Eblasakimab for Eczema
Recruiting in Palo Alto (17 mi)
+32 other locations
Age: 18+
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase 2
Recruiting
Sponsor: Aslan Pharmaceuticals
Prior Safety Data
Trial Summary
What is the purpose of this trial?This trial is testing a new medication called eblasakimab for people with moderate-to-severe atopic dermatitis who have already tried another treatment called dupilumab. The medication aims to reduce skin inflammation and improve symptoms. The study will last for several months, including a treatment period and a follow-up.
Do I need to stop my current medications to join the trial?
The trial requires you to stop using certain medications before joining. You must stop immunosuppressive/immunomodulating drugs, JAK inhibitors, or phototherapy 4 weeks before the trial. You also need to stop using topical corticosteroids, calcineurin inhibitors, phosphodiesterase inhibitors, and topical JAK inhibitors 1 week before randomization. Allergen immunotherapy should be stopped 6 months before joining.
What data supports the idea that Eblasakimab for Eczema is an effective drug?
The available research shows that Eblasakimab, when tested in a study with healthy volunteers, effectively blocked a specific receptor involved in inflammation, which is a key factor in eczema. This suggests that Eblasakimab could be a promising treatment for eczema. However, the research does not provide direct comparisons with other treatments like Tralokinumab, which has shown significant improvements in eczema symptoms in clinical trials. Therefore, while Eblasakimab shows potential, more research is needed to confirm its effectiveness compared to other existing treatments.
12345What safety data is available for Eblasakimab in treating eczema?
Eblasakimab, also known as ASLAN004, has been evaluated in a phase 1a study involving healthy male volunteers. The study found that single ascending doses of Eblasakimab, administered either intravenously or subcutaneously, did not result in any serious treatment-emergent adverse events. The treatment effectively blocked the IL-13Rα1 receptor and inhibited STAT6 phosphorylation, supporting its further clinical development for atopic dermatitis. Additionally, Eblasakimab is part of a class of IL-13 inhibitors, which have generally been shown to be well-tolerated in clinical trials for atopic dermatitis, with other similar treatments like tralokinumab demonstrating safety profiles comparable to placebo.
23467Eligibility Criteria
Adults with moderate-to-severe atopic dermatitis who've tried Dupilumab without success can join. They should have a significant area of skin affected, a certain severity score, and be able to follow the study plan. Excluded are those on recent immunotherapies or drugs that affect the immune system, uncontrolled asthma or chronic diseases, liver issues, HIV, hepatitis B/C infections, active COVID-19 infection.Inclusion Criteria
I am 18 years old or older.
Willing and able to comply with clinic visits and study-related procedures
I have been treated with dupilumab under specific conditions.
+5 more
Exclusion Criteria
My doctor is concerned about my organ function or lab results.
I do not have active tuberculosis or it has been adequately treated.
I have recently been treated with experimental drugs.
+9 more
Participant Groups
The trial is testing Eblasakimab (ASLAN004) against a placebo in people with stubborn eczema despite previous treatment. Participants will randomly receive either the drug or placebo for 16 weeks and then be monitored for another 8 weeks to check effectiveness and safety.
2Treatment groups
Experimental Treatment
Placebo Group
Group I: ASLAN004Experimental Treatment1 Intervention
Week 0, 1: LD of 600 mg; Week 2 through Week 15 QW: 400 mg dose
Group II: PlaceboPlacebo Group1 Intervention
Placebo loading dose equivalents at Baseline and Week 1, then placebo dose equivalents every week (QW) from Week 2 to Week 15
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
ASLAN Investigative SiteTampa, FL
ASLAN Investigative SiteHollywood, FL
ASLAN Investigative SiteCharlotte, NC
ASLAN Investigative SiteWebster, TX
More Trial Locations
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Who Is Running the Clinical Trial?
Aslan PharmaceuticalsLead Sponsor
ASLAN PharmaceuticalsLead Sponsor
References
Tralokinumab for the Treatment of Atopic Dermatitis. [2022]Atopic dermatitis (AD) is a relapsing or chronic heterogeneous inflammatory skin disorder with a substantial economic and social impact. AD is a multifactorial disease regulated by a diverse set of environmental and genetic determinants. The main factors involved in the pathogenesis of AD are epidermal barrier dysfunction, immune dysregulation, and dysbiosis. Current data have valued interleukin (IL)-13 as conceivably the crucial cytokine in the underlying inflammation of AD. Advances in understanding AD pathophysiology have driven the progress of targeted immunomodulatory treatments for the treatment of AD, including tralokinumab, a selective IL-13 inhibitor. A phase IIb clinical trial showed that a dosing regimen of 150 or 300 mg every 2 weeks effectively treated moderate-to-severe AD in adults with an acceptable tolerability profile. Phase III clinical trials demonstrated that results with tralokinumab in monotherapy were superior to those with placebo at 16 weeks of treatment. It was also well tolerated up to 52 weeks in the vast majority of patients. In addition, in association with topical corticosteroids, tralokinumab was well tolerated and effective and had a favorable risk-benefit profile. These data provide additional evidence that IL-13 is central to AD pathogenesis, suggesting that tralokinumab may be seen as an innovative option for the treatment of moderate-to-severe AD.
