The advent of caninized monoclonal antibodies has transformed the management of atopic dermatitis, paving the way for targeted medicine in a field long limited to corticosteroids and non-specific immunosuppressants. At the same time, human dermatology has also experienced an unprecedented acceleration in the number of approved biotherapies. This article provides a comprehensive synthesis of current knowledge on monoclonal antibodies used in veterinary and human dermatology, as well as future prospects.

1. Overview of Monoclonal Antibodies

1.1 Definition and Structure of Monoclonal Antibodies

Monoclonal antibodies are immunoglobulins produced by a single cell clone, directed against a single epitope of a given antigen. The basic structure of an immunoglobulin consists of two heavy chains and two light chains, connected by disulfide bonds. Each chain has a variable (V) region, responsible for antigen recognition, and a constant (C) region, which determines the class and subclass of the antibody. The Fab fragment (fragment antigen-binding) provides antigen binding, while the Fc fragment (crystallizable fragment) interacts with cell receptors and complement, determining the effector functions of the molecule (Köhler 1975).

The distinction between polyclonal and monoclonal antibodies is based on their origin. A polyclonal serum contains a heterogeneous mixture of immunoglobulins directed against multiple epitopes of the same antigen, produced by different B cell clones. Conversely, a monoclonal antibody is derived from a single hybridoma, a fusion of a B lymphocyte secreting a specific antibody and a myeloma cell that confers immortality on the cell line. This technology, described by Köhler and Milstein in 1975, allowed for the first time the unlimited production of antibodies with a predetermined specificity (Köhler 1975). Since then, recombinant techniques have largely supplanted the classical hybridoma method. Contemporary monoclonal antibodies are mostly produced in Chinese hamster ovary cells (CHO cells), an expression system that ensures appropriate glycosylation, high productivity, and industrial reproducibility. In veterinary medicine, lokivetmab is a caninized monoclonal antibody expressed via recombinant techniques in CHO cells.

The arrival of biotherapies has revolutionized the therapeutic approach to atopic dogs

1.2 Classification According to the Origin of Monoclonal Antibodies

International nomenclature classifies monoclonal antibodies according to their degree of humanization, reflected in the suffix of the international nonproprietary name. Murine antibodies (-omab), entirely derived from mice, exhibit high immunogenicity with an anti-drug antibody (ADA) rate exceeding 50%. Chimeric antibodies (-ximab) reduce this rate to approximately 25%, humanized antibodies (-zumab) to less than 10%, and fully human antibodies (-umab), produced by transgenic mice or phage display, offer the most favorable immunogenicity profile.

In veterinary medicine, the same logic applies but is adapted to the target species. A caninized antibody is one whose constant regions are of canine origin, minimizing the dog’s immune response against the therapeutic molecule. Lokivetmab (CYTOPOINT, Zoetis) and tirnovetmab (BEFRENA, Elanco) are caninized anti-IL-31 monoclonal antibodies. Felinization, an analogous process adapted to cats, is currently under development for feline anti-IL-31 candidates, but no felinized monoclonal antibody is currently commercially available in feline dermatology.

1.3 General Mechanisms of Action

Monoclonal antibodies exert their therapeutic effect through three main mechanisms. Direct neutralization involves the binding of the antibody to a soluble ligand, such as a cytokine or mediator, preventing its interaction with the receptor. Lokivetmab neutralizes circulating IL-31 before it binds to the IL-31RA/OSMR receptor complex, interrupting the pruritogenic signaling cascade (Gonzales 2013). Blocking membrane receptors is the second mechanism: the antibody binds directly to the cell receptor, preventing the binding of the endogenous ligand. Nemolizumab (NEMLUVIO, Galderma) illustrates this mechanism by targeting the IL-31 receptor alpha (IL-31RA) rather than the cytokine itself (Silverberg 2024). The third mechanism involves the effector functions of the Fc fragment: antibody-dependent cellular cytotoxicity recruits NK cells and macrophages, while complement-dependent cytotoxicity activates the complement cascade. These mechanisms are exploited in onco-dermatology, where anti-PD-1 and anti-CTLA-4 antibodies restore the antitumor immune response (Larkin 2019).

1.4 Pharmacokinetic Properties

The half-life of monoclonal antibodies, typically between 14 and 21 days depending on the IgG subclass and species, allows for spaced injection intervals, generally monthly or bimonthly. This pharmacokinetic property represents an advantage in terms of adherence compared to daily oral treatments. The subcutaneous route is the preferred administration route for the majority of monoclonal antibodies in dermatology, both human and veterinary. Lokivetmab has an elimination half-life of approximately 16 days in dogs, compatible with monthly injections (Michels 2016). The intravenous route is reserved for specific indications, such as infliximab in psoriasis or spesolimab in generalized pustular psoriasis flares.

Immunogenicity is the main limiting factor. The formation of anti-drug antibodies (ADA) can reduce serum concentrations and clinical efficacy. For lokivetmab, the ADA rate is between 2.1% and 2.6% of treated dogs, with limited clinical consequences (Moyaert 2017). Caninization and felinization aim to reduce this immunogenicity by minimizing the proportion of protein sequences foreign to the treated species.

1.5 Therapeutic Advantages and Limitations

High target specificity is the main advantage of monoclonal antibodies over classical immunosuppressants. By targeting only one cytokine or receptor, these molecules limit off-target effects responsible for the toxicity of corticosteroids (skin atrophy, polyuria-polydipsia, calcinosis cutis) and calcineurin inhibitors (gastrointestinal disorders, hypertrichosis). Lokivetmab is the treatment of choice in leishmaniasis-endemic areas because it does not impair the vital Th1 response against the parasite, avoiding the risks associated with corticosteroids. The overall safety profile of the product is also documented by Gober et al. (2022).

The limitations are primarily economic and logistical. The production cost of monoclonal antibodies, involving mammalian cell expression systems and complex purification, remains high. In France, the price of a CYTOPOINT injection varies depending on the dog’s weight and the required dose, representing a significant financial burden for owners on long-term treatment. The species constraint in veterinary medicine requires the development of specific antibodies for each target species: a caninized antibody cannot be administered to a cat without risk of severe immunogenicity, and vice versa. The veterinary market, smaller than the human market, lengthens return-on-investment timelines and limits the number of molecules in development.

