Delving into the Latest Updates on Abatacept with Synapse

Overview

Basic Info

Drug Type

Fc fusion protein

Synonyms

Abatacept (Genetical Recombination), CTLA4-Ig(Bristol-Myers Squibb), CTLA4Ig

+ [14]

Target

CD80 x CD86

Action

modulators

Mechanism

CD80 modulators(Cluster of differentiation 80 modulators), CD86 modulators(Cluster of differentiation 86 modulators)

Therapeutic Areas

Immune System DiseasesInfectious DiseasesSkin and Musculoskeletal Diseases+ [8]

Active Indication

Acute Graft Versus Host DiseaseJuvenile Idiopathic ArthritisArthritis, Psoriatic+ [11]

Inactive Indication

acute leukemiaAcute Lymphoblastic LeukemiaAcute Myeloid Leukemia+ [51]

Originator Organization

Bristol Myers Squibb Co.

Active Organization

Bristol-Myers Squibb Pharma EEIG

Bristol Myers Squibb Co.

Baker Heart & Diabetes Institute

+ [3]

Inactive Organization

Jiangsu Simcere Pharmaceutical Co., Ltd.

License Organization

Repligen Corp.

Ono Pharmaceutical Co., Ltd.

Simcere Pharmaceutical Co., Ltd.

+ [2]

Drug Highest PhaseApproved

First Approval Date

United States (23 Dec 2005),

Rheumatoid Arthritis

RegulationOrphan Drug (United States)

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Structure/Sequence

Sequence Code 19593

Source: *****

The purpose of this study it to evaluate a reduced toxicity conditioning regimen for haploidentical donor HCT followed by a GVHD prophylaxis regimen comprising of post-transplant cyclophosphamide, sirolimus and abatacept with the goal to improve the GVHD-free rejection-free survival (GRFS) to greater than 90% after haploidentical donor HCT in children and young adults with SCD.
Primary Objective:
- To assess the GVHD-free and rejection free survival (GRFS) after haploidentical donor HCT in children and young adults with SCD.
Secondary Objectives:
* Assess the overall survival (OS) and disease-free survival (DFS) after haploidentical donor HCT for SCD.
* Estimate incidence and severity of acute and chronic GVHD after haploidentical donor HCT for SCD.
* Assess the neutrophil and platelet engraftment kinetics after haploidentical donor HCT for SCD.

Start Date01 Sep 2026

Sponsor / Collaborator

St. Jude Children's Research Hospital, Inc.

NCT07599176

/ RecruitingPhase 1/2IIT

Matched Related Donor Non-myeloablative Hematopoietic Cell Transplantation With Alemtuzumab, 400 cGy TBI, and Abatacept for Sickle Cell Disease and Beta-Thalassemia

This is a non-ablative (partial) stem cell transplant for patients with severe sickle cell disease or beta-thalassemia requiring red cell transfusions. The intensity of the transplant is slightly increased from our previous transplant regimens. The goal is to aim for higher percentage of donor cells to stably remain in the recipients long term.

Start Date08 Jul 2026

Sponsor / Collaborator

National Heart, Lung & Blood Institute

100 Clinical Results associated with Abatacept

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100 Translational Medicine associated with Abatacept

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100 Patents (Medical) associated with Abatacept

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2,961

Literatures (Medical) associated with Abatacept

07 Sep 2026·Journal of Human Immunity

A homozygous CTLA-4 variant causes CTLA-4 deficiency with severe immune dysregulation

Article

Author: Bayram Catak, Feyza ; Bozkurtlar, Emine ; Koc, Ahmet ; Hubrack, Satanay ; Elmi, Asha ; Catak, Mehmet Cihangir ; Can, Salim ; Yilmaz, Baris ; Lo, Bernice ; Yorgun Altunbas, Melek ; Babayeva, Royala ; Baris, Safa ; Ertem, Deniz ; Erman, Batu ; Ozen, Ahmet ; Bilgic Eltan, Sevgi ; Amirov, Razin ; Karakoc-Aydiner, Elif

