Aclaris Therapeutics at HCW Conference: Strategic Moves and Future Plans

On Monday, 30 June 2025, Aclaris Therapeutics (NASDAQ:ACRS) presented at the HCW Annual Inflammation & Immunology Virtual Conference 2025. The development-stage biotech company, led by CEO Dr. Neil Walker, highlighted its robust financial position and strategic advancements. With over $190 million in cash reserves, Aclaris is well-positioned to pursue its clinical and preclinical goals through the first half of 2028. However, the company faces challenges in securing partnerships for its respiratory indications.

Key Takeaways

• Aclaris has over $190 million in cash, ensuring financial stability until 2028.
• The company is advancing three clinical assets: ATI-2138, ATI-45, and ATI-52.
• Aclaris is actively seeking partners for ATI-45’s respiratory applications outside China.
• Upcoming milestones include data from ATI-2138’s Phase 2a study in atopic dermatitis.

Financial Results

• Cash reserves exceed $190 million.
• Financial runway extends through the first half of 2028.
• Future funding includes potential nondilutive capital sources.

Operational Updates

• Clinical Trials:

- ATI-45: Phase 3 in China for severe asthma and CRS with NP, Phase 2 in COPD.

- ATI-45: Global Phase 2 in atopic dermatitis underway.

- ATI-52: Phase 1 SADMAD study initiated.

- ATI-2138: Phase 2 study completed, awaiting final PD data.

• Key Personnel:

- Dr. Jesse Hall appointed as Chief Medical Officer.

- Cash runway extended by a quarter and a half.

Future Outlook

• Upcoming Catalysts:

- Imminent release of ATI-2138 Phase 2a data in atopic dermatitis.

- Clinical study for alopecia areata with ATI-2138 to commence post-data release.

- ATI-52 SADMAD data expected at the turn of the year.

- IND filing for next-gen ITK molecule anticipated in 2026.

• Strategic Focus:

- Developing ATI-52 for atopic dermatitis, severe asthma, and COPD.

- Targeting ITK and JAK3 inhibition with ATI-2138 for alopecia areata and vitiligo.

Q&A Highlights

• Dr. Walker emphasized the strong clinical response in ATI-45’s Phase 2a study for atopic dermatitis, with significant EASI-75 and IgA response rates.
• The company aims to leverage its balanced portfolio and upcoming IND to drive growth through 2025 and 2026.

For a deeper dive into Aclaris Therapeutics’ strategic plans and clinical progress, readers are encouraged to refer to the full conference call transcript.

Full transcript - HCW Annual Inflammation & Immunology Virtual Conference 2025:

Operator: Four.

Jade Montgomery, Associate Research Analyst, H. C. Wainwright: Hi, everyone, and welcome to the HC Wainwright inflammation and immunology Day. I’m Doctor. Jade Montgomery, an associate research analyst for H. C. Wainwright, and it’s my pleasure today to welcome our speaker, from Aclaris Therapeutics, CEO, Doctor.

Neil Walker. Neil?

Operator: Thank you, Jade, and thank you for having us here today. Good morning, everybody. My name is Doctor. Neil Walker, and I’m the Chairman and CEO of Aclaris Therapeutics. Aclaris is a development stage biotech focused on developing potential best in class large and small molecule therapeutics.

Underpinning our portfolio, we have world class expertise in both large and small molecule drug development as well as a proprietary drug discovery engine. Importantly, our team has both large and small company experience. Many ex Pfizer as well as ex J and J executives are on our team. Currently, we have three assets in clinical development, which include ATI-twenty one thirty eight, which is an oral small molecule ITK JAK3 inhibitor with unique pharmacology, ATI-forty five, a uniquely potent monoclonal antibody targeting T slip, a key alarmin involved in numerous diseases, and ATI-fifty two, a bispecific antibody targeting t slip and IL4R, which are two key components of Th2 mediated diseases. In addition, we have a preclinical portfolio highlighted by our next gen ITK inhibitor, where we have engineered out the JAK3 component as well as a few novel bispecific constructs that are in early stage development.

Our portfolio is complemented by a strong balance sheet with over 190,000,000 in cash and runway through the first half of twenty twenty eight with additional visibility on incremental nondilutive capital in the future. Our pipeline is broad and includes highly differentiated large and small molecule assets, all with multi indication potential, targeting multibillion dollar target addressable markets. As I mentioned, we have three clinical stage assets. ATI-forty five is in phase three clinical studies in China in severe asthma and CRS with NP, as well as a phase two clinical study in COPD. As a reminder, we are currently seeking ex China partners for these indications.

