Will targeted therapies transform the treatment of atopic dermatitis?
New targeted treatments look set to transform the treatment of moderate to severe atopic dermatitis. As Dupixent (dupilumab; Regeneron/Sanofi) gains traction, older, more toxic immunosuppressant options will lose ground as treating physicians seek better efficacy and safety elsewhere. But as the market evolves, and more treatments are approved, clinical and commercial differentiation will become key. Key opinion leaders expect similar clinical profiles from tralokinumab (AstraZeneca/Leo Pharma) and lebrikizumab (Dermira), both anti-IL-13 monoclonal antibodies (mAbs). Moreover, other pipeline programmes, including mepolizumab (anti-IL-5; GSK) and nemolizumab (anti-IL-31; Galderma/Chugai) could potentially become niche options based on their respective mechanisms of action. Oral JAK inhibitors may also provide alternatives for treating atopic dermatitis.
Learn how KOLs see the market evolving, how current products can protect market share, and how developers can differentiate their pipeline therapies.
Twelve North American and European KOLs provide their insight on 2 marketed products, 11 pipeline programmes and 4 early-stage mechanisms of action.
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Take a tour of the report now:
- The table of contents
- The key business questions answered
- The key KOL quotes
- See the therapies covered
- Find out who the 6 EU & 6 US KOLs are
- Review an extract from the report - 1 drug profile
- Will traditional treatment options be side-lined by Dupixent (dupilumab; Sanofi/Regeneron) and other novel therapies? Find out how KOLs see the treatment paradigm for atopic dermatitis changing in the near-term as physicians look for greater efficacy and better safety.
- Pfizer's Eucrisa (crisaborole) has been launched in the US, but what do KOLs think about it? A welcome addition, say some KOLs, but what's the overarching view of Eucrisa's efficacy compared to more traditional treatments?
- Are AstraZeneca/Leo Pharma's tralokinumab and Dermira's lebrikizumab sufficiently different to Dupixent and themselves to carve out a place in the treatment paradigm? Both agents target IL-13, Dupixent targets both IL-13 and IL-4. What do KOLs think about that, and do they have any reservations about clinical similarity?
- Mepolizumab (anti-IL-5; GSK) and nemolizumab (anti-IL-31; Galderma/Chugai) target different cytokines, but which option is most appealing? Or will each of these treatment options only be able to carve out a small niche for themselves based on their respective mechanisms of action (MOA)?
- Oral JAK inhibitors may provide alternatives for treating atopic dermatitis, but will safety concerns limit uptake? With several JAK inhibitors in development, R&D investment in this MOA is high. But do KOLs have any safety concerns? Or will the convenience of oral treatment be sufficient to support clinical adoption?
- Will differentiation within the treatment landscape become increasingly challenging as the market grows? Several clinical and commercial tactics are available to companies in order to differentiate themselves. The question becomes, are these tactics enough? As physicians become more selective, and payers become less willing to pay, which tactics will become more influential in the future?
"There's a long list [of factors that influence treatment choice]. A lot of it will depend on what they've been on before. Some of it's going to be about severity, what their history is, patient preference, how old they are, what areas we're going to be treating. So a long list of factors come into our choice. I will say that some of it's going to be what I can get for the patient, because in the United States, access is an issue." US Key Opinion Leader.
"Provided that no other clinical side-effects pop up over time, and the conjunctivitis problems are not so severe, I could imagine that dupilumab might become a kind of blockbuster drug for the treatment of atopic dermatitis from the data which are available now." European Key Opinion Leader.
