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Turning standard radiotherapy into a precision therapeutic weapon through nanoparticle activation.

The platform

RadioLite's core technology is a novel class of radiation-activated nanoparticles designed to amplify the therapeutic effect of clinical radiotherapy while sparing healthy tissue. The platform is built on PEG-PLGA nanospheres (~100 nm diameter) that encapsulate both a scintillator core and a photosensitizer coating.

Unlike conventional photodynamic therapy (PDT), which requires visible light that cannot penetrate deep tissue, our nanoparticles are activated by ionizing radiation — the same radiation already used in cancer treatment. This means the therapy works deep inside the body, at the tumor site, without additional light sources or invasive procedures.

Key advantages

  • Works with existing clinical radiotherapy — no new equipment needed
  • Activates only within the radiation field, ensuring spatial precision
  • Nanoparticles are biocompatible and non-toxic until activated
  • Can be combined with standard-of-care chemoradiation protocols
  • Scalable manufacturing using established nanoparticle synthesis methods
  • Demonstrated >90% encapsulation efficiency in preclinical studies
  • Low polydispersity — easy to scale from small to large production
RadioPDT Nanoparticle Platform Diagram

The mechanism

When ionizing radiation (X-rays, 6 MV) interacts with our proprietary LaF3:Ce3+ scintillator nanoparticles, it triggers a cascade of energy transfer events. The scintillator core absorbs X-ray energy and emits luminescence (UV/visible photons) within picoseconds. This luminescence is harvested via Förster Resonance Energy Transfer (FRET) to activate nearby Protoporphyrin IX (PPIX) photosensitizers.

The activated photosensitizers generate highly reactive oxygen species (ROS) — primarily singlet oxygen (1O2) and hydroxyl radicals (·OH). These ROS species are lethal to cancer cells. They damage DNA, disrupt cell membranes, and trigger apoptotic pathways. Because the ROS are generated locally at the nanoparticle surface (range ~40 nm), their effect is limited to the immediate tumor microenvironment, minimizing off-target effects.

What makes it different

  • Depth-independent activation: Ionizing radiation penetrates deeply; visible light does not. Enables treatment of deep-seated tumors like GBM.
  • Spatial precision: Activation only occurs where the radiation beam intersects the tumor — millimeter-level accuracy.
  • Temporal control: Activation happens only during scheduled radiotherapy sessions, not between treatments.
  • Enhanced EPR effect: Nanoparticles preferentially accumulate in tumor vasculature due to leaky tumor blood vessels, peaking at 24h in mice.
  • Low-dose efficacy: Preclinical studies show efficacy at 0.5–2 Gy single doses, far below standard RT total doses (60–80 Gy).
  • Minimal toxicity: Acute toxicity dose-escalation in C57BL/6 mice showed no histopathologic toxicity and no weight loss at therapeutic doses.
X-ray Activation
FRET Energy Transfer
ROS Generation (Singlet Oxygen)
Targeted Cell Death

Made to scale

Uniform particles, and the same chemistry from a bench batch to a production batch.

Low polydispersity

The particles come out the same size, batch after batch. Mean diameter ~92 nm with tight size distribution. Demonstrated >90% encapsulation efficiency.

Scales cleanly

Small-batch production carries through to large-batch using established nanoparticle synthesis methods. Low polydispersity means easy scale-up from bench to GMP production.

Electron micrograph of nanoparticles Nanoparticle size distribution

Built to behave

It survives circulation, collects in tumours, gets taken up by cancer cells, and does nothing at all until it is switched on.

Stable for 24 hours

Survives circulation, then collects in tumours through the enhanced permeability and retention (EPR) effect. Peaks in tumour at 24 hours — the window when radiation is delivered.

Taken up by cancer

Surface chemistry drives active uptake into cancer cell lines. Accumulates in phagolysosomes and endoplasmic reticulum, driven by the particle's surface chemistry.

Quiet until fired

Minimal toxicity across normal and cancer cell lines while the particle is inactive. Only turns on where radiation energy is targeted. No off-target activity.

Biodistribution data showing tumour accumulation

Mouse biodistribution studies, four to forty-eight hours after injection. Peaks in tumour at 24 hours.

No toxicity. No weight loss.

Acute toxicity dose-escalation of the RadioPDT nanoparticle, injected intravenously into C57BL/6 mice.

No damage found

Histopathology across lung, kidney, liver and spleen shows no tissue damage at therapeutic doses.

No weight loss

Normalised weight held flat across the dose escalation. No appreciable toxicity in preclinical models at therapeutic doses.

Clears the body

Post-mortem fluorescence shows clearance through the spleen and liver. Safely broken down by noncancerous cells.

Histopathology showing no tissue damage Weight loss safety data

It works where radiation alone gives up.

Robust data from in vitro and in vivo models supports the therapeutic potential of the platform. A dual-specific mechanism: the biochemical selectivity of the nanoparticle plus the spatial selectivity of the beam, producing a specific and synergistic kill.

Stops tumour growth

Where radiation alone cannot. Tumour volume held flat while the radiation-only arm keeps climbing. Strong anti-cancer effect beyond radiation alone.

Double the therapeutic effect

RadioPDT combined with radiation produces significantly greater tumour control than radiation alone. Faster tumour destruction with less cancer resistance.

No appreciable toxicity

In preclinical models at therapeutic doses. Only turns on where radiation energy is targeted. No off-target activity.

Tumour growth and survival preclinical data

Preclinical tumour volume and survival data: Control, Nanoparticles alone, Radiation alone, and RadioPDT.

A paradigm shift, not a tweak.

No one else is doing radiation-activated photodynamic therapy in an agent that can actually reach the clinic.

Regulatory & manufacturing

FDA-approved components with proven scalability. PEG-PLGA, LaF3:Ce3+, and PPIX are all well-characterized materials with established safety profiles.

Targeting & mechanism

Superior selectivity, and a faster cancer cell kill. Dual specificity: biochemical selectivity of the nanoparticle plus spatial selectivity of the radiation beam.

Safety & integration

Fewer permanent radiation "late effects," and it complements the radiotherapy clinics already deliver. No new equipment, no new clinical workflows.