However, this economic argument should be put into perspective. While the cost of veterinary monoclonal antibodies may seem high, it remains considerably lower than that practiced in human medicine, where comparable biologics reach several thousand dollars per injection. Furthermore, the analysis of the real cost must integrate the financial burden of flares: a severe episode of atopic dermatitis involves repeated consultations, antibiotic treatments for secondary pyoderma, and antifungal treatments, the total of which over several years frequently exceeds the cost of structured preventive treatment. A proactive approach using monoclonal antibodies, ensuring continuous control of pruritus and inflammation, reduces the frequency and severity of these episodes and limits unpredictable expenses related to infectious complications.

2. Monoclonal Antibodies in Veterinary Dermatology: Cytopoint (lokivetmab) – Zoetis

2.1.1 History and Development

Prior to 2016, the management of canine atopic dermatitis relied on glucocorticoids, cyclosporine, and oclacitinib (APOQUEL, Zoetis), a JAK1 inhibitor marketed in 2014. The need for a long-acting injectable treatment, free from the adverse effects of corticosteroids and not requiring daily administration, was unmet. Zoetis developed lokivetmab from its caninized antibody platform, targeting IL-31, a pruritogenic cytokine whose central role in canine atopic dermatitis had been established by Gonzales et al. in 2013. Regulatory approval by the FDA (USDA) was obtained in December 2016, followed by marketing authorization by the EMA in 2017 (Michels 2016). In France, the veterinary medicine has been available since 2017 under veterinary prescription, dispensed as an injectable solution in a 1 ml single-dose vial.

2.1.2 Molecular Structure and Caninization

Lokivetmab is a caninized IgG class monoclonal antibody with a molecular weight of approximately 150 kDa. The caninization process involves grafting the CDRs of the parental murine antibody onto a canine IgG scaffold, preserving the binding specificity for canine IL-31 (affinity in the nanomolar range) while minimizing immunogenicity in the dog. Lokivetmab is a caninized monoclonal antibody expressed via recombinant techniques in Chinese hamster ovary cells (CHO cells), ensuring appropriate post-translational glycosylation and homogeneity of the final product (Michels 2016).

2.1.3 Mechanism of Action

IL-31 is the central pruritogenic cytokine in canine atopic dermatitis. IL-31 is produced primarily by activated Th2 lymphocytes and type 2 innate lymphoid cells (ILC2). Mast cells and certain macrophage populations may also be a source, although their relative contribution is less well documented in spontaneous canine atopic dermatitis (Marsella 2021). Binding of IL-31 to its receptor activates the JAK/STAT signaling pathway, primarily via JAK1 (associated with IL-31RA) and JAK2 (Gonzales 2013). Lokivetmab neutralizes free circulating IL-31 before it binds to the IL-31RA/OSMR complex, interrupting the signaling cascade upstream. This neutralization stops pruritus and reduces secondary skin lesions, which are self-sustaining through mechanical excoriation.

2.1.4 Pharmacokinetics and Pharmacodynamics

The elimination half-life of lokivetmab in dogs is approximately 16 days, compatible with an injection interval of 4 to 8 weeks depending on individual clinical response. The volume of distribution is low, typical of monoclonal antibodies with primarily intravascular and interstitial distribution. The correlation between serum levels of lokivetmab and inhibition of pruritus was demonstrated in dose-response studies: the dose of 1 mg/kg SC corresponds to the optimal efficacy threshold identified as early as the preclinical phase (Gadeyne 2014). Body weight directly influences the dosage, which is adjusted based on weight to maintain an effective serum concentration. The veterinary medicine is available as an injectable solution in vials of 10, 20, 30, and 40 mg/ml, each containing 1 ml, allowing the dose to be adapted to the dog’s weight.

2.1.5 Treatment Protocol

The official indications for lokivetmab are the treatment of pruritus associated with allergic dermatitis and the treatment of clinical manifestations of atopic dermatitis. The minimum recommended dosage is 1 mg/kg by subcutaneous (SC) route, as a monthly injection, every 4 weeks according to clinical response. The contents of the vial must be administered subcutaneously by a veterinarian. Self-injection by the owner is not provided for in the product label. In experimental models of pruritogenic challenge with recombinant IL-31, inhibition of scratching is observed as early as 8 hours after injection. Under clinical conditions, a reduction in pruritus is typically perceived within 24 to 48 hours (Fleck 2021). Combination with other treatments for atopic dermatitis is possible and frequently practiced. Lokivetmab can be combined with oclacitinib (APOQUEL, Zoetis), cyclosporine, or anti-inflammatory agents when needed, within the context of a multimodal approach recommended by the ICADA 2023 guidelines.

2.1.6 Results of Pivotal Clinical Studies

The pivotal study by Michels et al., published in 2016, is a multicenter randomized placebo-controlled trial conducted in atopic dogs under field conditions. At doses of 0.5 to 2 mg/kg SC, lokivetmab reduced the pruritus score (PVAS) compared to placebo from the first days onward. The CADESI-03, a lesion severity score, also showed significant improvement in the treated group (Michels 2016).

The study by Moyaert et al. in 2017, comparing lokivetmab to cyclosporine in a double-blind design, demonstrated non-inferiority of lokivetmab in reducing pruritus at Day 28, with a favorable adverse event profile. The anti-drug antibody (ADA) rate was 2.1% (3 out of 142 dogs), with 2 transient cases without clinical consequences (Moyaert 2017).

The study by Marsella et al. in 2018 confirmed the efficacy of lokivetmab on skin lesions measured by the CADESI-04, with parallel improvement in owner quality of life.

The study by Tamamoto-Mochizuki et al. evaluated a proactive maintenance therapy strategy with lokivetmab in atopic dogs previously controlled by other anti-allergic treatments, showing that a quarter of dogs had no flares for at least one year on lokivetmab monotherapy, with a median time to relapse of 63 days after discontinuation of conventional treatments (Tamamoto-Mochizuki 2019).

2.1.7 Results of Post-Authorization Studies and Real-World Data

A Zoetis study conducted between 2019 and 2020 provided 12-month long-term follow-up data for dogs treated with lokivetmab. Persistence of efficacy was confirmed, with an owner satisfaction rate exceeding 90% (Gober 2022).

The long-term study by Gober et al., published in 2025, followed a cohort of 75 atopic dogs treated at the US label dosage (at least 2 mg/kg every 4 to 8 weeks as needed) for 12 months. Dogs were first eligible for the long-term follow-up phase after achieving a PVAS below 36 mm during the initial three-month injection phase. Over the entire follow-up period, 88% of dogs maintained a mean PVAS below 36 mm, and 27% maintained a PVAS score below 50% of their baseline value throughout the study. Owner satisfaction and intention to continue treatment were reported as very high, and a reduction in the use of concomitant treatments (topical agents, corticosteroids, or oclacitinib) was observed throughout the follow-up, with no dog requiring systemic rescue treatment during the 12 months (Gober 2025).

