Dark Blue Therapeutics LogoDark Blue Therapeutics
Dark Blue Therapeutics Logo

Exploiting the Achilles heels in cancer requires deep understanding and precision

Many cancers become dependent on specific biological processes or signalling pathways for growth and survival. These represent Achilles heel vulnerabilities that can be exploited with precision medicines. At Dark Blue Therapeutics we work closely with world leading academics to identify novel approaches to exploit these dependencies and vulnerabilities.

Mutations that confer growth and survival advantage can drive exploitable vulnerabilities.

Genetic instability is a fundamental hallmark of cancer resulting in the accumulation of mutations across the genome of cancer cells, from small single nucleotide mutations to wholesale chromosomal rearrangements. These mutations can directly alter the function of critical genes to confer a growth or survival advantage to the cancer cell or can force the cancer cell to adapt the function of other genes to survive. This in turn can lead the cell to become dependent on specific proteins or pathways for survival,  exposing a potentially exploitable vulnerability.  This acts to molecularly mark the cancer cell as being differentiated from normal cells, providing opportunities for precision targeting. It is this combination of precision medicines to target cancer cells vulnerabilities that Dark Blue Therapeutics pursues.

Normal
cell
Cell
Genome
instability
Arrow
Acquired
mutations
Tumour
Tumour
Arrows going in 2 directions
Arrow going left and downArrow going right and down
Specific mutations to key proteins can cause
constitutive pathway activity and tumorigenesis
Tumorigenic illustration
Tumorigenic
Precision medicine
to block the mutant
protein or pathway
Tumour
Mutations can drive the cancer to adapt and
become dependent on specific signaling pathways
Precision medicine
to block the
adaptive response
Growth and survival illustrationCAncer cell - Adapted biologyCancer cell - Exploit vulnerability
Normal cell
Cancer cell

Adapted biology
Cancer cell

Exploit vulnerability

Delivering precision medicines with transformative benefit and a clear line of sight to approval.

At Dark Blue Therapeutics we are committed to delivering medicines that transform the outcomes for cancer patients. We work across a variety of biological mechanisms to identify and pursue only cancer targets that have the highest transformative potential. Proprietary chemical and functional genomics are central to our approach to drive a comprehensive understanding of the targets we work on and the drug candidates we discover. We use these insights to inform the optimal mechanism of action e.g. inhibition vs degradation; to validate the therapeutic hypothesis for single-agent activity, to establish opportunities for mechanism based combinations, and to identify optimal dosing schedules.

Most notably, our deep target understanding enables us to molecularly define patient populations predicted to benefit from our medicines. This insight - coupled with companion biomarkers - enables rapid and focussed clinical proof-of-concept studies and to support early regulatory approval.

For all our programs we prioritise opportunities for single agent activity in molecularly defined high unmet need patients that provide a clear line of sight to an approved medicine.

Precision medicines with clear markers to predict patient responders can increase response rate

Predictive markers enable potential
responsive patients to be enriched

Graphic of people in order

75% response rate in target population

Lack of predictive markers make it hard
to enrich for responsive patients

A graphic with people placed randomly

30% response rate in unselected target population

Our portfolio

Pipeline

Program

Target
Validation

Hit
Discovery

Hit
Validation

Hit
to Lead

Lead Optimization

Lead Opt.

IND
enabling

Transcriptional driver

RNA editing

Smoothened pathway

Early portfolio

Program

Target
Validation

Hit
Discovery

Hit
Validation

Hit
to Lead

Lead Opt.

IND
enabling

Transcrip-
tional driver

RNA editing

Smoothened pathway

Early
portfolio