Ab-LNP_mRNA
Platform validatedIn-situ cell engineering — instructing pathological cells to express therapeutic proteins locally.
Every nucleated cell can read an RNA instruction. Very few can be reached by one. Our platform is built around that gap.
~10¹³
Cells in an adult body
<1%
Reached by untargeted LNP outside liver and spleen
Ribosomes translate messenger RNA into protein in every nucleated cell in the body. Because the instruction itself is universal, the same molecular format can drive a cytotoxic response, restore a missing enzyme, or shut down a pathological programme — the outcome depends only on which cell receives it.
That universality is why RNA therapeutics are described as programmable. It is also why delivery, rather than design, decides which programmes ever become medicines.
After intravenous dosing, lipid nanoparticles are cleared by the liver and spleen. Reaching a tumour, an atherosclerotic lesion or inflamed mucosa requires an active targeting strategy — not a larger dose.
Attaching antibodies to a nanoparticle tends to destabilise the particle, obscure the binding site, or introduce batch-to-batch variation that is difficult to control at scale.
A conjugation step that works in a microcentrifuge tube rarely survives process transfer. Historically, every new antibody risked becoming a new process.
Promax has built an antibody-conjugated lipid nanoparticle platform — Ab-LNP — that treats the antibody as an interchangeable targeting module rather than a new product. A simplified, stable labelling chemistry anchors the antibody to the particle surface while preserving both binding avidity and payload integrity.
On top of that chemistry sits a tuned universal protein corona: a controlled surface composition that reduces unproductive clearance and keeps the targeting antibody available to its receptor. The practical consequence is a platform where changing the antibody changes the destination, without rebuilding the process.
Two payloads run on this backbone today. mRNA drives in-situ cell engineering, validated at platform level. CRISPR sgRNA drives in-situ gene editing, currently in development. Both share the same conjugation chemistry, the same analytical toolkit and the same production line.
In-situ cell engineering — instructing pathological cells to express therapeutic proteins locally.
In-situ gene editing — correcting or disabling a disease-driving locus inside the target cell.
Each component is developed in-house and validated against the same performance standard: does it make the next program faster without making it less precise?
Synthetic modified RNA carries the critical information that produces an antigen or a therapeutic protein. Getting it into a particle is straightforward. Getting the particle to a chosen cell is not.
Our conjugation chemistry attaches the antibody through a simplified, stable labelling process that preserves particle size distribution, encapsulation efficiency and antibody orientation. Because the bond is stable through formulation, lyophilisation and storage, the targeting function survives the manufacturing process rather than degrading inside it.
The payload determines what the cell becomes. We design mRNA sequences for high translation efficiency and controlled duration, using computational screening to balance expression level against innate immune activation.
For gene-editing programs, guide RNA is designed and ranked in silico, then validated for on-target activity and off-target risk. Both payload classes share one quality framework: defined integrity, defined potency, defined impurity profile.
When a nanoparticle enters circulation it is immediately coated by plasma proteins. That corona — not the particle itself — is what the immune system and the clearance organs actually see. An uncontrolled corona is the most common reason a well-targeted particle still ends up in the liver.
We engineer a tuned universal corona: a defined surface composition that reduces opsonisation and non-specific uptake while leaving the targeting antibody accessible. In practice this preserves receptor availability at the target site and widens the therapeutic window between local effect and systemic exposure.
Cell therapy works, but it is built outside the body: cells are collected, engineered, expanded and returned. That model is powerful and constrained — by time, by cost, by the biology of the cells that can be extracted.
In-situ engineering keeps the cell where it is. The Ab-LNP carries the instruction directly to the pathological population, so the cell that causes the disease becomes the cell that produces the therapy. Because the target is the disease site rather than the whole patient, the safety question changes from systemic exposure to local specificity.
Programmes in exploration
Most AI in drug discovery stops at prediction. We apply it to the operation itself: a six-layer system that spans laboratory hardware, drivers, data, applications, AI decision-making and governance, with validation built into every layer.
Instruments report into a governed data layer; the application layer schedules runs, analyses results and generates reports; the AI layer manages decisions, people, pipeline, materials and budget against the same record. Quality management is not a parallel track — system, algorithm and method validation are defined inside the architecture.
Each layer is validated before the layer above depends on it.
Modularity is a process decision, not only a scientific one. Because the antibody is a configurable input rather than a new product architecture, a new program reuses existing formulation, analytics and equipment — what we call line-agnostic adaptation.
The manufacturing approach is built for transfer: defined unit operations, in-line process control, and analytical methods that are the same from preclinical batches to clinical supply. Scale-up changes throughput, not the chemistry.
Illustrative comparison of biodistribution strategy, not clinical data.
We evaluate antibody candidates, payload configurations and process transfers with academic and industry partners.