A new imaging-drug collaboration aims to show whether progression of Parkinson’s disease can be slowed, not just managed.
For people living with Parkinson’s disease, the hardest part isn’t just the tremors, stiffness or slowness of movement. It’s the invisible damage happening inside the brain. Until recently, researchers could only guess whether experimental therapies were slowing the disease, because the toxic protein clumps driving it couldn’t be seen in living patients.
That’s changing now. SynuSight Biotech, ABLi Therapeutics and XingImaging have teamed up to bring a new imaging technology into clinical trials of risvodetinib, a therapy designed to stop or even reverse the progression of Parkinson’s [1].
The collaboration’s aim is to watch, in real time, whether the drug is reducing the toxic alpha-synuclein protein clumps that are thought to drive nerve cell damage – and if we can measure and intervene in neurodegeneration as it occurs, we could move closer to slowing or even preventing aging-related brain disease.
At the heart of the partnership is ¹⁸F-FD4, a PET imaging tracer developed by SynuSight. FD4 binds specifically to alpha-synuclein aggregates – the “toxic clumps” that mark Parkinson’s progression – and makes them visible on a PET scan. In other words, it turns the invisible visible.
SynuSight has licensed FD4 to ABLi Therapeutics, which is developing risvodetinib, and to XingImaging, which will manufacture the tracer in the US XingImaging will use it with their NeuroEXPLORER, an ultra-high-resolution brain PET scanner housed in their new facility in New Haven, Connecticut.
“This collaboration represents a key milestone in the global development of FD4,” said Roger Fan, CEO of SynuSight. “By integrating molecular imaging technologies with rigorously designed clinical trials and longitudinal follow-up, the partnership aims to directly interrogate the disease-modifying potential at the pathological level.”
Instead of relying solely on symptom improvement, researchers can now track what’s happening at the root of the disease.
Parkinson’s symptoms appear because dopamine-producing neurons are dying, but the damage often begins years earlier. Alpha-synuclein proteins misfold and form clumps, which slowly poison the brain’s nerve cells.
Until now, these clumps could only be confirmed after death. FD4 changes that, offering a window into the disease process while patients are alive and still able to respond to treatment.
Being able to see this process matters not just for one drug, but for the whole field of neurodegeneration and aging research. It’s a chance to move from indirect measures to real biological evidence.
ABLi plans to deploy FD4 in two clinical trials starting later this year.
The first, ABILITY-PD, will re-enroll 120 participants from a previous Phase 2a study completed in 2024 [1]. Over 12 months, researchers will track alpha-synuclein in the brain, along with blood and tissue biomarkers, and functional measures like movement, non-motor symptoms, and dopamine-specific activity. The goal is to determine whether changes in these markers align with improvements in patients’ function.
The second trial, CAMPD, is a larger Phase 2b/3 study. Up to 500 participants with untreated Parkinson’s will receive either risvodetinib or a placebo in a double-blind design, considered the gold standard for testing whether a therapy truly works [1].
“ABLi has been expanding its portfolio of disease-related biomarkers, with both blood-borne and tissue measures of alpha-synuclein pathology and is excited to add alpha-synuclein PET imaging to this panel to expand our understanding of the potential disease-modifying effect of risvodetinib in PD,” said Dr Milton Werner, Chairman and CEO of ABLi.
Risvodetinib works by blocking c-Abl kinases, enzymes involved in cell stress and neurodegeneration. Unlike current Parkinson’s treatments, which manage symptoms, risvodetinib aims to slow or even reverse the underlying disease process. In an earlier trial, it improved quality of life while also reducing alpha-synuclein pathology, a rare combination in neurodegenerative research.
The collaboration also signals a shift in how we think about aging and brain health. Imaging tools like FD4 allow researchers to track disease progression and therapeutic response directly, helping to identify interventions that genuinely modify biology rather than just treat symptoms.
“This represents a pivotal opportunity to advance one of the most promising alpha-synuclein PET tracers in humans with the potential disease-modifying effect of risvodetinib in PD,” said Gilles Tamagnan, CEO of XingImaging.
With clinical trials launching in the US and China in early 2026, backed by funding from the Michael J Fox Foundation, this partnership could mark a turning point not only for Parkinson’s patients but for the broader goal of extending healthy brain function and longevity.