Eblasakimab, a novel IL-13 receptor alpha 1 monoclonal antibody, blocks STAT6 phosphorylation with low dose in human volunteers. [2023]Eblasakimab is a first-in-class monoclonal antibody under investigation for the treatment of atopic dermatitis (AD), which targets IL-13Rα1, a subunit of the Type 2 receptor complex. IL-13Rα1 stimulates phosphorylation of signal transducer and activator of transcription 6 (STAT6) to drive inflammation. This brief report investigates the mechanistic basis of eblasakimab and its effects on IL-13Rα1 signaling as part of a phase 1a, open-label, single ascending dose study. Single ascending doses of eblasakimab were administered by intravenous or subcutaneous injection to healthy male volunteers. The impact of eblasakimab on IL-13Rα1 receptor occupancy and STAT6 phosphorylation was assessed in participant blood monocytes. No serious treatment emergent adverse events were reported. Eblasakimab effectively blocked the IL-13Rα1 receptor and inhibited STAT6 phosphorylation with single doses of 3 mg/kg intravenously and 300 mg subcutaneously. Results support further clinical development of eblasakimab as a novel biologic for AD, with potential for 2- to 4-week dosing regimens.
Targeting Interleukin 13 for the Treatment of Atopic Dermatitis. [2023]Atopic dermatitis (AD) is a common chronic inflammatory skin condition that has a significant impact on a patient's quality of life and requires ongoing management. Conventional topical and systemic therapies do not target specific components of AD pathogenesis and, therefore, have limited efficacy and may be associated with long-term toxicity. Thus, AD management is challenging, with a significant proportion of patients not achieving clear skin or a reduction in pruritus. There remains a large unmet need for effective therapeutic strategies with favorable safety profiles that can be used long-term in patients with refractory AD. The emergence of targeted biological and small molecule therapies has effectively broadened available treatment options for moderate-to-severe AD. Most recently, interleukin 13 (IL-13) inhibitors were shown to be efficacious and well-tolerated, with tralokinumab already approved for use in this patient population. It is important for dermatologists to be aware of the evidence behind this emerging class of biologic agents to guide treatment choices and improve outcomes in patients with AD. The main objective of this paper is to review the current literature regarding the efficacy and safety of current and emerging anti-IL-13 monoclonal antibodies, including tralokinumab, lebrikizumab, cendakimab, and eblasakimab, for the treatment of moderate-to-severe AD.
Tralokinumab therapy for moderate-to-severe atopic dermatitis: Clinical outcomes with targeted IL-13 inhibition. [2023]Atopic dermatitis (AD) is a chronic, inflammatory, intensely pruritic skin disorder associated with significant patient burden. Interleukin (IL)-13 is a cytokine that acts as a driver of immune dysregulation, skin-barrier dysfunction, and microbiome dysbiosis that characterizes AD, and is consistently overexpressed in AD skin. Tralokinumab is a fully human immunoglobulin (Ig) G4 monoclonal antibody that binds specifically to IL-13 with high affinity, thereby inhibiting subsequent downstream IL-13 signaling. Three pivotal phase 3 clinical trials demonstrated that tralokinumab 300 mg every other week, as monotherapy or in combination with topical corticosteroids as needed, provides significant improvements in signs and symptoms of moderate-to-severe AD, as measured by Investigator's Global Assessment 0/1 (clear/almost clear) and Eczema Area and Severity Index-75 at Week 16. Improvements were observed soon after tralokinumab initiation and were maintained over 52 weeks of therapy. Tralokinumab significantly improved patient-reported outcomes such as itch and sleep, and demonstrated a safety profile comparable with placebo; conjunctivitis during tralokinumab therapy was generally mild. Similar results were observed in a phase 3 adolescent trial. The role of IL-13 in the pathophysiology of AD justifies a targeted approach and a wealth of clinical data supports tralokinumab as a new therapeutic option for people with moderate-to-severe AD.
