UNIQUE MECHANISM
OF ACTION

Name: Nemluvio HCP
Creator: Nemluvio

NEMLUVIO is the first and only neuroimmune-targeted treatment to directly block IL‑31RA^1,2

NEMLUVIO^® disrupts PN and AD from the inside and outside by blocking IL-31 signaling

NEMLUVIO first and only to block IL-31RA. Itch, Inflammation, Skin Barrier Dysfunction, and Fibrosis.

Mechanism of disease

Unlike other cytokines, overexpression of IL-31 and IL-31RA has been shown to be a direct driver of itch and more. IL‑31 binds to receptors across multiple cell types to drive PN and AD^1,2

Mechanism of action

NEMLUVIO targets an IL-31 receptor, blocking signaling that drives itch, inflammation, skin barrier dysfunction, and fibrosis^1,2

NEMLUVIO is the first-of-its-kind, neuroimmune-targeted treatment to block IL‑31 signaling in four ways^1,2

NEMLUVIO blocks the urge to scratch and helps the skin heal from within at the same time^1,2

Hover over or click each card to reveal NEMLUVIO's action in each pathway

itch^1,2

Blocks the urge
to scratch

Helps block the urge to scratch in the sensory nerves in the skin and on the dorsal root ganglion^1,2

inflammation^1‑4

PROMOTES SKIN
HEALING THROUGH
DOWNREGULATION

Promotes skin healing by downregulating multiple inflammatory pathways including type 2 inflammation (such as IL‑13)^1‑4

SKIN BARRIER DYSFUNCTION^1‑5

HELPS RESTORE THE SKIN
BARRIER FROM WITHIN

Helps restore the skin barrier from within by blocking IL-31RA on keratinocytes^1‑5

FIBROSIs^1‑5

BLOCKS DRIVERS OF
SKIN THICKENING

Blocks IL-31RA on fibroblasts, which are drivers of skin thickening and lichenification^1‑5

WATCH THE VIDEO BELOW TO LEARN MORE ABOUT HOW NEMLUVIO WORKS

NEMLUVIO is a humanized IgG2 monoclonal antibody.¹

Transcript

IL-31, the neuroimmune cytokine, directly drives disease processes by binding to IL-31 receptor alpha to: activate sensory nerves in the skin and on the dorsal root ganglion to amplify the itch signal to the brain, which compels the patient to scratch, interact with multiple cell types to drive TH2 and non-TH2 inflammation, interfere with keratinocyte differentiation that leads to skin barrier dysfunction, stimulate fibroblasts to induce collagen deposition and tissue remodeling that result in fibrosis.

NEMLUVIO is the first and only neuroimmune treatment that targets IL-31 signaling to work across four disease processes: blocking signals in the sensory nerves and uniquely on the dorsal root ganglion to directly suppress itch, blocking IL-31 receptor alpha to disrupt a key cause of harmful inflammation in the immune system, blocking the IL-31RA on keratinocytes to normalize the skin barrier, and finally, NEMLUVIO blocks the IL-31RA on fibroblasts to inhibit pro-fibrotic and inflammatory responses to heal nodules.

Fast Itch Relief¹²

See how NEMLUVIO significantly improved itch in both pivotal and long-term studies^12,13

VIEW THE DATA

Patient Profiles

Take a closer look at the types of patients who may benefit from NEMLUVIO

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Sign up now for more information about NEMLUVIO for PN

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AD=atopic dermatitis; IL-31=interleukin‑31; IL‑31RA=interleukin‑31 receptor alpha; PN=prurigo nodularis.

