101 results about "Inducer Cells" patented technology

The application discloses a photosensitizer conjugate for targeted treatment of tongue squamous cell carcinoma and a preparation method and application thereof, and belongs to the technical field of biological medicines. A novel PROTAC-PDT conjugate Gef-PRO-SS-TPE is synthesized, and the compound connects a PROTAC molecule Gef-PRO targeting EGFR and an AIE photosensitizer TPE derivative through a breakable disulfide bond. On one hand, Gef-PRO can specifically degrade EGFR and block tumor cell proliferation signals; on the other hand, the TPE derivative can generate ROS under light conditions and induce cell apoptosis. More importantly, the disulfide bond can be broken in response to high concentrations of glutathione (GSH) in tumor cells, realizing controllable release of Gef-PRO and TPE molecules, so as to exert a synergistic anti-tumor effect.

The application provides a kind of HLA-A24:02 APC cell preparation method and application, it is related to cell preparation technical field.The present application constructs the APC cell (K562-HLA-A24:02) that can replace HLA-A24:02 subtype DC cell, fills the blank of HLA-A24:02 subtype special engineering APC cell, and the cell can realize the antigen presentation function consistent with natural HLA-A24:02 subtype DC cell, provides special tool cell for the immune research for the HLA subtype;The present application constructs APC cell with K562 cell line as base, K562 cell can be in vitro permanent passage amplification, without repeatedly separating and inducing DC cell from human peripheral blood, reduces the use amount of peripheral blood, reduces the raw material dependence and cost of cell acquisition, while avoiding the influence of individual difference of peripheral blood source on experimental results.

The present application discloses an antiviral fusion protein. Specifically, the present application provides an antiviral fusion protein, which comprises a cell death inducing domain (lethal domain), a domain inhibiting the activity of the lethal domain (inhibitory domain) and a protease recognition sequence capable of removing or destroying the function of the inhibitory domain; the fusion protein has the activity of inducing cell death after being cut by a specific viral protease, thereby killing the cells infected by the virus in a targeted manner. The present application also discloses a programmable method for inducing the death of virus-infected cells, which comprises transferring the above-mentioned fusion protein or nucleic acid into cells so that the cells die before replication and assembly after being infected by the virus, thereby achieving timely and effective elimination of the virus.

The present invention relates to a method of inducing mesenchymal-epithelial transition (MET) in a basal-like (or mesenchymal-like) cancer cell by contacting the cancer cell with an inducer of mesenchymal-epithelial transition for a time and under conditions sufficient to induce MET in the cell. Additionally, there is also provided a method of inhibiting epithelial-mesenchymal transition (EMT) of a cancer in a subject, the method comprising administering an inhibitor or regulator of lipid metabolism for a sufficient time and under conditions to inhibit epithelial mesenchymal transition (EMT) of the cancer in the subject.

This invention relates to the field of bioactive peptide preparation technology, and discloses a method for preparing and applying a bifunctional antioxidant and anti-inflammatory peptide based on porcine skin collagen. The bifunctional peptide has the amino acid sequence GPSGPPGEKGP. Through peptidomics and computer simulation screening, this invention identified five novel antioxidant peptides with good solubility, non-sensitizing properties, and non-toxicity. Using an AFB1-induced HuH7 cell oxidative damage model, in in vitro cell experiments, GP-11 was shown to significantly reduce ALT, AST activity, and ROS levels, enhance the activity of SOD, CAT, and GSH-Px antioxidant enzymes, and activate the Keap1-Nrf2 pathway. It also reduced the levels of inflammatory factors TNF-α and IL-6 by downregulating the classical cGAS-STING inflammatory pathway. GP-11 exhibits both significant antioxidant effects and the ability to reduce the levels of inflammatory factors, demonstrating a dual function of antioxidation and anti-inflammation.

