Fortitude Biomedicines to Present FTB-918 Preclinical Data for Axial Spondyloarthritis at ACR Convergence 2026
Fortitude Biomedicines, Inc., a biopharmaceutical company focused on developing precision antibody-based therapies for autoimmune diseases and cancer, has announced that its investigational candidate FTB-918 has been selected for an oral presentation at the American College of Rheumatology (ACR) Convergence 2026. The presentation will highlight preclinical findings supporting the development of FTB-918 as a potential treatment for axial spondyloarthritis (axSpA), a chronic inflammatory disease that primarily affects the spine and sacroiliac joints.
ACR Convergence 2026 will take place in Orlando, Florida, from November 6 to November 11, 2026. The meeting brings together rheumatologists, clinical researchers, healthcare professionals, and industry representatives to discuss advances in the understanding and treatment of rheumatic and musculoskeletal diseases. Fortitude’s participation will provide an opportunity to share the scientific rationale behind FTB-918 and its potential to address important limitations associated with existing axSpA therapies.
FTB-918 is the company’s lead development program and has demonstrated promising preclinical biological activity. The investigational therapy has been engineered as a first-in-class, dual-targeting antibody fusion designed to address two disease-related mechanisms simultaneously: the depletion of pathogenic CD8+ T cells expressing the TRBV9 gene segment and the neutralization of interleukin-17A (IL-17A), an inflammatory cytokine implicated in axSpA.
By combining targeted immune-cell depletion with cytokine inhibition in a single therapeutic candidate, Fortitude aims to develop a differentiated approach to disease management. The company believes that this dual mechanism could provide potential clinical benefits beyond those achieved with therapies that focus exclusively on inflammatory cytokines or individual cellular targets.
The oral presentation will be delivered by Atul Deodhar, M.D., Professor of Medicine and Medical Director of Rheumatology Clinics in the Division of Arthritis & Rheumatic Diseases at Oregon Health & Science University. The presentation, titled “FTB-918: A Dual Targeting Antibody With TRBV9+ T Cell Depletion and IL-17A Neutralization for the Treatment of Axial Spondyloarthritis,” is scheduled for Wednesday, November 11, 2026, from 9:30 a.m. to 9:45 a.m. Eastern Time. The abstract number is 2941, and the presentation will be included in the Spondyloarthritis Including Psoriatic Arthritis – Treatment session.
Addressing Unmet Needs in Axial Spondyloarthritis
Axial spondyloarthritis is a chronic inflammatory condition characterized by inflammation involving the axial skeleton, particularly the spine and sacroiliac joints. The disease can cause persistent back pain, stiffness, reduced mobility, and limitations in daily activities. In some patients, ongoing inflammation may contribute to structural changes in the spine and long-term functional impairment.
The disease can substantially affect quality of life, particularly when symptoms remain inadequately controlled over extended periods. Treatment generally aims to reduce inflammation, relieve pain and stiffness, preserve physical function, and prevent or limit disease-related complications.
Over the past two decades, advances in biologic therapies and targeted treatments have expanded the options available to patients with axSpA. Current approaches include therapies directed against tumor necrosis factor-alpha (TNF-alpha), inhibitors of IL-17, and targeted synthetic disease-modifying antirheumatic drugs where appropriate.
These treatments work by interfering with inflammatory pathways involved in disease activity. However, despite the availability of multiple therapeutic options, a considerable proportion of patients do not achieve sufficient disease control or lose their response over time.
This persistent treatment gap underscores the need for therapies that address additional mechanisms involved in the initiation and progression of axSpA. For patients who do not respond adequately to existing treatments, new approaches capable of targeting the underlying biological drivers of inflammation could provide an important advance.
Fortitude is developing FTB-918 in response to this unmet need. Rather than relying exclusively on the inhibition of inflammatory cytokines, the candidate is designed to combine cytokine neutralization with the removal of a specific population of immune cells associated with axSpA.
The company’s strategy reflects an effort to address both the inflammatory signals contributing to symptoms and the pathogenic immune-cell populations that may play a role in sustaining disease activity.
Targeting Pathogenic TRBV9-Positive CD8+ T Cells
A central element of Fortitude’s development strategy is the targeting of CD8+ T cells expressing the TRBV9 gene segment. These cells have been found at elevated levels in the circulation of patients with axSpA and in the synovial fluid of inflamed joints.
CD8+ T cells are part of the adaptive immune system and normally contribute to immune surveillance and responses to infected or abnormal cells. However, particular T-cell populations may become associated with pathological immune responses and contribute to chronic inflammatory disease.
