A neoantigen produced by a mutation that recurs across many patients' tumors — so a single off-the-shelf product can target it, instead of a vaccine built per person.
Most neoantigens are private: they come from mutations unique to one patient's tumor, which is why a personalized neoantigen vaccine has to be manufactured individually. But some cancer mutations are not random — they recur at the same position across thousands of patients. The neoantigens those recurrent mutations produce are called shared, or public, neoantigens.
The classic examples sit in the genes mutated most often in cancer: specific hotspots in TP53 (such as R175H) and KRAS (such as G12D and G12V). Because the same mutated peptide appears in many people, a shared neoantigen can be targeted by an off-the-shelf product — a single vaccine, or a single engineered T-cell receptor — rather than a bespoke design per patient. The catch is that the target still has to be presented on the patient's HLA, so a given shared-neoantigen therapy usually works only for patients carrying both the mutation and a compatible HLA allele.
Shared neoantigens are commercially attractive for exactly this reason: they trade the breadth of a personalized approach for the manufacturing simplicity of one product for many patients. ASCO 2026 featured both a shared-neoantigen vaccine (NOUS-209, for frameshift neoantigens) and a shared-neoantigen cell therapy (NT-175, against TP53 R175H).
A shared (public) neoantigen is a tumor-specific peptide created by a mutation that recurs across many patients — for example hotspot mutations in TP53 or KRAS. Because the same target appears in many people, it can be addressed with one off-the-shelf product rather than a vaccine built individually per patient.
A personalized (private) neoantigen comes from a mutation unique to one patient's tumor and requires a bespoke, per-patient product. A shared neoantigen is the same recurrent mutation found across many tumors, so a single product can treat many patients — though they still must carry the right HLA allele to present it.
They are the most frequently mutated genes in cancer, and their mutations cluster at a few hotspot positions (e.g. TP53 R175H, KRAS G12D/G12V). That recurrence means the same mutated peptide appears in large numbers of patients, making it worth developing one therapy — a vaccine or an engineered T-cell receptor — against it.