Regarding our internal programs, we recently initiated a global phase two study in atopic dermatitis with sites in The US, Canada, and Europe, and that study is ongoing. In addition, the IND for our bispecific t slip IL4R was recently allowed, and the phase one SADMAD work has begun. Finally, ATI-two thousand one hundred thirty eight, our oral small molecule ITK JAK3 inhibitor, is currently in phase two. We recently completed this study, and we are awaiting final PD data so top line data will be reported imminently. Since the close of our transaction with Biogen in November of last year, we have been busy executing on our plan.

We have hired a CMO, Jesse Hall. We have extended our cash runway by a quarter and a half and have continued to deliver on our clinical and preclinical plans. We have made good progress this year with a rich catalyst calendar expected in 2026. Our next update will be presenting top line data from our 2138 POC study in AD, which, as I said before, is imminent. Post reporting this top line data, we look to initiate a clinical study in alopecia areata with 02/1938, report top line data for ATI-fifty two SADMAD work at the turn of the year, followed by phase 1b POC results in the second half of twenty twenty six.

We will also report ATI-forty five AD data in the second half of ’twenty six and deliver an IND with our next gen ITK selected in the same year. Turning to ATI-forty five or Osacatug, our potential best in class t slip monoclonal antibody. Mosacitug is a humanized antibody targeting t slip, which is a key alarm and involved in pushing t h two inflammation relevant to a number of skin, GI, and respiratory diseases. T slip is a pleiotropic mediator with broad activity acting on a wide array of adaptive, innate, and structural cells. In addition to working on Th2 inflammatory pathways, it is also involved in a few non Th2 processes.

The expression of t slip is elevated in both respiratory and skin diseases, and therefore this represents a great target to inhibit, either alone as a monoclonal antibody or in a bispecific construct, and we have both. TESSFIRE is obviously approved in severe asthma and has been studied in a number of indications to date. So how is our molecule different? As a reminder, prior to consummating our transaction with Biogen last year, we tested bosacotug in numerous assays, comparing it not only to tezepelumab, but also a number of clinical development candidates head to head. In all cases, we demonstrated enhanced potency with bosacotug.

Here we show Osacatug versus tezepelumab demonstrating a greater than 60 x inhibition of CCL 17 production by human PBMCs. We believe this high potency is due to the very unique binding characteristics to tSlim. Osaka tug has an extremely low dissociation rate from t slip, leading to long residence time and enhanced neutralization activity, which we then quantified. To quantify the residence time, we utilize the TR FRET assay, where we are measuring dissociation time of from bisacatug in various competitor molecules. As you can see, we have an extremely long residence time of over four hundred hours in contrast to tezepelumab at fourteen hours and others at twenty hours or less.

This means we bind and stay bound, which we believe is very likely important in an alarming based mechanism of action. You want to make sure that once the antibody binds to the alarming, it doesn’t quickly cycle off and remain free to bind to a receptor, which then perpetuates inflammation. So why is this high infinity and long residence time important? Well, here we show that the potency is a funk in a functional assay measuring CCL 17 production from human PBMCs is quite robust versus the comparator molecules. So we know in vitro that we are driving a more robust effect in functional assays.

The next question that we had to answer was how does this enhanced potency translate to clinical effect in patients? Prior to our license deal with Biogen, the company conducted a 22 patient single arm study to answer that question. A phase two a POC study was initiated in The US with mosacetag in patients with moderate to severe AD. Mosacetag was dosed over twenty four weeks with a twelve week follow-up. In this study, we demonstrated a strong clinical response as measured by mean change from baseline and EZ score, which actually continued to peak through week twenty eight after dosing was complete at week twenty four.

In fact, e c seventy five response was maintained after the last dose for several weeks support supporting the potential for longer dosing intervals. The effect was rapid and sustained showing the clinical translation of the potency that I’ve already covered. Equally as impressive was the responder analysis. Strong responder rates were observed for an e z seventy five, e z ninety, e z one hundred, and IgA. Although this was a single arm study with all the caveats that that entails, rates of ninety four percent on e z seventy five and eighty eight percent on IgA response are very high in moderate to severe AD patients, which we believe further validates the enhanced potency of dosagetub relative to the competitive landscape.

In this graph, we are comparing our results to those of dupilumab and tezepelumab. It is notable that the response is rapid and similar to DUPI, but in contrast, bosacotub drives a deeper and more durable response over time when looking at mean change from baseline in EASI scores. On the heels of this impressive phase two a data, we have initiated global phase two study in atopic dermatitis. We’ll be enrolling approximately ninety patients with moderate to severe AD with a two to one randomization. Treatment will continue through week twenty ’2 with a ten week follow-up period.

