Corvus Pharmaceuticals, Inc. · NASDAQ:CRVS

Corvus Pharmaceuticals — Technical Presentation (May 2026)

14 slides from Corvus Pharmaceuticals's technical presentation, May 2026

  1. Slide 1: Immunologic and Clinical Activity of Soquelitinib, a Selective ITK Inhibitor, in Atopic Dermatitis

    Society for Investigative Dermatology 2026, ID # 0483 Immunologic and Clinical Activity of Soquelitinib, a Selective ITK Inhibitor, in Atopic Dermatitis Kavita Sarin, MD, PhD Professor of Dermatology Stanford University Medical Center Kavita Sarin1, Albert Chiou1, Michael Cameron2, Jennifer L. Paris

  2. Slide 2: Disclosures

    Disclosures Consultant for Nflection Therapeutics, Biossil, Springworks, Color Health, Kamal Therapeutics. Corvus Pharmaceuticals is the sponsor of the soquelitinib clinical trial (CPI-818-003).

  3. Slide 3: ITK is an Immune Regulator

    ITK is an Immune Regulator TH1 T-bet • Interleukin-2-inducible T cell kinase (ITK) is APC expressed in T, NK and ILC-2 cells Naïve TH2 • ITK is involved in TCR signaling and cell ITK CD4+ T cell GATA3 differentiation: inhibition leads to – Decreased Th2 and Th17 – Th1 skewing (via RLK sparing) TH17

  4. Slide 4: Why This Matters in Atopic Dermatitis

    Why This Matters in Atopic Dermatitis • AD is primarily Th2-driven disease • Current therapies suppress inflammation Th17 Cell Th2 Cell • ITK inhibition can lead to upstream immune reprogramming Front Pharm. 2020 Jul 31;11:1086. (DOI: 10.3389/fphar.2020.01086)

  5. Slide 5: Atopic Dermatitis Placebo Control Phase 1 Design

    Atopic Dermatitis Placebo Control Phase 1 Design Soquelitinib 100 mg BID Cohort 1 Randomized N = 12 Clinical Trial Design 3:1 4 weeks N =16 Placebo treatment N=4 • N = 72, moderate–severe atopic dermatitis Soquelitinib 200 mg QD Cohort 2 Randomized 3:1 N = 12 • Randomized, placebo- Participants N =

  6. Slide 6: Durable Responses After Drug Withdrawal

    Durable Responses After Drug Withdrawal 4-week Treatment Regimen 8-week Treatment Regimen No rebound! No rescue therapy! No rebound observed ≥90 days of follow-up No rebound observed ≥30 days of follow-up No patients received rescue meds No patients received rescue meds Improvement persists ≥30–90 d

  7. Slide 7: Mechanism-Driven Biomarker Strategy

    Mechanism-Driven Biomarker Strategy Biomarker Assessments Based on MOA, we evaluated effects on ITK TH2 Th1, Th2, Th17, and Tregs: GATA3 • Serum cytokines (MSD) • Blood flow cytometry (Foxp3) • PBMC single cell RNAseq Treg TH17 Treg RORγΤ Foxp3 suppresses BACH2 AD disease

  8. Slide 8: Effects on Th2 Related Immunology

    Effects on Th2 Related Immunology ITK TH2 IL-4 Th2 drives AD disease GATA3 IL-5 IL-13 Dose-dependent Reduction in Significant reduction in IL-4, IL-5, IL-13 and TARC Proliferating Th2* Cohort 3 Cohort 4 % change in proliferating Th2 150 200 mg BID for 28 days 200 mg BID for 56 days % change from bas

  9. Slide 9: Soquelitinib Treatment Leads to Increase in Persistent Tregs

    Soquelitinib Treatment Leads to Increase in Persistent Tregs Tregs (CD4+, CD25 hi, Foxp3+) persist beyond treatment Cohort 3 – 200 mg BID Cohort 4 – 200 mg BID Cohort 3+4* – 200 mg BID 0.0737 200 300 200 % change from baseline % change from baseline % change from baseline 150 200 150 28 Days 100 100

  10. Slide 10: Inhibiting ITK Regulates Switch to Treg from Th17

    Inhibiting ITK Regulates Switch to Treg from Th17 Increased BACH2 and reduced RORγT expression ITK Treg TH17 Foxp3 RORγΤ BACH2 Treg BACH2 increases at 200 mg BID dose RORγT decreases at 200 mg BID dose BACH2 in Tregs 200 mg BID RORγT in TH17 200 mg BID Paired t-test p = 0.14 Paired t-test p < 0.05 1

  11. Slide 11: Potential Mechanism of Treg Stabilization

    Potential Mechanism of Treg Stabilization Untreated Treg Soquelitinib Treg Soquelitinib • Increased BACH2 expression promotes Treg survival • ITK signaling prevents nuclear localization of BACH2 • ITK inhibition promotes BACH2 nuclear localization and activation of Foxp3 gene Unstable Treg Long-live

  12. Slide 12: Soquelitinib Upregulates SOCS3 and Reduces JAK1 in T helper Cells

    Soquelitinib Upregulates SOCS3 and Reduces JAK1 in T helper Cells Modulation of the JAK-STAT Pathway SOCS3 increases in circulating T cells SOCS3 in Th2 SOCS3 in Th1 SOCS3 in Tc17 150 200 p = 0.0614 200 p = 0.2166 p = 0.0452 % change from baseline % change from baseline % change from baseline 150 15

  13. Slide 13: Conclusions

    Conclusions Soquelitinib: Immune Reprogramming for Durable Control of Atopic Dermatitis Immune Targeted Mechanism Pathway Modulation Clinical Impact Reprogramming Soquelitinib is a Treg rebalancing: Soquelitinib modulates Durable Remissions selective, covalent the JAK-STAT pathway in Continued impro

  14. Slide 14: We thank the clinical trial participants and collaborating sites

    We thank the clinical trial participants and collaborating sites: Apex Clinical Research, Arkansas Research Trials, Best Skin Research, Cahaba Dermatology and Skin Health Research Center, Center For Dermatology Clinical Research, Empire Clinical Research, Equity Medical - New York and Kentucky, Nobl

Corvus Pharmaceuticals — Technical Presentation (May 2026) on 6ix