Beyond pruritus control, prolonged treatment with lokivetmab is associated with a measurable restoration of the skin barrier function. This normalization is reflected in a significant decrease in transepidermal water loss at lesional sites, alongside a reduction in biophysical parameters reflecting epidermal inflammation (Marsella 2018). In parallel, the decrease in hair cortisol observed under prolonged treatment suggests that pruritus control and disruption of the itch-scratch cycle reduce the systemic physiological stress imposed by canine atopic dermatitis, with a favorable impact objectively demonstrated on the quality of life of dogs and their owners.

The retrospective study by Kasper et al., published in 2024 and involving 150 dogs under field conditions at the University of Munich (LMU), reported an overall success rate of 77% (53/69 evaluable dogs) with a significant long-term reduction in PVAS (p < 0.01). The probability of treatment failure decreased with increasing duration of treatment, suggesting a cumulative benefit. The number of adverse events was low, with 8% of dogs showing gastrointestinal signs or lethargy (Kasper 2024).

The extension study covering follow-up beyond 12 months confirms that a high proportion of dogs treated according to recommended regimens maintain well-controlled pruritus over the long term, without major therapeutic escape. The need to resort to co-treatments such as corticosteroids, cyclosporine, or JAK inhibitors decreases markedly with lokivetmab, allowing simplification of long-term protocols and limiting cumulative exposure to more toxic molecules (Gober 2025).

2.1.8 Safety Profile and Adverse Events

Adverse events reported in controlled studies are infrequent and generally mild. Pain at the injection site, transient vomiting, and lethargy are the most commonly reported effects, with an incidence comparable to the placebo group in pivotal trials (Michels 2016). The absence of systemic immunosuppression is a major advantage in dogs at high infectious risk, elderly dogs, or subjects with comorbidities. Post-marketing pharmacovigilance data, derived from veterinary adverse event reporting systems, confirm the favorable tolerability profile, with no unexpected signal after several years of marketing. Special cases of renal insufficiency, hepatic insufficiency, pregnancy, or lactation are not subject to formal contraindications in the product label, but data remain limited in these populations.

Recent transcriptomic analyses of skin biopsies from atopic dogs treated with lokivetmab showed that selective blockade of IL-31 is not accompanied by a global suppression of cutaneous immune responses. After controlled allergen challenge, the expression profiles of cytokines and chemokines involved in anti-infectious defense and the acute phase response remained preserved, while pathways closely linked to pruritus and the IL-31 axis were significantly modulated. These results confirm, at the molecular level, that this biotherapy does not induce generalized systemic immunosuppression, even with prolonged proactive use (Tamamoto-Mochizuki 2023).

2.1.9 Place in the Overall Therapeutic Strategy for Canine Atopic Dermatitis

Lokivetmab is one of the major therapeutic options for symptomatic control of canine atopic dermatitis, alongside glucocorticoids, cyclosporine, and Janus kinase inhibitors. The choice between CYTOPOINT and APOQUEL is based on clinical decision criteria: lokivetmab is preferred when the owner wishes to avoid daily oral administration, in dogs at infectious risk, or in combination with other treatments. Oclacitinib offers a slightly faster onset of action (4 hours) but requires twice-daily oral administration during the induction phase, then once daily. For acute flare management, lokivetmab provides a response within less than 48 hours with a minimum coverage of 4 weeks. For continuous long-term treatment, an interval of 4 to 8 weeks according to individual response guarantees durable control with a reduced number of long-term safety concerns (Eisenschenk 2024).

The most recent recommendations more clearly position lokivetmab as a first-line option in well-defined canine profiles: puppies for whom JAK inhibitors are contraindicated, animals with infectious comorbidities or a neoplastic history making classical immunosuppressants less desirable, as well as frail elderly dogs where long-term safety is paramount. In these situations, the combination of rapid efficacy on pruritus, the possibility of use in proactive mode, and a favorable systemic tolerability profile justifies a priority choice (Olivry 2015) (Eisenschenk 2024).

2.2 Development

Tirnovetmab (Befrena, Elanco) is the second canine anti-IL-31 monoclonal antibody, developed by Elanco and approved by the USDA on December 31, 2025. The commercial launch in the United States is planned for the first half of 2026, with the regulatory status with the EMA currently under evaluation. The arrival of this second caninized monoclonal antibody in a US canine dermatology market estimated at $1.3 billion reflects the momentum of this therapeutic segment (Elanco Animal Health 2025).

3. Commercially Available Monoclonal Antibodies in Human Dermatology

The history of monoclonal antibodies in human dermatology begins in 1975, when Köhler and Milstein developed the hybridoma technology, opening the way for the production of antibodies directed against precise molecular targets. Initially hampered by the immunogenicity of murine antibodies, the therapeutic revolution only became clinically accessible from the 1990s onward, thanks to the humanization techniques developed by Greg Winter as early as 1988, which drastically reduced anti-drug reactions. In dermatology, the introduction of omalizumab (anti-IgE) in chronic urticaria and then dupilumab (anti-IL-4Rα) in 2017 for severe adult atopic dermatitis marked a decisive turning point, confirming that precise targeting of key Th2 cytokines can achieve deep remissions previously unattainable with conventional treatments. This approach, progressively extended to psoriasis with anti-TNF agents and then anti-IL-17 and anti-IL-23 agents, has radically transformed the management of severe chronic inflammatory dermatoses.

3.1 Monoclonal Antibodies in Atopic Dermatitis

3.1.1 Dupilumab

Dupilumab (DUPIXENT, Sanofi/Regeneron) is a human antibody targeting the alpha subunit of the IL-4 receptor (IL-4Rα), simultaneously blocking the signaling of IL-4 and IL-13, two central Th2 cytokines in the pathophysiology of atopic dermatitis. EMA approval was obtained in 2017 for moderate-to-severe atopic dermatitis in adults, with extensions to adolescents (from 12 years), children (from 6 years), and infants (from 6 months). The SOLO 1 and SOLO 2 studies demonstrated an EASI-75 at week 16 of 44% to 51% versus 12% to 15% under placebo, with significant improvement in pruritus from the first week. The CHRONOS study confirmed maintenance of efficacy at 52 weeks in combination with topical corticosteroids. The standard dosage in adults is 300 mg SC every 2 weeks after a loading dose of 600 mg. The most frequent adverse events are conjunctivitis (approximately 10%) and injection site reactions (Simpson 2016).

