Dr Martin Dahl Discusses the Pathophysiology of AD and Benefits of ANB032

EP: 1.Ruxolitinib Cream Improves AD Across Body Regions, Shows Efficacy, Safety in Black Patients

EP: 2.Upcoming Generics Provide New Considerations and Opportunities for Savings

EP: 3.Managed Care Has a Key Role in Biosimilar Adoption, Says Cardinal's Oskouei

EP: 4.Dr John Harris: There Are a Lot of Reasons to Talk About Vitiligo at This Year’s AAD Meeting

EP: 5.Dermatologists’ Focus to Delve Below the Skin at Annual Conference

EP: 6.Experts Herald “Year of the JAK Inhibitor” in Dermatology

EP: 7.Dr Monica Li Highlights Advances in Microneedling

EP: 8.Dr Eva Parker: Climate Change Has Been Impacting Skin Diseases for Years

EP: 9.Dermatology Data Can Direct Policy Priorities, but Gaps Reflect Inequities of Care

EP: 10.Dr John Harris Outlines the Outcomes of Stopping Treatment With Ruxolitinib Cream for Vitiligo

EP: 11.Late-Breaking Abstracts Demonstrate Value of Persistence With Ruxolitinib Cream for Vitiligo

EP: 12.Examining Dermatological Care for Transgender Patients

EP: 13.How Our Understanding of Inflammatory Skin Disease Has Evolved From the 4 Humors to Targeted Therapies

EP: 14.Dr Haley Naik Discusses Using Biologics and the Drug Pipeline for Hidradenitis Suppurativa

EP: 15.Drs Dellavalle and Rodriguez Discuss Disparities in Prescription Patterns for Atopic Dermatitis

EP: 16.Posters Show Success of Ruxolitinib Cream in Alleviating Facial Vitiligo Symptoms, Reducing Noticeability

EP: 17.Investigators Highlight Disparities Evident in Skin Disease Care, Data Collection

EP: 18.Studies Presented at AAD Examine Safety and Satisfaction of Tildrakizumab for Psoriasis

EP: 19.Patients With AD Have More Options With Biologics, JAK Inhibitors, Says Dr Emma Guttman-Yassky

EP: 20.Dermatologists Looking to the Future Will Need to Be Their Own Advocates, Panel Says

EP: 21.Teledermatology Can Increase Access for Patients With High-Risk Melanoma: Erik Jaklitsch

EP: 22.Dr Sancy Leachman: Melanoma Metastasizes Quickly, Needs to Be Caught Early

EP: 23.Panel Discusses Treating Acne, Psoriasis in Dermatology Patients

EP: 24.New and Upcoming Treatment for Vitiligo, Atopic Dermatitis

EP: 25.Long-Term Safety of Dupilumab in Adults With Moderate to Severe Atopic Dermatitis

EP: 26.Evaluating Label Warnings, Switching Rates in Patients With Psoriasis Initiating New Treatment

EP: 27.ICYMI: Highlights From RAD 2023

EP: 28.AAD 2024 to Feature Topics Including JAK Inhibitors, Biologics

EP: 29.Dr Amy Paller Previews the 2024 AAD Annual Conference

EP: 30.Ruxolitinib Reduces Extent, Severity of AD and Need for Other Treatments

EP: 31.Dr Raj Chovatiya Outlines Who Is a Good Candidate for Oral JAK Inhibitors

EP: 32.Atopic Dermatitis in Adults: Challenges and Treatment Strategies

EP: 33.Dr Robert Sidbury: Understanding What Makes a Dermatology Practice Successful

EP: 34.Dr Monica Li Discusses Tailoring Microneedling Treatments to Meet Each Patient's Need

EP: 35.Skin Tone Bias Persists in Google Searches for Vitiligo

EP: 36.Management of HS Requires Both Coordination, Communication Between Patients and Providers

EP: 37.Dr Jonathan Silverberg Discusses Findings on the Safety, Efficacy of Nemolizumab at 48 Weeks

EP: 38.Biologic, Topical Therapies Both Effective in Treating AD in Skin of Color

EP: 39.Late-Breaking Abstracts Highlight Promising Therapies in AD, Hidradenitis Suppurativa

EP: 40.Dr Jeff Stark: Pain Reduction With Bimekizumab-bkzx in Patients With HS

Now Viewing

EP: 41.Dr Martin Dahl Discusses the Pathophysiology of AD and Benefits of ANB032

EP: 42.New Study Links Social Factors to Hidradenitis Suppurativa Severity

EP: 43.Dr Laura Ferris Discusses Safety, Efficacy of JNJ-2113 in Patients With Plaque Psoriasis

EP: 44.Dr Shawn Kwatra Shares Efficacy, Safety Data of Nemolizumab in Patients With PN

EP: 45.Brodalumab Is Effective, Safe in Patients With Moderate to Severe Psoriasis

EP: 46.Patients With Vitiligo Suffer Heightened Stigma, Mental Health Risks

EP: 47.Racial Variations in Cardiovascular Outcomes Found in Hidradenitis Suppurativa Study