CTLA-4 is a critical immune checkpoint that maintains self-tolerance by regulating immune activation. Here, we describe the first case of homozygous CTLA-4 deficiency (CTLA4S172P/S172P), presenting with early-onset autoimmunity, lymphoproliferation, and growth failure. Immunological profiling revealed profound T- and B-cell dysregulation, characterized by T-cell hyperproliferation, a TH1-skewed helper T-cell phenotype, and expansion of activated and atypical B-cell subsets. The identified variant led to impaired CTLA-4 protein stability and enhanced lysosomal degradation, resulting in significantly reduced but still detectable total and surface expression and defective CD80 transendocytosis. Abatacept (CTLA-4-Ig) therapy effectively restored immune regulation and controlled disease activity. These findings expand the clinical and mechanistic spectrum of CTLA-4–related disorders, linking residual CTLA-4 function with the severity of immune dysregulation and emphasizing the therapeutic potential of targeted CTLA-4 modulation.

01 Sep 2026·AUTOIMMUNITY REVIEWS

Unraveling giant cell arteritis: From immunopathology to emerging targeted therapies (2026 update)

Review

Author: Parreau, Simon ; Ly, Kim ; Gallet, Francois ; Cayrou, Cory ; Bouanat, Sacha ; Fauchais, Anne-Laure

Giant cell arteritis (GCA) is the most common systemic vasculitis in the elderly mainly because of cellular senescence and "inflammaging" It results from granulomatous inflammation primarily affecting the aorta and its major branches. Recent advances highlight vascular dendritic cell (DC) activation via TLRs as the initiating event, leading to chemokine-mediated recruitment and polarization of CD4+ T cells mainly into Th1/Th17 subsets. These effector T cells drive monocyte differentiation into pro-inflammatory macrophages and giant cell formation, with subsequent matrix metalloproteinase production causing elastic lamina destruction and vascular remodeling. This vascular remodeling involves activation of endothelial cells, fibroblasts and smooth muscle cells followed by a differentiation in myofibroblast in the intima. Neutrophils may play an underestimated role. Current treatments remain limited to glucocorticoids, methotrexate and tocilizumab though relapse rates remain high. This narrative review synthesizes the DC-T-macrophage-fibroblast cascade and evaluates emerging biologics: abatacept showed phase 2 efficacy but real-world inferiority to tocilizumab; ustekinumab yielded conflicting results across small series; secukinumab failed phase 3 despite promising phase 2 data; anakinra lacked benefit in a truncated trial. In contrast, Mavrilimumab, an anti-GM-CSF-R, is showing promising results. JAK inhibitors such as upadacitinib (a JAK1 inhibitor; SELECT-GCA phase 3) are also promising, having demonstrated superior sustained remission compared with placebo, leading to regulatory approvals in 2025. These findings underscore opportunities to target upstream DC activation, macrophage polarization, and vascular remodeling pathways, potentially transforming GCA management beyond IL-6 inhibition.

01 Aug 2026·JOURNAL OF THE AMERICAN DENTAL ASSOCIATION

Effectiveness of biological drugs in the treatment of xerostomia and salivary hypofunction in patients with Sjögren disease

Review

Author: Seoane-Romero, Javier ; Varela-Centelles, Pablo ; Castelo-Baz, Pablo ; Bello-Castro, Alba ; Gancedo-Gancedo, Tania ; García-Pola, María José ; Seoane-Romero, Juan Manuel

BACKGROUND:

Sjögren disease (SjD) can involve systemic complications. Advances in understanding its pathophysiology and the development of novel biological agents could herald new possibilities for managing salivary dysfunction in SjD. This investigation was conducted to assess the effectiveness of biological agents in the treatment of xerostomia and hyposalivation in patients with SjD.

TYPES OF STUDIES REVIEWED:

A systematic review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses methodology. The inclusion criteria were randomized clinical trials (RCTs) involving adult patients who received a diagnosis of SjD, with information on unstimulated whole salivary flow or stimulated whole salivary flow or xerostomia measured using a visual analog scale. The quality of evidence and risk of bias were assessed using the Grading of Recommendations Assessment, Development and Evaluation and Cochrane Collaboration tools, respectively.

