A new immunotherapy has produced early signs of activity in people whose solid tumours had resisted multiple treatments, including immune checkpoint drugs. In a first-in-human Phase I/II trial, invikafusp alfa—shortened to invika—shrunk measurable tumours by at least 30% in four of 27 participants treated at the study’s selected biological doses.
The peer-reviewed results, published in Nature Medicine on 23 October 2026, are notable because the drug does not target a single cancer mutation. Instead, it selectively activates two families of T cells that already exist in the immune system.
This is an early, single-arm trial across several tumour types. It establishes a dose and provides preliminary evidence—not proof that invika improves survival or outperforms existing treatment.
A narrower way to press the immune accelerator
Checkpoint inhibitors work by releasing brakes that cancers use to suppress T cells. Invika takes a different approach. It is a bispecific antibody designed to bind and activate T cells carrying the Vβ6 or Vβ10 forms of the T-cell receptor while also providing a co-stimulatory signal.
Those subsets contain many different tumour-recognising T cells. The strategy aims to expand a useful slice of the existing immune repertoire rather than activating every T cell indiscriminately or manufacturing a personalised cell product.
Blood and tumour analyses showed dose-dependent expansion of the intended Vβ6 and Vβ10 populations, many with memory-like features. Interferon-gamma and soluble CD25, markers of immune activation, rose in a similar dose range.
The response signal came from a small selected group
Phase I enrolled 34 people across six dose levels, from 0.01 to 0.16 milligrams per kilogram. The initial Phase II portion enrolled another 18. Most participants had antigen-rich solid tumours that were resistant to immune checkpoint blockade.
At the two optimal biological doses—0.08 and 0.12 milligrams per kilogram—16 of 27 participants, or 59.3%, had no disease progression at the reported assessment. Four, or 14.8%, had confirmed partial responses. Responses included microsatellite-stable colorectal cancer and PD-L1-negative non-small-cell lung cancer, tumour settings that are often difficult to treat with existing checkpoint immunotherapy.
No objective responses occurred below 0.08 milligrams per kilogram. That dose-response pattern supports biological activity, but the small numbers make every percentage unstable. One additional response or progression would noticeably change the headline rate.
Safety was manageable in this dataset, not settled
The trial did not reach a maximum tolerated dose. Two participants experienced reversible dose-limiting toxicities, one at 0.08 and one at 0.16 milligrams per kilogram. Cytokine release syndrome—an inflammatory reaction caused by rapid immune activation—was the most common treatment-related adverse event and was mainly grade 1 or 2.
The paper reports no treatment-related deaths and no treatment-related non-laboratory grade 4 adverse events. That is encouraging for dose selection, but uncommon harms often emerge only after many more people are treated. Participants in early oncology trials are also closely monitored at specialist centres.
Why Phase II and randomised evidence matter
The data cutoff was 12 March 2025, even though the paper appeared in 2026. START-001 remains ongoing under ClinicalTrials.gov identifier NCT05592626. The reported population mixed cancer types, previous treatments and dose levels, and there was no control group.
Stable disease can be meaningful in heavily treated cancer, but it can also reflect natural variation or selection of slower-growing tumours. A response rate cannot by itself show longer survival or better quality of life.
The next tests are larger tumour-specific cohorts, durability of response, combinations with other therapies and eventually randomised comparisons. The NIH summary describes the activity as early, which is the right frame: invika has demonstrated that its mechanism can work in people, not that resistant cancer has been solved.
Featured image: National Cancer Institute/Unsplash. Contextual cell-culture photograph; not START-001 trial evidence.
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