About

David Pearson, MD, is an Associate Professor in the Department of Dermatology at the University of Minnesota. He provides individualized, evidence-based care for patients with autoimmune connective tissue diseases and autoimmune bullous diseases. His clinical interests include dermatomyositis, cutaneous lupus, systemic sclerosis, pemphigoid, pemphigus, severe cutaneous drug reactions, and morphea. Dr. Pearson is affiliated with the U of MN Medical Center (UMMC) and specializes in immunology and research related to autoimmune conditions. His professional focus encompasses both patient care and research in dermatology, contributing to the academic and clinical excellence of the department.

Research topics

• Medicine
• Dermatology
• Internal medicine
• Oncology
• Botany
• Ecology
• Biology

Selected publications

• A Phase 3 Trial of Brepocitinib in Dermatomyositis

  New England Journal of Medicine · 2026-03-28 · 4 citations

  articleOpen access

  BACKGROUND: Brepocitinib is a first-in-class, oral, selective TYK2-JAK1 inhibitor that blocks cytokine signaling, which has been implicated in dermatomyositis. METHODS: In this phase 3, double-blind, randomized, placebo-controlled trial, adults with dermatomyositis were assigned in a 1:1:1 ratio to receive once-daily oral brepocitinib at a dose of 30 mg, brepocitinib at a dose of 15 mg, or placebo for 52 weeks. Standard therapies were continued, and glucocorticoids were tapered. The primary end point was the Total Improvement Score, a validated composite myositis index (with scores ranging from 0 to 100 and higher scores indicating greater improvement) at week 52. Key secondary end points, including skin disease activity, glucocorticoid tapering, and physical function, were tested in a multiplicity-controlled sequence. RESULTS: A total of 241 patients underwent randomization: 81 to receive brepocitinib 30 mg, 81 to receive brepocitinib 15 mg, and 79 to receive placebo. At week 52, the mean Total Improvement Score was 46.5, 37.5, and 31.2, respectively (difference with brepocitinib 30 mg vs. placebo, 15.3; 95% confidence interval [CI], 6.7 to 24.0; P<0.001; difference with brepocitinib 15 mg vs. placebo, 6.3; 95% CI, -2.4 to 14.9). Brepocitinib 30 mg was superior to placebo across all nine key secondary end points, including skin disease activity, systemic glucocorticoid tapering, and functional disability, with improvements observed as early as week 4. Serious infections were more frequent in the brepocitinib 30-mg group than in the placebo group (10% vs. 1%). No deaths occurred during the trial. CONCLUSIONS: In adults with dermatomyositis that was resistant to previous therapy, the use of brepocitinib at a dose of 30 mg (but not at a dose of 15 mg) resulted in significant benefits with respect to a composite myositis index, skin disease severity, glucocorticoid tapering, and functional disability. (Funded by Priovant Therapeutics; ClinicalTrials.gov number, NCT05437263.).

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• PO:11:280 Randomized, placebo-controlled, double-blind phase 1b/2 study to explore safety, pharmacokinetics, and initial efficacy of DS-7011a, an anti-toll-like receptor 7 monoclonal antibody, in SLE patients

  2026-03-01

  articleOpen access

  Objectives Toll-like receptor (TLR)7 is a pattern recognition receptor that contributes to SLE pathogenesis.DS-7011a is an anti-TLR7 monoclonal antibody (mAb) that inhibits TLR7 signaling.The aim of this study was to explore safety and PK and to detect initial efficacy of DS-7011a in SLE patients.Methods This was a randomized, placebo-controlled, double-blind Phase 1b/2 study [NCT05638802].Patients were: 1) globally enrolled and randomized 2:1 to DS-7011a or placebo; 2) required to have definite SLE according to the 2019 EULAR/ ACR criteria, active CLE (CLASI-A score of at least 4), and no or inactive LN; 3) given DS-7011a (20 mg/kg) or placebo IV 3 times Q4W starting at Week 0; and 4) followed until Week 16 to assess treatment effect.Study primary objective was safety and secondary objectives were PK and initial efficacy.