Sample of therapies covered
- Dupixent (dupilumab; Regeneron/Sanofi)
- Eucrisa (crisaborole; Pfizer)
Pipeline (P2/P3) Therapies
- Tralokinumab (anti-IL13; AstraZeneca/Leo Pharma)
- Lebrikizumab (anti-IL13; Dermira)
- Mepolizumab (anti-IL5; GSK)
- Nemolizumab (anti-IL31; Galderma)
- ANB 020 (anti-IL33; AnaptysBio)
- Upadacitinib (JAK inhibitor; AbbVie)
- Ruxolitinib (JAK inhibitor; Incyte)
- PF 04965842 (JAK inhibitor; Pfizer)
- Baricitinib (JAK inhibitor; Eli Lilly/Incyte)
- ALX 101 (Liver X receptor agonist; Alexar)
- GBR 830 (Anti-OX40R mAb; Glenmark)
Early Stage MOAs (P1/P2)
- Tezepelumab (anti-TSLP; Amgen/AstraZeneca)
- Fevipiprant (CRTH2 antagonist; Novartis)
- GR MD 02 (Galectin 3 inhibitor; Galectin)
- Anti-GATA3 gene therapy (Sterna Biologicals)
KOLs from North America
- Mark Boguniewicz. Professor Division of Paediatric Allergy & Clinical Immunology, Department of Pediatrics, Denver, CO
- Raymond Cho. Associate Professor Dermatology, UCSF School of Medicine, San Francisco CA
- Peck Ong. Associate Professor of Clinical Pediatrics at University of Southern California, Los Angeles, CA
- Amy S Paller. Professor of Dermatology and Pediatrics. Chair, Department of Dermatology, Director, Northwestern University Skin Disease Research Center, Chicago, IL
- Jonathan Spergel. Professor of Pediatrics, Chief of the Allergy Section, Children's Hospital of Philadelphia. Philadelphia, PA
- Jeffrey M Weinberg. Associate Clinical Professor Dermatology, Kimberly and Eric J. Waldman Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY
KOLs from Europe
- Gianfranco Cimmino. Associate Professor in Dermatology at the University of Naples Federico II, Italy
- Graham Ogg. MRC Programme Leader, Professor of Dermatology, University of Oxford Consultant Dermatologist, Oxford University Hospitals NHS Trust, UK
- Odile Picard. Consultant at Saint Antoine Hospital in Paris, Professor of Dermatology at University of Saint-Antoine, Paris, France
- Richard Warren. Reader and Honorary Consultant Dermatologist, Division of Musculoskeletal & Dermatological Sciences, University of Manchester, UK
- Anonymous German KOL. Professor for Immunology, Department of Dermatology at a leading medical School in Germany
- Anonymous German KOL. Professor and Director In Dermatology at a leading university in Germany
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Table of Contents
1. Executive summary
2. Research objectives and focus
- 2.1. Research objectives
- 2.2. Research focus
3. Current treatment strategies
- 3.1. Overview
- 3.2. Dupixent (dupilumab; Sanofi/Regeneron)
- 3.2.1. Key insights summary
- 3.2.2. Drug summary
- 3.3. Eucrisa (crisaborole; Pfizer)
- 3.3.1. Key insights summary
- 3.3.2. Drug summary
4. Selected late-stage pipeline programmes
- 4.1. Tralokinumab (AstraZeneca/Leo Pharma)
- 4.1.1. Key insights summary
- 4.1.2. Drug summary
- 4.2. Lebrikizumab (Dermira)
- 4.2.1. Key insights summary
- 4.2.2. Drug summary
- 4.3. Mepolizumab (Nucala; GSK)
- 4.3.1. Key insights summary
- 4.3.2. Drug summary
- 4.4. Nemolizumab (Galderma/Chugai)
- 4.4.1. Key insights summary
- 4.4.2. Drug summary
- 4.5. ALX-101. (Ralexar Therapeutics)
- 4.5.1. Key insights summary
- 4.5.2. Drug summary
- 4.6. GBR 830. (Glenmark Pharmaceuticals)
- 4.6.1. Key insights summary
- 4.6.2. Drug summary
- 4.7. Tezepelumab (Amgen/AstraZeneca)
- 4.7.1. Key insights summary
- 4.7.2. Drug summary
- 4.8. SB011. (Sterna Biologicals)
- 4.8.1. Key insights summary
- 4.8.2. Drug summary
- 4.9. JAK inhibitors
- 4.9.1. Key insights summary
- 4.9.2. Overview
- 4.9.3. Olumiant (baricitinib; Eli Lilly/Incyte)
- 4.9.4. PF-04965842(Pfizer)
- 4.9.5. Ruxolitinib (Jakavi; Incyte) and Upadacitinib (AbbVie)
5. Other early stage pipeline programmes
- 5.1. Prostaglandin DP2 receptor antagonists
- 5.1.2. Fevipiprant (Novartis)
- 5.2. Galectin 3 inhibitors
- 5.2.1. GR-MD-02 (Galectin Therapeutics)
- 5.2.2. ANB020 (AnaptysBio)
6. Evolution of the atopic dermatitis treatment landscape
- 6.1. Current and future treatment pathways
- 6.1.2. Key insights summary
7. Future of the atopic dermatitis treatment paradigm
- 8.1. KOL details
- 8.1.1. US KOLs
- 8.1.2. European KOLs