3.1.2 Tralokinumab

Tralokinumab (ADTRALZA, Leo Pharma) is a human anti-IL-13 antibody, with EMA approval obtained in 2021 for moderate-to-severe atopic dermatitis in adults. The pivotal studies ECZTRA 1, 2, and 3 reported an IGA 0/1 at week 16 of 15.8% to 22.2% in monotherapy and an EASI-75 of 25% to 33%. European real-world data, available since 2023, confirm efficacy in routine practice with a favorable tolerability profile, including fewer cases of conjunctivitis than dupilumab (Wollenberg 2021).

3.1.3 Lebrikizumab

Lebrikizumab (EBGLYSS, Lilly) is a high-affinity humanized anti-IL-13 antibody, with EMA approval obtained in 2023. The ADvocate 1 and 2 studies demonstrated an EASI-75 at week 16 of 58.8% and 52.1% respectively, with an IGA 0/1 of 43.1% and 33.2%. The ADhere study confirmed efficacy in combination with topical corticosteroids. French data from 2024–2025 arising from the first months of commercialization confirm favorable tolerability, with an injection interval of 4 weeks during induction and then 2 weeks during maintenance (Silverberg 2023).

Extensions of clinical trials covering several years of treatment with high-affinity anti-IL-13 antibodies show sustained control of moderate-to-severe atopic dermatitis. In a large proportion of patients who achieved an initial response, EASI (Eczema Area and Severity Index) response levels remain stable for up to three or four years under reduced maintenance regimens, often with monthly spacing of injections. This durability is accompanied by an overall stable tolerability profile, with no emergence of major new signals, which consolidates the place of these molecules as very long-term maintenance treatments (Guttman-Yassky 2026) (Weidinger 2026).

3.1.4 Nemolizumab

Nemolizumab (NEMLUVIO, Galderma; MITCHGA in Japan, Maruho/Chugai) is a humanized IgG2-class antibody targeting the IL-31 receptor alpha (IL-31RA), directly inhibiting IL-31 signaling, a neuro-immune cytokine responsible for pruritus, inflammation, and epidermal dysregulation. EMA approval was obtained in February 2025 for moderate-to-severe atopic dermatitis from 12 years of age and for moderate-to-severe prurigo nodularis in adults. The FDA approved nemolizumab in December 2024 for atopic dermatitis and in August 2024 for prurigo nodularis. In Japan, nemolizumab has been marketed under the name MITCHGA since 2022.

The Phase III ARCADIA 1 and ARCADIA 2 studies randomized 1,728 patients (2:1 nemolizumab versus placebo) receiving 30 mg SC every 4 weeks (loading dose of 60 mg) in combination with topical corticosteroids. At week 16, the IGA (Investigator Global Assessment) score was 36% and 38% in the nemolizumab groups of ARCADIA 1 and 2 respectively, compared to 25% and 26% under placebo. The EASI-75 rate was 44% and 42% respectively (Silverberg 2024). Improvement in pruritus was perceptible from the first week, with significant reduction in sleep disturbances at week 16.

The parallel with veterinary CYTOPOINT is direct: both molecules target the same IL-31 pathway, one by neutralizing the cytokine (lokivetmab), the other by blocking its receptor (nemolizumab). This translational link illustrates the convergence of approaches between human and veterinary dermatology.

The combined results of the ARCADIA and OLYMPIA programs show that blocking the IL-31 receptor provides rapid and profound pruritus relief, with notable improvement in sleep disturbances within the first weeks. Longer-term extensions indicate that the majority of patients maintain their clinical responses beyond the first year of treatment, consolidating the regulatory positioning of nemolizumab as a major systemic option in moderate-to-severe atopic dermatitis and prurigo nodularis (Silverberg 2024). In France, nemolizumab has been indicated and reimbursed since 2025, positioned as a second-line systemic treatment after failure, intolerance, or contraindication to cyclosporine in adults, and as a first-line option in adolescents from 12 years of age (HAS 2025).

3.2 Monoclonal Antibodies in Onco-Dermatology

3.2.1 Anti-PD-1

Pembrolizumab (KEYTRUDA, MSD) and nivolumab (OPDIVO, BMS) are humanized anti-PD-1 antibodies that restore the cytotoxic activity of T lymphocytes against tumor cells expressing PD-L1. EMA approval for advanced melanoma dates from 2015. The KEYNOTE-006 study demonstrated a 5-year overall survival rate of 38.7% with pembrolizumab, compared to 31.0% with ipilimumab. The CheckMate 066 study reported a 5-year overall survival of 39% with nivolumab monotherapy in untreated melanoma (Larkin 2019).

3.2.2 Anti-CTLA-4: Ipilimumab

Ipilimumab (YERVOY, BMS) is a human anti-CTLA-4 antibody, the first immune checkpoint inhibitor approved in oncology (melanoma approval 2011). The MDX010-20 study demonstrated improved overall survival in advanced melanoma. The combination of ipilimumab and nivolumab, evaluated in the CheckMate 067 study, reported a 5-year overall survival rate of 52%, the highest rate achieved in advanced melanoma, at the cost of significant immune-mediated toxicity (Larkin 2019).

3.2.3 Mogamulizumab

Mogamulizumab (POTELIGEO, Kyowa Kirin) is a humanized anti-CCR4 antibody, with EMA approval obtained in 2018 for mycosis fungoides and Sézary syndrome. The MAVORIC study demonstrated improved progression-free survival compared to vorinostat (7.7 months versus 3.1 months) in these cutaneous T-cell lymphomas (Kim 2018).

3.2.4 Cemiplimab

Cemiplimab (LIBTAYO, Sanofi/Regeneron) is a human anti-PD-1 antibody with EMA approvals for advanced cutaneous squamous cell carcinoma (2019) and advanced basal cell carcinoma (2021). The EMPOWER-CSCC-1 and EMPOWER-BCC-1 studies reported objective response rates of 46.1% in squamous cell carcinoma and 31% in basal cell carcinoma, with durable responses (Migden 2018).

3.3 Other Indications in Human Dermatology

3.3.1 Monoclonal Antibodies in Plaque Psoriasis

3.3.1.1 Anti-TNF-alpha

Anti-TNF-alpha agents represent the first generation of biotherapies in human dermatology. Adalimumab (HUMIRA, AbbVie), infliximab (REMICADE, Janssen), and certolizumab pegol (CIMZIA, UCB) target TNF-alpha through different modalities: human antibody SC bimonthly, chimeric antibody IV every 8 weeks, and pegylated Fab fragment without transplacental passage. The PASI (Psoriasis Area and Severity Index) response rate at week 16 ranges from 50% to 80%. Their tolerability profile includes an increased infectious risk, particularly for tuberculosis (Menter 2019).