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• Enpatoran, a Toll-like receptor 7/8 inhibitor, in moderate-to-severe systemic lupus erythematosus: findings from Cohort B of a multicentre, international, double-blind, placebo-controlled dose-finding phase 2 trial

  The Lancet · 2026-05-01 · 2 citations

  articleOpen access

  BACKGROUND: Toll-like receptors (TLR) 7 and 8 (TLR7/8) are activators of innate and adaptive immunity contributing to lupus pathogenesis. In Cohort B of WILLOW, a phase 2, randomised, placebo-controlled, double-blind, basket, dose-finding study, enpatoran, an oral small molecule inhibitor of TLR7/8, was evaluated in participants with active systemic lupus erythematosus (SLE). METHODS: Participants were eligible if they were aged 18-75 years with moderate-to-severe SLE, with or without cutaneous manifestations, had a disease duration of at least 6 months, and were receiving a stable dose of medication before the screening period. Participants were recruited from 132 centres in 22 countries. In Part 1, participants were randomly allocated in a 1:2 ratio to receive either placebo or 100 mg enpatoran, both twice-daily. Following the enrolment of 60 participants, Part 2 was activated and additional participants were randomly allocated in a 1:1:1:1 ratio to 25 mg, 50 mg, or 100 mg of enpatoran or placebo, all twice-daily, for 24 weeks. Random allocation was stratified by region, biomarker status, and hybrid Safety of Estrogens in Lupus Erythematosus National Assessment-SLE Disease Activity Index score. The primary objective was to evaluate the dose-response relationship of enpatoran, using British Isles Lupus Assessment Group-based Composite Lupus Assessment (BICLA) response rate at week 24, based on multiple comparison procedure-modelling analysis. Study visits were scheduled from week 0 to week 24, followed by a 2-week safety follow-up period for participants who chose not to enter the long-term extension. From weeks 2 to 12, glucocorticoid doses were tapered to a prednisone-equivalent dose of no more than 5 mg/day, as clinically tolerated. Adverse events were monitored continuously throughout the study; safety parameters (including physical examination, vital signs, and routine chemistry and haematology) were assessed at all study visits. The trial was registered at ClinicalTrials.gov (NCT05162586) and a long-term extension study is ongoing. FINDINGS: Between May 4, 2022, and Feb 6, 2024, participants were screened for eligibility for WILLOW cohorts A and B; 715 participants were screened and 354 were randomly allocated and included in the Cohort B safety population (95 to placebo, 71 to 25 mg enpatoran, 74 to 50 mg enpatoran, and 114 to 100 mg enpatoran). One patient allocated to the placebo group was found to be ineligible and was excluded from the full analysis set for the efficacy analyses. 335 (95%) of 353 participants were female, 18 (5%) were male, and median age was 41 years (IQR 33-51). At week 24, the study did not meet its primary objective of identifying a statistically significant dose-response relationship for enpatoran in BICLA response rate (p=0·14). BICLA response rates at week 24 were higher with all doses of enpatoran (25 mg: 41 [58%] of 71; odds ratio [OR] vs placebo 2·2 [95% CI 1·1-4·0], 50 mg: 36 [49%] of 74; OR 1·5 [95% CI 0·8-2·8], and 100 mg: 56 [49%] of 114; OR 1·6 [95% CI 0·9-2·8]) versus placebo (37 [39%] of 94). The most common treatment-emergent adverse event was diarrhoea, in four (6%) of 71, two (3%) of 74, and two (2%) of 114 participants in the 25 mg, 50 mg, and 100 mg enpatoran groups, respectively, and seven (7%) of 95 participants in the placebo group. Serious adverse events were reported in one (1%) of 71, three (4%) of 74, five (4%) of 114, and three (3%) of 95 participants treated with 25 mg, 50 mg, and 100 mg enpatoran and placebo, respectively. INTERPRETATION: In this study of participants with moderate-to-severe SLE, enpatoran improved BICLA response rates versus placebo; however, the primary objective of a statistically significant dose-dependent effect on disease activity based on BICLA response was not met. Enpatoran was well tolerated across all dose groups. FUNDING: Merck Healthcare (Darmstadt, Germany).