RESULTS:

Fourteen RCTs were identified, including 4 focused on rituximab (RTX), 1 focused on infliximab, 1 focused on baminercept, 2 focused on abatacept, 1 focused on tocilizumab, 1 focused on remibrutinib, 1 focused on iscalimab, 1 focused on seletalisib, 1 focused on petesicatib, and 1 focused on human interferon (IFN)-α. Twelve were double-blind studies, 1 was double-blind during the first period of the study and open-label during the second period, and 1 was a triple-blind study. Most of the studies were classified as multicenter. The included studies comprised a total of 1,772 patients, with 1,012 in the intervention groups and 760 in placebo groups. RTX, iscalimab, and IFN-α had significant differences reported in 4 RCTs, with an increase in unstimulated whole salivary flow and a significant improvement in dry mouth sensation reported in 1 RCT. No relevant adverse effects were observed.

CONCLUSIONS AND PRACTICAL IMPLICATIONS:

RTX, iscalimab, and IFN-α have potential benefits in management of salivary gland dysfunction in SjD. Adequate methodological trials are needed to clarify the role of these agents in SjD. The research protocol was planned and registered with PROSPERO, an international systematic review registry (CRD42024596176), and it was not modified throughout the study.

92

News (Medical) associated with Abatacept

18 Jun 2026

·www.businesswire.com

Coya Therapeutics to Present ALSTARS Trial Design at the ENCALS 2026 Meeting

HOUSTON--(BUSINESS WIRE)--Coya Therapeutics, Inc. (NASDAQ: COYA) (“Coya” or the “Company”), a clinical-stage biotechnology company developing biologics intended to enhance T-cell (Treg) function in patients with neurodegenerative disorders, announces that the Company will present an overview of the ongoing ALSTARS trial, outlining its design and approach to targeting neuroinflammation, at the European Network to Cure ALS (ENCALS) Meeting 2026 which will take place June 24–26, 2026, in Madrid, Spain. The details for the poster presentation, which will be presented by Tyrell Simkins, D.O., Ph.D., Senior Director, Clinical Development, are below: Poster Title: ALSTARS: A Precision Immunomodulatory Phase 2 Trial Of Coya 302 Targeting Regulatory T Cells And Neuroinflammation In ALS Authors: Tyrell J. Simkins, DO, PhD; Fred Grossman, DO; Stanley Appel, MD; Karen King, MS; and James D. Berry, MD Date of Presentation: Wednesday, June 24, 2026, 11:20 am – 1:00 pm ET (5:20 pm – 7:00 pm Madrid) Session: ENCALS Research Forum – Posters Session About Coya Therapeutics, Inc. Headquartered in Houston, TX, Coya Therapeutics, Inc. (Nasdaq: COYA) is a clinical-stage biotechnology company developing proprietary treatments focused on the biology and potential therapeutic advantages of regulatory T cells (“Tregs”) to target systemic inflammation and neuroinflammation. Dysfunctional Tregs underlie numerous conditions, including neurodegenerative, metabolic, and autoimmune diseases. This cellular dysfunction may lead to sustained inflammation and oxidative stress resulting in lack of homeostasis of the immune system. Coya’s investigational product candidate pipeline leverages multiple therapeutic modalities aimed at restoring the anti-inflammatory and immunomodulatory functions of Tregs. Coya’s therapeutic platforms include Treg-enhancing biologics, Treg-derived exosomes, and autologous Treg cell therapy. For more information about Coya, please visit www.coyatherapeutics.com. About COYA 302 COYA 302 is an investigational and proprietary biologic combination therapy with a dual immunomodulatory mechanism of action intended to enhance the anti-inflammatory function of regulatory T cells (Tregs) and suppress the inflammation produced by activated monocytes and macrophages. COYA 302 comprises proprietary low dose interleukin-2 (LD IL-2) and CTLA-4 Ig and is being developed for subcutaneous administration for the treatment of patients with ALS and other neurodegenerative diseases. These mechanisms may have additive or synergistic effects. Coya is currently conducting the ALSTARS Trial, a Phase 2, randomized, multi-center, double-blind, placebo-controlled study to evaluate the efficacy and safety of COYA 302 for the treatment of ALS (ClinicalTrials.gov Identifier: NCT07161999). COYA 302 is an investigational product not yet approved by the FDA or any other regulatory agency. Forward-Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Statements in this press release that are not statements of historical fact are forward-looking statements. Such forward-looking statements include, without limitation, statements regarding: expectations of Coya Therapeutics, Inc. (the “Company”) regarding the potential benefits, effectiveness and safety of its product candidates; the significance and potential benefits associated with the FDA’s Fast Track designation for COYA 302; the Company’s ability to advance its product candidates through the preclinical and clinical development processes; the Company’s expectations regarding, quality, timing and availability of data from the Company’s clinical trials; the timing of announcements, updates and results of the Company’s clinical trials and related data; the Company’s future results of operations and financial position, including cash runway; and the potential therapeutic benefits and economic value of the Company’s product candidates. These forward-looking statements are based on the beliefs of the management of the Company as well as assumptions made by and information currently available to the Company. Such statements reflect the current views of the Company with respect to future events and are subject to known and unknown risks and uncertainties. In light of these risks and uncertainties, the events or circumstances referred to in the forward-looking statements may not occur. These and other factors that may cause the Company’s actual results to differ from current expectations are discussed in the Company’s filings with the Securities and Exchange Commission (the “SEC”), including the section titled “Risk Factors” in the Company’s Annual Report on Form 10-K for the year ended December 31, 2025. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date this press release is given. Except as required by law, the Company undertakes no obligation to publicly update any forward-looking statements, whether as a result of new information, future events or otherwise.

