Loading
AKT1 E17K is a single hotspot mutation, in about 3 to 5 percent of hormone-receptor-positive breast cancers, that switches on the AKT kinase directly. It is one of the three alterations that qualify a patient for capivasertib.
The E17K substitution in the pleckstrin homology domain sends AKT1 to the membrane without PIP3. Capivasertib (Truqap) is labelled with fulvestrant for HR-positive HER2-negative advanced breast cancer with one or more PIK3CA, AKT1 or PTEN alterations as detected by an FDA-approved test (CAPItello-291); FoundationOne CDx carries the three-gene claim. AKT1 E17K also appears in endometrial and rarer cancers, where it is a trial marker only.
In plain words · AKT is a central survival kinase downstream of PI3K, blocked by capivasertib in breast and now prostate cancer.
An AKT1 E17K result in hormone-receptor-positive breast cancer qualifies you for capivasertib with fulvestrant once hormone therapy has stopped working, the same as a PIK3CA mutation or PTEN loss would. Alpelisib and inavolisib are not approved for AKT1 mutations on their own.
Written only from the label or guideline text cited on this page. Not medical advice; your own report and the reading your team gives it come first.
The AKT1 c.49G>A (p.E17K) substitution by sequencing of tumour tissue or plasma, reported with PIK3CA and PTEN as the capivasertib selection set.
“PIK3CA/AKT1/PTEN alterations”
FDA: List of FDA-Authorized Companion Diagnostic Devices| Threshold | Drug | Cancer | Regulator | Source |
|---|---|---|---|---|
| AKT1 alteration (with PIK3CA and PTEN as the qualifying set) | Capivasertib | HR-positive / HER2-negative breast cancer | FDA | label |
| Device | Maker | Indication and sample | Drug | PMA / 510(k) |
|---|---|---|---|---|
| FoundationOne CDx | Foundation Medicine | Breast Cancer - Tissue | CapivasertibFulvestrant | P170019/S048 (11/16/2023) |
Matched on the name and aliases of the readout in the title, setting and summary of each trial; a match is a mention, not proof the readout was an entry criterion.
PAKT gives the trial-based prevalence of PI3K-pathway alteration in first-line metastatic TNBC (one in five) and the strongest signal for AKT inhibition in that subgroup; the phase 3 CAPItello-290 did not confirm it.
This is the sourced bridge between expression subtype and mutation: it tells a clinician that a LAR tumour is the one to sequence for PIK3CA and AKT1, and that immunomodulatory biology is a favourable prognostic group before any immunotherapy.
Shares Capivasertib, Endometrial cancer, HR-positive / HER2-negative breast cancer and the tag biomarker.
Shares Endometrial cancer, HR-positive / HER2-negative breast cancer and the tag biomarker.
Shares FoundationOne CDx / Liquid CDx and the tag biomarker.
Shares Triple-negative breast cancer (TNBC), HR-positive / HER2-negative breast cancer and the tag biomarker.
Shares FoundationOne CDx / Liquid CDx and the tag biomarker.
Shares Triple-negative breast cancer (TNBC), HR-positive / HER2-negative breast cancer and the tag biomarker.
Shares Endometrial cancer, Triple-negative breast cancer (TNBC) and the tag biomarker.
Shares FoundationOne CDx / Liquid CDx, Endometrial cancer, Triple-negative breast cancer (TNBC) and the tag biomarker.