Solid tumours are never still.
Most oncology programs test candidates in static conditions. Real tumours are under constant force. NeoMag® controls it.
Cancer is a mechanical problem.
You already know a static well cannot tell you the whole story. In a real tumour, growth, CAF contractility, matrix remodelling, compression, confinement, interstitial flow, fibrosis and inflammation deform cancer, stromal and immune cells every day, and that is what drives proliferation, invasion, immune exclusion and drug response. Stiffness is part of it; dynamic deformation and loading are what decide cell behaviour. We give you control of both.
What force controls
Forces rewire cell fate
Compression, tension, shear and confinement act through integrins (FAK/Src, YAP/TAZ, Piezo1 and the LINC complex), reaching chromatin and shifting proliferation, EMT, stemness and therapy resistance.
The cytoskeleton drives invasion
Actin contractility, microtubules and vimentin let cancer cells deform, shield the nucleus and degrade matrix; CAF traction and interstitial flow carve the tracks that guide metastasis.
Fibrosis & inflammation are mechanically driven
Desmoplasia stiffens the stroma, feeding a fibrosis (inflammation) stiffness loop that hardens the tumour against treatment.
Tumour mechanics block therapy
Crosslinked collagen, solid stress and interstitial pressure compress vessels, block drug penetration and exclude T cells.
Immune cells feel force
Stiff, deforming matrix impairs T-cell infiltration and drives exhaustion via chronic Piezo1 signalling; relieving load improves anti-PD-1 response.
Static culture hides the forces that decide how a tumour behaves.
Why this matters for your pipeline
ADCs depend on mechanical state
Antigen accessibility, binding, internalisation and lysosomal trafficking shift under load. An ADC that looks promising in 2D can fail in a loaded microenvironment.
Anti-fibrotic & anti-CAF therapies need load
Loading the stroma shows whether a candidate truly normalises matrix, lowers pressure and reopens drug and immune access.
Cytoskeleton- & invasion-targeting drugs are force-dependent
Migrastatics and actomyosin/ROCK, microtubule or intermediate-filament agents engage fully only under load; loaded models expose their potency.
Mechanical context decides efficacy
Understand why a drug shifts a marker yet fails to control the tumour, and find combinations that restore drug penetration and immune response.
Mechanical response profiling, not another fixed-stiffness model.
Applies real forces
Defined deformation, compression, tension, frequency and duration on living tumour models (cells, CAF co-cultures, organoids, ECM gels, immune cells, ± drug).
More controlled than in vivo
Each force is a precise, repeatable parameter, isolated from systemic confounders.
Scalable
Screen many candidates under identical, quantified loading regimes for robust head-to-head ranking.
Complements, doesn't replace
Layers onto molecular, organoid and animal models across solid tumours, ADCs, immuno-oncology and the tumour microenvironment.