41 results about "AKT1" patented technology

The invention provides a plant lactobacillus IOB602 for down-regulating an angiotensin receptor gene expression level and an application thereof, and relates to the technical field of microorganisms, the classification name of the plant lactobacillus IOB602 is plant lactobacillus, the plant lactobacillus IOB602 is preserved in China General Microbiological Culture Collection Center on June 29, 2018, called CGMCC for short, and the preservation number of the plant lactobacillus IOB602 is CGMCC. The preservation address is No.3, Yard 1, Beichen West Road, Chaoyang District, Beijing, and the preservation number is CGMCC No.16021. By down-regulating the expression level of an angiotensin II receptor type 1 AT1R gene, a PI3K / AKT1 / eNOS / NO signal channel is activated, the activity of angiotensin converting enzyme is inhibited, vasodilation is enhanced, and blood pressure is reduced.

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.

The invention discloses application of melastoma dodecandrum lour in preparation of antihypertensive drugs and drugs for treating hypertension complications. It is found for the first time that by means of melastoma dodecandrum extract treatment, AKT1 and EGFR protein expression related to hypertension can be lowered, blood pressure (Plt, 0.05) and cardiac fibrosis degree (Plt, 0.01) of spontaneously hypertensive rats (SHR) can be remarkably lowered, inflammatory response (Plt, 0.05) can be inhibited, and the effect of treating the melastoma dodecandrum extract can be achieved. The melastoma dodecandrum not only has the effect of reducing blood pressure, but also has the functions of improving myocardial fibrosis and inhibiting inflammatory response; moreover, the melastoma dodecandrum lour has no toxic or side effect on the body, is safe and reliable to use, shows that the melastoma dodecandrum lour has good research and development prospects of reducing blood pressure, improving myocardial fibrosis and resisting ventricular remodeling, and provides a new effective way for hypertension and corresponding complications.

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 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 compositions and methods for the treatment of cancer. Said compositions comprise a AKT1 inhibitor. Some embodiments comprise combination therapy featuring the AKT1 inhibitor with at least one additional oncology therapeutic agent.

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.

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.

The invention discloses a biological marker, a therapeutic drug and an action target spot for traumatic brain injury, and belongs to the technical field of biological medicine. The miRNA is selected from one or more of rno-miR-382-3p, rno-miR-21-5p, rno-miR-370-3p and the like, and the miRNA is one or more of the following components: the rno-miR-382-3p and the like. The invention also provides an application of the ginsenoside Rg1 in preparing a medicine for regulating and controlling the expression quantity of the miRNA in the claim 1 and an action target of the ginsenoside Rg1 for treating TBI by regulating and controlling the expression quantity of the miRNA in the claim 1, wherein the action target mainly comprises AKT1, EGFR, MMP9, SRC, STAT3 and CASP3. The method has the beneficial effects that the miRNAs expression change of exosomes in plasma after traumatic brain injury is evaluated through a high-throughput RNA sequencing technology, and 14 miRNAs are screened and proposed and can be used as biomarkers for diagnosing traumatic brain injury; and the influence of the Rg1 on the expression of the miRNAs in the plasma after trauma is further researched so as to determine the effectiveness and the targeting action way of treating the trauma by the Rg1.

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.

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.

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.

Described herein are compounds and methods for the modulation of AKT1 proteins, such as AKT1 E17K. In some aspects, the present disclosure provides an AKT1 protein, wherein a compound is bound to a lysine residue of the AKT1 protein. In another aspect, the present disclosure provides compounds of Formula (I) and (II), useful for the modulation of AKT1 proteins. In another aspect, the instant disclosure provides a method of attenuating AKT1 activity using the compounds described herein.

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 relates to solid state forms of 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 and salts thereof. Such solid state forms are useful in preparation of pharmaceutical compositions and dosage forms for the treatment of disease.

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

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.