The identification of expanded TRBV9-positive CD8+ T-cell populations in axSpA has drawn attention to a potential disease-associated cellular target beyond the inflammatory cytokines commonly addressed by current therapies.
According to Fortitude, FTB-918 has been engineered to selectively deplete these pathogenic TRBV9+ CD8+ T cells. The objective is to intervene in a cellular mechanism associated with the disease rather than solely suppressing the inflammatory signals generated through downstream pathways.
This approach could be important because cytokine inhibition and pathogenic-cell depletion address different aspects of disease biology. While cytokine-targeted treatments can reduce inflammation, they do not specifically remove the TRBV9-positive T cells that Fortitude is seeking to target.
The company’s research therefore explores whether eliminating this particular immune-cell population, alongside blocking a key inflammatory mediator, could produce a more comprehensive therapeutic effect.
However, the clinical significance of this approach remains to be established. The preclinical findings provide a scientific basis for further development, but clinical studies will be required to determine whether selective TRBV9+ T-cell depletion translates into improved disease control, functional outcomes, or longer-lasting responses in patients.
Combining T-Cell Depletion With IL-17A Neutralization
The second component of FTB-918 is the neutralization of IL-17A, an inflammatory cytokine involved in the biological processes underlying axSpA.
IL-17A contributes to inflammatory signaling and has an established role in the treatment landscape for axSpA. Approved IL-17 inhibitors have demonstrated clinical benefits in appropriate patient populations, providing a therapeutic foundation for targeting this pathway.
Nevertheless, IL-17A inhibition does not specifically eliminate pathogenic TRBV9-positive CD8+ T cells. Similarly, an approach focused only on depleting these T cells may not fully address the inflammatory activity associated with other disease pathways.
FTB-918 is designed to bring these two complementary mechanisms together in a single antibody fusion molecule.
Through its dual-targeting design, the candidate aims to deplete TRBV9+ CD8+ T cells while simultaneously neutralizing IL-17A. Fortitude believes this combination could address both a disease-associated cellular mechanism and an inflammatory pathway known to contribute to axSpA.
The strategy is intended to overcome the limitations of addressing either mechanism independently. By combining the two activities, FTB-918 may have the potential to influence disease processes at more than one level.
This design distinguishes the candidate from therapies that primarily block a single cytokine pathway. It also differentiates the program from approaches focused solely on the depletion of a particular immune-cell population.
The upcoming presentation at ACR Convergence 2026 will provide an opportunity for the rheumatology community to examine the scientific rationale for this approach and assess the preclinical evidence supporting further investigation.
At this stage, FTB-918 remains investigational. Its potential safety, tolerability, effectiveness, durability of response, and comparative benefits will need to be evaluated through clinical development.
Company and Clinical Expert Highlight the Scientific Rationale
Commenting on the presentation, Dr. Joseph Leveque, Chief Medical Officer of Fortitude, emphasized the potential value of combining the two mechanisms in one therapeutic candidate.
“We are excited to showcase FTB-918 and to share compelling preclinical data supporting its advancement into the clinic in the first half of 2027,” Leveque said.
He noted that TNF-alpha and IL-17 inhibitor-based therapies are used to block inflammatory cytokine pathways that contribute to axSpA symptoms. However, these approaches do not remove the pathogenic T cells believed to be involved in initiating and driving disease progression.
Leveque also explained that depleting TRBV9+ T cells alone addresses part of the underlying disease biology but may not provide the broad and durable disease control that patients need.
FTB-918 was developed to combine these approaches, potentially offering a broader strategy for addressing axSpA. Leveque added that Fortitude believes the dual mechanism could potentially be applicable to other diseases driven by TRBV9-positive T cells.
This broader possibility could be relevant to the company’s long-term research strategy, although additional scientific and clinical evidence would be necessary to establish the suitability of the approach in other indications.
Dr. Atul Deodhar also highlighted the continuing treatment challenges associated with axSpA and the potential importance of identifying new therapeutic targets.
“Despite advances in the treatment of axSpA over the past two decades, many patients still do not reach low disease activity or inactive disease by validated measures such as Ankylosing Spondylitis Disease Activity Score (ASDAS), highlighting the unmet need in this condition,” Deodhar said.
He explained that the identification of TRBV9+ CD8+ T-cell expansion in axSpA has opened the possibility of targeting a specific immune-cell population beyond conventional cytokine blockade.
