23 results about "Syk" patented technology

The invention relates to the field of stem cell biomedicine, and provides a stem cell biological preparation, a preparation method and application of the preparation as a rhinitis treatment medicine in order to solve the problem that when a Syk inhibitor is independently used, the recovery time of rhinitis is long, and the preparation method comprises the steps that S100, a lipidosome entrapped with the Syk inhibitor is prepared through a film dispersion method; s200, mixing the monoclonal antibody with N-hydroxysuccinimide ester according to a molar ratio of 1: (20-40), and obtaining a micelle solution through an incubation process; s300, mixing the liposome and the micelle solution according to a volume ratio of (40-70): 1 to obtain a first effective preparation; and S400, mixing the first effective preparation with the stem cell solution to obtain the stem cell biological preparation. Through cooperation of the Syk inhibitor and the stem cell repair function, the rhinitis recovery effect is improved, the Syk inhibitor is coated with the isolation layer, the action time and the action position of the Syk inhibitor are regulated and controlled, and the influence on the stem cells is reduced; due to modification of the lipidosome, the lipidosome has targeting property, and the influence on the stem cells can be reduced.

Provided herein are methods to treat neurodegenerative disease.

The invention relates to the field of antitumor drugs, in particular to a benzimidazole spleen tyrosine kinase inhibitor as well as a preparation method and application thereof. The inhibitor has a molecular structure as shown in a formula 1, in the formula 1, an R0 group is an R1 group containing an amide group, the R1 group is selected from at least one of the following groups, and an R3 group is selected from at least one of the following groups: H, F, Cl and Br; according to the benzimidazole inhibitor, the structure of the benzimidazole inhibitor can be optimized by introducing the R1 group of acylamino and the R2 group of multiple cyclic structures, so that efficient selective inhibition on spleen tyrosine kinase (Syk) is realized.

Provided are methods for determining if an individual is likely to experience immune-related adverse events (irAEs) if treated for melanoma with a combination of immune checkpoint inhibitors that are an anti-Cytotoxic T-Lymphocyte-Associated Protein 4 (CTLA-4) antibody and an anti-programmed death-ligand 1 (PD-1) antibody. The methods include determining differential gene signatures as between individuals who had melanoma and were treated with a combination of a CTLA-4 antibody and an PD-1 antibody but did not experience severe irAEs after the treatment, with the gene signature for an individual who has melanoma but was not treated with an immune checkpoint inhibitor.

The application belongs to the field of biomedical technology, and particularly relates to application of Cevidoplenib in preparation of drugs for treating periodontitis, and discloses for the first time that Cevidoplenib can inhibit Selp-induced neutrophil extracellular trap, and Cevidoplenib can inhibit the rising trend of free DNA (cf-DNA) and MPO-DNA complex caused by neutrophil extracellular trap (NETs). Experiments show that Cevidoplenib can inhibit Selp-mediated neutrophil extracellular trap (NETs) by inhibiting Syk phosphorylation, and in a periodontitis mouse model, alveolar bone absorption of the Cevidoplenib intervention group is significantly reduced, and bone parameters are obviously improved. The application provides a brand-new drug strategy for treating periodontitis related to abnormal formation of NETs.

The present invention relates to pyrazolyl-pyrimidine derivatives, methods for their preparation, pharmaceutical compositions comprising them, and their use as therapeutic agents. These compounds are kinase inhibitors, particularly inhibitors of spleen tyrosine kinase (SYK), and can be used to treat cancer, cell proliferative disorders, viral infections, immune disorders, neurodegenerative disorders, and cardiovascular diseases.