Phase 2Fast TrackCell TherapyImmunotherapy

08 Jun 2026

·www.businesswire.com

Coya Therapeutics Announces the First Cohort of Patients in the ALSTARS Trial Have Begun the Blinded Active-Treatment Extension Phase

HOUSTON--(BUSINESS WIRE)--Coya Therapeutics, Inc. (NASDAQ: COYA) (“Coya” or the “Company”), a clinical-stage biotechnology company developing biologics intended to enhance Treg function, announces the initiation of the blinded extension phase of the ALSTARS Trial (ClinicalTrials.gov Identifier: NCT07161999). Patients who complete the 24-week placebo-controlled double-blind phase enter the blinded extension phase of the study and continue on their regimen from the first phase; placebo patients are re-randomized to receive one of the two pre-specified dosing regimens of COYA 302 for a total of 24-weeks to provide a total of up to 48 weeks of data on COYA 302. To learn more about the study, please visit ALSTARS Trial. Fred Grossman, DO, FAPA, President and Chief Medical Officer of Coya said, “We are very pleased with the progress of this important clinical study of COYA 302 in people with ALS that we hope may ultimately lead to a transformational new treatment. We would like to thank the patients, families, and caregivers for their ongoing support and contribution to the ALSTARS Trial.” About Coya Therapeutics, Inc. Headquartered in Houston, TX, Coya Therapeutics, Inc. (Nasdaq: COYA) is a clinical-stage biotechnology company developing proprietary treatments focused on the biology and potential therapeutic advantages of regulatory T cells (“Tregs”) to target systemic inflammation and neuroinflammation. Dysfunctional Tregs underlie numerous conditions, including neurodegenerative, metabolic, and autoimmune diseases. This cellular dysfunction may lead to sustained inflammation and oxidative stress resulting in lack of homeostasis of the immune system. Coya’s investigational product candidate pipeline leverages multiple therapeutic modalities aimed at restoring the anti-inflammatory and immunomodulatory functions of Tregs. Coya’s therapeutic platforms include Treg-enhancing biologics, Treg-derived exosomes, and autologous Treg cell therapy. For more information about Coya, please visit www.coyatherapeutics.com. About COYA 302 COYA 302 is an investigational and proprietary biologic combination therapy with a dual immunomodulatory mechanism of action intended to enhance the anti-inflammatory function of regulatory T cells (Tregs) and suppress the inflammation produced by activated monocytes and macrophages. COYA 302 comprises proprietary low dose interleukin-2 (LD IL-2) and CTLA-4 Ig and is being developed for subcutaneous administration for the treatment of patients with ALS and other neurodegenerative diseases. These mechanisms may have additive or synergistic effects. Coya is currently conducting the ALSTARS Trial, a Phase 2, randomized, multi-center, double-blind, placebo-controlled study to evaluate the efficacy and safety of COYA 302 for the treatment of ALS (ClinicalTrials.gov Identifier: NCT07161999). COYA 302 is an investigational product not yet approved by the FDA or any other regulatory agency. Forward-Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Statements in this press release that are not statements of historical fact are forward-looking statements. Such forward-looking statements include, without limitation, statements regarding: statements regarding the design, conduct, timing, progress and potential results of the ALSTARS Trial and its blinded extension phase; expectations regarding enrollment, treatment, dosing, data collection and the availability, timing, quality or interpretation of clinical trial data; the potential benefits, effectiveness, safety and regulatory pathway of COYA 302; and the potential therapeutic benefits and economic value of the Company’s product candidates.. These forward-looking statements are based on the beliefs of the management of the Company as well as assumptions made by and information currently available to the Company. Such statements reflect the current views of the Company with respect to future events and are subject to known and unknown risks and uncertainties. In light of these risks and uncertainties, the events or circumstances referred to in the forward-looking statements may not occur. These and other factors that may cause the Company’s actual results to differ from current expectations are discussed in the Company’s filings with the Securities and Exchange Commission (the “SEC”), including the section titled “Risk Factors” in the Company’s Annual Report on Form 10-K for the year ended December 31, 2025. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date this press release is given. Except as required by law, the Company undertakes no obligation to publicly update any forward-looking statements, whether as a result of new information, future events or otherwise.