According to Deodhar, the scientific rationale for FTB-918 lies in its combination of targeted cell depletion and IL-17A neutralization. Although each approach addresses an important component of the disease process, using either mechanism alone may leave other pathways unaddressed.
Combining both activities in a single therapeutic candidate could therefore have the potential to deliver more meaningful benefits for patients, provided that the proposed effects are confirmed in clinical studies.
The perspectives of both Fortitude and Deodhar underscore the importance of investigating treatment strategies that address multiple aspects of axSpA biology rather than focusing exclusively on established inflammatory pathways.
FTB-918 Development Plans and Next Steps
Fortitude has indicated that it plans to advance FTB-918 into clinical development in the first half of 2027. The preclinical findings selected for presentation at ACR Convergence 2026 represent an important step in communicating the program’s scientific rationale before the anticipated transition into human studies.
The next phase of development will be critical for evaluating whether the candidate’s dual-targeting mechanism can be translated into a clinically meaningful treatment approach.
Clinical studies will need to assess the therapy’s safety and tolerability, its ability to engage the intended targets, and its effects on disease activity. Investigators will also need to determine whether the combined mechanism provides advantages over existing treatment strategies and whether any benefits can be maintained over time.
Validated measures such as the Ankylosing Spondylitis Disease Activity Score may help assess disease activity during clinical development. Additional evaluations could examine pain, stiffness, physical function, inflammatory markers, and other relevant clinical outcomes, depending on the study design.
The extent to which FTB-918 selectively depletes TRBV9-positive CD8+ T cells, as well as the contribution of IL-17A neutralization to its overall activity, will also be important scientific questions.
As with other investigational biologic therapies, the candidate’s safety profile will be a central consideration. Researchers will need to evaluate the implications of targeting a specific immune-cell population alongside inhibition of an inflammatory cytokine, including potential effects on normal immune function.
Although the company’s preclinical results support further investigation, the findings do not yet establish that FTB-918 will be effective or superior to existing therapies in patients. Its clinical value will depend on the results of appropriately designed and conducted trials.
Oral Presentation at ACR Convergence 2026
The presentation of FTB-918 at ACR Convergence 2026 will bring the candidate’s dual-targeting strategy before a scientific audience specializing in rheumatology and inflammatory diseases.
The meeting provides a forum for discussing emerging therapeutic approaches, evaluating research findings, and exploring opportunities to improve care for people living with rheumatic conditions.
Presentation details:
- Presentation title: FTB-918: A Dual Targeting Antibody With TRBV9+ T Cell Depletion and IL-17A Neutralization for the Treatment of Axial Spondyloarthritis
- Presenter: Atul Deodhar, M.D., Oregon Health & Science University
- Session: Spondyloarthritis Including Psoriatic Arthritis – Treatment
- Date: Wednesday, November 11, 2026
- Time: 9:30 a.m. to 9:45 a.m. Eastern Time
- Abstract number: 2941
- Conference: ACR Convergence 2026
- Location: Orlando, Florida
- Conference dates: November 6–11, 2026
Fortitude’s selection for an oral presentation highlights the scientific interest in its approach to targeting pathogenic immune cells and inflammatory signaling simultaneously. The findings may contribute to further investigation of the role of TRBV9-positive CD8+ T cells in axSpA and the development of therapies designed to address multiple disease mechanisms.
With clinical development anticipated to begin in the first half of 2027, FTB-918 represents Fortitude’s lead effort to explore a differentiated antibody-based treatment strategy for axSpA. The program’s progress will depend on demonstrating that its dual-targeting design can deliver acceptable safety and meaningful clinical benefits.
If successful in clinical development, FTB-918 could offer a new approach to addressing the persistent treatment gaps in axSpA. For now, its preclinical findings provide the foundation for the next stage of research into whether combining pathogenic T-cell depletion with IL-17A neutralization can improve disease management for patients who continue to face challenges with existing treatment options.
About Fortitude Biomedicines
Fortitude Biomedicines is a leading biotechnology company headquartered in Waltham, Massachusetts, pioneering next-generation immune cell targeting biologics and an antibody–drug conjugate (ADC) platform powered by proprietary molecular glue payloads.
By integrating the precision targeting of ADCs with the catalytic power of targeted protein degradation, the company is developing transformative therapies with the potential to expand the therapeutic window of ADCs, overcome resistance mechanisms, and unlock new target space. Leveraging a robust discovery engine and an experienced team of drug hunters, Fortitude is building a differentiated pipeline of biologics and ADCs aimed at delivering meaningful benefits to patients with high unmet medical need.