References: 1. NEMLUVIO (nemolizumab-ilto) injection 30 mg Prescribing Information. Dallas, TX: Galderma Laboratories, L.P. 2. Nemmer JM, Kuchner M, Datsi A, et al. Interleukin-31 signaling bridges the gap between immune cells, the nervous system and epithelial tissues. Front Med (Lausanne). 2021;8:639097. doi:10.3389/fmed.2021.639097 3. Tsoi LC, Hacini-Rachinel F, Fogel P, et al. Transcriptomic characterization of prurigo nodularis and the therapeutic response to nemolizumab. J Allergy Clin Immunol. 2022;149(4):1329-1339. doi:10.1016/j.jaci.2021.10.004 4. Galderma Laboratories, L.P.; data on file. 5. Ma F, Gharaee-Kermani M, Tsoi LC, et al. Single-cell profiling of prurigo nodularis demonstrates immune-stromal crosstalk driving profibrotic responses and reversal with nemolizumab. J Allergy Clin Immunol. 2024;153(1):146-160. doi:10.1016/j.jaci.2023.07.005 6. Dubin C, Del Duca E, Guttman-Yassky E. The IL-4, IL-13 and IL-31 pathways in atopic dermatitis. Expert Rev Clin lmmunol. 2021;17(8):835-852. doi:10.1080/1744666X.2021.1940962 7. Feld M, Garcia R, Buddenkotte J, et al. The pruritus- and TH2-associated cytokine IL-31 promotes growth of sensory nerves. J Allergy Clin lmmunol. 2016;138(2):500-508.e24. doi:10.1016/j.jaci.2016.02.020 8. Gibbs BF, Patsinakidis N, Raap U. Role of the pruritic cytokine IL-31 in autoimmune skin diseases. Front lmmunol. 2019;10:1383. doi:10.3389/fimmu.2019.01383 9. Hänel KH, Pfaff CM, Cornelissen C, et al. Control of the physical and antimicrobial skin barrier by an IL-31-I L-1 signaling network. J lmmunol. 2016;196(8):3233-3244. doi:10.4049/jimmunol.1402943 10. Mousa A, Bakhiet M. Role of cytokine signaling during nervous system development. Int J Mol Sci. 2013;14(7):13931-13957. doi:10.3390/ijms140713931 11. Bewley A, Homey B, Pink A. Prurigo nodularis: a review of IL-31RA blockade and other potential treatments. Dermatol Ther (Heidelb). 2022;12(9):2039-2048. doi:10.1007/s13555-022-00782-2 12. Ständer S, Elmariah SB, Kwatra SG, et al. Rapid improvement of itch with nemolizumab in atopic dermatitis and prurigo nodularis phase 3 studies. J Eur Acad Dermatol Venereol. 2025;00:1-9. doi:10.1111/jdv.70250 13. Kwatra SG, Legat FJ, Reich A, et al. Nemolizumab long-term safety and efficacy up to 148 weeks in the OLYMPIA open-label extension study in patients with prurigo nodularis. Presented at: 2026 Winter Clinical Miami; February 27-March 1, 2026; Aventura, FL.

IMPORTANT SAFETY INFORMATION

INDICATIONS: NEMLUVIO^® (nemolizumab-ilto) is an interleukin-31 receptor alpha antagonist indicated for:

the treatment of adults and pediatric patients 12 years of age and older with moderate-to-severe atopic dermatitis in combination with topical corticosteroids and/or calcineurin inhibitors when the disease is not adequately controlled with topical prescription therapies.
the treatment of adults with prurigo nodularis.

CONTRAINDICATION: NEMLUVIO is contraindicated in patients with known hypersensitivity to nemolizumab-ilto or to any of the excipients in NEMLUVIO.

WARNINGS AND PRECAUTIONS:
Hypersensitivity reactions have been reported with NEMLUVIO use. If clinically significant hypersensitivity reaction occurs, immediately institute appropriate therapy, and discontinue NEMLUVIO. Avoid use of live vaccines during treatment with NEMLUVIO.

ADVERSE REACTIONS:
Most common adverse reactions (incidence ≥1%) are:

Atopic Dermatitis: headache (including migraine), arthralgia, urticaria, and myalgia.
Prurigo Nodularis: headache, dermatitis atopic, eczema, and eczema nummular.

USE IN SPECIFIC POPULATIONS:
Pregnancy: There are no adequate and well-controlled studies on NEMLUVIO in pregnant women. The limited available information on NEMLUVIO use during pregnancy is not sufficient to inform a drug-associated risk of major birth defects or miscarriage in humans. Human IgG antibodies are known to cross the placental barrier; therefore, NEMLUVIO may be transmitted from the mother to the developing fetus.

Lactation: There are no data on the presence or transfer of NEMLUVIO in human milk, the effects on the breastfed infant, or the effects on milk production. Human IgG is known to be present in human milk. The effects of local gastrointestinal and limited systemic exposure to NEMLUVIO on the breastfed infant are unknown. NEMLUVIO has not been administered to nursing/lactating women. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for NEMLUVIO and any potential adverse effects on the breastfed child from NEMLUVIO or from the underlying maternal condition.

Pediatric Use: The safety and effectiveness of NEMLUVIO have not been established in pediatric patients younger than 12 years of age for the treatment of moderate-to-severe atopic dermatitis or pediatric patients younger than 18 years of age for the treatment of prurigo nodularis.

Please see full Prescribing Information, including Patient Information.

UNIQUE MECHANISM OF ACTION

NEMLUVIO is the first and only neuroimmune-targeted treatment to directly block IL‑31RA1,2