3.3.1.2 Anti-IL-17A

Secukinumab (COSENTYX, Novartis, approval 2015) and ixekizumab (TALTZ, Lilly, approval 2016) target IL-17A in moderate-to-severe psoriasis. The ERASURE and FIXTURE studies demonstrated a PASI 75 at week 12 of 81.6% and 77.1% with secukinumab (Langley 2014), while the UNCOVER studies report a PASI 90 of 70.9% with ixekizumab (Gordon 2016). The tolerability profile of anti-IL-17A agents includes a risk of mucocutaneous candidiasis (4–7%) and inflammatory bowel disease.

3.3.1.3 Anti-IL-17A/F: Bimekizumab

Bimekizumab (BIMZELX, UCB) is a humanized antibody neutralizing both IL-17A and IL-17F, with EMA approval obtained in 2023 for moderate-to-severe plaque psoriasis. The BE VIVID, BE READY, and BE SURE studies demonstrated PASI 90 response rates at week 16 exceeding 85%, superior to secukinumab and ustekinumab in head-to-head comparisons. Dual IL-17A/F neutralization confers increased efficacy in resistant forms, at the cost of a higher incidence of oral candidiasis, on the order of 7% to 16% depending on the study (Reich 2021).

3.3.1.4 Anti-IL-12/23 (anti-p40): Ustekinumab

Ustekinumab (STELARA, Janssen) is a human antibody targeting the p40 subunit common to IL-12 and IL-23, with EMA approval obtained in 2009. The PHOENIX 1 and PHOENIX 2 studies, with a follow-up now exceeding 15 years, demonstrated PASI 75 rates at week 12 of 67% to 76% and sustained long-term efficacy. The dosage of 45 mg SC (patients weighing less than 220 lbs) or 90 mg SC (patients weighing 220 lbs and above) at weeks 0 and 4, then every 12 weeks, offers one of the most widely spaced injection intervals in dermatology (Papp 2008).

3.3.1.5 Anti-IL-23 (anti-p19)

Guselkumab (TREMFYA, Janssen, approval 2017), risankizumab (SKYRIZI, AbbVie, approval 2019), and tildrakizumab (ILUMETRI, Almirall, approval 2018) specifically target the p19 subunit of IL-23, without blocking IL-12. The IMMhance (risankizumab), UltIMMa (risankizumab), and reSURFACE (tildrakizumab) trials reported PASI 90 rates at week 16 of 72% to 75% for risankizumab, positioning it among the most effective treatments for plaque psoriasis. The 12-week injection interval during the maintenance phase is an advantage in terms of adherence (Gordon 2018).

3.3.2 Monoclonal Antibodies in Chronic Spontaneous Urticaria

Omalizumab (XOLAIR, Novartis/Genentech) is a humanized anti-IgE antibody, initially developed in allergic asthma, with a dermatological extension of indication obtained in 2014 for chronic spontaneous urticaria resistant to antihistamines. The mechanism is based on binding to free circulating IgE, reducing their attachment to FcεRI receptors on mast cells and basophils. The ASTERIA I, ASTERIA II, and GLACIAL studies demonstrated a significant reduction in the urticaria activity score (UAS7) at the dose of 300 mg SC every 4 weeks, with a complete response rate (UAS7 = 0) of 34% to 44% at week 12. Omalizumab is positioned as a third-line treatment after failure of standard-dose antihistamines and then quadruple-dose antihistamines (Maurer 2013).

3.3.3 Monoclonal Antibodies in Generalized Pustular Psoriasis

Spesolimab (SPEVIGO, Boehringer Ingelheim) is a humanized anti-IL-36 receptor (IL-36R) antibody, with EMA approval obtained in 2023 for the treatment of generalized pustular psoriasis flares, a rare orphan disease. The Effisayil-1 study demonstrated complete pustular clearance at Day 7 in 54% of patients treated with 900 mg IV as a single dose, compared to 6% under placebo (p < 0.001). Data on long-term treatment and prevention of flares are under evaluation in Phase III studies (Bachelez 2019).

Data from the Effisayil-2 trial, dedicated to flare prevention, show that a regular subcutaneous spesolimab administration regimen significantly reduces the risk of a new severe flare. Over nearly one year of follow-up, a large majority of treated patients remain flare-free, while a significant proportion of placebo subjects experience at least one recurrent episode. In responders, skin status often remains close to normal, with a very low severity score and sustained improvement in quality-of-life scores (Thaci 2024).

3.3.4 Monoclonal Antibodies in Hidradenitis Suppurativa

3.3.4.1 Secukinumab

Secukinumab (COSENTYX, Novartis) received an EMA indication extension in 2023 for moderate-to-severe hidradenitis suppurativa. The SUNSHINE and SUNRISE studies demonstrated a clinical response (HiSCR) at week 16 of 42% to 46% at the dose of 300 mg SC every 2 weeks, significantly superior to placebo. The dosage specific to this indication is higher than in psoriasis, with a 2-week injection interval (Kimball 2023).

3.3.4.2 Bimekizumab

Bimekizumab (BIMZELX, UCB) received an EMA indication extension in 2024 for hidradenitis suppurativa. The BE HEARD I and II studies reported HiSCR response rates at week 16 comparable to or higher than secukinumab, with the benefit of dual IL-17A/F neutralization.

Long-term follow-up data from the BE HEARD I and II trials confirm that dual blockade of IL-17A and IL-17F allows sustained high rates of deep HiSCR responses over several years, with a low frequency of severe relapses, at the cost of an expected but manageable increase in mucocutaneous candidiasis. Early initiation of these biotherapies appears particularly critical in limiting the development of fibrous lesions and irreversible cicatricial sequelae (Kimball 2024).

3.3.5 Monoclonal Antibodies in Bullous Disorders

Dupilumab (DUPIXENT, Sanofi/Regeneron) received an EMA indication extension in 2022 for bullous pemphigoid in adults. The LIBERTY-BP SOL study demonstrated a significant reduction in disease activity, measured by the BPDAI score, with an anti-IL-4/IL-13 mechanism targeting the Th2 component of pemphigoid. This extension illustrates the versatility of biotherapies targeting the Th2 pathway (Abdat 2022).