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• Efficacy and safety of enpatoran, a Toll-like receptor 7/8 inhibitor, in patients with skin manifestations of cutaneous lupus erythematosus or systemic lupus erythematosus: findings from Cohort A of a multicentre, international, double-blind, placebo-controlled, dose-finding phase 2 trial

  The Lancet Rheumatology · 2026-05-01

  articleSenior author
  PublisherDOI

• S1:04 Enpatoran, a toll-like receptor 7/8 inhibitor, in skin manifestations of cutaneous lupus erythematosus or systemic lupus erythematosus: pooled safety data from the phase 2 willow trial

  Oral Presentations · 2026-03-01

  articleOpen accessSenior author

  Objectives Fatigue, a debilitating symptom, is the most common symptom reported among patients with systemic lupus Abstract S1:04 Table 1 Pooled safety data from WILLOW cohorts A and B for participants with CLE/SLE and cutaneous manifestations a Lupus Science & Medicine: first published as 10.

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• Evaluating heterogeneity in MDA‐5+ dermatomyositis through cluster analyses

  Journal of the European Academy of Dermatology and Venereology · 2026-01-12

  articleOpen access1st authorCorresponding

  Dermatomyositis is a multisystem autoimmune disease that may affect the skin, musculoskeletal system, respiratory system and others. There is significant heterogeneity in clinical manifestations, prognosis and response to treatment. Despite limitations, clinical phenotypes are often associated with individual myositis-specific antibodies (MSA). Patients with MSA directed against Melanoma Differentiation Antigen-5 (MDA-5) may develop rapidly progressive interstitial lung disease (RP-ILD), the leading cause of death in this subset, with a mortality risk that may exceed 80% within 3 months of diagnosis.1, 2 However, significant heterogeneity exists among patients with MDA-5 autoantibodies. Prior studies of Chinese1 and predominantly northern European and Black2 cohorts have employed unsupervised cluster analyses to identify three similar clinical phenotypes: (1) Patients who develop RP-ILD and experience high mortality; other notable features included mechanic's hands, elevated inflammatory markers, and lower likelihood of proximal myositis (32% vs. 18% of patients in each study, respectively). (2) Patients with lower rates of RP-ILD and more typical cutaneous and proximal muscle symptoms (27% vs. 55%). (3) Patients at lower risk of RP-ILD but demonstrable vasculopathy, with cutaneous ulcers, Raynaud's phenomenon, and proximal myositis (41% vs. 27%). He et al.'s study3 is an important addition to this growing literature because it builds upon methodology and rigour. It also identifies three phenotypes, though they differ somewhat from those previously described. Utilizing unsupervised cluster analysis followed by a robust sensitivity analysis, they define: (1) a similar high-risk RP-ILD cohort; (2) a dermato-rheumatologic cohort with typical skin and musculoskeletal involvement and lower risk of RP-ILD and (3) a novel, low-risk group with the lowest rate of RP-ILD and dermato-rheumatologic manifestations. The difference in 3-month all-cause mortality between these groups is striking: 88.7% vs. 4.3% vs. 2.4%, respectively, and mirrors rates of RP-ILD (84.9% vs. 18.1% vs. 17.1%). An important strength of this study is its inclusion criterion of radiographically demonstrated ILD by high-resolution computed tomography. As He et al. discusses, these features are critical in the early diagnosis of RP-ILD and carry important prognostic implications. While reduction in dimensionality through application of principal component (PC) analysis allowed for incorporation of these data into the cluster analysis, and functions as a critical component of the model, it does pose a challenge for clinicians: how do we easily calculate the PC1 score in the office for our patients? Further refinement of this model, hopefully without loss of integrity, may prove a highly useful bedside tool. The heterogeneity of patients with MDA-5 autoantibodies, and dermatomyositis in general, is further complicated: how well can we as clinicians rely on commercially available MSA testing? Lack of standardization among commercial antibody panels, lack of widespread availability of gold standard immunoprecipitation testing for MSA, and challenge in identifying patients with high pretest probability all influence the positive and negative predictive values of these tests. In comparison to immunoprecipitation, line immunoassay (LIA) and enzyme-linked immunosorbent assays (ELISA) do not perform equally across MSAs; a recent meta-analysis4 found better agreement with immunoprecipitation for MDA-5 autoantibodies (LIA, sensitivity 82.8%, specificity 96.3%; ELISA, sensitivity 95.7%, specificity 99.7%) versus transcriptional intermediary factor 1-γ (TIF1γ) autoantibodies (LIA, sensitivity 63.8%, specificity 96.5%). A lack of positive antibodies does not eliminate risk of severe outcomes; Chen et al.5 found an incidence of ILD of 46.8%; 25% of these patients demonstrated RP-ILD. In summary, phenotypic differentiation of dermatomyositis is crucial in identifying high-risk patients, and He et al. expands the literature in defining these groups. Accurate modelling and biomarkers will allow us to better care for high-risk patients, and above all, we must remain vigilant for RP-ILD in all our dermatomyositis patients, even those who do not have positive MSAs. Grants or contracts: Daiichi Sankyo Company Ltd., EMD Serono Inc., Nkarta Inc., Priovant Therapeutics. Consulting: AstraZeneca plc, Biogen Inc., Merck & Co Inc., Pfizer Inc. Board membership: Minnesota Dermatological Society. Steering committee membership: EMD Serono Inc. Data sharing is not applicable to this article as no datasets were generated or analysed during the current study.

