New precompetitive effort aims to standardize how senescence is measured, bringing regulators, academia and industry into alignment.
Senescence has had a good decade. Once a somewhat esoteric corner of cell biology, it now sits squarely in the translational spotlight – implicated in everything from fibrosis to cancer progression to the slow erosion of tissue function that accompanies aging. Therapeutic programs are moving forward. Clinical trials are underway. The ambition is no longer theoretical.
And yet… Ask a deceptively simple question – what, precisely, is a senescent cell in a human patient? – and the answers begin to diverge.
The launch of the Senotherapeutics Biomarker Consortium (SBC), introduced by Marco Quarta, Nicola Neretti, Heinrich Jasper and Marco Demaria, under the umbrella of the Phaedon Institute, is an attempt to bring those answers back into alignment. Framed as a precompetitive collaboration, it brings together academia, industry and regulators to do something less glamorous than drug discovery, but arguably more necessary – to agree on how senescence should be measured, validated and ultimately trusted in the clinic.
Longevity.Technology: There is something quietly paradoxical about a field trying to develop exquisitely precise therapies for senescent cells while still arguing about how to recognize one when it sees it; but that is more or less where senotherapeutics now finds itself. The launch of the Senotherapeutics Biomarker Consortium feels less like a nice-to-have than a necessary moment of alignment – an acknowledgment that the real bottleneck is not a lack of therapeutic ambition, but a lack of shared, reliable ways to measure what is, by its nature, a deeply context-dependent biology. Senescence is not one thing, expressed one way, in one tissue, at one moment, for one consequence; it can suppress tumors, support repair and shape development – or, when persistent and dysregulated, drive fibrosis, frailty and disease. That makes biomarker development far more than just a technical exercise; it is an attempt to distinguish between transient, functional programs and those that have tipped into pathology, and to do so with enough precision for trials, regulators and clinicians to act with confidence. In that sense, SBC signals a maturation point for the field – if the first chapter of senotherapeutics was about establishing relevance, this next phase will depend on whether we can measure it well enough to intervene intelligently.
A field outgrowing its tools
The accompanying Nature Aging paper is unusually direct about the problem. The field, the authors write, has reached a “translational inflection point” – a moment where therapeutic ideas are proliferating faster than the infrastructure needed to evaluate them [1].
Put less formally: the biology is moving quickly but the measurement is not keeping up.
Across laboratories, assays differ, and across disease areas, definitions shift. What counts as senescence in one context may not translate cleanly into another, and the result of all this is a kind of methodological patchwork – workable in discovery, less so in clinical development, where comparability and reproducibility are not luxuries but requirements.
The consequences ripple outward. Trial readouts become harder to interpret. Cross-study comparisons start to blur. Regulators, faced with heterogeneous endpoints, hesitate.
Not one state but many
Part of the difficulty is conceptual. Senescence resists simplification.
Writing on LinkedIn, Demaria put it plainly: “senescence is, on the contrary, profoundly context-dependent.” It can suppress tumorigenesis; it can coordinate tissue repair; it can even play a role in embryonic development. Under different conditions, the same program contributes to fibrosis, metabolic dysfunction and frailty.
Same label. Different biology.
Speaking to Longevity.Technology, Quarta said the field is entering the clinic with remarkable speed – but the measurement toolkit remains comparatively immature.
“That gap matters, because senescence is increasingly understood not as one fixed cell fate, but as a diverse family of states that vary across tissues, disease contexts, and stages of progression,” he explained. “In practical terms, this means that negative or modest trial signals should be interpreted cautiously: they may indicate limitations of the therapeutic approach, but instead also an incomplete ability to identify the relevant senescent cell populations, measure target engagement, and link biological modulation to meaningful clinical change. This heterogeneity complicates patient selection, target engagement assessment, and endpoint interpretation, and reinforces the need for multimodal biomarker strategies that can resolve which senescent cell states are being modulated, in which tissues, and with what biological consequence.”
That variability makes the continued reliance on single markers feel increasingly strained. “We know that p16 and SA-βgal are not enough,” Demaria wrote on LinkedIn – a line that lands because it captures a quiet consensus in the field. Markers detect presence. They do not necessarily capture function.
And function is the point.
From markers to meaning
SBC’s answer is not to search for a better single biomarker, but to move beyond the idea that one could exist. Following the launch, the plan is to make assay selection this year, followed by multicenter validation and biorepositories next year and submission of surrogate endpoints to regulators in 2029. The consortium’s roadmap centers on multimodal panels – molecular signatures, imaging modalities, histological features, functional readouts – stitched together into something closer to a biological profile than a binary signal. Critically, this includes functional readouts: moving past the static question of whether a cell “looks” senescent to measuring how it actually behaves and disrupts its environment. As the consortium notes, the goal is to capture markers that reflect cellular heterogeneity and context dependence across different tissues. [1].
Messier, perhaps. Also more faithful to the biology.
Quarta, writing on LinkedIn, framed the issue with characteristic clarity: “a central bottleneck is straightforward, and solvable: we still lack robust, standardized, clinically validated biomarkers to measure senescence in humans.” Without them, he noted, interpreting clinical signals becomes an exercise in ambiguity – not ideal when regulatory decisions are at stake.
So the consortium sets out to build the missing layer. Shared assays. Shared datasets. Shared expectations.
Aligning before competing
There is a quiet pragmatism to the consortium’s precompetitive structure. Competitors, for a time, agreeing not to compete.
In practice, that means aligning on the fundamentals – how to measure senescence, how to validate it, what endpoints might satisfy regulators – before diverging again at the level of therapeutics. No one is giving up their molecules or their pipelines. What is being shared is the measuring stick.
It is not a new model, but it is a necessary one. Without it, each program risks generating its own internal logic, its own assays, its own interpretation of success – difficult to reconcile, harder still to approve.
Within SBC, that alignment takes form through working groups focused on biomarker development, data integration, regulatory engagement and standard setting. Engagement with the FDA and EMA is built in from the outset; not an afterthought, but part of the design [1].
Which, in this field, is telling.
A more disciplined phase
Something else is shifting here. Tone, perhaps.
The early years of senescence research were expansive – mapping pathways, identifying targets, exploring possibilities. Now the constraints are different. Reproducibility matters. Definitions matter. Endpoints matter.
The authors argue that harmonized biomarkers will do more than smooth regulatory pathways; they will sharpen the science itself [1]. Better stratification. Cleaner trials. Faster learning cycles – including from failure, which becomes more interpretable when measured against shared standards.
Less noise. More signal.
Where this leaves the field
SBC will not solve senescence. It is not meant to.
What it may do is something subtler – to give the field a common language, one that allows in vitro observations, in vivo models and clinical data to speak to each other with fewer distortions. To make results legible across institutions. To reduce the interpretive drift that has, until now, been tolerated.
Quiet work but fundamentally foundational. And, if it succeeds, the kind that rarely makes headlines – but tends to determine which ideas make it through to the clinic, and which do not.
For those looking to help build this foundational layer, the SBC is actively welcoming collaborators – from academic labs to big pharma – who can contribute assays or expertise. Enquiries can be directed to sbc@phaedon.institute ahead of the first general meeting in 2026.