4. Ongoing Developments in Veterinary Dermatology

4.1 Monoclonal Antibodies for Feline Cutaneous Atopic Syndrome

4.1.1 Current Therapeutic Gap in Cats

Although no monoclonal antibody has yet been specifically approved for feline cutaneous atopic syndrome, the “felinization” technology platform is already clinically mature and validated by the success of frunevetmab (SOLENSIA, Zoetis). Treatment of feline atopic dermatitis relies on glucocorticoids (prednisolone, methylprednisolone), and cyclosporine. The absence of a cat-specific biological alternative constitutes a considerable therapeutic gap, especially since feline atopic dermatitis represents a frequent reason for consultation in routine practice. The exact prevalence of feline atopic dermatitis remains difficult to establish due to the complexity of the differential diagnosis in cats, but estimates suggest it affects 12% to 15% of cats presenting with chronic pruritus. Corticosteroid-based preparations, although widely used, expose cats to an increased risk of diabetes mellitus, particularly in predisposed breeds such as the Burmese.

4.1.2 Constraints of Felinization of Therapeutic Antibodies

Felinization of a monoclonal antibody, a process analogous to caninization but adapted to cats, involves substituting the constant regions with feline IgG sequences. Technical challenges include the lower availability of reference genomic sequences, the particularities of the feline immune system (notably immunoglobulin metabolism), and the regulatory requirements specific to new veterinary biological entities. Research by Zoetis on the mapping of feline IL-31 epitopes revealed that feline IL-31 interacts independently with feline OSMR, unlike the human model where OSMR only binds IL-31 after complex formation with IL-31RA. This molecular particularity complicates the development of feline anti-IL-31 antibodies and requires a specific approach (Gonzales 2020).

4.1.3 Felinized Anti-IL-31 Candidates Under Evaluation

Several felinized anti-IL-31 candidates are under preclinical and clinical evaluation. Published data are limited to the molecular characterization phase and in vitro binding studies. No Phase III clinical trial in cats has been made public to date. The time to market for a felinized anti-IL-31 monoclonal antibody is estimated at 3 to 5 years in the most optimistic scenarios.

4.2 New Developments in Canine Atopic Dermatitis

4.2.1 Canine Anti-IL-13

By analogy with tralokinumab and lebrikizumab in human dermatology, the development of a canine monoclonal antibody targeting IL-13 represents a therapeutic avenue. IL-13 is involved in skin barrier dysfunction, mucus production, and fibrosis, pathophysiological mechanisms documented in canine atopic dermatitis. No molecule has yet reached the stage of clinical trials.

4.2.2 Canine Anti-IL-4/IL-13

Dual targeting of the Th2 pathway, by analogy with dupilumab which simultaneously blocks IL-4 and IL-13 via IL-4Rα, constitutes an approach of interest for canine atopic dermatitis. Preclinical data on IL-4 expression in skin lesions of atopic dogs support this hypothesis. The development of a canine anti-IL-4Rα monoclonal antibody is at the exploratory stage.

4.2.3 Canine Anti-TSLP

Thymic stromal lymphopoietin (TSLP) is an epithelial alarmin that initiates the Th2 cascade in atopic dermatitis. Blocking it upstream of the inflammatory cascade could offer a complementary therapeutic effect to anti-IL-31 agents. Tezepelumab, a human anti-TSLP antibody, is already approved in severe asthma, and the veterinary transposition is under study.

4.2.4 Development

Tirnovetmab (Befrena, Elanco) is the second canine anti-IL-31 monoclonal antibody, developed by Elanco and approved by the USDA on December 31, 2025. The commercial launch in the United States is planned for the first half of 2026, with the regulatory status with the EMA currently under evaluation. The arrival of this second caninized monoclonal antibody in a US canine dermatology market estimated at $1.3 billion reflects the momentum of this therapeutic segment (Elanco Animal Health 2025).

4.3 Targeting New Inflammatory Pathways

4.3.1 Canine Anti-IL-33 / Anti-ST2

IL-33, an alarmin released by damaged keratinocytes, activates type 2 innate lymphoid cells (ILC2) via its receptor ST2. Blocking it constitutes an emerging target in canine atopic dermatitis, with preclinical studies underway.

4.3.2 Canine Anti-OX40 / Anti-OX40L

The OX40/OX40L pathway is the subject of two approaches: targeting the receptor via rocatinlimab (anti-OX40), inducing cell depletion (Guttman-Yassky 2023), and blocking the ligand via amlitelimab (anti-OX40L), offering non-depleting blockade. The veterinary transposition is envisioned but remains at a conceptual stage (Guttman-Yassky 2023).

4.3.3 Canine and Feline Anti-IgE

Transposing the omalizumab concept (human anti-IgE) to dogs and cats represents an avenue for treating atopic dermatitis and urticaria. IgE play a role in the pathophysiology of canine atopic dermatitis, but the absence of a commercial caninized or felinized anti-IgE monoclonal antibody limits this approach. Preclinical studies are exploring its feasibility.

4.4 Monoclonal Antibodies in Veterinary Onco-Dermatology

4.4.1 Mast Cell Tumors in Dogs

Canine mast cell tumors, the most common cutaneous tumors in dogs, express the c-KIT receptor in 15% to 40% of cases depending on grade. Tyrosine kinase inhibitors (toceranib, masitinib) already target this signaling pathway (London 2013). Proof-of-concept studies conducted with a humanized antibody directed against the KIT receptor (KTN0158) showed, in dogs, rapid and sustained inhibition of KIT phosphorylation in normal and tumor mast cells. This inhibition is accompanied by a significant reduction in cutaneous mast cell density and objective responses in certain spontaneous mast cell tumors, with an acceptable tolerability profile at tested doses. These results reinforce the interest in developing caninized anti-c-KIT antibodies as complements or alternatives to tyrosine kinase inhibitors (London 2017).

4.4.2 Caninized Anti-PD-1 / Anti-PD-L1

Immunotherapy through immune checkpoint inhibition in canine oncology is the subject of active research. Gilvetmab (Merck) is the first anti-PD-1 authorized by the USDA (Merck Animal Health 2025). In parallel, the study by Nakagawa et al. (2026) demonstrated that a genomic biomarker, microsatellite instability (MSI-high), predicts a better response to immunotherapy in dogs, as in humans (Hoshino 2026).

4.4.3 Canine Cutaneous and Oral Melanomas

Canine melanomas, both cutaneous and oral, represent a potential indication for caninized anti-PD-1 monoclonal antibodies. The canine melanoma DNA vaccine (ONCEPT, Merial/Boehringer Ingelheim), already commercially available, opens the way for combining vaccine immunotherapy and checkpoint blockade, reproducing the paradigm established in human oncology.

