CancerFax
DISEASE GUIDE

ONCOLYTIC VIRUS FOR
BRAIN TUMOURS

GBM has failed every immune approach β€” except this one. PVSRIPO's 21% OS at 36 months against 4% historical control is the most important signal to emerge from recurrent GBM research.

Reviewed by: CancerFax Medical Team, Oncology & Haematology SpecialistsLast reviewed: April 16, 202612 min read

Why GBM Is the Strongest Rationale

GBM is one of oncology's most immunologically cold tumours β€” dominated by immunosuppressive M2 macrophages and myeloid-derived suppressor cells. Checkpoint inhibitors have failed in multiple Phase III trials. Extreme cold tumour biology is exactly where oncolytic virus mechanism has the strongest theoretical rationale.

β€œThe blood-brain barrier is irrelevant here β€” the neurosurgeon already operates on the tumour. PVSRIPO and DNX-2401 are delivered by direct intratumoral injection during or after surgery.”

Key GBM Data

  • 21%OS at 36 months (PVSRIPO)Versus ~4% historical control in recurrent GBM.
  • ~12%3-year OS (DNX-2401)Versus near-zero historical baseline.
  • Phase IIIPVSRIPO StatusOngoing at Duke and affiliated sites.

GBM Oncolytic Virus Programmes

  • PVSRIPO

    Poliovirus with IRES replaced by rhinovirus 2 IRES β€” eliminates neurovirulence, preserves oncolysis. Targets CD155 on GBM cells and immunosuppressive macrophages. Pre-treatment polio vaccination required. Phase III ongoing at Duke.

  • DNX-2401 (Tasadenoturev)

    Adenovirus selective for Rb-deficient cells (majority of GBM). ~12% 3-year OS. Being combined with pembrolizumab β€” viral inflammation + checkpoint inhibition.

  • G207 (HSV-1 Derivative)

    Most significant data from paediatric high-grade glioma trials. Phase II showed radiological and clinical responses in children with DIPG β€” a disease where nothing currently produces objective responses.

Frequently Asked Questions

GBM Questions

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