Provided are salt forms, crystal forms, and preparation methods of pyrazole-substituted imidazo[1,2-a]quinoxaline derivatives, specifically the salt forms, crystal forms, and preparation methods of the compound of formula (I), and their use in preparing drugs related to dual inhibitors of spleen tyrosine kinase (Syk) and vascular endothelial growth factor 2 (VEGFR2). #imgabs0#

Provided herein are methods of using (S)-2-(2,6-dioxopiperidin-3-yl)-4-((2-fluoro-4-((3-morpholinoazetidin-1-yl)methyl)benzyl)amino)isoindoline-1,3-dione, or an enantiomer, mixture of enantiomers, tautomer, isotopolog, or pharmaceutically acceptable salt thereof, in combination with a second active agent for treating, preventing or managing hematological malignancies. The second active agent is one or more of an HDAC inhibitor, a BCL2 inhibitor, a BTK inhibitor, an mTOR inhibitor, a PI3K inhibitor, a PKCβ inhibitor, a SYK inhibitor, a JAK2 inhibitor, an Aurora kinase inhibitor, an EZH2 inhibitor, a BET inhibitor, a hypomethylating agent, a DOT1L inhibitor, a HAT inhibitor, a WDR5 inhibitor, a DNMT1 inhibitor, an LSD-1 inhibitor, a G9A inhibitor, a PRMT5 inhibitor, a BRD inhibitor, a SUV420H1 / H2 inhibitor, a CARM1 inhibitor, a PLK1 inhibitor, an NEK2 inhibitor, an MEK inhibitor, a PHF19 inhibitor, a PIM inhibitor, an IGF-1R inhibitor, an XPO1 inhibitor, a BIRC5 inhibitor, or a chemotherapy.

The invention provides an ITK-SYK fusion gene detection kit and detection method based on ultra-high depth sequencing, the ITK-SYK fusion gene detection kit comprises a plurality of primers, the detection method uses obtained cf-RNA as a template to amplify a target sequence and build a library, the obtained library is sequenced, offline data is analyzed, and the detection result of the ITK-SYK fusion gene detection kit based on ultra-high depth sequencing is obtained. And calculating the relative proportion of the ITK-SYK fusion gene. According to the detection method, the limit of digital PCR is broken through, the designed amplified fragment is shorter, the detection sensitivity is further improved, an SE50-SE75 short read length mode is used during sequencing, ultrahigh sequencing depth is achieved under the condition of extremely small data volume, 10 <-6 > low-frequency fusion mutation can be detected, the time required by the overall experimental process is as short as 1 day, and the report period is greatly shortened. The method is high in specificity, high in sensitivity, simple, convenient and rapid to operate and rigorous and reliable in result, provides a reliable method for related research of ITK-SYK gene fusion diseases, and is a convenient and non-invasive detection technology.

Methods for treating leukemia are disclosed based on detecting specific cell states and transcriptional programs within leukemic cells. This disclosure presents a novel therapeutic method for treating acute lymphoblastic leukemia (ALL), including BCR-ABL positive and BCR-ABL1-like ALL subtypes. The method involves detecting specific cell states and transcriptional programs in patient samples and administering targeted therapies based on these characteristics. For a pre-B cell-like state or pre-BCR signaling program, a combination of tyrosine kinase inhibitor (TKI) and SYK inhibitor is used. Conversely, a progenitor-like state or stress-autophagy program is treated with a TKI and a p38 MAPK inhibitor. This approach aims to improve treatment efficacy by tailoring therapy to the leukemia's unique molecular and cellular features, particularly in relapsed cases or when minimal residual disease is present.

The present disclosure describes novel compounds, or their pharmaceutically acceptable salts, pharmaceutical compositions containing them, and their medical uses. Compounds of the disclosure have activity as dual modulators of Janus kinase (JAK), alone, or in combination with one or more of an additional mechanism, including a tyrosine kinase, such as TrkA or Syk, and PDE4, and are useful in the in the treatment or control of inflammation, auto-immune diseases, cancer, and other disorders and indications where modulation of JAK would be desirable. Also described herein are methods of treating inflammation, auto-immune diseases, cancer, and other conditions susceptible to inhibition of JAK and PDE4 by administering a compound herein described.

