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Can ARG-007 Overcome the Challenges of Treating Traumatic Brain Injury?

Biotechnology By Ada Torres 3 min read

Argenica Therapeutics reports compelling preclinical evidence that its lead candidate ARG-007 significantly reduces brain cell damage and inflammation in moderate traumatic brain injury models, marking a promising step toward new TBI treatments.

  • ARG-007 reduces axonal injury and neuroinflammation to levels seen in non-injured animals
  • Significant improvements observed in motor function and behavioural tests in treated rats
  • ARG-007 prevents acute increase of neurofilament light protein, a key TBI biomarker
  • Treatment accelerates weight recovery post-injury, indicating systemic benefits
  • Findings replicate and expand on previous pilot studies in rats and ferrets

A Promising Advance in TBI Therapeutics

Argenica Therapeutics Limited (ASX, AGN) has unveiled significant new preclinical data demonstrating the neuroprotective effects of its lead peptide candidate, ARG-007, in a rat model of moderate traumatic brain injury (TBI). The study, conducted at Curtin University and the Perron Institute, confirms that ARG-007 markedly reduces brain cell damage and neuroinflammation, key drivers of the acute and chronic consequences of TBI.

Traumatic brain injury affects millions globally each year, often resulting in long-term neurological impairments. Despite this, effective pharmacological treatments targeting the secondary injury processes such as axonal damage and inflammation remain elusive. Argenica’s ARG-007 aims to fill this critical gap.

Robust Neuroprotection Confirmed

The study showed that a single intravenous dose of ARG-007 administered 30 minutes post-injury significantly reduced levels of neurofilament heavy protein (NF-H) and amyloid precursor protein (APP), biomarkers indicative of axonal injury and neurodegeneration. Remarkably, these biomarker levels in treated animals were comparable to those in non-injured controls, suggesting near-complete protection of brain cells.

Additionally, ARG-007 prevented the acute rise of neurofilament light protein (NF-L) in plasma, a biomarker increasingly recognised for its predictive value in human TBI outcomes. The peptide also significantly lowered Iba1 levels, a marker of microglial activation and neuroinflammation, which is implicated in secondary brain injury progression.

Functional and Systemic Benefits

Beyond biochemical markers, ARG-007-treated rats exhibited improved motor coordination and behavioural outcomes, as measured by standard tests. The treatment also mitigated weight loss commonly associated with moderate TBI, with treated animals regaining their pre-injury weight faster than controls. These findings suggest ARG-007’s benefits extend beyond cellular protection to functional recovery and systemic health.

Building on Previous Research

This larger study replicates and expands upon earlier pilot studies in rats and ferrets, reinforcing the consistency and robustness of ARG-007’s neuroprotective effects. Argenica plans to continue rigorous preclinical validation, including studies on repeated mild TBIs and dosing regimens, in collaboration with research partners at the University of Adelaide and Curtin University.

Dr Liz Dallimore, Managing Director, emphasised the significance of these findings, stating that ARG-007 consistently reduces key pathological markers to near-normal levels and holds promise as a therapeutic candidate for moderate TBI.

Looking Ahead

With a Phase 2 clinical trial underway for acute ischemic stroke and ongoing preclinical work in other neurological conditions, Argenica is positioning ARG-007 as a versatile neuroprotective agent. The company’s progress in TBI models adds a compelling dimension to its pipeline, addressing a major unmet medical need.

Bottom Line?

ARG-007’s compelling preclinical results set the stage for critical clinical trials that could redefine TBI treatment.

Questions in the middle?

  • How will ARG-007 perform in human clinical trials for traumatic brain injury?
  • What are the timelines and endpoints for upcoming larger animal and repeated dosing studies?
  • Could ARG-007’s neuroprotective effects extend to other neurodegenerative conditions?