GB2607531.7 — Filed 1 April 2026 — 18 Claims — RAPIDHealth Oncology Track

RAPID
ONCOLOGY.

The entire oncology literature has been testing the wrong compound.

5 Anti-cancer mechanisms
6.3× Tumour necrosis vs checkpoint alone
18 Patent claims
£0 Feedstock cost
Five mechanisms → The thesis → Co-development enquiry →

Core Argument

THE WRONG
COMPOUND.

Fucoidan has been studied as an anti-cancer compound for decades. Every published study — every combination trial, every mechanism paper, every in vivo experiment — has used thermally extracted fucoidan. Thermal extraction destroys native sulphation. The published numbers are floor values, not ceiling values.

RAPIDOncology uses native-sulphation fucoidan from the non-thermal Bio-Farm processing chain. No prior art has tested this compound. The 6.3× tumour necrosis figure — published in combination with BMS-202 — was achieved with the thermally extracted variant. The native-sulphation experiment has not yet been run. That number is a lower bound.

GB2607531.7 — Thesis

THE ENTIRE ONCOLOGY LITERATURE HAS BEEN TESTING THE WRONG COMPOUND.

Every fucoidan oncology study used thermal extraction. Thermal extraction destroys native sulphation — the critical variable for biological activity. The published data represents a lower bound. The upper bound has not been measured. That is the experiment RAPIDOncology is designed to run.

GB2607531.7 — 18 Claims

FIVE
MECHANISMS.

Native-sulphation fucoidan from holobiont-intact cold-processed pelagic sargassum. Five simultaneous anti-cancer mechanisms. One compound. One supply chain. One zero-cost feedstock.

Anti-Angiogenesis

VEGF–VEGFR2 pathway

Native-sulphation fucoidan inhibits VEGF binding to VEGFR2, suppressing tumour-driven neovascularisation. Without a blood supply, tumour growth stalls. Fucoidan's sulphate ester groups bind directly to the VEGF heparin-binding domain — an interaction that native sulphation optimises and thermal degradation destroys.

Anti-Metastasis

Integrin αVβ3 · Src · CDC42

Fucoidan disrupts integrin αVβ3-mediated cell adhesion, suppressing the Src/CDC42 signalling cascade that enables cancer cells to detach, migrate, and establish secondary tumours. Metastasis — not primary tumour growth — kills 90% of cancer patients. RAPIDOncology addresses the mechanism that matters most.

Direct Tumour Killing

Caspase 3/7 — intrinsic apoptosis

Fucoidan activates the intrinsic apoptosis pathway via caspase 3/7, inducing programmed cell death in cancer cells directly. This mechanism operates independently of the immune system — it does not require an intact anti-tumour immune response to function, making it relevant across a wide range of cancer types and immunosuppressed patients.

Warburg Suppression

SIRT6 · HIF-1α pathway

Cancer cells preferentially ferment glucose even in the presence of oxygen — the Warburg effect — to generate building blocks for rapid proliferation. SIRT6 activation via native fucoidan suppresses HIF-1α, the transcription factor that drives the Warburg metabolic switch. Cutting the fuel supply starves tumour growth independent of its mutational profile.

Checkpoint Potentiation

NK cells · Macrophage · PD-1/PD-L1

Fucoidan activates NK cells and macrophages while simultaneously potentiating PD-1/PD-L1 checkpoint inhibition. The published combination study with BMS-202 (PD-1 inhibitor) achieved 6.3× tumour necrosis versus checkpoint inhibition alone. That data used thermally extracted fucoidan. The native-sulphation comparison has not been run. That number is a lower bound.

Published Data — Thermally Extracted Fucoidan

THE FLOOR,
NOT THE CEILING.

Every published fucoidan oncology study used thermally extracted material. These numbers represent the biological activity of a degraded compound. Native sulphation amplifies these effects — by how much is the experiment that RAPIDOncology is designed to run.

Combination study — BMS-202 (PD-1 inhibitor) + thermally extracted fucoidan

6.3×

Tumour necrosis vs checkpoint inhibition alone — thermally extracted fucoidan — native sulphation experiment not yet run

Active Trials — Cancer Cachexia — Thermally Extracted Fucoidan

Two active clinical trials are using thermally extracted fucoidan for cancer cachexia. Both represent direct supply upgrade opportunities — replace degraded feedstock with native-sulphation material from the Bio-Farm cold-processing chain.

Trial ID Indication Compound Used Opportunity
NCT05616507 Cancer cachexia Thermally extracted fucoidan Supply upgrade — native sulphation
NCT05623852 Cancer cachexia Thermally extracted fucoidan Supply upgrade — native sulphation

Co-Development

SEEKING
PHARMA PARTNERS.

RAPIDOncology is not being developed as a standalone pharmaceutical product by NeuroSync. The IP position is filed. The mechanisms are described. The co-development partnership provides the clinical infrastructure to run the native-sulphation experiments and advance to Phase I.

Bristol-Myers Squibb

Checkpoint combination data — BMS-202

The published 6.3× tumour necrosis data was achieved in combination with BMS-202, a BMS checkpoint inhibitor. The logical next experiment — native sulphation + BMS-202 — is a BMS decision.

Merck / MSD

Pembrolizumab + fucoidan combination

PD-1/PD-L1 checkpoint potentiation is mechanism five. Pembrolizumab is the world's leading checkpoint inhibitor. The combination experiment defines the upper limit of the potentiation effect.

Roche · AZ · Pfizer

VEGF, metastasis, apoptosis pipeline

Anti-angiogenesis (VEGF-VEGFR2), anti-metastasis (integrin αVβ3), and direct apoptosis (caspase 3/7) mechanisms map directly to existing oncology pipeline programmes across all three organisations.

GB2607531.7 — 18 Claims — Filed 1 April 2026

PCT FILING WITHIN 12 MONTHS

NDA-protected full mechanism data, preclinical package, and co-development terms available to qualified pharma contacts.

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