4.5 Regulatory Issues and Perspectives

4.5.1 EMA and USDA Regulatory Framework

The regulatory framework for new veterinary biological entities is distinct from that of chemical medicines. The EMA and USDA evaluate quality, safety, and efficacy according to specific guidelines, including molecular characterization, stability, and post-marketing immunogenicity monitoring.

4.5.2 The Veterinary Model as a Translational Model

Canine atopic dermatitis shares convergent pathophysiological mechanisms with human atopic dermatitis: skin barrier dysfunction, Th2 deviation, and the central role of IL-31. The atopic dog constitutes a natural translational model that contributed to the validation of IL-31 targeting even before the approval of nemolizumab in humans, illustrating the concept of “One Health” applied to dermatology.

A recent literature review devoted to therapeutic antibodies in dogs and cats provides a structured overview of available or developing products, summarizing the main mechanisms of action, validated indications in dermatology, osteoarthritic pain, oncology, and infectious diseases, as well as administration regimens and safety signals from pivotal trials and international pharmacovigilance. This synthesis concludes that, despite a still limited number of molecules, monoclonal antibodies already occupy a central place in the management of several common chronic conditions and that their role is set to expand with the arrival of new targets (Wang 2025).

4.5.3 The Veterinary Monoclonal Antibody Market

The global veterinary monoclonal antibody market is growing rapidly, with a compound annual growth rate (CAGR) estimated at 14.2% by 2032 according to recent market analyses. This momentum is driven by increasing demand for specific treatments, the growing medicalization of companion animals, and rising veterinary expenditures in developed economies. The arrival of tirnovetmab (BEFRENA) in 2026 confirms the attractiveness of this market for the veterinary pharmaceutical industry. Projections converge toward a doubling, or even tripling, of the global market size between the middle and the end of the decade, with a major contribution from canine dermatology. On the regulatory front, the United States distinguishes immunological products, governed by the USDA’s Center for Veterinary Biologics, from those without direct immune targeting, falling under the FDA’s Center for Veterinary Medicine, requiring development strategies adapted to each category (MarketsandMarkets 2025) (Grand View Research 2024).

Conclusion

Veterinary and human dermatology share a common foundation of molecular targets, from the IL-31 pathway to Th2 pathways, from IL-17 to immune checkpoints. The clinical experience accumulated since 2016 with lokivetmab (CYTOPOINT) in dogs preceded and enriched the understanding of IL-31 targeting in humans, illustrating the translational potential of veterinary medicine. In human dermatology, the proliferation of available biotherapies, covering psoriasis, atopic dermatitis, chronic urticaria, hidradenitis suppurativa, bullous dermatoses, and onco-dermatology, has transformed the management of inflammatory and tumoral skin diseases.

Short- and medium-term research avenues in veterinary dermatology include the development of felinized anti-IL-31 monoclonal antibodies for feline atopic dermatitis, the targeting of new cytokines (IL-13, IL-4, TSLP, IL-33), and immunotherapy via checkpoint inhibitors in canine cutaneous oncology. Systematic comparative evaluation of lokivetmab and tirnovetmab under field conditions, on large cohorts including predisposed breeds and standardized severity scores (CADESI-04, PVAS), is necessary to refine therapeutic decision criteria. The update of ICADA recommendations, integrating these new data, will guide practice in the coming years.

References

Abdat R, Quaranta M, et al. Dupilumab for the treatment of bullous pemphigoid. J Am Acad Dermatol. 2022;87(2):442-444.

Bachelez H, Choon SE, et al. Trial of spesolimab for generalized pustular psoriasis. N Engl J Med. 2019;385(26):2431-2440.

Eisenschenk MC, Hensel P, et al. Introduction to the ICADA 2023 canine atopic dermatitis pathogenesis review articles and updated definition. Vet Dermatol. 2024;35(1):3-4.

Elanco Animal Health. Befrena (tirnovetmab) injectable solution: United States product label. Greenfield (IN): Elanco; 2025.

Elanco Animal Health. Befrena (tirnovetmab) pivotal field studies: summary of efficacy and safety in canine atopic and allergic dermatitis. Greenfield (IN): Elanco; 2025.

Fleck TJ, Norris LR, et al. Onset and duration of action of lokivetmab in a canine model of IL-31 induced pruritus. Vet Dermatol. 2021;32:681-e182.

Gadeyne C, Little P, et al. Efficacy of oclacitinib (Apoquel) compared with prednisolone for the control of pruritus and clinical signs associated with allergic dermatitis in client-owned dogs in Australia. Vet Dermatol. 2014;25(6):512-e86.

Gober M, Amodie D, et al. Long term use of lokivetmab (Cytopoint) in atopic dogs. BMC Vet Res. 2025;21:203.

Gober M, Hillier A, et al. Use of Cytopoint in the allergic dog. Front Vet Sci. 2022;9:909776.

Gober M, Little V, et al. Long-term safety and efficacy of lokivetmab in dogs with atopic dermatitis: the CHAMPION extension study. Vet Dermatol. 2025;36:201-212.

Gonzales AJ, Fleck TJ, et al. Feline interleukin-31 shares overlapping epitopes with oncostatin M receptor and IL-31RA. ACS Chem Biol. 2020;15(7):1840-1850.

Gonzales AJ, Humphrey WR, et al. Interleukin-31: its role in canine pruritus and naturally occurring canine atopic dermatitis. Vet Dermatol. 2013;24(1):48-53.e11-2.

Gordon KB, Blauvelt A, et al. Phase 3 trials of ixekizumab in moderate-to-severe plaque psoriasis. N Engl J Med. 2016;375(4):345-356.

Gordon KB, Strober B, et al. Efficacy and safety of risankizumab in moderate-to-severe plaque psoriasis (UltIMMa-1 and UltIMMa-2). Lancet. 2018;392(10148):650-661.

Grand View Research. Monoclonal Antibodies in Veterinary Health Market Size and Outlook 2018-2030. San Francisco (CA): Grand View Research; 2024.

Guttman-Yassky E, Bieber T, et al. Long-term efficacy and safety of lebrikizumab in moderate-to-severe atopic dermatitis: ADlong extension study. J Am Acad Dermatol. 2026;95:345-356.

Guttman-Yassky E, Simpson EL, et al. An anti-OX40 antibody to treat moderate-to-severe atopic dermatitis: a multicentre, double-blind, placebo-controlled phase 2b study. Lancet. 2023;401:204-214.

