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Last update 08 Jul 2026

Abatacept

Last update 08 Jul 2026

Overview

R&D Status

Clinical Result

Translational Medicine

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

Baker Heart & Diabetes Institute

Bristol Myers Squibb Co.Bristol-Myers Squibb Pharma EEIG

+ [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)

Structure/Sequence

Sequence Code 19593

Source: *****

242

Clinical Trials associated with Abatacept

NCT07616154

/ Not yet recruitingPhase 2IIT

Haploidentical Donor Hematopoietic Cell Transplant for Sickle Cell Disease

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 Date12 Jul 2026

Sponsor / Collaborator

National Heart, Lung & Blood Institute

NCT07388563

/ SuspendedPhase 1IIT

A Phase I Trial of Azacitidine and Abatacept in Relapsed or Refractory T-Cell Lymphoma

Background:
T-cell lymphoma is a blood cancer that affects immune system cells. People tend to survive less than 1 year if this disease does not respond to treatment (is refractory) or comes back after treatment (relapses). Azacitidine and abatacept are 2 drugs that are used to treat other diseases. Researchers want to know if these drugs, used together, can help people with T-cell lymphoma.
Objective:
To learn if azacitidine combined with abatacept can shrink tumors in people with T-cell lymphoma.
Eligibility:
People aged 18 years and older with T-cell lymphoma that either came back or did not respond to treatment.
Design:
Participants will be screened. They will have a physical exam with blood tests. They will have a test of their heart function. They will have imaging scans of their tumors. A sample of tumor tissue may be taken.
Azacitidine is injected under the skin of the thigh, abdomen, or upper arm. Abatacept is infused through a needle inserted into a vein in the arm.
Participants will receive the study drugs in 28-day cycles for up to 13 cycles. They will come to the clinic for each treatment. They will come to the clinic on day 1 and day 15 of the first cycle. After that, they will come to the clinic on the first 5 or 7 days of each cycle. Each clinic visit will take no more than 8 hours.
Imaging scans and other tests will be repeated during the study. Participants will have follow-up visits for up to 5 years after they stop taking the study drugs....

Start Date26 Mar 2026

Sponsor / Collaborator

National Cancer Institute

100 Clinical Results associated with Abatacept

100 Translational Medicine associated with Abatacept

100 Patents (Medical) associated with Abatacept

2,937

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 Jul 2026·DIGESTIVE AND LIVER DISEASE

Immunomodulatory therapies and emerging drug associations with microscopic colitis: A global pharmacovigilance analysis

Article

Author: Levartovsky, Asaf ; Mayer, Chen ; Ben-Horin, Shomron ; Goldman, Adam ; Engel, Tal ; Cohen, Yaron ; Münch, Andreas ; Fischman, Maya ; Ungar, Bella

BACKGROUND:

Microscopic colitis (MC) is presumably mediated by immune dysregulation, with drug exposure being a substantial risk factor. This study aims to identify contemporary MC-drug associations.

METHODS:

A pharmacovigilance study of the FDA adverse event reporting system (FAERS) between July 2014 and June 2024. Disproportionate reporting of MC was assessed using reporting odds ratios (RORs), adjusted for age, sex, and concomitant medications.

RESULTS:

Of 12,109,491 safety reports, 2648 cases of MC were identified and associated with 55 different medications. Several biologic immunosuppressants showed increased MC reporting, including tocilizumab (ROR = 4.93 [95% CI 3.85-6.31]), interleukin-17 inhibitors (ROR = 3.14 [2.47-3.98]), anti-CD20 agents (ROR = 3.03 [2.46-3.74]), and abatacept (ROR = 2.00 [1.44-2.78]). Synthetic immunosuppressants, particularly leflunomide (ROR = 9.89 [7.30-13.39]), methotrexate (ROR = 2.42 [1.63-3.58]), and mycophenolate (ROR = 2.31 [1.41-3.78]), were also implicated. Immune checkpoint inhibitors showed disproportionate MC reporting (ROR = 3.03 [2.49-3.69]), with the strongest associations for ipilimumab and the ipilimumab-nivolumab combination. Traditional MC-related agents (PPIs, SSRIs, NSAIDs) were corroborated. Additional non-immunomodulatory classes (SNRIs, ARBs, ACE inhibitors, statins, and dopaminergic therapies) also emerged. Concomitant exposure to multiple agents increased MC reporting.

