University of South Florida

Yale University

Other

University of Florida Research Foundation Inc

Jin Q. Cheng

Said M. Sebti

Jin Q Cheng

Said M Sebti

Andrew D Hamilton

Katherine J Kayser-Bricker

Mei Sun

This application relates to combination therapies including triciribine compounds and epidermal growth factor receptor inhibitor compounds, particularly erlotinib-like compounds and compositions with reduced toxicity for the treatment and prevention of tumors, cancer, and other disorders associated with abnormal cell proliferation.

Compositions including triciribine and epidermal growth factor receptor inhibitor compounds or salts thereof and methods of use thereof

Methods of treating breast cancer that overexpress AKT kinase

The inventors have determined, contrary to the prior art and experience, how to successfully use triciribine to treat ovarian cancer by one or a combination of (i) administering triciribine only to patients which according to a diagnostic test described below, exhibit enhanced sensitivity to the drug; (ii) use of a described dosage level that minimizes the toxicity of the drug but yet still exhibits efficacy; or (iii) use of a described dosage regimen that minimizes the toxicity of the drug.

Effective treatment of ovarian cancer using triciribine and related compounds

Disclosed herein is a species of peptide and non-peptide inhibitors of Akt, an oncogenic protein. Beginning with a residue of Akt target substrate GSK-3, the functional domains of the GSK-3 residue were characterized. Functionally homologous non-peptide groups were substituted for the amino acids of the GSK-3 creating a hybrid peptide-non-peptide and non-peptide compounds capable of binding to Akt. The non-peptide compounds show increased stability and rigidity compared to peptide counterparts and are less susceptible to degradation. The bound non-peptide compounds exhibit an inhibitory effect on Akt, similar to peptide-based Akt inhibitors.

Substrate-mimetic AKT inhibitor

The inventors have determined, contrary to the prior art and experience, how to successfully use triciribine to treat tumors and cancer by one or a combination of (i) administering triciribine only to patients which according to a diagnostic test described below, exhibit enhanced sensitivity to the drug; (ii) use of a described dosage level that minimizes the toxicity of the drug but yet still exhibits efficacy; or (iii) use of a described dosage regimen that minimizes the toxicity of the drug.

Effective treatment of tumors and cancer with triciribine and related compounds

This invention encompasses combination therapies including TCN, TCN-P, TCN-PM and/or related compounds and one or more additional anti-cancer agents, for example, taxanes a molecule that modulates the HER2/neu (erbB2) receptor, anthracyclin compounds, epidermal growth factor receptor inhibitor compounds, one or more platinum compounds and bortezomib and derivatives thereof and compositions with reduced toxicity for the treatment and prevention of tumors, cancer, and other disorders associated with abnormal cell proliferation.

Compositions including triciribine and methods of use thereof

This application relates to combination therapies including triciribine and related compounds and taxanes and compositions with reduced toxicity for the treatment and prevention of tumors, cancer, and other disorders associated with abnormal cell proliferation.

Compositions including triciribine and taxanes and methods of use thereof

This application relates to combination therapies including triciribine and related compounds and bortezomib and derivatives thereof analogs and compositions with reduced toxicity for the treatment and prevention of tumors, cancer, and other disorders associated with abnormal cell proliferation.

Compositions including triciribine and bortezomib and derivatives thereof and methods of use thereof

This application encompasses combination therapies including triciribine and related compounds and one or more platinum compounds and compositions with reduced toxicity for the treatment and prevention of tumors, cancer, and other disorders associated with abnormal cell proliferation.

Compositions including triciribine and one or more platinum compounds and methods of use thereof

This application relates to combination therapies including triciribine and related compounds and trastuzumab or a salt thereof and compositions with reduced toxicity for the treatment and prevention of tumors, cancer, and other disorders associated with abnormal cell proliferation.

Compositions including triciribine and trastuzumab and methods of use thereof

The inventors have determined, contrary to the prior art and experience, how to successfully use triciribine to treat esophogeal adenocarcinoma by one or a combination of (i) administering triciribine only to patients which according to a diagnostic test described below, exhibit enhanced sensitivity to the drug; (ii) use of a described dosage level that minimizes the toxicity of the drug but yet still exhibits efficacy; or (iii) use of a described dosage regimen that minimizes the toxicity of the drug.

Effective treatment of esophageal adenocarcinoma using triciribine and related compounds

Substrate-mimetic Akt inhibitor

MicroRNAs (miRNAs) represent a novel class of genes that function as negative regulators of gene expression and have recently been implicated in several cancers. However, aberrant miRNA expression and its clinicopathological significance in human ovarian cancer have not been well documented. Numerous miRNAs are shown altered in human ovarian cancer, significantly miR-214, -199a*, -200a, -100, -125b, -30d, -221, -222, -126, and -24. Four miRNAs (miR-221, miR-222, miR-126, and miR-24) were found to be deregulated in all four histological types of ovarian carcinoma (serous, mucinous, endometrioid, and clear cell). Frequent deregulation of miR-214, -199a*, -200a and -100 was demonstrated in ovarian cancers. Significantly, miR-214 induces cell survival and cisplatin resistance through targeting down-regulation of proteins activating the Akt pathway. Inhibition of Akt using Akt inhibitor, API-2/triciribine, or PTEN cDNA lacking 3'UTR largely abrogates miR-214 induced cell survival. These findings indicate that deregulation of miRNAs is a recurrent event in human ovarian cancer and that miR-214 induces cell survival and cisplatin resistance primarily through targeting the PTEN/Akt pathway.

Growing community of inventors

Tampa, FL, United States of America

Jin Q Cheng