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• 0007 Anifrolumab for adult patients with refractory juvenile dermatomyositis

  Journal of Investigative Dermatology · 2025-07-21 · 1 citations

  articleOpen accessSenior author
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• Abstract 4369748: Race Differences in Acute Chest Pain Care in a Multisite U.S. Cohort

  Circulation · 2025-11-03

  article

  Introduction: Race-based differences in cardiovascular care are well described. However, data examining differences in cardiac testing and death or myocardial infarction (MI) rates among U.S. emergency department (ED) patients with acute chest pain by race are limited. Research Question: Do safety and healthcare utilization differ by race among patients with chest pain in a multisite U.S. ED cohort? Methods: We conducted a multisite observational study using the Wake Forest Chest Pain Registry, including patients ≥18 years old who were evaluated for possible acute coronary syndrome from 1/1/2021–12/31/2021 across 25 EDs. Each ED used the same high-sensitivity troponin protocol for chest pain evaluations. Race was determined by patient self-report in the electronic health record and reported as White non-Hispanic, Black non-Hispanic, Hispanic, and Other. The primary safety outcome was 30-day all-cause death or MI. Healthcare utilization outcomes included 30-day hospitalizations and objective cardiac testing (OCT), which was defined as non-invasive testing (NIT: stress testing and coronary computed tomography angiography) and invasive coronary angiography. Outcomes between races were compared using chi-square tests. Multivariable logistic regression models were used to assess the association between race and outcomes adjusting for sex, age, obesity, smoking, rurality, prior coronary artery disease, diabetes, hypertension, hyperlipidemia, insurance status, ED site, and initial troponin, with White race as the reference group. Results: Among 40979 patients, 58.7% were White, 32.9% Black, 5.4% Hispanic, and 3.0% Other. At 30 days, death or MI occurred in 4.6% (1,097/24063) of White patients compared to 2.2% (301/13480) of Black and 1.6% (36/2195) of Hispanic patients (p&lt;0.001). Compared to White patients, the odds of 30-day death or MI were lower among Black (aOR 0.51, 95%CI: 0.43-0.60) and Hispanic (aOR 0.65, 95%CI: 0.44-0.97) patients. OCT at 30 days occurred in 19.8% (4756/24063) of White, 13.1% (1765/13480) of Black, and 10.7% (234/2195) of Hispanic patients (p&lt;0.001). Compared to White patients, after adjusting for confounders, the odds of 30-day OCT were lower among Black (aOR 0.73, 95%CI: 0.68-0.78) and Hispanic (aOR 0.83, 95%CI: 0.71-0.97) patients. Table 1 describes OCT and hospitalization rates by race. Conclusion: Black and Hispanic patients with chest pain had lower rates of 30-day death or MI and OCT compared to White patients.

