The Promise and the Problem
Checkpoint inhibitors like pembrolizumab and nivolumab have revolutionized cancer treatment. For some patients, these drugs produce responses that last years—turning a terminal diagnosis into a manageable condition.
But here's the challenge: only 20-30% of patients actually respond. The rest experience the side effects—sometimes severe—without the benefit. And our current testing methods can't reliably tell us who will be in which group.
Expression ≠ Function
Current PD-L1 tests measure how much protein is present. But a protein can be present without being active. It can be in the wrong location. It might not be engaged with its binding partner.
Missing Responders
24% of patients who could benefit from immunotherapy have low PD-L1 expression. They're denied treatment based on a test that measures the wrong thing.
Treating Non-Responders
18% of patients with high PD-L1 expression don't respond to treatment. They endure toxicity without benefit because the test said they should respond.
No Mechanism Insight
Expression testing tells you a protein exists. It doesn't tell you if the immune evasion mechanism is actually active—the very thing the drug is designed to block.
"If a drug works by blocking an interaction, we should measure whether that interaction is happening—not just count molecules."
Two Approaches, Different Answers
There's a Better Way
What if we measured what actually matters—whether immune checkpoint proteins are actively engaged? Not just present, but functioning. Not just expressed, but interacting.
That's exactly what functional biomarkers do. By measuring protein-protein interaction at nanometer resolution, we can see whether the immune evasion mechanism is truly active—and predict whether blocking it will help.
(31 vs 10 months)
See the Evidence
Real clinical data showing how functional biomarkers change patient outcomes.