16 results about "Activating transcription factor" patented technology

The invention discloses an anti-TL1A antibody or an antigen binding fragment thereof and application of the anti-TL1A antibody or the antigen binding fragment thereof. The anti-TL1A antibody or the antigen binding fragment thereof comprises HCDR1: X1YX2MH, hCDR2: X < 3 > X < 4 > NPYX < 5 > X < 6 > X < 7 > TX < 8 > YX < 9 > X < 10 > KFKG; hCDR3: X < 11 > X < 12 > X < 13 > X < 14 > X < 15 > X < 16 > X < 17 > X < 18 > X < 19 > Y; lCDR1: X < 20 > ASX < 21 > X < 22 > VX < 23 > X < 24 > X < 25 > X < 26 > X < 27 >; lCDR2: X < 28 > X < 29 > X < 30 > X < 31 > X < 32 > X < 33 > X < 34 >; and LCDR3: QQX35SSX36PX37T, and LCDR3: The anti-TL1A antibody or the antigen binding fragment thereof provided by the invention has TL1A binding affinity, especially can be specifically bound with TL1A, and can be used for detecting TL1A; the compound also can block the activity of a TL1A activated transcription factor NF [kappa] B, has an effect of inhibiting IFN-gamma, and can be used for preventing and / or treating TL1A mediated related diseases.

The present disclosure provides genetically modified iPSC-derived γδT cells and their precursors. A double genomic disruption in the suppressor of cytokine signaling 1 (SOCS1) gene and the cytokine-inducible sh2-containing protein (CISH) gene are provided, as is a triple genomic disruption in genes for SOCS1, CISH, and Bcl-2 interacting mediator of cell death (BIM), as is a quadruple genomic disruption in genes for SOCS1, CISH, BIM, and cell surface death receptor (FAS), as is a quintuple genomic disruption in genes for SOCS1, CISH, BIM, β-2-Microglobulin (B2M), and class II transactivator (CITTA), as is a sextuple genomic disruption in genes for SOCS1, CISH, BIM, B2M, CITTA, and FAS. Also provided is genetically modified iPSC-derived γδT cells and their precursors with improved proliferation and tumor killing activity. Also provided are genetically modified iPSC-derived γδT cells and their precursors further comprising CD19 CAR. The present disclosure further provides methods making and using such cells, as well as gene editing systems.

The present disclosure provides genetically modified iPSC-derived γδT cells and their precursors. A double genomic disruption in the suppressor of cytokine signaling 1 (SOCS1) gene and the cytokine-inducible sh2-containing protein (CISH) gene are provided, as is a triple genomic disruption in genes for SOCS1, CISH, and Bcl-2 interacting mediator of cell death (BIM), as is a quadruple genomic disruption in genes for SOCS1, CISH, BIM, and cell surface death receptor (FAS), as is a quintuple genomic disruption in genes for SOCS1, CISH, BIM, β-2-Microglobulin (B2M), and class II transactivator (CIITA), as is a sextuple genomic disruption in genes for SOCS1, CISH, BIM, B2M, CIITA, and FAS. Also provided is genetically modified iPSC-derived γδT cells and their precursors with improved proliferation and tumor killing activity. Also provided are genetically modified iPSC-derived γδT cells and their precursors further comprising CD19 CAR. The present disclosure further provides methods making and using such cells, as well as gene editing systems.

Compounds as inhibitors of Activating Transcription Factor 6 (ATF6) are provided. The compounds may find use as therapeutic agents for the treatment of diseases or disorders mediated by ATF6 and may find particular use in the treatment of viral infections, neurodegenerative diseases, vascular diseases, or cancer.

The invention discloses an anti-TL1A antibody or an antigen binding fragment thereof and application thereof. The anti-TL1A antibody comprises at least one of the following CDRs: a heavy chain variable region CDR: an amino acid sequence as shown in SEQ ID NO: 1-3, SEQ ID NO: 7-9 or SEQ ID NO: 13-15; and the light chain variable region CDR has an amino acid sequence as shown in SEQ ID NO: 4-6, SEQ ID NO: 10-12 or SEQ ID NO: 16-18. The anti-TL1A antibody or the antigen binding fragment thereof provided by the invention has TL1A binding affinity, especially can be specifically bound with TL1A, and can be used for detecting TL1A; the compound also can block the activity of a TL1A activated transcription factor NF [kappa] B, has an effect of inhibiting IFN-gamma, and can be used for preventing and / or treating TL1A mediated related diseases.