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• RANDOMIZED, PLACEBO-CONTROLLED PHASE II STUDY OF ENPATORAN, A SMALL MOLECULE TOLL-LIKE RECEPTOR 7/8 INHIBITOR, IN CUTANEOUS LUPUS ERYTHEMATOSUS: RESULTS FROM COHORT A

  The Journal of Rheumatology · 2025-05-20 · 12 citations

  articleOpen access1st authorCorresponding

  O010 / #827 Topic: AS07 - Cutaneous Lupus Late-Breaking Abstract ABSTRACT CONCURRENT SESSION 01: FINDINGS FROM LUPUS CLINICAL TRIALS 22-05-2025 1:40 PM - 2:40 PM Background/Purpose No treatment is approved for cutaneous lupus erythematosus (CLE), which may occur in the presence or absence of systemic lupus erythematosus (SLE). Enpatoran is an oral small molecule toll-like receptor 7/8 inhibitor, with potential to modulate processes central to CLE and SLE pathophysiology. WILLOW ( NCT05162586 ) is a Phase II randomized double-blind placebo-controlled dose-finding parallel adaptive study in adults with SLE or CLE receiving standard of care to evaluate the efficacy and safety of enpatoran. WILLOW Cohort A enrolled patients with CLE or SLE who had active lupus rash. Methods Patients with Cutaneous Lupus Disease Area and Severity Index-Activity (CLASI-A) score ≥ 8 CLE were enrolled; they had CLE only, or SLE with mild or no extramucocutaneous disease activity [British Isles Lupus Assessment Group 2004 &lt; 1B, C, D]). Patients were randomized 1:1:1:1 to 1 of 3 doses of enpatoran or placebo for 24 weeks, with an additional 2-week safety follow-up for patients not choosing to enter the long-term extension. The primary objective was to evaluate the dose-response relationship of enpatoran in reducing disease activity, based on change from baseline in CLASI-A score at Week 16. Secondary endpoints included change from baseline in Physician’s Global Assessment at Weeks 16 and 24, clinically meaningful corticosteroid (CS) reduction, and occurrence of Cutaneous Lupus Activity-Investigator Global Assessment 0 or 1 at Week 16 and Week 24. Exploratory endpoints included CLASI-A improvement ≥ 50%/70% (CLASI-50/70). Treatment-emergent adverse events (TEAEs), serious TEAEs, TEAEs of special interest and laboratory parameters were collected from Day 1 to the end of safety follow-up. Results 102 patients were randomized, and 100 patients were included for efficacy evaluation (placebo n = 26; enpatoran low dose n = 23; mid dose n = 25; high dose n = 26). 77.0% of patients were female, and 58.0% had CLE only. At baseline, 59.0% of patients were receiving systemic CS, 38.0% immunosuppressants and 76.0% antimalarials; 71% had moderate-to-severe disease (CLASI-A ≥ 10). The primary outcome was achieved. At Week 16, a significant dose response for enpatoran in reducing CLASI-A from baseline was detected (p = 0.0002) (Table 1). Table 1 Dose-response relationship of enpatoran in reducing disease activity based on change from baseline in CLASI-A score at Week 16 (FAS; N = 100) Furthermore, up to 91.3% of patients receiving enpatoran achieved CLASI-50, and up to 60.9% achieved CLASI-70 at Week 16, compared with 38.5% and 11.5% of patients, respectively, receiving placebo. Enpatoran was well tolerated across all study doses. High-dose enpatoran was associated with a higher rate of TEAEs (Table 2) than lower doses or placebo; the most frequently reported TEAEs were infections and infestations. Table 2 Treatment-emergent adverse events (SAS; N = 102) Conclusions Enpatoran demonstrated a significant dose response in change from baseline in CLASI-A compared with placebo at Week 16 in patients with CLE or SLE and was well tolerated. Acknowledgments: The authors wish to thank Dominika Weinelt for their support with the study conduct and analysis. Medical writing support was provided by Nicole Jones on behalf of Amica Scientific, Macclesfield, UK, and sponsored by the healthcare business of Merck KGaA, Darmstadt, Germany.