Phase 2Cell TherapyImmunotherapy

01 Jun 2026

·www.sciencedaily.com

This drug delayed rheumatoid arthritis for years after treatment ended

A promising new study suggests rheumatoid arthritis may not be as inevitable as once thought for people at high risk. Researchers found that just one year of treatment with the immune-targeting drug abatacept delayed the onset of rheumatoid arthritis by up to four years, with benefits lasting long after treatment ended.People at high risk of developing rheumatoid arthritis (RA) may be able to postpone the disease for years with early treatment, according to new research from King's College London. The study found that a one year course of the biologic drug abatacept significantly delayed the onset of rheumatoid arthritis, with benefits continuing long after treatment ended. Published in The Lancet Rheumatology, the research extends findings from an earlier clinical trial reported by King's researchers in 2024. The original study followed 213 participants from the UK and the Netherlands for two years. The latest analysis tracked participants for between four and eight years, making it one of the longest follow up studies ever conducted in people at risk of rheumatoid arthritis. Early Treatment Delays Rheumatoid Arthritis Rheumatoid arthritis is a long term autoimmune disease that affects roughly half a million people in the UK. The condition occurs when the immune system mistakenly attacks the joints, leading to pain, swelling, fatigue, and, over time, permanent joint damage and disability. People who are at risk of developing rheumatoid arthritis often experience challenges even before receiving a diagnosis. Many leave the workforce before the disease fully develops, creating financial and employment difficulties. Although several treatments are available for people who already have rheumatoid arthritis, no approved therapy currently exists to prevent the disease in people who are known to be at high risk. The researchers found that participants who received abatacept for 12 months developed rheumatoid arthritis much later than those who received a placebo. In some cases, the disease was delayed by as much as four years beyond the treatment period. The drug did not completely stop rheumatoid arthritis from developing. However, the results suggest that intervening before the disease appears can meaningfully alter its course, potentially reducing the number of years people spend living with symptoms and related complications. Professor Andrew Cope, Professor of Rheumatology in the Centre for Rheumatic Diseases at King's College London and lead author of the study, said: "Intervening early in people at high risk of RA can have lasting benefits. We have shown that this approach is safe and can prevent disease while patients are on treatment as well as substantially relieve symptoms. Importantly, it can also delay the onset of RA for several years, even after treatment has stopped. This could reduce how long people live with symptoms and complications, drastically improving their quality of life." Greatest Benefit Seen in Highest Risk Patients The study found that abatacept worked best in people with the highest likelihood of developing rheumatoid arthritis. These individuals were identified through blood tests that detected specific autoantibodies associated with the disease. While this group faced the greatest risk of progressing to rheumatoid arthritis, they also experienced the largest benefits from early treatment. During the period before rheumatoid arthritis developed, participants treated with abatacept reported improvements in symptoms such as joint pain and fatigue, along with better overall well-being. However, after treatment ended, symptom levels eventually became similar between the abatacept and placebo groups. According to the researchers, this suggests that ongoing immune system modulation may be needed to maintain symptom relief. Long Lasting Effects With No New Safety Concerns Researchers also reported that abatacept appeared to be safe. Serious adverse events occurred at similar rates in both the treatment and placebo groups, and no new safety issues linked to the drug were identified. The team believes the findings strengthen the case for treating autoimmune diseases before they fully emerge. They say the results provide important evidence that targeted immune therapies can delay rheumatoid arthritis in people at highest risk and support further research into preventive strategies for autoimmune conditions.

