apolipoprotein
target · ANGPTL3 — chr 1p31.3A single-edit therapy for homozygous familial hypercholesterolemia. Reduces LDL by silencing ANGPTL3 in hepatocytes — durable, one-time treatment.
Codon turns rare-disease genetics into clinical programs. A therapeutics company brand and design language for science that has to read as both rigorous and human.
Codon's platform is built on a quiet truth: gene editing is at its most powerful when it is restrained. One sequence, one cut, one repair. The brand carries that discipline through every surface.
A guide RNA — twenty bases long, a near-perfect match to the target locus — directs Cas9 to a single position in three billion. The enzyme reads, confirms, and cuts. The cell repairs. What changes is precise. What is left is everything else.
The system below — sketched at the level of visible, not literal — anchors every Codon surface: investor decks, regulatory submissions, the patient registry, the lobby glass at HQ.
Codon advances rare-disease therapeutics where the genetics are well-characterised and the unmet need is total. Each program targets a single locus with a single edit.
A single-edit therapy for homozygous familial hypercholesterolemia. Reduces LDL by silencing ANGPTL3 in hepatocytes — durable, one-time treatment.
Ocular gene editing for Leber congenital amaurosis. Locally delivered, single-injection, restores rhodopsin cycling in retinal pigment epithelial cells.
Reactivation of fetal haemoglobin via a precise enhancer disruption. In vivo delivery to hematopoietic stem cells, building on the Vertex / CRISPR Tx blueprint.
A continuously-improving toolkit of tissue-targeted delivery vehicles. Each new program contributes back into the library; each future program inherits.
The visual system reads as scientific without reading as clinical-cold. Editorial spreads, clinical one-pagers, and a patient registry portal share the same restraint.