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• OP0079 Clinical, Cellular Kinetics, Pharmacodynamics and Biomarker Data Up to 12 Months After YTB323 (Rapcabtagene Autoleucel), a Rapidly Manufactured CD19 CAR-T Therapy, From an Open-Label, Phase 1/2 Study in Severe Refractory SLE

  Annals of the Rheumatic Diseases · 2025-06-01 · 7 citations

  articleOpen access

  <h2>Abstract</h2><h3>Background:</h3> Patients with severe refractory systemic lupus erythematosus (srSLE) are those who do not respond to standard of care treatments, resulting in progressive organ damage, morbidity and mortality. Current evidence suggests that B cell depletion through CD19-directed chimeric antigen receptor T cell (CAR-T) therapies can induce marked clinical improvements in patients with srSLE [1]. However, data from formal clinical trials assessing efficacy and safety of CAR-T therapies in multicentre settings and long-term outcomes are needed. YTB323 (rapcabtagene autoleucel) is a rapidly manufactured, autologous CD19 CAR-T therapy that has so far demonstrated favourable risk/benefit in haematological malignancies [2]. Here we report results from this phase 1/2 open-label study investigating YTB323 in patients with srSLE which has recently completed enrolment [3]. <h3>Objectives:</h3> To describe clinical, cellular kinetics, pharmacodynamics and biomarker outcomes up to 12 months after YTB323 treatment of patients with srSLE. <h3>Methods:</h3> This open-label, single-arm, multicentre phase 1/2 study (NCT05798117) to assess the safety, efficacy and cellular kinetics of YTB323 in patients with srSLE (defined as SLE disease activity index 2000 [SLEDAI-2K] ≥8 with organ involvement, having failed to respond to ≥2 standard immunosuppressive therapies and ≥1 biological agent) is fully enrolled (n = 21) and currently ongoing [3]. YTB323 treatment was administered in a single dose of 12.5 × 10⁶ CAR-positive viable T cells, following lymphodepletion with cyclophosphamide/fludarabine. Efficacy assessments included the SLEDAI-2K. Cellular kinetics were monitored by quantitative polymerase chain reaction and flow cytometry; pharmacodynamics and biomarker assessments included levels of anti-dsDNA, complement C3 and C4, IgG, IgA, and IgM. <h3>Results:</h3> To date, data from 13 patients in the study have been analysed and detailed below. Data from all enrolled patients (n = 21) and longer follow-up data will be available at the time of presentation. At baseline, the median age was 36 (range: 24–54) years, and 12 of 13 patients were female. The median duration of follow-up was less than 4 months, with 1 patient with follow-up data at 12 months and 3 patients with follow-up data at 9 months (Table 1). In the 3 patients with a follow-up of at least 9 months, marked improvement from baseline in disease activity was observed with a mean SLEDAI-2K decrease of 14.7 points, decrease in anti-dsDNA antibodies (geometric mean ratio to baseline of 8.4%), and increase in complement C3 (geometric mean ratio of 130%) at 9 months. Cellular kinetics and pharmacodynamics data from 13 patients revealed peak expansion of CAR-T cells 2-3 weeks post-infusion and B cell depletion, with subsequent B cell recovery occurring 60 to 90 days after CAR-T administration in most patients. Analysis of early reconstituted B cells showed a dominant naive phenotype, with a drastic reduction in memory B cell subsets and plasmablasts. Safety data from 13 patients indicated that YTB323 was generally well tolerated. Transient lymphodepletion-related cytopenia (grade 3/4) was observed in all patients. No patient had grade 4 neutropenia or lymphopenia lasting >28 days. Grade 1/2 cytokine release syndrome (CRS) was observed in 8 of 13 patients; all