EP: 48.Autoimmune Comorbidities Prevalent in Patients With Vitiligo

EP: 49.Skin Cancer Incidence Highest Among Rural, SOC Individuals

EP: 50.Dupilumab Considered Safe, Effective Treatment for Adolescent, Adult Patients With AD

EP: 51.Gaps in Skincare Knowledge, Sun Protection Practice Exist Among Patients With Lupus

EP: 52.Dr Raj Chovatiya Provides Evidence Supporting Oral JAK Inhibitor Use to Treat AD

EP: 53.Undertreatment, Biologic Access Gaps Identified in Psoriasis Treatment

EP: 54.Dr Raj Chovatiya Explains Oral JAK Inhibitor Monitoring Protocols for AD Treatment

EP: 55.Dr Monica Li Lists Microneedling Considerations, Precautions

EP: 56.Dr Jonathan Silverberg Describes AD Diagnosis, Treatment in Children vs Adults

EP: 57.Dr Lawrence Eichenfield Discusses Positive Results of Roflumilast Cream 0.05% in Pediatric Patients With AD

EP: 58.Dr Robert Sidbury on Implementing Value-Based Care Initiatives in a Pediatric Dermatology Practice

EP: 59.Dr Monica Li Explains Efficacy, Safety Differences Between Different Microneedling Techniques

EP: 60.Dr Lawrence Eichenfield Hopeful for New Pediatric AD Treatment Option

EP: 61.Dr Martina Porter Shares Findings on Ruxolitinib Cream in Patients With HS

This content was produced independently by The American Journal of Managed Care^® and is not endorsed by the American Academy of Dermatology.

ANB302 is a novel non-depleting antibody that has the potential to treat many systemic inflammatory diseases.

In a poster presented at the American Academy of Dermatology (AAD), ANB302 was associated with reduced inflammatory cytokines that drive the pathophysiology of atopic dermatitis (AD), according to Martin Dahl, PhD, senior vice president of research, AnaptysBio.

Transcript

What are the primary mechanisms underlying the pathophysiology of AD, including the role of immune dysregulation, skin barrier dysfunction, and genetic predisposition?

We find that in atopic dermatitis, it's a T-cell driven disease. So, when we look in the skin, we can see a lot of T cells that accumulate in the skin and they can be a heterogeneous population of T-cells, sometimes Th1 [T helper cell 1], sometimes Th2, sometimes Th17, sometimes Th22, or sometimes a mix of all of those types. [Emma Guttman, MD, PhD, professor, Icahn School of Medicine at Mount Sinai; director of the Occupational Dermatitis Clinic and director of the Laboratory for Inflammatory Skin Diseases] had a really great publication back in 2008, where she showed in histology, the presence of a high number of T cells. Not only are there a high number of T cells, [but] she also showed a really dense population of dendritic cells that are in the skin driving that inflammatory T-cell process.

Can you please provide an overview of the study presented at AAD on ANB032 for patients with AD?

At this meeting, we presented a poster on ANB032 around the dendritic cell biology in atopic dermatitis. In the past, we and others have shown that BTLA expression on T cells represents an immune checkpoint that can be added agonized to turn off the T-cell function. And what that does, it reduces T-cell proliferation, migration into tissue, and reduction of inflammatory cytokines across a broad panel of cytokines.

In this study, what we've done is we've moved on to the dendritic cell. We can see not only are there a lot of dendritic cells in the skin and patients, but we can take those dendritic cells, we can purify them, and when we stimulate them with an immune stimulant like LPS [lipopolysaccharide] to mature them, they upregulate a lot of BTLA on the surface, which allows us to engage that dendritic cell and try to turn it off through the agonistic mechanism.

What we did in this poster was we took immature dendritic cells, matured them overnight in LPS and looked at the upregulation of BTLA expression. Then we repeated the study by adding an ANB032 to agonize BTLA. In that process overnight, even in the presence of LPS, ANB032 agonized the dendritic cells and prevented them from maturing. So, we see a reduction in the number of cells that mature, a reduction in MHC [major histocompatibility complex] class 2 expression, which is needed for T-cell activation, and a reduction in the costimulatory molecules CD80, CD86, and CD40.

The combination of that effect should reduce T-cell priming and reduce the activity and the ability of dendritic cells to activate T cells downstream. We then took those dendritic cells that were cultured with ANB032 overnight and they were in the immature state. We washed off all the drug and we took those DCs [dendritic cells] and put them in a culture with naive T cells. And that's a mixed lymphocyte reaction, where typically the dendritic cell will activate the T-cells and drive an inflammatory process.

If we pretreat those DCs with ANB032, what we saw was the induction of a large number of regulatory T cells that express FOXP3 and CD25. And those regulatory T cells contributed to reducing the inflammatory cytokines from other T cells in that culture. So, we saw reductions in IL-17, reduction of interferon gamma, and reductions of IL-5; all common T-cell cytokines that drive the pathology of atopic dermatitis.