Eblasakimab is a novel biologic in development for moderate-to-severe AD, with the potential to deliver a monthly dosing regimen from initiation with no compromise on efficacy

In July 2023, we announced positive data from TREK-AD, a Phase 2b study of eblasakimab in adults with moderate to severe atopic dermatitis (AD), that showed eblasakimab has the potential to deliver a monthly dosing regimen from initiation without compromising on efficacy. Eblasakimab was well tolerated and doses of 600mg Q4W (every 4 weeks), 400mg Q2W (every 2 weeks) and 300mg Q2W, met the primary endpoint of percent change from baseline in the Eczema Area and Severity Index (EASI) score.

Plans to advance eblasakimab into a pivotal Phase 3 study in moderate-to-severe AD are underway.

Eblasakimab is currently in clinical development in the TREK-DX study, a Phase 2 study in dupilumab experienced AD patients and a positive outcome could strengthen the positioning of eblasakimab as a biologic of first choice in AD.

About eblasakimab

Eblasakimab is a novel, fully human, monoclonal IgG4 antibody that binds specifically to the Interleukin (IL)-13 receptor (IL-13R), preventing signaling of IL-4 and IL-13 through the Type 2 receptor.  

The role of the Type 2 receptor in driving allergic conditions

The Type 2 receptor is a heterodimer comprising of the IL-4 receptor (IL-4R) and the IL-13 receptor (IL-13R). Cytokines IL-4 and IL-13 signal through the Type 2 receptor and are key drivers of inflammation, central to triggering symptoms of allergy in Type 2-driven diseases such as AD, asthma and COPD.

Eblasakimab’s Mechanism of Action in AD

Eblasakimab is the only known antibody targeting the IL-13 receptor in clinical development for the treatment of moderate-to-severe AD.

By targeting the IL-13 receptor, eblasakimab’s novel approach selectively blocks the Type 2 receptor, preventing signaling through both IL-4 and IL-13.

Watch the following video to learn more about eblasakimab’s mechanism of action in AD:

What makes eblasakimab different?

Eblasakimab and dupilumab both block Type 2 receptor signaling, but – unlike dupilumab –  eblasakimab spares the Type 1 receptor

Recently published translational data demonstrates that blocking the IL-13R with eblasakimab resulted in lower levels of allergy-related Th2 cytokines and pro-inflammatory Th1 cytokines when compared to blockade of the IL-4R, the target of dupilumab.

By sparing the Type 1 receptor, eblasakimab may offer a differentiated therapeutic approach with a better safety profile.

Eblasakimab may be effective against other allergic co-morbidities, unlike drugs targeting the IL-13 ligand

Drugs targeting the IL-13 ligand, like lebrikizumab and tralokinumab, do not inhibit IL-4 signaling through the Type 2 receptor, which also contributes to inflammation in AD and other allergic conditions.

81% of AD patients have Type 2 inflammatory comorbidities like asthma and allergic rhinitis[1]. By blocking both IL-4 and IL-13 signaling through the Type 2 receptor, eblasakimab has the potential to be efficacious in a broad range of allergic co morbidities in AD, unlike drugs targeting the IL-13 ligand.

A proven molecular basis for directly attenuating itch

Using human sensory neurons, blocking IL-13R with eblasakimab has been shown in data published by ASLAN to significantly reduce cytokine-driven amplification of itch and spontaneous activation of neurons.

Itch is a key burdensome symptom in patients with AD and these results suggest a molecular basis for the significant reduction of pruritus scores observed in clinical studies of eblasakimab.

Posters on translational studies presented at international scientific conferences can be viewed on our publications page.

You can also view data from our previous studies on eblasakimab by clicking the links below.

Phase 2b: TREK-AD topline readout
Phase 1b: Multiple Ascending Dose study publications