Corporate presentation
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Evommune (EVMN) Corporate presentation summary

Event summary combining transcript, slides, and related documents.

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Corporate presentation summary

5 Nov, 2026

Portfolio and catalysts

  • Three programs target distinct pathways: EVO301 IL-18BP for inflammatory disease, EVO756 oral MRGPRX2 for migraine, and EVO646 oral TLR7/8 for autoimmune disease.

  • EVO301 Phase 2b in atopic dermatitis is planned for mid-2027, with data anticipated in 2028; EVO756 migraine Phase 2b topline is expected in 2027; EVO646 Phase 1 is planned for 1H 2027.

  • Cash and investments of ~$287M are expected to fund operations into 2029; new research programs are anticipated to enter the clinic at a steady cadence.

EVO301 in atopic dermatitis

  • Phase 2a met its primary endpoint: placebo-adjusted EASI improvement was 34% at Week 8 and 33% at Week 12 after dosing at Weeks 0 and 4.

  • At Week 12, 23% achieved IGA 0/1 vs. 0% on placebo; EASI reductions were highly significant vs. placebo at Weeks 4, 8 and 12.

  • No treatment-related serious or severe adverse events or conjunctivitis; PK supported at least Q4-week dosing.

  • Planned Phase 2b dose-ranging trial: 180 adults, three EVO301 regimens plus placebo, with Week 16 EASI change as the primary endpoint; Q2W and Q4W regimens to be explored.

  • Subcutaneous formulation work is complete, with trial initiation on track for mid-2027; nonclinical serum exposure was described as consistent with IV dosing.

EVO756 in migraine

  • Oral MRGPRX2 antagonist designed to modulate peripheral sensory neurons and mast cells; estimated preventive-therapy eligibility is ~30M patients across the US, EU5 and Japan.

  • Phase 2b migraine trial began in July 2026; 330 adults with refractory migraine are assigned to 25 mg BID, 50 mg BID or placebo, with topline data expected in 2027.

  • Phase 1 findings included tolerability, target engagement, ~70% human-skin penetration and PK supporting target coverage at doses as low as 25 mg BID.

  • Rationale centers on MRGPRX2 signaling in trigeminal neurons and meningeal mast cells; PACAP, VIP and substance P are identified as migraine-triggering ligands.

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