<?xml version="1.0" encoding="UTF-8"?><ns2:project xmlns:ns1="http://gtr.rcuk.ac.uk/gtr/api" xmlns:ns2="http://gtr.rcuk.ac.uk/gtr/api/project" xmlns:ns3="http://gtr.rcuk.ac.uk/gtr/api/fund" xmlns:ns4="http://gtr.rcuk.ac.uk/gtr/api/person" xmlns:ns5="http://gtr.rcuk.ac.uk/gtr/api/project/outcome" xmlns:ns6="http://gtr.rcuk.ac.uk/gtr/api/organisation" ns1:created="2026-06-03T15:52:43Z" ns1:href="http://gtr.ukri.org/gtr/api/projects/DD66ED5B-6248-4157-9BA6-643E5DCF7E69" ns1:id="DD66ED5B-6248-4157-9BA6-643E5DCF7E69"><ns1:links><ns1:link ns1:href="http://gtr.ukri.org/gtr/api/persons/69EB0E93-8BD0-4CE6-A6E0-475C5032D790" ns1:rel="PM_PER"/><ns1:link ns1:href="http://gtr.ukri.org/gtr/api/organisations/50F457E7-653B-4A9F-82DB-C21E6ED94382" ns1:rel="LEAD_ORG"/><ns1:link ns1:href="http://gtr.ukri.org/gtr/api/organisations/50F457E7-653B-4A9F-82DB-C21E6ED94382" ns1:rel="PARTICIPANT_ORG"/><ns1:link ns1:end="2022-03-30T23:00:00Z" ns1:href="http://gtr.ukri.org/gtr/api/funds/498BAE4B-1055-4447-B80C-30C6D3157531" ns1:rel="FUND" ns1:start="2019-06-30T23:00:00Z"/></ns1:links><ns2:identifiers><ns2:identifier ns2:type="RCUK">105199</ns2:identifier></ns2:identifiers><ns2:title>Clinical validation of a revolutionary multi-analyte companion diagnostic platform technology and treatment algorithm for precision medicine</ns2:title><ns2:status>Closed</ns2:status><ns2:grantCategory>Collaborative R&amp;D</ns2:grantCategory><ns2:leadFunder>Innovate UK</ns2:leadFunder><ns2:abstractText>&amp;quot;Acute myeloid leukaemia (AML) is an aggressive form of blood cancer, where only about 20% of patients are expected to survive for 5 or more years after diagnosis. A new drug called midostaurin can triple survival times for some patients and is now available on the NHS. However, only a subgroup of AML patients (~30%) are eligible to receive this treatment and approximately 50% of those will experience no benefit; therefore, only about 15% of AML patients overall actually benefit from treatment. Consequently, many patients are exposed to unnecessary side-effects, are denied the opportunity to be recruited on trials for drugs that may be effective, and the NHS are subjected to unnecessary costs (\&amp;gt;&amp;pound;23M/year) treating patients that fail to benefit.

The diagnostic test used to determine patient eligibility to receive midostaurin is called LeukoStrat(r), which assesses whether an AML patient's cancer cells have mutations in a gene called FLT3\. Patients who are positive for this &amp;quot;&amp;quot;biomarker&amp;quot;&amp;quot; will receive midostaurin.

Early clinical trials and a recent pre-clinical study by Kinomica's Founders showed that 42-65% of patients _without_ the FLT3 mutation biomarker (representing 70% of all AML patients) responded well to midostaurin, so there is likely a significant number of patients currently classified as ineligible who could benefit from treatment. Midostaurin is currently in the very advanced stages of clinical trials for use in patients without the FLT3 mutation biomarker. Thus the importance of identifying those who will benefit from treatment becomes even greater, as the cost to the NHS to treat patients who will not benefit could triple.

The variable response rates for midostaurin treatment in AML (with and without mutated FLT3), suggest that the current FLT3 mutation biomarker and medical test to detect this marker (LeukoStrat(r)) are severely limited. Kinomica's Founders have developed a new and much more accurate way to predict whether an AML patient will respond to midostaurin. Kinomica's approach involves measuring the activity of an important group of proteins called kinases, within a patient's cancer cells. This readout can then better predict whether midostaurin will destroy those cells. Funding is sought so that Kinomica can develop the technology into a clinical test. The realisation that kinase activities are better predictors of therapeutic response than genetic alterations will likely have far wider implications for the development of personalised therapies across many cancer types.&amp;quot;</ns2:abstractText></ns2:project>