Biologic Therapies in Dermatology
Introduction
Biologic therapies have revolutionized the treatment of inflammatory skin diseases by targeting specific cytokines, receptors, and immune cell populations. Unlike traditional immunosuppressants that broadly suppress immune function, biologics offer precise modulation of pathogenic pathways with often superior efficacy and improved safety profiles.
This chapter provides a comprehensive overview of biologic agents used in dermatology, organized by mechanism of action.
Overview of Biologic Classes
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TNF-α Inhibitors
Mechanism and Agents
| Agent | Structure | Half-life | Approved Indications (Derm) |
|---|
| Etanercept | Fusion protein (TNFR2-Fc) | 3-5.5 days | Psoriasis, psoriatic arthritis |
| Infliximab | Chimeric mAb | 8-10 days | Psoriasis, psoriatic arthritis |
| Adalimumab | Fully human mAb | 14 days | Psoriasis, PsA, HS, pyoderma gangrenosum |
| Certolizumab | PEGylated Fab' | 14 days | Psoriasis, PsA (no placental transfer) |
| Golimumab | Human mAb | 14 days | Psoriatic arthritis |
TNF-α in Psoriasis
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Safety Considerations
| Risk | Monitoring |
|---|
| Infections (esp. TB, fungal) | TB screening before and during; watch for signs |
| Malignancy (lymphoma) | Baseline and ongoing assessment |
| Heart failure | Contraindicated in NYHA III/IV |
| Demyelinating disease | Rare; avoid in MS history |
| Injection site reactions | Common with SC agents |
| Autoantibody formation | ANA, anti-dsDNA (usually asymptomatic) |
IL-17 Inhibitors
Agents and Targets
| Agent | Target | Structure | Indications |
|---|
| Secukinumab | IL-17A | Human mAb | Psoriasis, PsA, AS |
| Ixekizumab | IL-17A | Humanized mAb | Psoriasis, PsA |
| Brodalumab | IL-17RA | Human mAb | Psoriasis |
| Bimekizumab | IL-17A + IL-17F | Humanized mAb | Psoriasis, PsA, HS |
IL-17 in Psoriasis
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Clinical Considerations
| Issue | Details |
|---|
| Efficacy | PASI 90+ in >70% (among highest for psoriasis) |
| Candidiasis | Increased risk (mucocutaneous); usually mild |
| IBD | New-onset or exacerbation (esp. brodalumab) |
| Suicidal ideation | Boxed warning for brodalumab |
| Speed of response | Rapid onset (visible improvement in 2-4 weeks) |
IL-23 Inhibitors
Agents
| Agent | Target | Structure | Dosing |
|---|
| Ustekinumab | IL-12/23 (p40 subunit) | Human mAb | Q12 weeks (after loading) |
| Guselkumab | IL-23 (p19 subunit) | Human mAb | Q8 weeks |
| Tildrakizumab | IL-23 (p19 subunit) | Humanized mAb | Q12 weeks |
| Risankizumab | IL-23 (p19 subunit) | Humanized mAb | Q12 weeks |
IL-23/IL-17 Axis
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Advantages of IL-23 Inhibitors
| Feature | Benefit |
|---|
| Durability | Some patients maintain response after discontinuation |
| Dosing interval | Q8-12 weeks maintenance (convenient) |
| Safety profile | Generally excellent; no TB reactivation signal |
| IBD | No increased risk (unlike IL-17 inhibitors) |
| Efficacy | PASI 90+ in 70-80% |
IL-4/IL-13 Inhibitors (Type 2 Targeting)
Dupilumab: Breakthrough for AD
| Feature | Details |
|---|
| Target | IL-4Rα (blocks IL-4 and IL-13) |
| Structure | Fully human mAb |
| Approved indications | Atopic dermatitis, asthma, CRSwNP, eosinophilic esophagitis, prurigo nodularis |
| Dosing | 300 mg SC q2 weeks |
Mechanism in Atopic Dermatitis
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Other Type 2 Agents
| Agent | Target | Status |
|---|
| Tralokinumab | IL-13 only | Approved for AD |
| Lebrikizumab | IL-13 only | Approved for AD |
| Nemolizumab | IL-31RA | Approved for prurigo nodularis, AD |
Dupilumab Adverse Effects
| Effect | Frequency | Notes |
|---|
| Conjunctivitis | 10-30% in AD | Less in asthma; mechanism unclear |
| Injection site reactions | Common | Usually mild |
| Facial erythema | Uncommon | "Dupilumab facial redness" |
| Infections | No significant increase | |
| Eosinophilia | Transient | Usually asymptomatic |
Anti-CD20: B Cell Depletion
Rituximab in Dermatology
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Indications in Dermatology
| Disease | Evidence | Typical Regimen |
|---|
| Pemphigus vulgaris | First-line with CS | 1g × 2 (days 1, 15) |
| Pemphigus foliaceus | First-line | Same |
| Bullous pemphigoid (refractory) | Second-line | Same |
| Dermatomyositis (refractory) | Case series | 375 mg/m² × 4 |
| Primary cutaneous B cell lymphomas | Standard | Various regimens |
Anti-IgE: Omalizumab
Mechanism
| Feature | Details |
|---|
| Target | IgE (Fc portion) |
| Effect | Binds free IgE; prevents binding to FcεRI |
| Result | Reduces IgE, downregulates FcεRI on mast cells/basophils |
Indications in Dermatology
| Condition | Evidence | Mechanism |
|---|
| Chronic spontaneous urticaria | High | Reduces IgE autoantibodies, FcεRI activation |
| Chronic inducible urticaria | Moderate | Same |
| Refractory atopic dermatitis | Limited | IgE reduction |
JAK Inhibitors (Targeted Synthetic)
Overview
JAK inhibitors are small molecules (not biologics) but target specific pathways similarly.
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JAK Inhibitors in Dermatology
| Agent | Target | Indication | Route |
|---|
| Tofacitinib | JAK1/3 | Psoriasis, PsA, off-label (AA, vitiligo) | Oral |
| Baricitinib | JAK1/2 | Atopic dermatitis, AA | Oral |
| Upadacitinib | JAK1 | Atopic dermatitis | Oral |
| Abrocitinib | JAK1 | Atopic dermatitis | Oral |
| Ruxolitinib | JAK1/2 | Atopic dermatitis, vitiligo | Topical |
| Deucravacitinib | TYK2 | Psoriasis | Oral |
Summary: Biologic Selection by Disease
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Key Clinical Pearls
| Topic | Pearl |
|---|
| IL-17 inhibitors | Highest PASI rates; watch for candidiasis and IBD |
| IL-23 inhibitors | Convenient dosing (q8-12 weeks); durable response |
| Dupilumab | Game-changer for AD; watch for conjunctivitis |
| Rituximab | First-line for pemphigus with corticosteroids |
| Omalizumab | Works in CSU regardless of IgE level |
| JAK inhibitors | Oral convenience; monitor for infections, VTE, malignancy |
| TB screening | Required before anti-TNF; consider for all biologics |
Cross-References
How to Cite
Cutisight. "Biologic Therapies." Encyclopedia of Dermatology [Internet]. 2026. Available from: https://cutisight.com/education/volume-03-skin-reactions-and-interactions/04-immunology/04-therapeutics/01-biologics/01-biologic-therapies
This is an open-access resource. Please cite appropriately when using in academic or clinical work.