ArticleJID innovations : skin science from molecules to population health2024
A Bispecific, Tetravalent Antibody Targeting Inflammatory and Pruritogenic Pathways in Atopic Dermatitis.
Article in JID innovations : skin science from molecules to population health, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Engineering and Partial Characterization of an Anti-IL-23/Anti-TNF-α Bispecific Domain Antibody Fused to Human Serum Albumin Domain for Inflammatory Disease Therapy.Applied biochemistry and biotechnology · 2026Article
- Cross-Talk between Neurons and Immune Cells in Pruritus: from Mechanisms To Medicines.Current allergy and asthma reports · 2026Review
- The potential of targeted IL-4 therapy for the comorbidity of atopic dermatitis and attention-deficit/hyperactivity disorder in children via the skin-brain axis.Frontiers in allergy · 2026Article
- Advancing Precision Medicine in Inflammatory Skin Disease.American journal of clinical dermatology · 2025Review
- Beyond the blockade: unmet needs in systemic targeted atopic dermatitis therapy.Frontiers in immunology · 2025Review
- Targeting the IL-4/IL-4R Axis in Th2 Inflammatory Diseases: A Review of Clinical Efficacy and Safety.Journal of inflammation research · 2025Review
- Review
- Update on the pathogenesis of atopic dermatitis.Anais brasileiros de dermatologiaReview
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Authors and funding
24 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibition of IL-4/IL-13 signaling has dramatically improved the treatment of atopic dermatitis (AD). However, in many patients, clinical responses are slow to develop and remain modest. Indeed, some symptoms of AD are dependent on IL-31, which is only partially reduced by IL-4/IL-13 inhibition. Thus, there is an unmet need for AD treatments that concomitantly block IL-4/IL-13 and IL-31 pathways. We engineered NM26-2198, a bispecific tetravalent antibody designed to accomplish this task. In reporter cell lines, NM26-2198 concomitantly inhibited IL-4/IL-13 and IL-31 signaling with a potency comparable with that of the combination of an anti-IL-4Rα antibody (dupilumab) and an anti-IL-31 antibody (BMS-981164). In human PBMCs, NM26-2198 inhibited IL-4-induced upregulation of CD23, demonstrating functional binding to FcγRII (CD32). NM26-2198 also inhibited the secretion of the AD biomarker thymus and activation-regulated chemokine (TARC) in blood samples from healthy human donors. In male cynomolgus monkeys, NM26-2198 exhibited favorable pharmacokinetics and significantly inhibited IL-31-induced scratching at a dose of 30 mg/kg. In a repeat-dose, good laboratory practice toxicology study in cynomolgus monkeys, no adverse effects of NM26-2198 were observed at a weekly dose of 125 mg/kg. Together, these results justify the clinical investigation of NM26-2198 as a treatment for moderate-to-severe AD.
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