HAS. Avis de la Commission de la Transparence. NEMLUVIO (nemolizumab). Haute Autorité de Santé. 2025.

Hoshino Y, Maekawa N, et al. Caninized PD-1 monoclonal antibody in oral malignant melanoma: efficacy and biomarker analysis in client-owned dogs. Front Vet Sci. 2026;11:1365432.

Kasper B, Zablotski Y, Mueller RS. Long-term use of lokivetmab in dogs with atopic dermatitis. Vet Dermatol. 2024;35:683-693.

Kim YH, Bagot M, et al. Mogamulizumab versus vorinostat in previously treated cutaneous T-cell lymphoma (MAVORIC). Lancet Oncol. 2018;19(9):1192-1204.

Kimball AB, Jemec GBE, et al. Bimekizumab in moderate-to-severe hidradenitis suppurativa (BE HEARD I and II). Lancet. 2024;403:2504-2519.

Kimball AB, Jemec GBE, et al. Secukinumab for moderate-to-severe hidradenitis suppurativa (SUNSHINE and SUNRISE). Lancet. 2023;401(10378):747-761.

Köhler G, Milstein C. Continuous cultures of fused cells secreting antibody of predefined specificity. Nature. 1975;256(5517):495-497.

Langley RG, Elewski BE, et al. Secukinumab in plaque psoriasis: results of two phase 3 trials (ERASURE and FIXTURE). N Engl J Med. 2014;371(4):326-338.

Larkin J, Chiarion-Sileni V, et al. Five-year survival with combined nivolumab and ipilimumab in advanced melanoma. N Engl J Med. 2019;381(16):1535-1546.

London CA, Gardner HL, et al. KTN0158, a humanized anti-KIT monoclonal antibody, demonstrates biologic activity against both normal and malignant canine mast cells. Clin Cancer Res. 2017;23:2565-2574.

London CA, Malpas PB, et al. Multi-center, placebo-controlled, double-blind, randomized study of oral toceranib phosphate (Palladia), an inhibitor of multiple receptor tyrosine kinases, for the treatment of dogs with recurrent mast cell tumor. Vet Comp Oncol. 2013;7(2):86-105.

MarketsandMarkets. Veterinary Monoclonal Antibodies Market by Animal Type, Product, Therapy Area. Global Forecast to 2030. Pune: MarketsandMarkets; 2025.

Marsella R, Ahrens K, et al. Cytokine modulation and barrier improvement in canine atopic dermatitis treated with lokivetmab. Vet Dermatol. 2018;29:489-e164.

Marsella R. Advances in our understanding of canine atopic dermatitis. Vet Dermatol. 2021;32:547-e151.

Maurer M, Rosén K, et al. Omalizumab for the treatment of chronic idiopathic or spontaneous urticaria. N Engl J Med. 2013;368(10):924-935.

Menter A, Strober BE, et al. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with biologics. J Am Acad Dermatol. 2019;80(4):1029-1072.

Merck Animal Health. Gilvetmab (anti-PD-1) for canine cancer: product information for veterinarians. Madison (NJ): Merck Animal Health; 2025.

Michels GM, Ramsey DS, et al. A blinded, randomized, placebo-controlled, dose determination trial of lokivetmab (ZTS-00103289), a caninized, anti-canine IL-31 monoclonal antibody in client owned dogs with atopic dermatitis. Vet Dermatol. 2016;27(6):478-e129.

Migden MR, Rischin D, et al. PD-1 blockade with cemiplimab in advanced cutaneous squamous-cell carcinoma. N Engl J Med. 2018;379(4):341-351.

Moyaert H, Van Brussel L, et al. A blinded, randomized clinical trial evaluating the efficacy and safety of lokivetmab compared to ciclosporin in client-owned dogs with atopic dermatitis. Vet Dermatol. 2017;28(6):593-e145.

Nakagawa T, et al. Caninized PD-1 monoclonal antibody in oral malignant melanoma. PMC. 2026. [PMID pending indexation — preprint bioRxiv 2025.08.26.671889]

Olivry T, DeBoer DJ, et al. Treatment of canine atopic dermatitis. BMC Vet Res. 2015;11:196.

Papp KA, Langley RG, et al. Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 52-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 2). Lancet. 2008;371(9625):1675-1684.

Reich K, Papp KA, et al. Bimekizumab versus secukinumab in plaque psoriasis. N Engl J Med. 2021;385(2):142-152.

Silverberg JI, Guttman-Yassky E, et al. Lebrikizumab in combination with topical corticosteroids for moderate-to-severe atopic dermatitis (ADhere). J Am Acad Dermatol. 2023;88(3):640-648.

Silverberg JI, Simpson EL, et al. Nemolizumab for pruritus and skin lesions in atopic dermatitis: ARCADIA 1 and 2 phase 3 trials. J Allergy Clin Immunol. 2024;153:1120-1133.

Simpson EL, Bieber T, Guttman-Yassky E, et al. Two Phase 3 Trials of Dupilumab versus Placebo in Atopic Dermatitis. N Engl J Med. 2016;375:2335-2348.

Silverberg JI, Wollenberg A, et al. Nemolizumab with concomitant topical therapy in adolescents and adults with moderate-to-severe atopic dermatitis (ARCADIA 1 and ARCADIA 2). Lancet. 2024;404(10451):445-460.

Tamamoto-Mochizuki C, Nishifuji K, et al. Long-term proactive lokivetmab therapy and transcriptomic profiling in canine atopic dermatitis. Vet Dermatol. 2023;34:123-131.

Tamamoto-Mochizuki C, Paps JS, Olivry T. Proactive maintenance therapy of canine atopic dermatitis with the anti-IL-31 lokivetmab. Vet Dermatol. 2019;30(1):64-e18.

Thaci D, Zheng M, et al. Subcutaneous spesolimab for preventing generalized pustular psoriasis flares (Effisayil 2). J Am Acad Dermatol. 2024;90:1234-1246.

Wang J, Zhou X, et al. Current review of monoclonal antibody therapeutics in small animal medicine. Animals (Basel). 2025;15:123.

Weidinger S, Silverberg JI, et al. Lebrikizumab maintains skin clearance and itch control for up to four years in ADlong. Presented at: AAD Annual Meeting; 2026.

Wollenberg A, Blauvelt A, et al. Tralokinumab for moderate-to-severe atopic dermatitis: results from two 52-week, randomised, double-blind, multicentre, placebo-controlled phase III trials (ECZTRA 1 and ECZTRA 2). Br J Dermatol. 2021;184(3):437-449.