events resolved with (n = 7) or without (n = 1) tocilizumab treatment. A single grade 2 event of immune cell-associated neurotoxicity syndrome (ICANS) presenting with ataxia, with immune effector cell-associated encephalopathy (ICE) score of 10 out of 10 (where 10 is least severe and 0 is most severe), was reported; the patient recovered 4 days after corticosteroid treatment was initiated. Three serious adverse events (treatment-related: n=2 [CRS and pneumonia]; non-related: n=1 [urinary tract infection]) were reported; all patients fully recovered. <h3>Conclusion:</h3> YTB323 treatment resulted in improved disease activity, effective B cell depletion and recovery of naive B cell phenotype. Early clinical data suggest remarkable efficacy in the srSLE population [4], and a safety profile that is in line with that reported for CD19 CAR-T therapy in autoimmune disease [1]. These data support the continued evaluation of YTB323 in srSLE. <h3>REFERENCES:</h3> [1] Müller et al. <i>N Eng J Med</i>. 2024;390;8:687-700. [2] Barba P et al. <i>Blood</i>. 2022;140;Suppl1:1056–59. [3] ClinicalTrials.gov. NCT05798117. Accessed January 7, 2025. https://clinicaltrials.gov/study/NCT05798117. [4] Kandane-Rathnayake R et al. <i>Ann Rheum Dis</i>. 2024;83,Suppl.1:399-400.<b>Table 1.</b> Patient baseline characteristics (n=13). <h3>Acknowledgements:</h3> The authors thank Rangariroyashe Chipika and Seonadh O'Leary (Novartis Ireland Limited, Dublin, Ireland) for editorial and medical writing support, which was funded by Novartis Pharma AG, Basel, Switzerland in accordance with the Good Publication Practice (GPP 2022) guidelines (http://www.ismpp.org/gpp-2022). This study was sponsored by Novartis Pharma AG, Basel, Switzerland. <h3>Disclosure of Interests:</h3> Eric Morand has received consulting fees and/or speaker honoraria from AstraZeneca, Biogen, Bristol Myers Squibb, DragonFly, Eli Lilly, EMD Serono, GlaxoSmithKline, Novartis, Remegen, Quell, UCB, and Zenas, has received consulting fees and/or speaker honoraria from AstraZeneca, Biogen, Bristol Myers Squibb, DragonFly, Eli Lilly, EMD Serono, GlaxoSmithKline, Novartis, Remegen, Quell, UCB, and Zenas, has received research funding from AbbVie, Amgen, AstraZeneca, Biogen, Bristol Myers Squibb, Eli Lilly, EMD Serono, Genentech-Hoffman La Roche, GSK, Janssen, Novartis, Takeda, and Union Chimique Belge, Rangi Kandane-Rathnayake has received research grants from BMS, GSK, and Novartis, Josefina Cortés-Hernández has received speaker fees from GSK, Zahir Amoura has received speaker fees and honoraria for advisory boards from AstraZeneca, BMS, GSK, Novartis, Merck, and Roche, has received speaker fees and honoraria for advisory boards from AstraZeneca, BMS, GSK, Novartis, Merck, and Roche, Julia Weinmann-Menke has received speaker fees and honoraria for advisory boards from AstraZeneca, Boehringer Ingelheim, GSK, Novartis, Otsuka, Takeda, and Vifor, has received consulting fees from Novartis, Boerhinger-Ingelheim, AstraZeneca, Otsuka and GSK, has received grant/research support from Toray, Miltenyi, Diamed, Britta Maurer has received lecturing fees from Boehringer Ingelheim, GaxoSmithKline, Novartis, Otsuka, and Merck Sharpe & Dohme, declares an mir-29 patent for the treatment of systemic sclerosis (US8247389, EP2331143), has received consulting fees from Novartis, Boehringer Ingelheim, Janssen-Cilag, financial support for congresses (ie, for registration fees and travel) from Medtalk, Pfizer, Roche, Actelion, Mepha, and Merck Sharpe & Dohme,and GaxoSmithKline, and has been on an advisory board for Janssen and Boehringer Ingelheim, has received research grants from AbbVie, Protagen, and Novartis Biomedical Research, Christophe Richez has received speaker fees