41 results about "HER Inhibitors" patented technology

The invention provides application of TRMT61A and its inhibitor tetramethylthiuram disulfide in tumor immunotherapy, and relates to the technical field of biological medicine, clinical research proves that RNA m1A methyltransferase TRMT61A is highly expressed in tumor tissues and is related to poor prognosis of tumor patients, and can be used as one of tumor therapy targets. Meanwhile, high expression of the TRMT61A is related to poor prognosis of a tumor patient receiving anti-PD-1 immunotherapy, and after anti-PD-1 antibody immunotherapy is carried out on the patient with low TRMT61A expression level in the tumor of the patient, pathological complete relief is easier. Tetramethylthiuram disulfide inhibits TRMT61A, inhibits m1A modification regulation of TRMT61A on PD-L1 mRNA, increases PD-L1 protein expression, and is combined with a PD-1 antibody drug to significantly enhance the immunotherapy effect of the anti-PD-1 immune checkpoint drug in treating malignant tumors.

The invention discloses annexin A2 (ANXA2) and application of an inhibitor thereof in diagnosis, treatment and / or prevention of pulmonary arterial hypertension. In particular discloses application of an ANXA2 inhibitor (including siRNA for silencing an ANXA2 gene, an ANXA2 antibody and a phosphorylation inhibitor) in preparation of a product for preventing and / or treating pulmonary arterial hypertension. Experiments prove that the ANXA2 inhibitor can significantly inhibit proliferation and migration of pulmonary artery smooth muscle cells, and significantly improve pulmonary arterial hypertension, pulmonary artery vascular remodeling and right ventricular hypertrophy. The ANXA2 or the Thr208 phosphorylation site of the ANXA2 protein can be used for diagnosis or auxiliary diagnosis of pulmonary arterial hypertension, or used for screening drugs for pulmonary arterial hypertension and developing new diagnosis and treatment methods and drugs. The therapeutic target and the ANXA2 inhibitor developed by the invention have wide clinical application value in the fields of diagnosis, prevention and treatment of pulmonary arterial hypertension.

The invention relates to application of mitochondrial E3 ligase MAPL and an inhibitor of the mitochondrial E3 ligase MAPL in preparation of a medicine for treating intervertebral disc degeneration. MAPL increases mitochondrial translocation of Drp1 by promoting SUMOylation modification of Drp1 to cause abnormal mitochondrial division of nucleus pulposus cells to play a pathophysiological role, and in-vivo inhibition of MAPL can significantly reverse the degeneration phenotype of intervertebral disc. Compared with the prior art, the invention focuses on the SUMOylation modification effect of MAPL on Drp1, and aims to reveal the molecular mechanism of the MAPL for influencing the IVDD process by regulating mitochondrial division, thereby providing an innovative theoretical basis for developing a precise targeted therapy strategy.

The invention relates to an LECT2 inhibitor and application of the LECT2 inhibitor in intervention of NETs formation and preparation of drugs for preventing and treating alcoholic hepatitis (AH), and provides application of the LECT2 inhibitor in preparation of drugs for intervention of NETs formation and further prevention and treatment of AH, and a foundation is laid for new drug screening. The LECT2 is positively correlated with the disease severity of AH, and the LECT2 inhibitor plays a role in preparing a medicine for intervening the generation of NETs so as to prevent and treat the progress of AH. An LECT2 inhibitor is AAV-shLECT2, the LECT2 shRNA is transfected into AAV-293 cells, the adeno-associated virus for inhibiting liver expression of LECT2 is prepared, liver expression and LECT2 secretion are inhibited by injecting the virus, then formation of NETs in the liver is reduced, and finally the effect of preventing and treating AH progress is achieved. LECT2 is combined with a neutrophile granulocyte receptor PHB2, so that generation of NETs in neutrophile granulocytes is increased, then liver injury is aggravated, and the generation of the NETs in the neutrophile granulocytes can be reduced by knocking down LECT2, so that AH development is prevented and treated.