The primary endpoint is mean change from baseline and EASI score. One key component of our study is the incorporation of a rigorous picture review process prior to enrolling patients. This will be conducted by an independent central reviewer and then sent to the company to review prior to enrollment. In this way, we hope to mitigate against the growing placebo responses seen in recent years in some studies. As I mentioned, next steps, we have initiated this first study in in atopic dermatitis with losacatug, plus first placebo controlled study, and we’ll look to report the top line data in the second half of twenty twenty six.

As a reminder, we are also actively seeking partners to develop losacatug in respiratory indications ex China. Now moving on to our bispecific, ATI o five two, which is our anti t slip IL four r bispecific, utilizing the same antibody binding regions of ATI-forty five combined with IL4R, which inhibits T slip upstream and clearly immune cells downstream of the Th2 cascade, which we believe is likely important for enhanced activity in atopic dermatitis, severe asthma, and COPD relative to targeting a single inflammatory mediator. In this construct, we continue to leverage the best in class potential of our t slip monoclonal antibody in terms of dissociation kinetics, residence time, and potency. This molecule is also half life extended and has the potential to show superior activity than the single target approach in a variety of diseases as I already mentioned. As we see here, o five two demonstrates far greater potency up to four x versus tezi and dupilumab combined in this functional assay looking at CCL seventeen release.

On the heels of this, we recently announced the initiation of a phase one program with our bispecific where we will look at safety, tolerability, PK, and immunogenicity VTI o five two. After completing the MAD portion of the study, which we’ll complete at the end of this year, we’ll move into a phase one b POC and a yet to be disclosed respiratory as well as a dermatology indication. So we’ll be doing two phase one b proof of concept studies post the MAD work. As we have previously announced, the IND was recently clear for o five two in April of this year. We’ve initiated activities in the phase one SADMAD program, and we expect top line results from the phase 1b portion in the second half of twenty twenty six.

Now moving to our small molecule programs. ATI-two thousand one hundred thirty eight is an oral small molecule covalent inhibitor of ITK and JAK3. It is highly potent on both targets and can be thought of in the same class as rituximab, which is Pfizer’s approved drug for alopecia areata. Although our pharmacology is quite unique and distinct from rituximab, which tends to more broadly inhibit members of the TET kinase family. As we can see here, we compare quite favorably to riclositinib in terms of potency in the JAK three assay, about a five x increase on the right hand side in potency and over 40 x on the left hand side, more potent in the ITKX assay, which gives us confidence when thinking about indications like alopecia areata, vitiligo, or atopic dermatitis.

Next, we show a potency comparison to CPI eight one eight, where across all measures of ITK enzyme activity, we’re showing that twenty one thirty eight is between fifteen and thirty x times more potent at inhibiting ITK, and that is shown on the left. In addition, 2,138 is also significantly more potent at blocking Th2 derived cytokines like IL4, IL5, and IL13. This positions us as the most potent and potential best in class molecule in targeting ITK. Last year, we embarked on a POC study with 2,138 in patients with moderate to severe atopic dermatitis. The study was twelve weeks in duration with the primary endpoint of safety and secondary endpoints of PKPD and efficacy.

Our main objective with this study was to demonstrate the unique pharmacology and safety profile of 2,138 relevant to indications such as atopic dermatitis and alopecia areata, demonstrate the importance of ITK through the PE analyses, which has been extensive, and bridge this data importantly to our next gen ITK selective molecule. The study enrolled 14 patients with moderate to severe atopic dermatitis. It is in fact complete, and the data will be available imminently once we receive the full set of PD data from our external partner. In terms of next steps, we look to report out top line data on our phase two a open label study of ATI-two thousand one hundred thirty eight. We’ll be focusing on the safety and efficacy and, again, importantly, the PD as it relates to both twenty one thirty eight and guidance, related to the ITK selective.

Next indication for us with twenty one thirty eight will be alopecia areata. We think that’s a better fit than, atopic dermatitis for this particular molecule given the JAK effect that we have. Now moving to our next gen ITK selective. ITK is an is important in driving both Th two and Th 17 inflammation. Blockade of ITK inhibits key cytokines like IL four and IL 13 involved in allergic and atopic diseases.

We plan to file an IND on our next gen ITK molecule in 2026 and begin phase one work. So in summary, we have a highly accomplished executive team with world class small and large molecule capability. We have a strong balance sheet with over a 190,000,000, which gives us a cash runway through midyear twenty twenty eight. We have a balanced portfolio of three clinical stage assets and a new IND coming into focus in 2026, along with multiple clinical catalysts in 2025 and 2026. Thank you for your attention.

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