As CEO of Coya Therapeutics, Dr Arun Swaminathan is steering the company’s lead programme, COYA 302, an immune-modulating combination designed to restore regulatory T-cell function and dampen neuroinflammation, through a pivotal stage of development in amyotrophic lateral sclerosis (ALS).
The FDA’s fast track designation (FTD) adds urgency and optionality to that journey, enabling closer regulatory engagement and opening potential routes such as rolling review, priority review, and accelerated approval if clinical evidence supports it.
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Swaminathan tells Pharmaceutical Technology how the designation shapes Coya’s near-term priorities, including completing enrolment in the ALSTARS study, advancing manufacturing readiness, and building mechanistic and biomarker datasets to strengthen the clinical narrative.
Salong Debbarma (SD): Following fast track designation for COYA 302, what are your key priorities over the next 6-12 months, and how does this designation change your development pathway?
Dr Arun Swaminathan (AS): Fast track designation is a very important milestone. Its primary purpose is to ensure that promising new therapies reach patients as quickly as possible through several key regulatory advantages, which include more frequent FDA interactions, potential for rolling review, and eligibility for expedited programmes such as accelerated approval and priority review.
Over the next 6-12 months, our priorities are clear. First, we are focused on completing full enrolment of ALSTARS in the second half of 2026. We recently amended the protocol, now cleared by both the FDA and Health Canada, to remove exclusions around antihypertensive medications and controlled autoimmune conditions, broadening the eligible population and we expect that to translate into higher enrolment rates. We currently have nearly 25 sites in the US and Canada actively recruiting in this trial.
Second, we plan to initiate our Phase IIa study of COYA 302 in frontotemporal dementia (FTD), also in the second half of 2026.
Third, we will continue to generate mechanistic and translational datasets, including single-cell proteomics and biomarker analyses, from completed investigator-initiated studies.
Operationally, we are advancing manufacturing readiness, and on the business development front, we continue to evaluate value-creating partnerships both for markets like Japan for COYA 302, but also for other innovative combinations using our COYA 301 as the backbone.
While fast track does not change our topline data guidance, which remains the first quarter of 2027, it strengthens the regulatory pathway following that readout.
SD: How does COYA 302’s immune-modulating approach translate into meaningful outcomes for ALS patients, and what clinical data supports this?
AS: For patients with ALS, the central question is whether a therapy can alter the relentless functional decline. This is typically about one ALSFRS-R point per month of decline. The goal is to slow or stop this decline.
Stopping neuroinflammation can prevent further damage and potentially slow disease progression. Regulatory T cells (Tregs) are both reduced and functionally impaired in ALS, leading to increased inflammation and subsequently patient decline. COYA 302 addresses this through a dual mechanism: low-dose IL-2 restores Treg number and function, while CTLA4-Ig dampens inflammation driven by activated monocytes and macrophages. We believe these effects are additive and potentially synergistic.
Our early human data are encouraging and internally consistent. In a proof-of-concept study of four ALS patients, who were declining at approximately 1.1 ALSFRS-R points per month pre-treatment, patient function remained stable over the first 24 weeks on therapy, with substantially slower decline through 48 weeks. We observed durable improvements in Treg suppressive function, alongside reductions in biomarkers of inflammation, oxidative stress, and neuronal injury.
Our recent publication in Annals of Clinical and Translational Neurology further demonstrated that these biomarkers correlate with survival and progression in ALS.
All these data points give us confidence in ALSTARS, our ongoing trial that is designed to demonstrate if COYA 302 is making a meaningful impact on disease progression.
SD: What endpoints and signals will determine whether COYA 302 demonstrates disease-modifying activity?
AS: The primary endpoint is change in ALSFRS-R at 24 weeks versus placebo, the most clinically meaningful and widely accepted measure in ALS. Given the typical progression of approximately one to one-and-a-half points of decline per month, our study is designed to show at least a 3-point difference between the treatment and placebo arms. The study also has an additional 24-week blinded extension.
Neurofilament light (NfL), a well-established marker of neuronal injury, is a marker the FDA recognises as a surrogate of efficacy as well and is our secondary endpoint. Of note, unique to our design, we are stratifying patients by the NfL levels to maintain uniformity in inflammatory status across the groups and reduce variability.
Other exploratory markers such as Treg number and suppressive function will help confirm target engagement while markers of inflammation and oxidative stress, such as LBP and 4-HNE, will assess downstream biological effects.
Clinically meaningful effects on ALSFRS-R, supported by biomarker data including NfL which is a secondary endpoint with a favourable safety profile could have a significant clinical impact on people with ALS and we would fully intend to discuss with the FDA a path towards approval.
SD: Assuming positive data, what is the most realistic pathway to approval and patient access?
AS: The pathway ultimately depends on ALSTARS outcomes. We expect topline data in the first quarter of 2027. If the results are positive and compelling, multiple regulatory options become viable.
Fast track designation enables rolling BLA submission and eligibility for priority review. Given ALS’ severity and limited treatment options, regulators have historically shown regulatory flexibility.
The path forward, whether through accelerated approval or additional studies, will depend on the strength and consistency of the clinical data, supportive biomarker findings, and feedback from the FDA on whether the ALSTARS data supports a BLA filing.
SD: How does COYA 302 support expansion into other indications, and what are your priorities?
AS: COYA 302 represents more than a single asset. Many major neurodegenerative diseases, including ALS, FTD, Alzheimer’s, and Parkinson’s, share a common upstream driver: dysregulated neuroinflammation linked to Treg dysfunction. If restoring Treg function and dampening inflammation can alter disease trajectory in ALS, the same mechanism may be applicable across these indications.
Our immediate expansion focus is FTD. We have an FDA-cleared IND, encouraging open-label Investigator Initiated Trial data with the Low dose IL-2/CTLA4 Combination showing Treg engagement and cognitive stability over 22 weeks, measured by MoCA and CDR-FTLD. The Alzheimer’s Drug Discovery Foundation supports this approach and has invested in Coya. We plan to initiate a Phase IIa study in the second half of 2026, and from a business perspective we retain full global rights to FTD.
Beyond this, the company’s additional candidate, COYA 303, a proprietary combination of low-dose IL-2 and a GLP-1 receptor agonist, is being explored in Alzheimer’s disease, where we believe combination therapy may address limitations observed with GLP-1 monotherapy and the additive/synergistic potential is supported by pre-clinical studies.
