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Frontiers in Lupus ·

Volume 4 - 2026 | https://doi.org/10.3389/flupu.2026.1800946

Safety and efficacy of novel therapeutics in lupus: a narrative review

  • Michael F. Loncharich1*corresponding author
  • Brenna E. Cafeo1
  • Evan B. Noble1
  1. Department of Medicine, Division of Rheumatology, Walter Reed National Military Medical Center, Bethesda, MD, United States
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Abstract

Systemic lupus erythematosus (SLE) poses diagnostic and management challenges to physicians given its protean manifestations and complex immune dysregulation. Numerous drugs are used in the management of lupus with a plethora under investigation for more effective, safe, and targeted therapies. This narrative review explores recent literature on the safety and efficacy multiple drug classes and gene therapy under investigation in the management of SLE. The findings in this review detail which new candidate drug and gene therapies are showing efficacy and safety in SLE management, and which are not.

Keywords

1 Introduction

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by complex dysregulation in both the innate and adaptive immune systems. The spectrum of symptoms and potential therapeutic targets pose significant management challenges. Approval of new therapeutic agents had been stagnant for a decade following belimumab's approval in 2011 until the FDA approved voclosporin and anifrolumab in 2021, followed by obinutuzumab late in 2025. Progress toward developing additional medications appears to be accelerating as researchers explore medications targeting B cells, interferons, and a wide array of cytokines. In this narrative review, we summarize recent research of novel therapeutic agents targeting B cells, plasmacytoid dendritic cells, Janus kinases (JAK), and tyrosine kinases (TYK) among other cytokines and review long-term data on the aforementioned approved medications. Additionally, we explore chimeric antigen receptor therapy (CAR T).

2 Methods

For this narrative review, the authors searched PubMed with the term “lupus” and applying filters limiting the search to clinical trials published in the past five years. Additionally, the authors searched clinicaltrials.gov using the term “lupus” and applying filters for “phase III” and “phase IV” with no date restrictions. All articles considered to be relevant were included, and phase I trials were excluded in the scope of this review. Finally, the authors searched the American College of Rheumatology Convergence 2025 lupus treatment abstract sessions for emerging literature.

3 Results

Table 1 summarizes the key findings of the studies reviewed in this manuscript.

Table 1. Key findings from included studies.

