Akt sensitization of cancer cells
US8828451B2 · kind B2 · utility
Assignee
Inventors
Key dates
| Filing date | Oct 4, 2007 |
| Grant date | Sep 9, 2014 |
| Priority date | — |
| Expiry date | Jan 15, 2028 |
Classification
- Technology area (CPC C)Chemistry; Metallurgy
- CPC primaryC07K2317/24
- WIPO fieldPharmaceuticals
- WIPO sectorChemistry
Abstract
Most human tumors find ways to resist anticancer drug monotherapy. Akt is considered a likely peptide providing such monotherapy drug resistance. Data indicates that Akt chemoresistance is induced in a p53-dependent manner and that inhibition of Akt may be an effective means of overcoming chemoresistance in cancer cells expressing wild-type p53. Breast, ovarian, lung cancer and leukemia cells lines were treated with combinations of Akt activation inhibitor Triciribine (TCN) or Triciribine phosphate (TCNP) and chemotherapeutic drugs to determine the efficiency of combination therapy. Additionally, cells were introduced into xenograft models to determine in vivo effects of combination treatment. Combining TCN or TCNP with other anticancer drugs overcame cytotoxic or treatment resistance. Thus, TCN and TCNP are shown to broaden the spectrum of human tumors that can be effectively treated.
Source: USPTO / EPO open patent data. Objective bibliographic and citation counts.