and honoraria for advisory boards from Abbvie, AstraZeneca, Amgen, BMS, Boehringer Ingelheim, GSK, Lilly, and Novartis, has received speaker fees and honoraria for advisory boards from Abbvie, AstraZeneca, Amgen, BMS, Boehringer Ingelheim, GSK, Lilly, and Novartis, Edouard Forcade has received speaker fees and honoraria for advisory boards from Novartis, Gilead, Alexion, GSK, MSD, Astellas, Jazz, and Sobi, has received speaker fees and honoraria for advisory boards from Novartis, Gilead, Alexion, GSK, MSD, Astellas, Jazz, and Sobi, Stephanie Finzel has received speaker honorarium from AbbVie, Alfasigma/Galapagos, Biotest, Celltrion, Chugai, Johnson&Johnson, Novartis, and UCB, has received consulting fees from Johnson & Johnson, Novartis, NovoNordisk, and UCB, has received meeting or travel grants from Biotest, Eli Lilly, Johnson&Johnson, Novartis, UCB, Galapagos, and Sobi, Jose-Maria Alvaro-Gracia has received speaker and consulting fees for AbbVie, AstraZeneca, BMS, Galapagos, GSK, Novartis, Pfizer, and UCB, has received speaker and consulting fees for AbbVie, AstraZeneca, BMS, Galapagos, GSK, Novartis, Pfizer, and UCB, Anne-Sophie Korganow was invited to congresses as an auditor, and conference-related fees were covered by CSL, LFB, BMS, GSK and Takeda, received grant/research support from CSL, Alberta Hoi is on advisory boards for AstraZeneca, GSK, and Janssen, has received sponsorship for the Australian Lupus Registry & Biobank and Asia Pacific Lupus Collaboration from AstraZeneca, BMS, Eli Lilly, and UCB and contract research from AstraZeneca and Merck Serono, Yannick D. Muller has received grant supports, speaker fees and honoraria for advisory boards from AstraZeneca, Takeda, Viatris, GSK, Sanofi, Thermofisher, and Blueprint Medicines, is an inventor of a CAR-T licence (US 2023/0340068 A1), has received grant supports, speaker fees and honoraria for advisory boards from AstraZeneca, Takeda, Viatris, GSK, Sanofi, Thermofisher, and Blueprint Medicines, has received grant supports, speaker fees and honoraria for advisory boards from AstraZeneca, Takeda, Viatris, GSK, Sanofi, Thermofisher, and Blueprint Medicines, Ozana Fischer may hold Novartis stocks, is an employee of Novartis, Beata Kovacs may hold Novartis stocks, is an employee of Novartis, Frédérique Chaperon may hold Novartis stocks, is an employee of Novartis, David Pearson may hold Novartis stocks, is an employee of Novartis, Adrienne Lefeber may hold Novartis stocks, is an employee of Novartis, Chih-Yung Sean Lee may hold Novartis stocks, is an employee of Novartis, Melissa Fernandes may hold Novartis stocks, is an employee of Novartis, Thomas Calzascia may hold Novartis stocks, is an employee of Novartis, Tamas Shisha may hold Novartis stocks, is an employee of Novartis, Richard Siegel may hold Novartis stocks, is an employee of Novartis, Peter Gergely may hold Novartis stocks, is an employee of Novartis. © The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Neither EULAR nor the publisher make any representation as to the accuracy of the content. The authors are solely responsible for the content in their abstract including accuracy of the facts, statements, results, conclusion, citing resources etc.

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Frequent coauthors

• Victoria P. Werth

  Philadelphia VA Medical Center

  81 shared

• Rebecca G. Gaffney

  Philadelphia VA Medical Center

  36 shared

• Carolyn J. Kushner

  33 shared

• M. Tarazi

  Columbia University Irving Medical Center

  31 shared

• Joyce Okawa

  Philadelphia VA Medical Center

  31 shared

• Basil Patel

  University of Florida

  27 shared

• D. L. Costill

  Ball State University

  27 shared

• Josef Symon S. Concha

  24 shared