DrugMechanism of actionStudiesPrimary endpointMet endpoint?Safety data
CAR T therapies
BCMA CAR TChimeric antigen receptor T-cell therapy targeting BCMA to kill B-cells.Hu et al. 2025—Phase 1, n = 7DORIS or LLDASYesOne patient had grade 1 CRS; no severe infections were reported; temporary lymphodepletion resolved within 4 weeks.
CD 19 CAR TChimeric antigen receptor T-cell therapy targeting CD19 to kill B-cells.Mackensen et al. 2022—Case series, n = 5DORIS remissionYesOne case of grade 1 CRS
Muller et al. 2024—Case series, n = 10DORIS and LLDASYesOne patient with grade 2 CRS, one patient with grade 1 immune effector cell-associated neurotoxicity syndrome, and one pneumonia resulting in hospitalization
Compound BCMA-CD19 cCAR TCompound CAR T therapy with dual targets: BCMA and CD19.Wang et al. 2024—Phase 1, n = 13DORIS and LLDASYesOne patient had grade 1 CRS; temporary neutropenia resolved within 6 weeks, and B-cells recovered within 7 months.
B cell Depleting Therapies
ObexelimabAnti-CD19/ FcγRIIb bifunctional monoclonal antibody.Merrill et al. 2023—Phase 2, n = 104No relapse by week 32NoSimilar rate of infections as placebo; some patients experienced infusion reactions.
OcrelizumabAnti-CD20 monoclonal antibody.Mysler et al. 2013—Phase 3, n = 89Renal response at week 48n/aDiscontinued early due to safety concerns.
ObinutuzumabHumanized glycoengineered type II anti-CD20 monoclonal antibody.Furie et al. 2022—Phase 2, n = 125CRR at week 52NoNo unexpected safety signals were identified.
Furie et al. 2025—Phase 3, n = 271CRR at week 76YesNo unexpected safety results, and fewer deaths or renal events occurred in the treatment group.
EpratuzumabAnti-CD22 (B-lymphocyte-restricted adhesion molecule) monoclonal antibody.Clowse et al. 2017—Phase 2, n = 793 and 791BILAG and BICLA responseNoNo new safety signals were identified.
Gottenberg et al. 2017—Post-hoc, n = 1,375BICLA and BILAGNon/a (post hoc of Clowse et al. 2017)
Wallace et al. 2013—Phase 2, n = 90BILAGNoAdverse event incidence was similar between treatment and placebo groups.
LitifilimabBlood dendritic cell antigen 2 (BDCA2) monoclonal antibody.Furie et al. 2022—Phase 2, n = 334Mean active joint countYesMore adverse events in the placebo group.
Werth et al. 2022—Phase 2, n = 132CLASI responseYesSimilar rates of adverse events in treatment and placebo groups.
BlisbimodBAFF inhibitor.Furie et al. 2015—Phase 2, n = 547SRI-5 responseNoNo significant difference in safety events with blisibimod versus placebo, but injection site reactions were reported more frequently.
Merrill et al. 2018—Phase 3, n = 442SRI-6 responseNoThe most common adverse events were upper respiratory tract infection, urinary tract infection, injection site erythema/reaction and diarrhea.
TabalumabAnti-BAFF IgG4 monoclonal antibody.Isenberg et al. 2016—Phase 3, n = 1,124SRI-5 responseYes (high dose)Similar rates of adverse events in treatment and placebo groups.
IanalumabBAFF receptor inhibitor.Agmon-Levin et al. 2025—Phase 2, n = 67SRI-4 response and CS reductionYesNot associated with increased serious adverse events or infections.
AtaciceptTransmembrane activator and calcium modulator fusion and IgG protein.Isenberg et al. 2015—Phase 2, n =Flare by week 52NoStopped early due to 2 deaths in high-dose treatment group.
Gordon et al. 2017—Phase 2, n =SRI-4 responseNoTwo deaths adjudicated to be non-treatment related.
TelitaciceptTransmembrane activator and calcium modulator fusion recombinant fusion protein.van Vollenhoven et al. 2025—Phase 3, n = 433SRI-4 responseYesSimilar nonserious infection risk to other B cell depleting therapies; no difference in serious infections vs. placebo.
Bruton's Tyrosine Kinase, Janus Kinase, and Tyrosine Kinase Inhibitors
BaricitinibSelective JAK1 and JAK2 inhibitor.Petri et al. 2023—Phase 3, n = 775SRI-4 responseYesConsistent with the known baricitinib safety profile.
Morand et al. 2023—Phase 3, n = 760SRI-4 responseNoNo new safety signals.
DeucravacitinibTyrosine Kinase 2 (TYK2) inhibitor.Morand et al. 2023—Phase 2, n = 363SRI-4 responseYesHigher rates of infections and cutaneous events with deucravacitinib.
ElsubrutinibBruton's Tyrosine Kinase (BTK) inhibitor.Merrill et al. 2023—Phase 2, n = 341SRI-4 response and CS reductionNoNo unexpected safety concerns were noted.
Type 1 Interferon Inhibitor
AnifrolumabGlobal type I interferon inhibitor.Furie et al. 2017—Phase 2, n = 305SRI-4 responseYesHigher rates of influenza and herpes zoster infections with anifrolumab.
Furie et al. 2019—Phase 3, n = 457SRI-4 responseNoSimilar to the phase 2 trial in the row above.
Morand et al. 2020—Phase 3, n = 362BICLA responseYesSimilar to other anifrolumab trials. One death from pneumonia.
Jayne et al. 2022—Phase 2, n = 145Change in 24 h proteinuriaNoNo new safety signals compared to other anifrolumab trials.
Cereblon Ligand
IberdomideCereblon ligand; degrades Ikaros (IKZF1) and Aiodolos (IKZF3).Furie et al. 2022—Phase 2, n = 42SafetyYesTolerable safety profile.
Merrill et al. 2022—Phase 2, n = 288SRI-4 responseYesOverall similar rates of adverse events to placebo, but more urinary tract infections, upper respirator tract infections, and neutropenia.

3.1 Calcineurin inhibitors

In 2021, the FDA approved voclosporin (VCS) in addition to background immunosuppression (IS) for active LN based on the AURA-LV, AURION, and AURORA trials, which showed complete renal remission (CRR) rates at one year of 41%–71% compared to 23% in placebo (1–3). In a pooled analysis of these trials, CRR at week 52 for VCS was 44 vs. 23% in PLACEBO (OR 2.76), and there were no new safety signals (4). Since its approval, a three-year safety study with repeat renal biopsy found no change in chronicity, no vascular lesions or tubular compartment changes on biopsy, indicating long-term tolerability (5).

