Trial reportLeukemia research2013
Phase I clinical, pharmacokinetic, and pharmacodynamic study of the Akt-inhibitor triciribine phosphate monohydrate in patients with advanced hematologic malignancies.
Trial report in Leukemia research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
- Oral MEK 1/2 Inhibitor Trametinib in Combination With AKT Inhibitor GSK2141795 in Patients With Acute Myeloid Leukemia With RAS Mutations: A Phase II Study.Clinical lymphoma, myeloma & leukemia · 2019Trial
- Multi-omics profiling identifies triciribine as a biomarker-guided antimetabolite therapy for acute lymphoblastic leukemia.NPJ precision oncology · 2026Article
- Targeting a Pleckstrin Homology Domain with a Lysine-Reactive Covalent Binder.Journal of medicinal chemistry · 2026Article
- Review
- AKT and DUBs: a bidirectional relationship.Cellular & molecular biology letters · 2025Review
- FGTI-2734 Inhibits ERK Reactivation to Overcome Sotorasib Resistance in KRAS G12C Lung Cancer.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2025Article
- Article
- Combination of triciribine and p38 MAPK inhibitor PD169316 enhances the differentiation effect on myeloid leukemia cells.PloS one · 2024Article
- Article
- Targeting PI3K/Akt signaling in prostate cancer therapy.Journal of cell communication and signaling · 2023Review
- Triciribine attenuates pathological neovascularization and vascular permeability in a mouse model of proliferative retinopathy.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- Augmenting Venetoclax Activity Through Signal Transduction in AML.Journal of cellular signaling · 2023Article
- Targeting PI3K/Akt signal transduction for cancer therapy.Signal transduction and targeted therapy · 2021Review
- Akt-independent effects of triciribine on ACE2 expression in human lung epithelial cells: Potential benefits in restricting SARS-CoV2 infection.Journal of cellular physiology · 2021Article
- ZNF217: the cerberus who fails to guard the gateway to lethal malignancy.American journal of cancer research · 2021Review
- The PI3K-Akt-mTOR Signaling Pathway in Human Acute Myeloid Leukemia (AML) Cells.International journal of molecular sciences · 2020Review
- Targeting AKT for cancer therapy.Expert opinion on investigational drugs · 2019Review
- Review
- The Akt pathway in oncology therapy and beyond (Review).International journal of oncology · 2018Review
- Protein Tyrosine Signaling and its Potential Therapeutic Implications in Carcinogenesis.Current pharmaceutical design · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Akt, a serine/threonine protein kinase, is constitutively phosphorylated and hyperactivated in multiple cancers, including acute myeloid leukemia. High levels are linked to poor survival and inferior responses to chemotherapy, making Akt inhibition an attractive therapeutic target. In this phase I/II study of TCN-PM, a small-molecule Akt inhibitor, TCN-PM therapy was well tolerated in patients with advanced hematological malignancies, and reduced levels of phosphorylation of Akt and its substrate Bad were shown, consistent with inhibition of this survival pathway and induction of cell death. Further investigation of TCN-PM alone or in combination in patients with high Akt levels is warranted.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.