The invention relates to application of a compound 101-mer in preparation of an influenza vaccine adjuvant and an influenza vaccine, and belongs to the technical field of biology. The compound 101-mer is used as an influenza vaccine adjuvant for preparing an influenza vaccine, the immune protection effect of the influenza vaccine can be improved, the specific total IgG antibody titer of an influenza antigen and IgG1, IgG2a, IgG2b and IgG3 subtype antibody levels are improved, complete protection is provided after challenge, tissue damage is relieved, and the antiviral activity is remarkably superior to that of compounds 18-mer, 19-mer, 27-mer and LPS; as an adjuvant, the compound 101-mer does not have observable toxicity, can still be well tolerated under a high dosage, and has relatively high safety, and the safety of the compound 101-mer is remarkably superior to that of LPS (Lipopolysaccharide); the action mechanism is clear, and the compound can be used as a Dectin-2 agonist to activate a host immune system through a Syk / NF-kappa B signal channel.

The present application provides a gene marker combination and a use thereof in an early-onset preeclampsia risk prediction model. The gene marker combination comprises at least one selected from a combination of GTF2H1, CD48, PBX1, PLA2G2A, ACVR1B, HMGB1, ERBB2, XRCC5, TGFBR2, NFKB1, EGF, TLR6, EZH2, IKZF1, EGFR, and CD36, a combination of HIPK1, MTHFR, IL6R, RAB27A, UBE2I, CREBBP, SOX8, HNF4A, ICOS, LIF, TMPRSS6, DNMT3A, WWTR1, RASSF1, FOXP1, TLR2, and MAPK14, a combination of AGRN, ATP2B1, ELAC2, HDAC5, GABARAP, FXR2, NFE2L2, DGCR2, MAPK1, CASR, MYLIP, TUBB, DOCK4, PTGS1, HSPA5, ABL1, and SYK, or a combination of chr1:110,000,000-115,000,000, chr4:150,000,000-155,000,000, chr6:160,000,000-165,000,000, chr6:60,000,000-65,000,000, and chr7:125,000,000-130,000,000.

Provided are a salt form and a crystal form of a pyrazole substituted imidazo[1,2-a]quinoxaline derivative, and a preparation method therefor. Specifically disclosed are a salt form and a crystal form of a compound of formula (I), and a preparation method therefor and the use thereof in the preparation of drugs related to dual inhibitors of spleen tyrosine kinase (Syk) and vascular endothelial growth factor 2 (VEGFR2).

Provided herein, inter alia, are methods of treating chemical or radiation-induced lung injury by administering to a subject Fosatinib, an active ingredient thereof, or a pharmaceutically acceptable salt thereof.

The present invention provides compounds of Formula (I) which can be used as Syk inhibitors and potently as therapeutic agents against diseases mediated by Syk.

The present invention relates to a SYK gene SNP primer and application related to the isovaleric acid content in musk deer, and belongs to the field of biotechnology. The present invention provides a SYK gene SNP primer related to the isovaleric acid content trait in musk deer, the deoxyribonucleotide sequence of the SNP primer is as shown in SEQ ID NO: 1 and SEQ ID NO: 2, the SNP is located at the 25879500th base of chromosome 7 of the musk deer reference genome, the base mutation is A or G, and the genotype is GG, AG. The detection method disclosed in the present invention is simple and easy to operate, can be carried out in the laboratory, and can also be applied to genomic breeding technology. Its beneficial effect is that it can efficiently and quickly identify the relative content trait of isovaleric acid in musk deer, providing a scientific basis for the early breeding of high-quality musk deer.