The present invention relates to novel compounds (I') which inhibit the Signal Transducer and Activator of Transcription protein 6 (STAT6). This invention also relates to pharmaceutical compositions containing them, processes for their preparation and their use in the treatment of several disorders.

To provide heme oxygenase 1 (HMOX 1) inducers.SOLUTION: There are provided compounds represented by structural formula (I) as heme oxygenase 1 (HMOX 1) inducers (Formula I) and a method of controlling the activity or the amount, or both the activity and the amount, of heme-oxygenase 1 in a mammalian subject. A pharmaceutical composition is provided for use in methods of increasing the activity of or the amount of HMOX1 in a human subject, methods of activating transcription factor Nrf2 in a human subject, and methods of reducing the amount of ROS in a human subject, wherein the pharmaceutical composition comprises the compounds, or a pharmaceutically acceptable salt thereof, and at least one pharmaceutically acceptable diluent or carrier.SELECTED DRAWING: None

The present invention relates to STAT3 degraders and methods of use thereof for treating diseases, disorders, or conditions in patients comprising one or more mutations to serine / threonine kinase 11 (STK11) or KRAS.

Compounds (I) that are modulators of activated transcription factor 6 (ATF6) are provided. These compounds can be used as therapeutic agents for treating diseases or disorders mediated by ATF6, and can be particularly used to treat viral infections, neurodegenerative diseases, vascular diseases or cancer. #imgabs0#

The present invention relates to novel compounds (I') which inhibit the Signal Transducer and Activator of Transcription protein 6 (STAT6). This invention also relates to pharmaceutical compositions containing them, processes for their preparation and their use in the treatment of several disorders.

The application discloses application of an anti-IFN-gamma antibody loaded hydrogel in preparation of a drug for treating bisphosphonate-related osteonecrosis of the jaw. The research result of the application shows that ZOL treatment can promote secretion of IFN-gamma by gamma delta T cells, enhance glycolysis of osteoclasts, induce histone H3K18 lactic acidification of lactic acid generated by glycolysis, activate transcription factor IKZF1 and downstream effector molecule ZBP1, finally drive necrotic apoptosis of osteoclasts and damage bone remodeling function. By locally applying GelMA@ab at a BRONJ lesion, controllable release of the anti-IFN-gamma antibody can be realized, IFN-gamma activity can be effectively blocked, necrotic apoptosis of osteoclasts and local inflammatory reaction can be significantly reduced, and a rat BRONJ-like lesion can be improved. Therefore, the application provides an effective strategy for treatment of BRONJ and provides experimental feasibility support for clinical conversion application of the composite hydrogel.

Compounds (1-2) as modulators of Activating Transcription Factor 6 (ATF6) are provided. The compounds may find use as therapeutic agents for the treatment of diseases or disorders mediated by ATF6 and may find particular use in the treatment of viral infections, neurodegenerative diseases, vascular diseases, or cancer. (Formula (1-2))

The invention belongs to the field of tobaccos, and provides an alginate oligosaccharide molecule for improving the sweetness of tobacco leaves by activating transcription factors. By screening alginate oligosaccharide fragment molecules and activating a signal channel, carbon and nitrogen metabolism of the tobacco leaves is promoted, degradation of macromolecular substances such as starch is promoted, a metabolic pathway of aroma substances such as flavone is activated, and the sweetness of the tobacco leaves is improved.

The disclosure relates to methods of inhibiting cellular senescence involving expressing Activating Transcription Factor 3 (ATF3) in a cell at a level sufficient to inhibit senescence of the cell. In some embodiments, ATF3 is delivered to a cell via administration of a messenger ribonucleic acid comprising an open reading frame encoding ATF3.

The present invention provides compositions and methods for the sensitization of tumor cells to immune killing and to improve anti-tumor immunotherapy. The methods of treating cancer include administering to the subject a therapeutically effective amount of an activator of Activating Transcription Factor 6 (ATF6). Methods and compositions for enhancing immune checkpoint blockade therapy in are also provided and include administering an effective amount of an activator of Activating Transcription Factor 6 (ATF6) before, during or after administration of an immune checkpoint blockade therapy.

The invention relates to ATF6 modulators and uses thereof. Compounds (I) are provided that are modulators of activating transcription factor 6 (ATF6). These compounds can be used as therapeutic agents for the treatment of diseases or disorders mediated by ATF6 and in particular for the treatment of viral infections, neurodegenerative diseases, vascular diseases or cancer. # imgabs0 #