Clinical ResultImmunotherapy

100 Deals associated with Abatacept

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External Link

KEGG	Wiki	ATC	Drug Bank
D03203	Abatacept	L04AA24	DB01281

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Acute Graft Versus Host Disease	United States	Bristol Myers Squibb Co.	15 Dec 2021
Juvenile Idiopathic Arthritis	United States	Bristol Myers Squibb Co.	25 Aug 2009
Arthritis, Psoriatic	European Union	Bristol-Myers Squibb Pharma EEIG	21 May 2007
Arthritis, Psoriatic	Iceland	Bristol-Myers Squibb Pharma EEIG	21 May 2007
Arthritis, Psoriatic	Liechtenstein	Bristol-Myers Squibb Pharma EEIG	21 May 2007
Arthritis, Psoriatic	Norway	Bristol-Myers Squibb Pharma EEIG	21 May 2007
Polyarticular Juvenile Idiopathic Arthritis	European Union	Bristol-Myers Squibb Pharma EEIG	21 May 2007
Polyarticular Juvenile Idiopathic Arthritis	Iceland	Bristol-Myers Squibb Pharma EEIG	21 May 2007
Polyarticular Juvenile Idiopathic Arthritis	Liechtenstein	Bristol-Myers Squibb Pharma EEIG	21 May 2007
Polyarticular Juvenile Idiopathic Arthritis	Norway	Bristol-Myers Squibb Pharma EEIG	21 May 2007
Rheumatoid Arthritis	United States	Bristol Myers Squibb Co.	23 Dec 2005

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Myocarditis	Phase 3	United States	Bristol Myers Squibb Co.	02 Jul 2022
Myocarditis	Phase 3	Canada	Bristol Myers Squibb Co.	02 Jul 2022
Polymyalgia Rheumatica	Phase 3	France	Bristol Myers Squibb Co.	13 Dec 2018
Giant Cell Arteritis	Phase 3	United States	Bristol Myers Squibb Co.	15 Jul 2017
Giant Cell Arteritis	Phase 3	Australia	Bristol Myers Squibb Co.	15 Jul 2017
Giant Cell Arteritis	Phase 3	Austria	Bristol Myers Squibb Co.	15 Jul 2017
Giant Cell Arteritis	Phase 3	Belgium	Bristol Myers Squibb Co.	15 Jul 2017
Giant Cell Arteritis	Phase 3	Bulgaria	Bristol Myers Squibb Co.	15 Jul 2017
Giant Cell Arteritis	Phase 3	Canada	Bristol Myers Squibb Co.	15 Jul 2017
Giant Cell Arteritis	Phase 3	Denmark	Bristol Myers Squibb Co.	15 Jul 2017