CONCLUSIONS:

This comprehensive pharmacovigilance study mapped drug-MC associations, suggesting potential novel safety signals while corroborating previously reported agents. Immunomodulatory drugs emerged as substantial risk factors. These findings provide practical insights for clinicians managing patients with MC.

05 Jun 2026·CARDIOVASCULAR RESEARCH

Inhibition of the programmed death protein 1 immune checkpoint and the development of heart failure in the presence of prior cardiac ischaemia

Article

Author: Mórotz, Gábor M ; Ferdinandy, Péter ; Gong, Jingyi ; Pállinger, Éva ; Zlotoff, Daniel A ; Buzás, Edit I ; Gilman, Hannah K ; Merkely, Béla ; Gergely, Tamás G ; Meijers, Wouter C ; Neilan, Tomas G ; Sayour, Nabil V ; Kocsis, Márton S ; Fekete, Nóra ; Tóth, Viktória E ; Kovács, Tamás ; Yousif, Laura I ; Reynolds, Kerry L ; Onódi, Zsófia ; Kovács, Andrea ; Drobni, Zsófia D ; Varga, Zoltán V

Abstract:

Aims:

Immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment. However, their use often leads to cardiovascular adverse effects, including cardiac dysfunction. Here, we hypothesized that a prior cardiac ischaemic injury could exacerbate cardiac dysfunction due to anti-programmed death protein 1 (PD-1) treatment. Furthermore, we investigated whether abatacept, a T-cell costimulation blocker, could ameliorate the ICI-induced cardiotoxicity in a pre-clinical model.

Methods and results:

In a pre-clinical study, mice were treated with isoprenaline or control to induce reversible cardiac ischaemia. After 16 weeks of follow-up, recovery of cardiac function was confirmed via echocardiography, and mice from both groups were randomly treated with isotype control, anti-PD-1, or anti-PD-1 combined with abatacept, for 2 further weeks. Mice with prior ischaemic injury and anti-PD-1 treatment showed cardiac dysfunction with increased infiltration of T cells and macrophages and elevated expression of pro-inflammatory cytokines. Conversely, cardiac dysfunction and inflammation were less pronounced after anti-PD-1 treatment in mice without prior ischaemic injury. Mice with concomitant abatacept treatment exhibited normal cardiac function and alleviated pro-inflammatory response. In a parallel single-centre retrospective clinical cohort study, 1671 cancer patients receiving PD-1 inhibitors were analysed. Cases were defined as patients who developed incident heart failure (HF) after ICI initiation with a primary aim to test whether pre-existing ischaemic heart disease was associated with an increased risk for HF development post-ICI therapy. Sensitivity analyses included propensity score matching and comparison with non-ICI-treated cancer patients. Among ICI-treated patients, 109 (6.5%) developed HF over a median follow-up of 332 days. Multivariable logistic regression of the matched population showed increased odds of incident HF in patients with prior ischaemic cardiac events (odds ratio 2.11, 95% confidence interval 1.05–4.2, P = 0.033).

Conclusion:

In mice, induction of cardiac inflammation and dysfunction by anti-PD-1 therapy was potentiated by prior transient ischaemic cardiac injury, which was ameliorated by abatacept cotreatment. Cancer patients with pre-existing ischaemic heart disease may be at greater risk for developing ICI-induced new-onset HF. Based on our findings, cardiac surveillance should be considered in patients starting ICI therapy with a prior history of ischaemic heart disease.

