potential $10B+ U.S. market opportunity in IgAN and pipeline autoimmune diseases1 LCM for BAFF and APRIL inhibition US Prevalence1 IgAN/IgAVN Sjögren’s pMN Nephrology Non-Nephrology ~500K ~700K gMG FSGS SLE MCD ITP AAV SSc LN 1. Vera Therapeutics corporate estimates for peak year market opportunity

  31. Slide 31: TRUTAKNA projected catalysts

    TRUTAKNA projected catalysts Catalyst 2026 2027 2028 US launch IgAN Phase 3 final efficacy analysis Projected full approval1 IgAN Clinical results IgAN, pMN, Clinical results FSGS, MCD Vera holds worldwide, exclusive rights to develop and commercialize TRUTAKNA 1. Subject to U.S. FDA review of full

  32. Slide 32: © 2026 Vera Therapeutics, Inc. Corporate Presentation

    © 2026 Vera Therapeutics, Inc. Corporate Presentation

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