| Treatment Category | Specific Agent/Approach | Mechanism of Action | Histologic Remission Rate (%) | Regulatory Status | Key Notes |
|---|---|---|---|---|---|
| Acid suppression / anti-inflammatory therapy (MAXO: proton pump inhibitor administration) | Proton pump inhibitors (PPIs; e.g., omeprazole, esomeprazole) | Reduce acid exposure and also exert anti-inflammatory effects, including suppression of Th2-associated inflammatory signaling beyond acid suppression | 41.7% in meta-analytic data; ~45–50.5% in recent reviews/real-world summaries | Used off-label but guideline-recommended first-line therapy for EoE | Clinical response reported around 60.8–71%; long-term histologic response ~60% in some cohorts; often first pharmacologic option (pqac-00000025, pqac-00000027, pqac-00000029, pqac-00000030) |
| Topical corticosteroid (MAXO: topical corticosteroid therapy) | Budesonide oral suspension (BOS; Eohilia) | Local glucocorticoid anti-inflammatory effect in esophageal mucosa via NR3C1 signaling | 53.1% | FDA-approved in the US for induction treatment in adolescents/adults; formulation-specific approval noted in recent reviews | Maintenance remission reported up to 83.3% at lower doses; adverse effects include esophageal candidiasis (pqac-00000027, pqac-00000029) |
| Topical corticosteroid (MAXO: topical corticosteroid therapy) | Budesonide orodispersible tablet (BOT; Jorveza) | Local glucocorticoid anti-inflammatory effect optimized for esophageal contact time | Up to 93% | Approved in Europe/Canada/Australia for adults in recent reviews | Sustained remission ~75% at 48 weeks; among the highest efficacy topical options reported (pqac-00000025, pqac-00000026) |
| Topical corticosteroid (MAXO: topical corticosteroid therapy) | Fluticasone swallowed from inhaler / esophagus-targeted preparation | Local glucocorticoid anti-inflammatory effect in esophageal epithelium | 64–71% | Commonly used off-label; guideline-recommended topical steroid option | Histologic remission superior to placebo; candidiasis reported in ~5–30% with topical steroids overall (pqac-00000029, pqac-00000030) |
| Biologic therapy (MAXO: monoclonal antibody therapy) | Dupilumab (anti-IL-4Rα) | Blocks IL-4/IL-13 signaling through IL4Rα, targeting core type 2 inflammatory pathway | 59–60% at 24 weeks; 100% in long-term open-label extension reported in review summary | FDA-approved for EoE since 2022; label expanded in 2024 to younger children; also approved in Europe/Canada per reviews | First disease-specific biologic for EoE; particularly useful in refractory disease and patients with atopic comorbidities; marked eosinophil reduction (~96%) reported (pqac-00000025, pqac-00000026, pqac-00000028, pqac-00000032) |
| Dietary therapy (MAXO: dietary modification) | Single-food elimination diet (often milk-first approach) | Removes food antigen triggers driving esophageal type 2 inflammation | 44–54% | Guideline-recommended first-line non-pharmacologic therapy | Less restrictive than broader elimination diets; requires serial endoscopy/biopsy to confirm remission and identify triggers (pqac-00000025, pqac-00000026, pqac-00000032) |
| Dietary therapy (MAXO: elimination diet) | Empiric multi-food elimination diet (e.g., 2-food, 4-food, 6-food elimination) | Sequential removal of common food allergens | Variable within broader dietary range; higher than 1-food approaches but below elemental diet in most summaries | Guideline-recommended first-line option | Common targets include dairy, wheat, egg, soy/legumes, nuts, fish/shellfish; adherence burden is substantial (pqac-00000026, pqac-00000032) |
| Dietary therapy (MAXO: elemental diet) | Elemental amino-acid formula diet | Complete removal of intact food antigens | 90–94% | Effective but limited by palatability, cost, and practicality | Highest remission rates among dietary therapies; often reserved for selected or refractory cases (pqac-00000025, pqac-00000026) |
| Endoscopic/mechanical therapy (MAXO: esophageal dilation) | Esophageal dilation for fibrostenotic disease | Mechanically disrupts strictures and increases luminal diameter; does not treat inflammation | Histologic remission: not applicable | Standard adjunctive interventional approach | Symptomatic relief ~85–95%; often targets 15–18 mm luminal diameter; repeat dilations common; perforation risk ~0.38%; should be combined with anti-inflammatory treatment (pqac-00000026, pqac-00000028) |
| Emerging biologic (MAXO: monoclonal antibody therapy) | Cendakimab (anti-IL-13) | Selectively blocks IL-13, aiming to reduce epithelial dysfunction, eotaxin-3 induction, and remodeling | 28.6% vs 2.2% placebo in review summary | Investigational / not broadly approved for EoE | Mechanistically attractive because IL-13 is central to EoE biology; under active clinical development (pqac-00000026) |
| Emerging biologic (MAXO: monoclonal antibody therapy) | Tezepelumab (anti-TSLP) | Blocks epithelial alarmin TSLP upstream of Th2 polarization and eosinophilic inflammation | Not established in the cited summaries | Investigational | Rationale is strong given TSLP genetic and mechanistic evidence in EoE, but robust remission data were not provided in the retrieved summaries (pqac-00000021, pqac-00000032) |
| Emerging biologic (MAXO: monoclonal antibody therapy) | Benralizumab (anti-IL-5Rα) | Depletes eosinophils by targeting IL-5 receptor alpha | Not recommended / no consistent efficacy for routine EoE treatment in recent reviews | Investigational; not approved for EoE | Despite a compelling eosinophil-depleting mechanism, recent reviews summarize insufficient clinical benefit for routine use in EoE (pqac-00000026, pqac-00000032) |


*Table: This table summarizes current and emerging treatment options for eosinophilic esophagitis, including mechanisms, remission rates, regulatory status, and practical notes. It is useful for comparing first-line therapies, procedural management, and biologic pipeline agents in one place.*