Defined target biology
PTPσ and inhibitory proteoglycans provide a specific molecular framework for programme design.
Lead proprietary programme
MK-1 is being developed within the proteoglycan–PTPσ biology that regulates axonal growth, plasticity and repair after nervous-system injury.
Programme rationale
Neural tissue can retain substantial capacity for repair after injury, but CSPG-rich extracellular matrix restricts the extension and reorganisation required for recovery. PTPσ is a central receptor in this inhibitory response and links matrix composition to growth-cone behaviour.
MK-1 applies peptide pharmacology to this target space. The programme is structured to connect molecular interaction with neurite growth, cellular repair and translational outcomes while building a proprietary data and intellectual-property position.
Programme profile
PTPσ and inhibitory proteoglycans provide a specific molecular framework for programme design.
Neurite extension under CSPG-conditioned inhibition provides a direct and reproducible functional readout.
The pathway is implicated in axonal repair, remyelination, plasticity and the post-injury microenvironment.
Maak controls programme strategy, experimental packages, resulting data and intellectual-property development.
Development work
The programme advances through specific experiments that show where MK-1 acts, what response it produces and how that response translates.
Characterise activity within the CSPG–PTPσ signalling environment using defined biochemical systems.
Quantify neurite extension and growth-cone response under controlled inhibitory conditions.
Evaluate neuronal and glial responses relevant to protection, plasticity and remyelination.
Test exposure, biomarkers, anatomy and function in models selected for pathway relevance.
Scientific foundation
The literature identifies PTPσ as a receptor for inhibitory CSPGs, explains how proteoglycan structure changes receptor organisation, and demonstrates peptide-mediated recovery of neurite growth and functional effects in preclinical neural-repair models. MK-1 advances this field as Maak's proprietary programme.
Primary literature
Work with Maak