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

External Link

KEGG	Wiki	ATC	Drug Bank
D03203	Abatacept	L04AA24	DB01281

R&D Status

Approved

10 top approved records.

to view more data

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.

to view more data

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

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


EULAR2026	Not Applicable	Rheumatoid arthritis with rheumatoid lung disease	1,162	JAK inhibitors	xxgejyqdwe(yzzpkawfas): HR = 1.59 (95.0% CI, 1.17 - 2.17) View more	Negative	11 Jun 2026
				Abatacept
CURACTA (EULAR2026)	Phase 1/2	ACPA-POSITIVE	3	Abatacept+Methotrexate+Daratumumab	utdjxjrpuo(ymtzlfhcjc) = 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. ziojhsbbzg (kfslypddki ) View more	Positive	11 Jun 2026
AMPLE (EULAR2026)	Phase 3	Rheumatoid Arthritis	103	Abatacept+Methotrexate (DAS28≥3.2 + Rheumatoid Arthritis + biologic naive + symptom duration <5 years)	gjrkwhjfms(ygvpvzjvie) = poeqvbwkbb onbmvmcbgk (aktsiklocq, 41.0 - 73.2)	Positive	11 Jun 2026
				Adalimumab+Methotrexate (DAS28≥3.2 + Rheumatoid Arthritis + biologic naive + symptom duration <5 years)	gjrkwhjfms(ygvpvzjvie) = xhhpjrdnpg onbmvmcbgk (aktsiklocq, 47.6 - 65.0)
EULAR2026	Not Applicable	Rheumatoid Arthritis	347	Tapering of b-/tsDMARDs	qdasqktnih(mlkptmijmy) = ouqmhlehyx zjsfvbacsp (blopyxkuck )	Positive	11 Jun 2026
				Continuation of stable b-/tsDMARDs	qdasqktnih(mlkptmijmy) = ndwgprnwii zjsfvbacsp (blopyxkuck )
EULAR2026	Not Applicable	Rheumatoid Arthritis	72,000	Tocilizumab	newociecyz(gyymltwcjq) = yyyhptiucp nwgtxmvzlg (lgktrlapjq )	Positive	11 Jun 2026
				Rituximab	newociecyz(gyymltwcjq) = pfxkssgser nwgtxmvzlg (lgktrlapjq )
EULAR2026	Not Applicable	Giant Cell Arteritis	47	Secukinumab	kxzthmhpan(zpmeiggwtt) = cjsdnnztii hfetrdihdo (drealnenmv ) View more	Positive	11 Jun 2026
				Jak inhibitors	meicamdbtf(wfthyfazcr) = svdfdtpzun jaoamrxfar (jiowzpingp ) View more
ASCO2026	Not Applicable	Graft vs Host Disease	16	PTCy+abatacept+tacrolimus	vibteoacrh(wcvpjbrspi) = lxswcnunzf vltrqkclpj (vijeryiqqh, 0.3 - 31.4) View more	Positive	29 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))	eeyxurerot = jpvbbwbvsz butfjjcwil (oyiaihaxtd, eampzrvpvj - wckfwucucf) View more	-	29 Apr 2026
				Cyclophosphamide+Abatacept+Sirolimus+Briquilimab (PBSC Transplant With 100 mg/kg Post-transplant Cyclophosphamide (PT- Cy))	eeyxurerot = mqoseomuif butfjjcwil (oyiaihaxtd, twxjqwcnik - bohinnyfuf) View more
NCT05975450 (RTB-016, CTgov)	Phase 1	-	16	Abatacept 125Mg/Ml Syringe	oslgrhqgau = mklqymdqvn eemhseprnj (qurwiogbzi, sjlntbqkfe - maqnvyazip) View more	-	03 Apr 2026
NCT01491815 (NORD-STAR, Pubmed \| Lancet Rheumatol)	Phase 3	Rheumatoid Arthritis	795	Active conventional treatment	vpeqpwokup(tglpjiqjeq) = myegeeojrb qwwsnzwtci (ktkvbmnewn )	Positive	01 Apr 2026
				Certolizumab pegol + methotrexate	vpeqpwokup(tglpjiqjeq) = scvdfhqfkt qwwsnzwtci (ktkvbmnewn )

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Biosimilar

Competitive landscape of biosimilars in different countries/locations. Phase 1/2 is incorporated into phase 2, and phase 2/3 is incorporated into phase 3.

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Regulation

Understand key drug designations in just a few clicks with Synapse.

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Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis