AAB builds genetically programmable nanovesicles from engineered human cell membranes. One platform carries small molecules, RNA and biologics, and releases them into the cytosol of a chosen cell.
Chemotherapy damages healthy tissue because it goes everywhere. Targeted agents often reach the right tissue but not the right compartment: most cargo carried by lipid nanoparticles is trapped and destroyed before it reaches the cytosol. The limiting step is rarely the drug. It is getting enough of it to the inside of the right cell, and nowhere else.
of patients do not respond to CD19 CAR-T, and have no established standard of care after it fails.
Previously treated metastatic PDAC, RAS G12 population
Nanovesicles are produced from engineered human cell membranes. Because the producing cells are genetically programmed, what sits on the vesicle surface is designed rather than inherited.
Antibodies or ligands displayed on the surface, multiplexed when no single marker is specific enough. CD19 today; TROP2 with cMET or EGFR for solid tumours.
Small molecules, RNA and biologics such as antibodies and enzymes. One platform, three classes, including agents too fragile or too toxic to give on their own.
Fusogenic proteins fuse the vesicle with the cell membrane and release cargo into the cytosol, bypassing the endosome that traps most lipid nanoparticle payloads.
Pancreatic cancer is the case that defeats most delivery technologies. Five-year survival in the UK remains near 7%, and tumour cells sit behind a dense extracellular matrix that drugs struggle to cross.
The platform was developed within the company. Earlier work was supported by SynbiCITE and by Accelerate@Babraham, both non-dilutive and neither holding any claim to the intellectual property.
Vesicle production and purification, RNA loading, and proof of target engagement on CD19-positive B cells by flow cytometry.
Selectivity and efficacy in patient-derived models, accessed through academic collaboration, then toxicity and efficacy in vivo.
A data and development package that pharmaceutical partners can evaluate, built around a defined cargo such as a KRAS or BTK inhibitor.
Regulatory toxicology and an MHRA clinical trial authorisation for one in-house candidate, into a phase 1a/1b trial.
Molecular biophysicist with over fifteen years across chemistry, structural biology and pharmacology. PhD in Chemistry from Utrecht University, where she pioneered dynamic nuclear polarisation for structural biology. Postdoctoral positions at AMOLF, Amsterdam, and the University of Nottingham. Twenty-four peer-reviewed papers and over 1,400 citations. Founded AAB and led it into Accelerate@Babraham with funded lab space. Secured a £400,000 MRC grant as co-investigator and a paid R&D collaboration with Boehringer Ingelheim.
Chair in Molecular and Cellular Pharmacology at the University of Nottingham and a member of the COMPARE Centre. Over 100 peer-reviewed publications and three decades in receptor biophysics, structural biology and drug discovery. Pioneered live-cell biophysical assays, including BRET and kinetic ligand-binding methods. Founder of Z7 Biotech, a precision pharmacology CRO. Long-standing collaborations with Roche, AstraZeneca and Boehringer Ingelheim.
If you hold a compound that cannot reach the inside of the right cell, that is the conversation we want. We are equally glad to hear from academic groups with disease-relevant models. We are raising pre-seed funding of £1M for in vivo proof of concept. SEIS and EIS eligible.
Occasional updates on the platform, data and partnerships. A few emails a year, nothing else.
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