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT05822583 (STRIVE, CTgov)	Phase 4	COVID-19	285	abatacept infusion (Active Treatment Group)	vpgrrymaof = vpsneixpxw klbovpcmgw (maxpgnyten, nrcpbtxqvi - piyfwbueez) View more	-	31 Aug 2026
				Placebo group (Control Group)	vpgrrymaof = wimnuybdvq klbovpcmgw (maxpgnyten, wnldzmprqd - awsupqcyrw) View more
EULAR2026	Not Applicable	Rheumatoid Arthritis	72,000	Tocilizumab	evjosvhouq(ymincrvtcw) = qcncftensx vsmbbydoyx (besfekjbtj )	Positive	11 Jun 2026
				Rituximab	evjosvhouq(ymincrvtcw) = xeohcnolng vsmbbydoyx (besfekjbtj )
AMPLE (EULAR2026)	Phase 3	Rheumatoid Arthritis	103	Abatacept+Methotrexate (DAS28≥3.2 + Rheumatoid Arthritis + biologic naive + symptom duration <5 years)	whqjnotyfz(mktnzfxnze) = suyusbntql athffcisny (ywolzvsvue, 41.0 - 73.2)	Positive	11 Jun 2026
				Adalimumab+Methotrexate (DAS28≥3.2 + Rheumatoid Arthritis + biologic naive + symptom duration <5 years)	whqjnotyfz(mktnzfxnze) = nufpenuapm athffcisny (ywolzvsvue, 47.6 - 65.0)
CURACTA (EULAR2026)	Phase 1/2	ACPA-POSITIVE	3	Abatacept+Methotrexate+Daratumumab	kcxkobxggw(nsrmjxmosc) = Most AEs were mild or moderate. All patients experienced transient non-severe symptoms indicative of systemic infusion-related reactions (IRR; e.g. erythema, hyperhidrosis), and one patient experienced local IRR. One patient had transient grade 4 neutropenia with leukopenia, which resolved without intervention. Total IgG levels decreased in all patients, and one patient received immunoglobulin replacement therapy due to IgG levels below 4g/l (week 24). No severe infections occurred. batfmnlqiv (hqlowigmav ) View more	Positive	11 Jun 2026
EULAR2026	Not Applicable	Giant Cell Arteritis	47	Secukinumab	tibxuouqbw(furudjijyk) = pmqbmnxdbu omyqussaff (gfnzeyjtzz ) View more	Positive	11 Jun 2026
				Jak inhibitors	rcbkvtotrd(eewsxekkqj) = dcnepjlxro ykrvwyijnm (rjlthfkxuz ) View more
EULAR2026	Not Applicable	Rheumatoid arthritis with rheumatoid lung disease	1,162	JAK inhibitors	yuryinoduy(gtdpdciyek): HR = 1.59 (95.0% CI, 1.17 - 2.17) View more	Negative	11 Jun 2026
				Abatacept
EULAR2026	Not Applicable	Rheumatoid Arthritis	347	Tapering of b-/tsDMARDs	oqhlzfnbht(qwcoqaksje) = uxypwwjzkt mtbbthjlnb (iouqgyzobt )	Positive	11 Jun 2026
				Continuation of stable b-/tsDMARDs	oqhlzfnbht(qwcoqaksje) = aegrskfilt mtbbthjlnb (iouqgyzobt )
ASCO2026	Not Applicable	Graft vs Host Disease	16	PTCy+abatacept+tacrolimus	bymjmsbxbp(ojplkfboqp) = ijojloxjni gvjniwzfjx (snftoximzf, 0.3 - 31.4) View more	Positive	29 May 2026
ARVO2026	Not Applicable	-	5	Abatacept 500mg (Refractory Birdshot Chorioretinopathy)	vggymmhrao(gvwvjmopng) = One patient reported mild oral ulcers, and no patients reported abatacept-related systemic toxicity or serious side effects. achgburlcj (dqwyjlmmiy )	Positive	03 May 2026
NCT06145282 (CTgov)	Phase 1/2	Acute Chest Syndrome \| Anemia, Sickle Cell	6	Cyclophosphamide+Abatacept+Sirolimus+Briquilimab (PBSC Transplant With 50 mg/kg Post-transplant Cyclophosphamide (PT- Cy))	lrymlpltyv = tacvwakuxk ikmikmfgxb (nusygrkuzj, fgetbshdpu - tnabvgwglv) View more	-	29 Apr 2026
				Cyclophosphamide+Abatacept+Sirolimus+Briquilimab (PBSC Transplant With 100 mg/kg Post-transplant Cyclophosphamide (PT- Cy))	lrymlpltyv = mbvvsufngq ikmikmfgxb (nusygrkuzj, qqpakbmuge - ecdsftgczp) View more

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