- 01261-patient study linked CCR2 activity to poorer FSGS outcomes.
- 02Supports DMX-200’s rationale, not efficacy.
- 03ACTION3 Phase 3 is fully recruited.
Dimerix (ASX: DXB) has gained fresh human evidence supporting the biological rationale for its investigational kidney disease treatment DMX-200 after researchers linked inflammatory pathway activity to poorer patient outcomes.
The independent analysis drew on 261 patients with focal segmental glomerulosclerosis (FSGS), a rare disease that damages the kidney’s filtering units and can lead to kidney failure.
Findings presented at Kidney Week 2026 in Denver on 22 October associated heightened activity of the C-C chemokine receptor type 2 (CCR2) pathway with declining kidney function.
The results support the treatment target being investigated in Dimerix’s ACTION3 trial but do not establish that DMX-200 is clinically effective.
Dimerix has filed a provisional patent application covering the findings, which it considers potentially supportive of future regulatory submissions if the ACTION3 trial succeeds.
Kidney Tissue Signalling
Research led by University of Michigan investigator Dr Sean Eddy used the Nephrotic Syndrome Study Network (NEPTUNE) cohort to explore CCR2 signalling in kidney tissue and urine biomarkers.
The Dimerix-funded study found CCR2-associated gene activity was higher in FSGS kidney samples than in healthy donor samples, and was negatively correlated with kidney function.
Researchers identified a network of 206 CCR2-associated genes and used it to construct a transcriptional activity score, with higher scores linked to lower estimated glomerular filtration rate.
They also found that urinary monocyte chemoattractant protein-1 (MCP-1), an inflammatory molecule that activates CCR2, was associated with a greater risk of kidney function deterioration or kidney failure.
These observational associations identify a biologically relevant pathway rather than demonstrating that blocking it changes clinical outcomes.
Trial Reinforces Rationale
DMX-200 is designed to inhibit CCR2, potentially reducing the inflammatory activity implicated in progressive kidney damage among patients with FSGS.
The new findings confirm biomarker findings from Dimerix’s earlier Phase 2 trial, in which urinary MCP-1 levels fell among DMX-200 recipients but rose among placebo recipients.
“These findings are significant because they provide independent human data linking activation of the CCR2 pathway to poorer outcomes in patients with FSGS,” chief executive officer Dr Nina Webster said.
“They further strengthen the scientific rationale for targeting CCR2 in FSGS as we continue progressing our fully recruited ACTION3 Phase 3 study.”
Phase Three Decisive
The ACTION3 Phase 3 trial is a randomised, double-blind, placebo-controlled study testing DMX-200 alongside stable angiotensin II receptor blocker treatment against placebo in patients with FSGS.
Its adult cohort has enrolled and dosed 333 patients across 219 sites in 21 countries, with the final adult patient entering treatment in March 2026.
That patient is expected to complete dosing in March 2028, while recruitment of a separate cohort aged 12 to 17 years continues.
The study measures proteinuria and the rate of kidney function change, seeking evidence sufficient to support a possible marketing approval application.
Dimerix is separately advancing DMX-652 towards Phase 2 development in acute kidney injury, but the efficacy of DMX-200 in FSGS remains dependent on ACTION3 outcomes.
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