MK-1. A proprietary peptide programme for neural repair.

MK-1 is being developed within the proteoglycan–PTPσ biology that regulates axonal growth, plasticity and repair after nervous-system injury.

Preclinical research programme

Target a defined extracellular barrier to regeneration.

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.

A focused asset in a biologically validated pathway.

01

Defined target biology

PTPσ and inhibitory proteoglycans provide a specific molecular framework for programme design.

02

Quantifiable phenotype

Neurite extension under CSPG-conditioned inhibition provides a direct and reproducible functional readout.

03

Translational relevance

The pathway is implicated in axonal repair, remyelination, plasticity and the post-injury microenvironment.

04

Proprietary development

Maak controls programme strategy, experimental packages, resulting data and intellectual-property development.

Mechanism connected
to measurable biology.

The programme advances through specific experiments that show where MK-1 acts, what response it produces and how that response translates.

01

Molecular interaction

Characterise activity within the CSPG–PTPσ signalling environment using defined biochemical systems.

02

Neurite outgrowth

Quantify neurite extension and growth-cone response under controlled inhibitory conditions.

03

Repair biology

Evaluate neuronal and glial responses relevant to protection, plasticity and remyelination.

04

Translational models

Test exposure, biomarkers, anatomy and function in models selected for pathway relevance.

Peer-reviewed research supports intervention at both the matrix and receptor level.

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.

TargetProteoglycan-regulated PTPσ signalling
Primary phenotypeNeurite growth under CSPG inhibition
Programme objectiveRestore a repair-supportive neural response

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