Provided herein are methods of using (S)-2-(2,6-dioxopiperidin-3-yl)-4-((2-fluoro-4-((3-morpholinoazetidin-1-yl)methyl)benzyl)amino)isoindoline-1,3-dione, or an enantiomer, mixture of enantiomers, tautomer, isotopolog, or pharmaceutically acceptable salt thereof, in combination with a second active agent for treating, preventing or managing hematological malignancies. The second active agent is one or more of an HDAC inhibitor, a BCL2 inhibitor, a BTK inhibitor, an mTOR inhibitor, a PI3K inhibitor, a PKCβ inhibitor, a SYK inhibitor, a JAK2 inhibitor, an Aurora kinase inhibitor, an EZH2 inhibitor, a BET inhibitor, a hypomethylating agent, a DOT1L inhibitor, a HAT inhibitor, a WDR5 inhibitor, a DNMT1 inhibitor, an LSD-1 inhibitor, a G9A inhibitor, a PRMT5 inhibitor, a BRD inhibitor, a SUV420H1 / H2 inhibitor, a CARM1 inhibitor, a PLK1 inhibitor, an NEK2 inhibitor, an MEK inhibitor, a PHF19 inhibitor, a PIM inhibitor, an IGF-1R inhibitor, an XPO1 inhibitor, a BIRC5 inhibitor, or a chemotherapy.

This invention belongs to the field of pharmaceutical synthesis technology, specifically relating to a compound containing an imidazo[1,2-a]pyrazine fragment, its preparation method, and its applications. The compound containing the imidazo[1,2-a]pyrazine fragment of this invention exhibits significant inhibitory activity against SYK, and also significantly inhibits the proliferation of tumor cells, particularly breast cancer cells, ovarian cancer cells, and liver cancer cells. Furthermore, it can induce apoptosis in ovarian cancer cells, thus providing a novel option for SYK inhibitors used in the treatment of solid tumors.

The present invention relates to a novel monoclonal antibody and its use in a specific method for the expansion of adaptive NK lymphocytes expressing the activating receptor CD94 / NKG2C. In particular, the invention relates to a monoclonal antibody designed for the selective expansion of adaptive NK lymphocytes NKG2C+CD57+NKG2A- selfKIR+ FcϵRy- / low and Syk- / Iow, characterized by the absence of the inhibitory receptor PD-1. The invention also describes a specific method for the expansion and selection of this particular cell population, as well as the use of the aforementioned population in the medical field.

The invention relates to the use of AT7867, MC1568, ACY-1215, AZD-4547, NPK76- II-72-1, tivozanib, SAR-245409, HG-9-91-01, BIX-01294, UNC-669, WZ-7043, dacomitinib, CC-401, UNC-0638, epigallocatechin gallate (-), SB-239063, GDC-0879, KIN001-260, quizartinib, CGK-733, UNC-1215, XMD11-85H, garcinol, PF-573228, veliparib, VE-821, NVP-TAE684, GSK-J2, masitinib, KU-55933, KIN001-127, KIN001- 270, vandetanib, CG-930, GNF-2, decitabine, SGI-1776, amuvatinib, BS-181, CTB, MGCD-265, olaparib, ZM-447439, AGK-2, bosutinib, JNJ-38877605, RG-108, SYK- inhibitor, AZ-20, and OSI-930 drugs, which aim to suppress immune system escape mechanisms in cancer treatment and reduce the proliferation and survival abilities of cancer cells by interacting with proteins involved in immune escape processes and / or neighbouring proteins of these proteins, in T-cell-based immunotherapies.

The invention provides a salt form, a crystal form and a preparation method of a pyrazole-substituted imidazo [1, 2-a] quinoxaline derivative, and particularly discloses a salt form, a crystal form and a preparation method of a compound shown in a formula (I), and application of the compound in preparation of spleen tyrosine kinase (Syk) and vascular endothelial growth factor 2 (VEGFR2) dual-inhibitor related drugs.

The present disclosure describes novel compounds, or their pharmaceutically acceptable salts, pharmaceutical compositions containing them, and their medical uses. Compounds of the disclosure have activity as dual modulators of Janus kinase (JAK), alone, or in combination with one or more of an additional mechanism, including a tyrosine kinase, such as TrkA or Syk, and PDE4, and are useful in the in the treatment or control of inflammation, auto-immune diseases, cancer, and other disorders and indications where modulation of JAK would be desirable. Also described herein are methods of treating inflammation, auto-immune diseases, cancer, and other conditions susceptible to inhibition of JAK and PDE4 by administering a compound herein described.