3.2 Chimeric antigen receptor T-cell therapy

Chimeric antigen receptor T-cell therapy (CAR T) is a rapidly expanding form of cell-based gene therapy initially developed to treat malignancies that is emerging as a novel option for treating autoimmune diseases. T-lymphocytes can be engineered to kill B cells. Common target antigens in SLE include CD19 and anti-B cell maturation antigen (BMCA) (6).

As discussed later in this paper, some B-cell depleting drugs have failed to show efficacy in treating SLE, which raises the question of if and how B-cell targeted CAR T would be effective. Two theories may explain the inefficacy of B-cell depleting drugs that would not hinder B-cell targeted CAR T. First, B cells can remain “hidden” from biologics in tissues such as the synovial membrane (7), tonsils (8), and lymph nodes (9). Second, plasma cells and pro B cells lack CD20, which protects them from depletion (10). CD19 or BCMA CAR T could penetrate these tissues and inhibit plasma cells and pro B cells.

In 2022, Mackensen et al. treated five patients with CD19 CAR T resulting in Definition of Remission in SLE (DORIS) remission in all patients within 3 months and a durable response of 5–18 months. The treatment regimen started with lymphodepleting chemotherapy with cyclophosphamide and fludarabine, followed by an infusion of 1 × 106 cells per kg autologous CD19 CAR T cells. The safety profile was acceptable; only one case of a mild cytokine-release syndrome occurred. Patients had disappearance of anti-dsDNA and anti-Smith autoantibodies (6).

In 2024, Muller et al. reported CD19 CAR-T treatment in eight patients with SLE. All eight patients met lupus low disease activity state (LLDAS) criteria and DORIS remission after six months with a durable response up to 29 months, when all SLEDAI-2K scores remained at 0. These patients similarly showed seroconversion of anti-dsDNA and anti-Smith autoantibodies (11).

Hu et al. recently completed an open-label, single-arm clinical trial of BCMA CAR T in seven patients with active lupus nephritis class III-V who failed treatment with glucocorticoids (GC) and at least two IS or biologics (12). Prior to leukapheresis, IS or biologics were discontinued, and GC was tapered below 10 mg, then completely discontinued within one month. The median SLEDAI improved from 18 at baseline to 0 at 6 months and remained at 0 for 4 years. Five patients achieved DORIS remission, and the two remaining patients met LLDAS criteria. One patient had grade 1 cytokine release syndrome (CRS), no severe infections were reported, and lymphodepletion resolved within 4 weeks in all patients (12).

Compound CAR (cCAR) T, which has two antigenic targets, BCMA and CD19, has also been investigated in a single-arm, open-label phase 1 trial of 13 participants (13). Nine participants met DORIS remission and twelve met LLDAS criteria. Eleven had significant improvements in eGFR and microproteinuria. Repeat renal biopsy of one patient in drug-free remission revealed clearance of glomerular IgG immunocomplexes. BCMA-CD19 cCAR was well-tolerated in all patients. One had grade 1 CRS. In all cases, neutropenia resolved within 6 weeks, and B cells recovered within 7 months (13).

3.3 B cell depleting therapies (BCDT)

3.3.1 Anti-CD19/ FcγRIIb

Obexelimab is a bifunctional monoclonal antibody that targets CD19 to enhance binding to the inhibitory Fc receptor, FcγRIIb (CD32b). Binding FcγRIIb downregulates B cell receptor (BCR) signaling, thus decreasing B cell response. A 2023 phase 2 trial (14) investigating obexelimab failed to meet its primary endpoint of 32 weeks follow up without relapse. Secondary analysis found a significant increase in the time it took for patients’ conditions to worsen in the obexelimab group vs. PLACEBO (230 vs. 131 days). During this trial, obexelimab had similar number infections as placebo, and seven patients were intolerant due to infusion reactions.

3.3.2 Anti-CD20

Prior literature on type I anti-CD20 agents, rituximab and ocrelizumab, have failed to show efficacy in treating SLE in the EXPLORER and LUNAR trials for rituximab (15, 16), and the BELONG trial for ocrelizumab were discontinued early due to safety concerns (17). In interim analysis, ocrelizumab outperformed cyclophosphamide, but not mycophenolate mofetil (17).