This invention relates to a novel compound derived from nutmeg and an anticancer composition comprising the same. The present invention isolates several novel compounds derived from nutmeg extract and confirms that most of these novel compounds exhibit cytotoxic activity against various cancer cell lines. Five compounds (3, 4, 6, 9, and 11) were identified as having high cytotoxic activity against gastric and colorectal cancers. In particular, the compound represented by chemical formula 3 was confirmed to not only effectively induce apoptosis by regulating the cell cycle of cancer cells but also effectively inhibit tumor growth in xenograft mouse models, thus making it an effective anticancer composition.

Generally, the present invention provides novel quinolone compounds and pharmaceutical composition thereof which may inhibit cell proliferation and / or induce cell apoptosis. The present invention also provides methods of preparing such compounds and compositions, and methods of making and using the same.

The present application belongs to the technical field of coordination chemistry and biomedical science, and provides a multifunctional iridium (III) complex, a preparation method and application thereof. The multifunctional iridium (III) complex (Mito-Ir) is composed of an iridium (III) complex cation and a coordination anion shown in the following formula. Mito-Ir can efficiently target mitochondria, and also has the abilities of phosphorescence imaging, type I and type II active oxygen generation, and photocatalytic oxidation of nicotinamide adenine dinucleotide. Under light irradiation, Mito-Ir triggers severe mitochondrial dysfunction through the above synergistic effect, and then specifically activates the caspase-3 / GSDME signaling pathway, and significantly induces pyroptosis; this pyroptosis-based cell death mechanism can effectively overcome the apoptosis tolerance of tumor cells, and is accompanied by the release of a large amount of inflammatory factors and damage-associated molecular patterns, stimulates immunogenic cell death, and activates the body's anti-tumor immune response.

This invention is related to the fields of medical biotechnology, nanobiotechnology, and nanomedicine. It involves a nanomedicine product that can release HOC1 (hypochlorous acid) at the tumor site in a controlled manner to treat lung cancer. HOC1 is a potent antimicrobial and antitumor agent that can target tumor tissues while minimizing damage to healthy tissues. The produced nanoparticles have a two-layer structure: the inner layer contains alginate, PFP (perfluoropentane), and Ca(OCl)2 to release HOC1, and the outer layer has a chitosan coating with folate and salicylic acid for targeting and proton release. The production process involves nanoemulsion and coating with the ionic gelation technique. When the nanoparticles are delivered to the lungs and targeted to cancer cells with folate, ultrasound radiation triggers the release of HOC1 to induce apoptosis and destroy cancer cells effectively, reducing side effects and improving treatment outcomes for lung cancer patients.

A method for the precise cellular destruction of an oncogenic non-coding RNA with a RNA-binding small molecule conjugated with bleomycin A5 is described. The method affords reversal of phenotype. Bleomycin A5 was coupled to an RNA-binding molecule that selectively binds the microRNA-96 hairpin precursor (pri-miR-96). By coupling of bleomycin A5's free amine to the RNA-binding molecule, its affinity for binding to pri-miR-96 is >100-fold stronger than to DNA. The conjugate compound selectively cleaves pri-miR-96 in triple negative breast cancer (TNBC) cells. Selective cleavage of pri-miR-96 enhances expression of FOXO1 protein, a pro-apoptotic transcription factor that miR-96 silences, and triggers apoptosis in TNBC cells. No effects were observed in healthy breast epithelial cells. This method provides programmable control for targeting RNA through the selection of an RNA-binding molecule / bleomycin A5 conjugate and provides a facile method of mapping the cellular binding sites of an RNA-binding molecule.

Disclosed herein are engineered polyfunctional CD4+ T cells / CAR T cells and methods of their use for the treatment of cancers. One embodiment provides a method of producing polyfunctional CD4+ T cells by constitutively activating STAT5A in the cells to induce a polyfunctional phenotype. Also provided is a method of reversing exhaustion in tumor-specific CD4+ T cells by engineering the cells to express Fos, Jun, Nr4a1, or combinations thereof but not express Tox, Pdcd1, Ctla4, Haver2, Lag3, Tigit, Slam6, Nrf4a2, and administering the engineered cells to a subject.

