Insights
The science of multispecific immune design — explained by the scientists who built the platform.
Same target, different outcome.
Multiple approved therapies target the same myeloma antigen. They do not perform the same. The variable is not the target — it is what was measured during design, and whether those measurements predicted the biology that determines clinical outcomes.
Read article →CAR-T or BiTE? The wrong question.
The debate misframes the choice. What matters is not the format — it's the biology it's designed to engage. The right question is what the disease requires at this stage of treatment, not which delivery mechanism wins.
Read article →Antigen escape isn't a biology problem. It's an engineering problem.
Tumours shed targeted antigens under selective pressure. The question is whether the therapy was designed for that reality — and the answer is determined at the engineering stage, before the first patient is dosed.
Read article →What functional data actually means — and why it changes what gets into the clinic.
Not all data predicts clinical performance. Most drug discovery measures the wrong thing. The infrastructure constraint that keeps the field optimising for binding has a solution — and it changes what clinical translation looks like.
Read article →From serums to T-cell engagers: how immunotherapy learned to direct the immune system.
A century of immunotherapy — from Coley's toxins to checkpoint inhibitors to programmable multispecifics. Each era solved one problem and revealed the next.
Read article →T-cell engager or CAR-T? In the same disease, targeting the same antigen, the outcomes still differ.
Both formats redirect T cells to the same target. The clinical results are not the same. Format matters less than most assume — and more than some claim.
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