19 results about "AKT1" patented technology

Provided herein are inhibitors of AKT1, pharmaceutical compositions comprising the inhibitory compounds, and methods for using the AKT1 inhibitory compounds for the treatment of disease.

Provided herein are pharmaceutical formulations of the AKT1 E17K selective inhibitor 4-((1-(4-(2-(2-aminopyridin-3-yl)-5-(5-fluoropyridin-2-yl)-3H-imidazo[4,5-b]pyridin-3-yl)benzyl)piperidin-4-yl)amino)pyrimidine-2-carbonitrile maleate.

The application belongs to the field of biological medicine, and particularly relates to a group of gene mutations and application thereof in diagnosis of pancreaticobiliary duct cancer. Specifically, the application provides a group of gene mutations for detecting pancreaticobiliary duct cancer, wherein the gene mutations include one or more of AKT1, KRAS, APC, NRAS, ARID1A, PIK3CA, AXIN1, PPP2R1A, BAP1, PTEN, BRAF, SMAD4, CDKN2A, TERT, TP53, EGFR, FBXW7, FGFR2, HRAS, IDH1 and IDH2.

The application discloses application of an AKT1 inhibitor in preparation of a medicine for treating pigmented villonodular synovitis. A person skilled in the art knows that high migration activity and high invasion activity of PVNS-FLSs are important reasons for causing the development of the disease. Experimental results of the application show that the migration and invasion activity of PVNS-FLSs can be effectively inhibited by silencing AKT1. Therefore, the AKT1 inhibitor has the prospect of being developed into a medicine for treating pigmented villonodular synovitis.

This invention discloses the application of lncRNA SVIL-AS1 as a target in AKT1E17K mutant tumors, belonging to the field of molecular biology technology. This invention provides the application of lncRNA SVIL-AS1-related biomaterials in the preparation of products for regulating the function of AKT1E17K mutant cells. This invention verifies that SVIL-AS1 can specifically bind to AKT1E17K mutants and inhibit their phosphorylation level and kinase function, thereby inhibiting the proliferation of AKT1E17K mutant cells, revealing the role of SVIL-AS1 in the treatment of AKT1E17K mutant tumors. This invention applies lncRNA SVIL-AS1 to the treatment of AKT1E17K mutant tumors, not only providing a new source for the preparation of materials for the prevention and treatment of AKT1E17K mutant tumors, but also exploring new pharmaceutical value of lncRNA SVIL-AS1.

Provided herein are fusion proteins having (i) a signaling activator comprising an AKT1 polypeptide, and (ii) a protein transduction domain. The fusion protein can activate cytokine pathway signaling in a cell independently of the binding of a cytokine to a cytokine receptor. Also provided herein are nucleic acids and vectors encoding the fusion proteins, as well as cells and compositions having the fusion proteins. In addition, provided herein are methods of using the fusion proteins to activate cytokine signaling in a cell, to prepare a therapeutic cell, and to treat a disease or condition in a subject.

The invention relates to the technical field of biological medicines, in particular to a cell-penetrating peptide targeting a UFL1-AKT signal axis and used for preventing and treating tumors as well as application and a pharmaceutical composition of the cell-penetrating peptide. The amino acid sequence of the cell-penetrating peptide is as shown in SEQ ID No. 1. The in-vitro and in-vivo progresses of other types of breast cancers such as triple negative breast cancers, hormone receptor positive breast cancers and HER2 receptor positive breast cancers can be remarkably inhibited by using the cell-penetrating peptide to destroy the interaction of UFL1-AKT. The discovery of the inventor reveals a key role of UFL1-AKT feedback circulation in other types of breast cancers such as triple negative breast cancers, hormone receptor positive breast cancers, HER2 receptor positive breast cancers and the like, and prompts that the target UFL1-AKT1 axis may provide a new strategy for cancer treatment.

The present disclosure provides a culture medium for cell culturing, the culture medium containing a combination of specific components. The present disclosure provides a culture medium which contains a combination of components selected from the group consisting of: (1) a halcinonide component; (2) an ALK4 / 7 inhibitor or a TGFβ receptor type-1 kinase inhibitor; (3) a BRD7 / 9 double degradation factor or a BRD7 / 9 binding molecule (degradation factor); (4) an LATS1 / 2 inhibitor, a PKA inhibitor, or an AKT1 inhibitor; (5) a CK1 / 2 inhibitor, an insulin receptor inhibitor, a Tyr kinase inhibitor, a PKA inhibitor or a PKC inhibitor, or an adenosine kinase inhibitor; (6) an E-selectin inhibitor, a VCAM1 inhibitor, or an ICAM1 inhibitor; and (7) an LATS1 inhibitor + an LATS2 inhibitor.

This invention relates to the application of hedera saponin A1 in the preparation of drugs for the prevention and / or treatment of seborrheic keratosis or its secondary lesions. Through molecular-level experiments, this invention verifies that hedera saponin A1 can directly bind to the AKT1 protein, inhibiting AKT1-induced upregulation of pro-apoptotic proteins, thereby initiating cell apoptosis. Compared with existing technologies, this invention is a non-invasive treatment, painless, non-invasive, and leaves no scars after healing. Furthermore, this invention has the dual efficacy of "treating seborrheic keratosis" and "chemopreventing malignant transformation." In addition, hedera saponin A1 has a significant killing effect on seborrheic keratosis lesion cells, exhibiting a killing effect on the epidermal layer of isolated seborrheic keratosis lesion tissue, but without inducing significant apoptosis in dermal cells.

The invention discloses application of AKT1-K189 / 276 / 297Ufm protein in cancer diagnosis and treatment, and belongs to the field of biological medicine. According to the application disclosed by the invention, the fact that UFMylatation modification (AKT1-K189 / 276 / 297Ufm) of AKT1 is a necessary condition for activating the AKT1 and is also necessary for growth and metastasis of breast cancer is proved for the first time in a cellular level and a mouse model. Therefore, the AKT1-K189 / 276 / 297Ufm protein can be used as a novel diagnostic marker for breast cancer generation and metastasis, the accuracy of predicting breast cancer metastasis in breast cancer diagnosis is improved, and the breast cancer diagnosis is quicker and more accurate. The AKT1-K189 / 276 / 297Ufm protein also provides a new molecular target for breast cancer treatment, and lays a theoretical foundation for developing a novel medicine for treating breast cancer. The application can be expanded to lung cancer and pancreatic cancer.