Provided are bispecific antibodies comprising first and second VIIII binding domains that specifically bind to the extracellular domains of interleukin- 10 receptor (IL-10R) alpha subunit (IL-10Rα) and beta subunit (IL-10Rβ), and that selectively suppress activation of myeloid cells and induce minimal or no direct activation of T cells or B cells.

The application discloses the application of Huaxingdan in the preparation of a glioma drug in the technical field of biology and medicine, detects the influence of Huaxingdan on the proliferation activity of glioma cells U251, U87 and A172 by using an MTT method in vitro, finds that Huaxingdan has a significant inhibitory effect on the proliferation of glioma cells, and is time and concentration dependent. The influence of Huaxingdan on the apoptosis of glioma cells U87 is detected by using a flow cytometry, and it is found that Huaxingdan can induce the apoptosis of U87 cells, and is concentration dependent. The animal experiment shows that Huaxingdan can effectively inhibit the growth of glioma cells in vivo, and the HE staining shows that Huaxingdan has no toxicity in vivo, and can be used as a drug for preventing and treating glioma.

The present invention relates to an isolated antigen-binding protein, which comprises a CD3-binding moiety, wherein the CD3-binding moiety comprises amino acid sequences having at least 95% identity to heavy chain variable regions HCDR1, HCDR2 and HCDR3; the amino acid sequence of the HCDR1 is set forth in any one of SEQ ID NOs: 1 and 2; the amino acid sequence of the HCDR2 is set forth in any one of SEQ ID NOs: 3, 4 and 5; the amino acid sequence of the HCDR3 is set forth in SEQ ID NO: 6; and / or, the CD3-binding moiety comprises amino acid sequences having at least 95% identity to light chain variable regions LCDR1, LCDR2 and LCDR3; the amino acid sequence of the LCDR1 is set forth in any one of SEQ ID NOs: 7, 8 and 9; the amino acid sequence of the LCDR2 is set forth in any one of SEQ ID NOs: 11 and 12; the amino acid sequence of the LCDR3 is set forth in SEQ ID NO: 13, wherein the CD3-binding moiety can induce T cell activation.

The present invention relates to a vaccine composition comprising a recombinant Nipah virus protein. The vaccine composition according to the present invention not only exhibits excellent immunogenicity against both the G protein and the F protein of Nipah virus, but also exhibits immunogenicity against the G protein and the F protein of Hendra virus, and thus can be used as a universal vaccine against Henipavirus. In addition, the vaccine composition has the characteristic of inducing cell-mediated immune responses, and therefore can be provided as a formulation for enhancing specific immune responses to an administered drug such as an adjuvant or a vaccine.

The present invention describes novel drug-carrying nanoparticles called bionanocarriers capable of modulating the cellular redox system and targeting the cancerous tumor.Specifically, the invention relates to a nanomedicine strategy for combating cancerous tumor cells, a strategy that aims to target the tumor, and consists of providing quercetin-linked magnetite nanoparticles (Q): (MNPs Q), and 3,5-dimaleylbenzoic acid-linked magnetite nanoparticles (A3'5DMB): (MNPs A3'5DMB)M; both types of nanoparticles were subsequently encapsulated with chitosan (Qs) and O-carboxymethyl chitosan (O-CMQs), functionalized with 11-mercaptoundecanoic acid (MUDA), and finally the anti-ABCC3 antibody was attached to the polymer phase, which was used as a selective driver of the delivery process of the encapsulated nanoparticles, thus carrying out the construction of the bionanocarriers: BNC-1: MNPs-Q-Ab; BNC-2: MNPs-a3'5DMB-Ab.Its manufacturing method and the tests of its biological functionality, its stability, the degradation of the encapsulation for the tumor microenvironment, the controlled release profile of the drugs Q and A3'5DMB, selective cell uptake, intracellular localization, cytotoxic effect on steroids of hepatocellular carcinoma cells with altered redox balance and induction of apoptosis, as well as its safety on normal cells, are described.