More recently, obinutuzumab, a humanized glycoengineered type II anti-CD20 drug, has shown promise in the NOBILITY and REGENCY studies (18, 19). Compared to the type I anti-CD20 drugs, obinutuzumab was designed for greater FcyRIIB affinity, which permits greater antibody-dependent cytotoxicity and less reliance on complement-mediated cytotoxicity. Additionally, it has less redistribution to membrane-bound lipid rafts, resulting in less internalization. The phase II NOBILITY trial failed to meet its primary endpoint of CRR at week 52. However, key secondary endpoints including CRR at week 104 and partial renal remission rates (PRR) did show significant improvements over placebo. No unexpected safety signals were identified (18). Later in the phase 3 REGENCY trial, obinutuzumab did meet its primary endpoint, showing higher rates of CRR at week 76 than placebo (45 vs. 33%). Key secondary endpoints including treatment failure and the need for rescue therapy also significantly favored obinutuzumab. There were no unexpected safety results, and fewer deaths or renal events occurred in the treatment group (19).

3.3.3 Anti-CD22

Epratuzumab, a B-lymphocyte-restricted adhesion molecule, failed to outperform placebo in clinical outcomes in the EMBODY 1 and 2 trials (20) despite depleting B-cell specific activity. post-hoc analysis of these trials selecting a subpopulation of patients with comorbid Sjogren's syndrome found a significantly better BICLA response in the epratuzumab group vs. placebo (73% vs. 40%) (21). While the mechanism of this response is unclear, participants with comorbid Sjogren's syndrome had a greater and earlier B-cell depletion than the SLE-only participants. Similarly, the ALLEVIATE trials also failed to find a significant clinical benefit of epratuzumab (22).

3.3.4 BDCA2

Litifilimab blocks blood dendritic cell antigen 2 (BDCA2), which is expressed on plasmacytoid dendritic cells. The LILAC trials explored the safety and efficacy of litifilimab in cutaneous lupus erythematosus (CLE) and SLE (23, 24). In CLE, litifilimab produced significantly better CLASI responses than placebo and had a tolerable safety profile (23). Similarly, in SLE, litifilimab produced greater improvements in swollen and tender joint counts, CLASI scores, SRI-4 response, and SLEDAI score than placebo, also with a tolerable safety profile (24).

3.3.5 B cell survival cytokines

B cell activating factor [BAFF; also known as B lymphocyte stimulator (BlyS)] and A Proliferation Inducing Ligand (APRIL) are promising targets for the treatment of SLE. Overexpression of BAFF promotes survival and maturation of immature B cells, thereby expanding overall B cell populations with dampened negative selection against autoreactivity within the germinal center, ultimately increasing autoantibody production (25, 26). APRIL modulates plasma cell survival and induces class switching.

3.3.5.1 Belimumab

In 2011, belimumab became the first FDA approved anti-BAFF agent for the treatment of active SLE and active LN based on the phase 3 trials, BLISS-52 and BLISS-76. Several long-term extension studies have assessed its long-term safety with follow up periods of 6–8 years (27–31). Across these studies, no new or unexpected safety signals emerged. The most common adverse events were infections, headaches and gastrointestinal symptoms. Discontinuation rates due to adverse events were as low as 9% (28). Efficacy had a durable response with flare rates as low as 15% over 7 years (29).

3.3.5.2 Blisbimod

The 24-week phase IIb PEARL-SC trial compared three doses of blisbimod, a BAFF inhibitor to placebo. This study failed to meet its primary endpoint of SRI-5 response at 24 weeks in the pooled blisbimod groups. However, patients in the 200 mg once weekly group did achieve significantly higher SRI-5 response rates at week 20 than placebo. Additionally, there were significant improvements in SLE biomarkers, including complement and anti-dsDNA antibodies. There was no significant difference in safety events with blisibimod vs. placebo, but injection site reactions were reported more frequently (32).

Subsequently, the phase III CHABLIS-SC1 trial further evaluated blisibimod in severe SLE and failed to meet its primary endpoint of significantly improved SRI-6 response at week 52 (33). However, blisibimod did achieve several secondary endpoints such as significantly reduced CS doses, improved SLE biomarkers, and proteinuria.

3.3.5.3 Tabalumab

The phase III ILLUMINATE trials studied tabalumab, an anti-BAFF IgG4 monoclonal antibody, at different doses (34, 35). Dosed monthly, tabalumab failed to show efficacy over placebo (Isenberg 2015). Dosed biweekly, tabalumab resulted in better SRI-5 response at week 52 (38% vs. 28%) than placebo, with a signal for improvement as early as week 26. When assessing secondary outcomes, no differences were observed in time to flare or CS sparing effects. There were no differences in adverse events between groups.

