<p><strong>Join us to build:</strong> we’re seeking entrepreneurially-minded scientists with deep technical expertise, who are eager to solve one of the most durable and consequential challenges in medicine through venture building. This role offers a unique opportunity to work at the forefront of CNS drug delivery, leading a company that makes it fundamentally easier, safer and more broadly applicable to get therapeutics into the brain.</p><p>The role is full-time, remote initially until venture incorporation and spin-out (circa end of 2027), location TBD.</p><h3>The Opportunity</h3><p>CNS diseases represent one of the largest and most persistent unmet needs in medicine. Over 1 billion people worldwide live with a neurological condition, yet disease-modifying treatments remain elusive for the vast majority - from Alzheimer’s and Parkinson’s to multiple sclerosis and rare paediatric neurological disorders. The failure rate in CNS drug development is among the highest of any therapeutic area, and a central reason is not a lack of therapeutic targets: it is our inability to reliably deliver drugs across the blood-brain barrier (BBB).</p><p>The BBB is a highly specialised endothelial barrier that protects the brain from pathogens and toxins - but in doing so, it excludes the vast majority of therapeutic molecules. Fewer than 2% of small molecules cross the BBB in meaningful quantities, and almost no large-format biologics - antibodies, proteins, nucleic acids - reach the brain parenchyma without specialised delivery mechanisms. This has forced the field into a narrow set of workarounds: direct intracranial injection, high-dose systemic administration with poor CNS penetration, or compromising on target biology to find something accessible.</p><p>The emergence of receptor-mediated transcytosis (RMT) as a BBB delivery strategy represented a genuine step forward. Pioneered clinically by approaches targeting TfR1 and CD98hc, RMT exploits the brain’s own endocytic transport machinery to carry therapeutic cargo across the BBB endothelium. Roche, Denali, and others have invested heavily in this paradigm, and early clinical data are encouraging. But the fundamental constraints of these approaches are becoming clearer: haematotoxicity arising from high peripheral expression of TfR1, receptor saturation by endogenous transferrin, inefficient endosomal tubule sorting leading to lysosomal degradation of cargo, and receptor downregulation under sustained high-affinity engagement. These are not engineering imperfections that can be tuned away - they are intrinsic consequences of repurposing receptors whose primary biological function is not transcytosis.</p><p>Much of the underlying biology that governs whether cargo successfully reaches the brain parenchyma, rather than being degraded en route, remains a relatively unexplored design space - distinct from the well-trodden ground around TfR1 and CD98hc. And beyond transcytosis, other constraints persist across the