Described herein are compounds that block the activity of LOX family members having good IC50 values, no cellular toxicity below 10 μM, induce sensitization of the cells to doxorubicin, strong activity in a recombinant LOX / LOXL2 activity, and a chemical structure that is drug-like and does not have a PAINS flag, as well as, methods of treatment using the compounds with respect to cancer, organ fibrosis, neurodegenerative and cardiovascular diseases.

This invention discloses a semi-sandwich structured ruthenium triphenylphosphine dithiocarboxylic acid complex with a simple preparation process and its applications. The complex has the structure shown in Figure (I), with the central ruthenium and... η 5 - Coordination with cyclopentadiene, triphenylphosphine, and dithiocarboxylic acid derivatives, wherein the dithiocarboxylic acid ligands are selected from ethyl xanthic acid, isopropyl xanthic acid, ... N,N Diethyldithiocarbamic acid, morpholine dithiocarbamic acid, and carbazole dithiocarbamic acid. This invention employs a simple one-step method of room temperature preparation and recrystallization purification using a ruthenium precursor and dithiocarbamic acid ligand. This method offers advantages such as readily available raw materials, mild reaction conditions, simple post-processing, and high yield. In vitro tests show that the complexes exhibit excellent anti-proliferative activity against non-small cell lung cancer A549 cells, significantly superior to cisplatin. The complexes demonstrate activity by reducing mitochondrial membrane potential, inducing intracellular reactive oxygen species accumulation, and arresting the cell cycle (G1 phase), leading to late apoptosis in A549 cells.

To provide a method and composition for generating induced non-pluripotent cells differentiated from single-cell induced iPSC (induced pluripotent stem cell) clone lines. [Solution] A method and composition are provided for obtaining functionally enhanced induced effector cells obtained from targeted differentiation of genome-manipulated iPSCs. The iPSC-induced cells provided herein have stable functional genome editing that results in improved or enhanced therapeutic effects. Therapeutic compositions and their use are also provided, comprising functionally enhanced induced effector cells alone or in combination therapy with antibodies or checkpoint inhibitors.

The application belongs to the technical field of biological medicine, and provides a photosensitizer, a targeted delivery nano platform and application. A preparation method of the photosensitizer comprises the following process: a Suzuki coupling reaction is used to synthesize an intermediate with an aldehyde group by taking a brominated or iodinated triphenylamine as a precursor and reacting with boric acid, and then a Knoevenagel condensation reaction is used to convert the terminal aldehyde group into a strong electron-withdrawing dicyanovinyl group by reacting the aldehyde group intermediate with malononitrile, so as to synthesize the photosensitizer PSs. The application takes a structure-optimized photosensitizer (used for generating ROS and inactivating viruses) and a STING agonist (used for activating the STING pathway and inducing cell death) as core treatment components, and takes a rabies virus glycoprotein peptide as a active targeting ligand, so that the "PDT-immune" synergistic inactivation of RABV can be realized.

The application relates to the technical field of biological medicine, and discloses application of Nilotinib in preparation of a drug for inhibiting p53-AKT interaction. Relying on a double-fluorescence reporting system NanoBRET system, high-throughput screening is completed at a live cell level, and it is determined that a tyrosine kinase inhibitor Nilotinib can inhibit p53-AKT interaction. Function verification shows that Nilotinib can dose-dependently destroy a p53-AKT complex in HEK293T tool cells and U87MG, T98G and other glioma cells, release the inhibition of p53 function, and induce cell apoptosis. The above results illustrate a new path of precise intervention with the "p53-AKT interface" as a target, and provide experimental basis for redirecting Nilotinib to overcome p53-related drug resistance.

This invention relates to antimony nanopowder, its preparation method, and its applications, belonging to the field of metal powder processing technology. The method includes dispersing antimony nanopowder in a solvent to obtain a dispersion, mixing the dispersion with 5-10 times the mass of nitrobenzene diazonium salt (p-NBD) of the antimony nanopowder, and reacting under light irradiation at 0-4°C for 30-60 hours to obtain passivated antimony nanopowder. The diazo chemical reaction forms stable covalent bonds on the surface of Sb NPs, blocking their interaction with respiratory cells. Compared with the original Sb NPs group, the nitrobenzene diazonium salt modification reverses the GPX4 activity inhibition effect, upregulates GPX4 protein expression and restores it to near the control group level, and eliminates the ability to induce ferroptosis, thus addressing the pulmonary toxicity problem of Sb NPs from the perspective of ferroptosis mechanism.

