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The Science of
Cancer Cell Plasticity

Understanding why some cancers stop responding to treatment — and how we can prevent it.

The Problem

Why Cancer Wins

Most cancer therapies are designed to hit a specific target, for example, a mutated gene, an overexpressed protein or a signalling pathway. They often work. But cancer adapts.

Through a process called cellular plasticity, tumour cells can change states to shift their identity, downregulate the targeted pathway, and re-emerge as a treatment-resistant population. This is not a rare event. It is an important mechanism of treatment failure across many cancer types.

Resistance does not arrive from outside the tumour. It is already there, encoded in the biological flexibility of cancer cells — waiting to be selected.

“Therapy resistance is responsible for the majority of cancer deaths worldwide. Plasticity is an engine that drives it.”

~90%

of metastatic cancer deaths involve treatment resistance

All types

Plasticity operates across virtually every solid tumour

Cancer Cells Can Change

Plasticity in Action

Understanding how plasticity works gives us a precise point of intervention.

Cancer Cells Are Plastic

Cancer cells are not fixed in their state. They can switch from a less aggressive form into a more aggressive, treatment-resistant one.

Chemotherapy Triggers the Switch

In some cancers, chemotherapy itself triggers this change by activating biological programs that make surviving cells harder to kill.

Resistance Emerges

Once cells have switched state, they are more likely to stop responding to treatment.

Why Plasticity Drives Resistance

An Active
Survival Strategy

CSC vs non-CSC cell state conversions

Cancer cell plasticity is not a side effect of treatment, rather it is an active survival strategy. When cancer cells sense a threat, they can reorganise their internal biology, switching on genes and pathways that protect them from that threat.

In triple-negative breast cancer, the subject of Kembi's existing Phase 2 clinical program, this switching is driven by androgen receptor signalling. When chemotherapy is administered, androgen receptor activation triggers cancer cells to change state and emerge as chemotherapy-resistant cells that are harder to target. Until recently, this process had no validated clinical intervention.

Kembi's Approach

Blocking
the Switch

Kembi's plasticity-targeting therapies are designed to block the switching mechanism before it can occur. This approach works alongside conventional cancer therapy, not instead of it.

Stop cell switch

What Seviteronel Does

  • Blocks the switch

    Inhibiting androgen receptor signalling with seviteronel stops the trigger for cancer cells to change state.

  • Prevents resistance from emerging

    Now when chemotherapy is used, the cancer cells are unable to use androgen receptor signalling to switch into a resistant state to evade the therapy.

  • Preserves chemotherapy effectiveness

    By preventing the switch, chemotherapy stays effective for longer.

Watch & Listen

Stopping plasticity to prevent resistance

Watch on YouTube

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