3.3.5.4 Inanlumab

Ianalumab has been studied in a phase II trial showing efficacy and safety as an add-on to standard of care treatment for SLE (36). The study met its primary endpoint, with a significantly higher proportion of patients treated with ianalumab achieving a SRI-4 response and a sustained reduction in CS use compared to standard therapy at 28 weeks. Clinical benefits were observed through week 52 during the open-label extension period. Ianalumab was not associated with increased serious adverse events or infections.

3.3.6 Transmembrane activator and calcium modulator fusion proteins

Atacicept first demonstrated efficacy in the treatment of SLE in the APRIL-SLE trial, which compared atacicept 75 mg and 150 mg against placebo with a primary endpoint of flare rate (37). There was no difference between the 75 mg group and placebo, but the 150 mg group suggested benefit in post hoc analysis. The 150 mg arm was discontinued prematurely due to two deaths. There was overall similarity between three arms of the study regarding adverse events. A follow up post hoc study of this trial found better response rates in the subgroup of participants with elevated baseline BAFF levels, regardless of APRIL levels (38).

The ADDRESS II trial evaluated atacicept 75 mg and 150 mg against placebo with a primary endpoint SRI-4 response at week 24 (39). Despite failing to meet the primary endpoint, there was signal of efficacy in high disease activity and serologically active subgroups on secondary analysis. Subsequently, a long-term extension study found that atacicept 150 mg had durable efficacy and a similar safety profile compared to the original trial at 84 weeks. Two deaths were noted in the atacicept group and were considered unrelated to treatment (40).

A recent phase III trial of telitacicept in China met its primary endpoint at week 52 with greater modified SRI-4 response of 67% for telitacicept vs. 33% for placebo a significant difference detected as early as week 4 (41). Telitacicept displayed similar nonserious infectious risk, injection site reactions, and hypogammaglobulinemia rates as other B cell depletion agents. There was no difference between telitacicept and placebo in serious infections. In 2021, after early trial data demonstrated improvement (42), telitacicept was approved for the treatment of SLE in China.

3.3.7 BTK, JAK, and TYK2 inhibitors

3.3.7.1 Bruton's tyrosine kinase inhibitors

The SLEeK study investigated the safety and efficacy of elsubrutinib, a BTK inhibitor, and ustekinumab, a selective JAK1 inhibitor (43). This trial was discontinued early when interim analysis showed a lack of efficacy. There were no unexpected safety concerns. Analysis revealed that the high-dose upadacitinib and elsubrutinib group had a better SRI-4 response and GC reduction at week 24 than placebo (55 vs. 37%). The trend held at 48 weeks. Given that the dose of elsubrutinib was the same across groups, it appears that the high dose of upadacitinib drove this result, which is supported by the SLEeK study's long-term extension, which found similar results for upadacitinib monotherapy (44). Considering pathophysiology, a potential explanation is that, in plasmacytoid dendritic cells, BTK inhibition blocks IFN-α production via TLR-9, but not via TLR-7. TLR-7 stimulation enhances the production of IFN-α by disinhibiting the BDCA-2 pathway (45).

3.3.7.2 Janus kinase inhibitors

The SLE-BRAVE studies explored the safety and efficacy of baricitinib, a selective JAK1 and JAK2 inhibitor, and found conflicting results (46, 47). In SLE-BRAVE 1, baricitinib 4 mg outperformed placebo as measured by SRI-4 at week 52; secondary endpoints failed to reach significance (48). In SLE-BRAVE 2, no dose of baricitinib had significantly better results than placebo (47). A follow-up post-hoc analysis combining data from both trials also found that baricitinib failed to outperform placebo, however they did report an unusually high placebo SRI-4 response rate of 46% (49).

3.3.7.3 Tyrosine kinase inhibitors

In comparison to JAK inhibitors, the TYK2 inhibitor, deucravacitinib, binds the inactive regulatory domains of its target kinases, theoretically permitting a more durable response. In the phase II PAISLEY study, low-, medium-, and high-doses of deucravacitinib showed better SRI-4 responses than placebo (58%, 50%, 45%, and 34%, respectively) at 32 weeks (46). Similarly, better responses in BICLA, CLASI, LLDAS, and swollen and tender joint counts were noted. The safety profile was comparable to prior literature on TYK2 and JAK inhibitors. Phase 3 trials are ongoing.