This specification discloses the use of alternating electric fields and DNA-dependent PK inhibitors for cancer treatment. This specification discloses the use of alternating electric fields and DNA-dependent PK inhibitors for inducing cell death. This specification discloses the use of alternating electric fields and DNA-dependent PK inhibitors to inhibit DNA repair in cancer cells having DNA strand breaks (e.g., double-strand DNA breaks). This specification discloses the use of alternating electric fields and DNA-dependent PK inhibitors to enhance the effectiveness of radiotherapy.

Provided is a cell culture membrane for use during a cell stretching process that stresses the cell to induce mechanical signaling and thus biochemical signals in the cell. A production method for the cell culture membrane includes: providing a mold assembly with a lower plate containing pin slots, an upper plate placed on the lower plate and including at least one window, pins to be placed in said pin slots, and a mold to be placed between the pins remaining in said window; placing pins in the pin slots remaining in the said window and placing a mold of primary length in the window; pouring the polydimethylsiloxane-solidifier mixture into the window in an amount that exceeds the primary length; eliminating the air bubbles in the mixture; baking the mold assembly in which said mixture is located, and then leaving the assembly to cool and removing it from the mold assembly.

This invention discloses the application of glycyrrhizin, an effective extract of licorice, in the preparation of drugs for the prevention, improvement, or treatment of hepatocellular carcinoma. This invention is the first to discover that glycyrrhizin possesses significant anti-hepatocellular carcinoma activity, significantly inhibiting the proliferation of human liver cancer cells HepG2 and Huh7, and inducing cell morphological shrinkage, decreased adhesion, and cell death. Transcriptome sequencing and network pharmacology combined analysis showed that glycyrrhizin exerts its effects by regulating the PI3K-Akt signaling pathway and cell cycle pathway, and regulates 10 core targets, including CCNA2, PLK1, AURKA, AKT1, EGFR, CASP3, BIRC7, HK1, PAEP, and ALDH3A1. Molecular docking confirmed the stable binding of glycyrrhizin to these targets. TCGA clinical database validation showed that the expression levels of these core targets were significantly correlated with the prognosis of hepatocellular carcinoma patients. This invention clarifies for the first time the pharmacodynamics and molecular mechanism of glycyrrhizin against hepatocellular carcinoma, providing a safe, efficient, multi-target natural small molecule anti-liver cancer candidate drug with significant clinical translational and application value.

The present invention relates to methods for identifying cancer, responders, predicting response and stratifying patients with respect to a combination therapy comprising the administration of a P2X4 receptor inhibitor and a cell death inducing chemotherapy. The methods according to the present invention are based on the detection of P2X4 receptor protein expression in cells of a patient-derived cancer sample, e.g. cells or organoids, to identify cancer, responders, predict responders and stratify patients, wherein an increase in protein expression identifies cancer, responders and predicts responders when applying the combination therapy and also allows to stratify the patients accordingly.

The application discloses a method for inducing Breg cell proliferation in vitro. The method comprises the following steps: (1) culturing B cells derived from mammals in a culture medium containing CD40 antibodies; (2) adding SARS-CoV-2 virus antigens to the culture system, wherein the SARS-CoV-2 virus antigens are selected from one or more of N protein, S protein specific epitope peptide segments or S1 subunits containing RBD regions of S protein; and (3) after 24-96 hours of culture, the induction of Breg cells is achieved. The application uses SARS-CoV-2 specific protein antigens to significantly improve the proportion of B cell conversion to Breg cells, and realizes the specific induction of Breg (CD19 + IL-10 + ) cell proliferation and differentiation under in vitro conditions.