IL-13 antagonists in the treatment of atopic dermatitis. [2022]Atopic dermatitis (AD) is a prevalent inflammatory skin disease. IL-13 contributes significantly to the pathogenesis of AD in several ways, and beneficial results have been demonstrated with anti-IL-13 therapies. Currently, the only monoclonal antibody (mAb) approved for AD treatment is dupilumab, an antagonist of the IL-4 receptor alpha (IL-4Rα) subunit common to IL-4 and IL-13 receptors, but clinical trials evaluating anti-IL-13 mAbs are providing promising results. The topics of this review will be mAbs targeting IL-13 for the treatment of AD such as dupilumab, tralokinumab and lebrikizumab, small molecules targeting the IL-13 pathway, and a brief explanation of therapies targeting IL-13 for the treatment of other skin diseases.
Rademikibart (CBP-201), a next-generation monoclonal antibody targeting human IL-4Rα: Two phase I randomized trials, in healthy individuals and patients with atopic dermatitis. [2023]IL-4 and IL-13 signaling via IL-4Rα plays key roles in the pathogenesis of atopic dermatitis (AD) and asthma. Rademikibart (formerly CBP-201), a next-generation human IgG4 kappa monoclonal antibody, blocks IL-4Rα-mediated signal transduction. We performed two phase I, randomized, double-blind, placebo-controlled trials. In a single-ascending dose trial, 40 healthy adults were randomized 3:1 to rademikibart (75-600 mg s.c., 300 mg i.v.) or placebo, with 12 weeks of follow-up. In the multiple-ascending dose trial, 31 adults with moderate-to-severe AD were randomized 4:1 to once weekly rademikibart (75-300 mg s.c.) or placebo for 4 weeks, plus 7 weeks of follow-up. Most treatment-emergent adverse events (TEAEs) were mild; none were serious. Two s.c. injection site reactions and one TEAE of conjunctivitis were reported, all were mild. Rapid and sustained improvements were observed in AD severity and in quality of life (QoL), without plateauing. At week 4, efficacy scores improved by a maximum of -74.4% (Eczema Area and Severity Index), -62.7% (body surface area), -52.8% (Pruritus Numerical Rating Scale [PNRS] severity), -54.4% (PNRS frequency), and - 69.9% (Dermatology Life Quality Index). Thymus activation regulated chemokine inflammatory biomarker concentrations decreased in both trials (-55.4% in the pooled rademikibart arms vs. +18.0% with placebo, at week 5, in patients with AD). Exposure to rademikibart increased in a greater than dose-proportional manner, suggesting nonlinear clearance. In summary, rademikibart was well-tolerated and associated with rapid and sustained improvements in eczematous lesions, pruritus, QoL, and inflammatory biomarker concentrations during 4 weeks of treatment. Efficacy responses did not plateau and were generally dose dependent. These promising findings support further development of rademikibart in patients with AD.
The efficacy and safety of IL-13 inhibitors in atopic dermatitis: A systematic review and meta-analysis. [2022]Several clinical trials have evaluated the efficacy and safety of interleukin-13 (IL-13) with lebrikizumab and tralokinumab in patients with moderate to severe atopic dermatitis (AD). However, the safety and efficacy of IL-13 inhibitors as a potent biologic for AD remain elusive.
Two Phase 3 Trials of Dupilumab versus Placebo in Atopic Dermatitis. [2022]Dupilumab, a human monoclonal antibody against interleukin-4 receptor alpha, inhibits signaling of interleukin-4 and interleukin-13, type 2 cytokines that may be important drivers of atopic or allergic diseases such as atopic dermatitis.
Monoclonal antibodies against interleukin 13 and interleukin 31RA in development for atopic dermatitis. [2019]The interleukin 13 (IL-13) and IL-31 cytokines and inflammatory pathways have been identified as important for the pathophysiology of atopic dermatitis (AD). Monoclonal antibodies against IL-13 have been studied for the treatment of asthma since 2011. More recently, 2 phase 2 trials have been completed with these antibodies in AD treatment. In both trials, significant reductions of Eczema Area and Severity Index scores were seen. IL-31 is thought to play a role transmitting itch sensation to the central nervous system, and blocking IL-31 activity reduces itch in patients with AD. One phase 2 trial has been completed for a humanized antibody against IL-31 receptor alpha, which is 1 subunit of the IL-31 receptor complex. This study showed significant dose-dependent reductions in pruritus, Eczema Area and Severity Index scores, and markers of sleep quality. Initial clinical trials for monoclonal antibodies against IL-13 and IL-31 receptor A all show promise, although long-term safety and efficacy data are lacking. Nevertheless, these medications will likely play a role in the treatment of moderate-to-severe AD.