3.3.8 Interferon inhibitors

Anifrolumab, a first in class global type I interferon inhibitor, received FDA approval for SLE without nephritis in 2021 based on results of the MUSE, TULIP-1, and TULIP-2 trials (50–52). Individually, the MUSE and TULIP-2 trials showed better response rates with anifrolumab than with placebo (50, 52), whereas the TULIP-1 trial failed to meet its primary endpoint of SRI-4 response (51). Subsequent post hoc studies pooling data from these trials found better response with anifrolumab than placebo, specifically noting 32% greater GC dose-reduction (53), multiple patient-reported outcomes (53), BICLA response (54), and SRI-7 and SRI-8 responses (54).

Following these positive results, a three-year open-label extension study of the TULIP trial found greater SLEDAI improvement, GC dose-reduction, and 50% lower annualized flare rate than placebo (55). Exposure-adjusted adverse event incident rates were marginally lower with anifrolumab, and there were no significant differences in rates of nonopportunistic infections.

These initial trials excluded patients with LN. The TULIP-LN trial and its two-year extension study explored this gap (56, 57). Neither trial found significant differences in the treatment group vs. placebo. Despite these null findings, research is ongoing with the IRIS phase III trial expected to complete in September 2026 (NCT05138133).

3.3.9 Other agents

Pharmaceutical research in the management of SLE remains robust. For example, B- and T-lymphocyte attenuator (BTLA; CD272) (58) and CD38 (59) have been proposed as novel immunologic targets. Considering previously identified immunologic targets, prior studies with ustekinumab, inhibiting IL-12 and IL-23 (60), with secukinumab, targeting IL-17 (61), and with dapirolizumab, targeting CD40 (62), failed to show efficacy over placebo. The multicenter phase II LUPIL-2 trial with IL-2 therapy failed to meet its primary endpoint on initial analysis (63). However, when excluding two sites with a 100% placebo response rate, the researchers found better SLEDAI response, SRI-7 and SRI-8 scores, greater GC dose-reduction, and higher percentage in clinical remission in the intervention group at 12 weeks with an overall estimated response rate of 30%.

Other agents that show early promise include sphingosine-1-phosphate receptor (S1P1) modulators and cereblon ligands. Cenerimod, a selective S1P1 receptor modulator, has shown 1.43-fold greater likelihood to respond than placebo (64) and phase III trials are ongoing (65, 66). The proposed mechanism entails “trapping” lymphocytes in lymphoid organs, preventing them from causing end-organ damage.

Iberdomide, a cereblon ligand, binds hematopoietic transcription factors Ikaros (IKZF1) and Aiodolos (IKZF3) for proteosomal degradation. Inhibiting IKZF1 and IKZF3 inhibits BAFF- and CD40L-induced cell proliferation. One phase II study exploring safety as its primary endpoint found a tolerable safety profile (67). Efficacy measures, such as SRI-4 response, PGA score, and CLASI score, numerically favored iberdomide but did not reach statistical significance; however, this trial was not powered to fully assess these secondary outcomes. Another phase II trial that was powered to assess efficacy as its primary endpoint found that high-dose iberdomide significantly outperformed placebo as measured by SRI-4, SLEDAI, and CLASI responses (68).

4 Discussion

This narrative review explored emerging literature on a variety of novel therapeutic agents for SLE as well as long-term data on recently approved medications. Long-term data on anifrolumab, belimumab, and voclosporin suggest that their efficacy holds with time without new safety concerns. Regarding newer agents, novel B-cell therapies show promise, specifically the type II anti-CD20 obinutuzumab and the TACI fusion protein telitacicept demonstrated safety and efficacy in phase III trials. Litifilimab, ianalumab, deucravacitinib, and iberdomide are showing promise in early phase II trials. Finally, data on CD19 and BCMA CAR T is mostly limited to case series and phase I trials, but early data shows significant improvements with sustained remission in refractory cases.

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Footnotes

Edited by: Charalampos Skarlis, University of Nicosia, Cyprus

Reviewed by: Xianrui Wu, Central South University, China

Statements

Conflict of interest

The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Funding

The author(s) declared that financial support was not received for this work and/or its publication.

Author contributions

ML: Conceptualization, Methodology, Supervision, Writing – original draft, Writing – review & editing. BC: Writing – original draft, Writing – review & editing. EN: Writing – original draft, Writing – review & editing.

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Citation

Loncharich, M. F., et al. (2026). Safety and efficacy of novel therapeutics in lupus: a narrative review. Frontiers in Lupus, Volume 4. https://doi.org/
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4 - 2026

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© 2026 Loncharich, Cafeo and Noble.

License: https://creativecommons.org/licenses/by/4.0/

*Correspondence: Michael F. Loncharich

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