The invention relates to the technical field of biological medicines, in particular to application of four micro RNAs (Ribonucleic Acid) of miR-92a, miR-25, miR-30d and miR-30c and inhibitors targeting the four micro RNAs to preparation of medicines for resisting metastasis of multiple cancer species such as breast cancer, colorectal cancer and melanoma. When the nucleic acid inhibitor anti-agomirs targeting at least one of a set consisting of miR-92a, miR-25, miR-30d and miR-30c is used for treating metastasis of multiple cancer species, the anti-metastasis effect is remarkable, the universality is high, and the nucleic acid inhibitor anti-agomirs can show a strong inhibition effect in three different tumor metastasis models of breast cancer, colorectal cancer and melanoma; especially, when the four inhibitors are combined for use, the synergistic effect is prominent, the colorectal cancer liver metastasis load can be reduced by 90% or above, the breast cancer metastasis rate is reduced by 80% or above, the melanoma metastasis inhibition rate is 65% or above, and the composition is suitable for treatment of multi-cancer metastasis.

According to the invention, a novel immune checkpoint molecule SIDT1 is found. The SIDT1 is a powerful T cell inhibition factor mainly expressed on CD8 < + > T cells. A series of SIDT1 inhibitors are identified in the invention. The SIDT1 inhibitor can enhance the anti-tumor CD8T cell reaction and limit tumor progression, so that a new thought is provided for treatment and prevention of related tumor patients with PD-1 treatment resistance.

This invention discloses the application of SDC1 in the diagnosis and treatment of breast cancer. Through bioinformatics analysis, cell function experiments, multi-omics analysis, and animal model validation, this invention reveals for the first time the high expression of SDC1 in breast cancer and its correlation with poor patient prognosis. It elucidates the molecular mechanism by which SDC1 promotes the malignant progression of breast cancer by regulating ECM remodeling, EMT, angiogenesis, and ferroptosis resistance, and verifies the therapeutic potential of MZ1 in inhibiting breast cancer growth and metastasis by downregulating SDC1 expression. This invention provides the application of reagents for detecting SDC1 expression levels in the preparation of diagnostic or prognostic kits for breast cancer, as well as the application of SDC1 inhibitors in the preparation of drugs for treating breast cancer. This invention provides new technical solutions for the diagnosis, prognostic assessment, and treatment of breast cancer.

The present invention belongs to the technical field of anti-tumor drug research, and specifically relates to a splicing factor WBP11 and uses of its inhibitors, and drugs for preventing or treating colorectal cancer. WBP11 Significantly inhibited the proliferation, invasion and migration of colorectal cancer cells, and WBP11 The expression level in colorectal cancer tissues is higher than that in corresponding normal tissues. WBP11 High expression of TNF-α leads to poor prognosis of colorectal cancer. WBP11 It has been confirmed that both siRNA and Cas knockdown plasmids have good effects in inhibiting tumor development and are expected to be used in the development of anti-colorectal cancer drugs.

The invention relates to the technical field of bioengineering, in particular to a Cs-NPF gene and a Cs-NPFR gene as well as an inhibitor and application thereof. The invention provides a nucleotide sequence of a Cs-NPF gene as shown in SEQ ID NO.1 (sequence identifier number 1) and a nucleotide sequence of a Cs-NPFR gene as shown in SEQ ID NO.6). The invention further provides a Cs-NPF gene inhibitor and a Cs-NPFR gene inhibitor, and the two inhibitors can be applied to induction of biological diapause. After the expression of the Cs-NPF gene and the Cs-NPFR gene is inhibited by dsRNA, the diapause of the coccinella septempunctata can be induced, the dsRNA of the Cs-NPF gene and the dsRNA of the Cs-NPFR gene can be used as related preparations and products for inducing the diapause of the coccinella septempunctata, the development of the natural enemy industry is promoted, and the application prospect is wide.

The invention belongs to the technical field of biological medicine, and relates to application of H1FX as a therapeutic target and application of three compounds as H1FX inhibitors in preparation of drugs for preventing and / or treating prostatic cancer. Experimental results show that up-regulation of H1FX expression level can promote proliferation of prostate cancer cells, and knock-down of H1FX can inhibit proliferation of prostate cancer cells. H1FX expression up-regulation can significantly promote generation and development of prostate cancer cell line nude mouse subcutaneous tumor formation. Researches show that the three compounds are specifically combined with H1FX, and proliferation of prostate cancer cells and growth of subcutaneous tumors of nude mice with prostate cancer cell strains are inhibited. Therefore, the invention provides a new target for the design of new anti-prostatic cancer drugs, and provides a new thought for the development and preparation of prostatic cancer prevention and / or treatment drugs.

This invention relates to the pharmaceutical applications of MRPS7 as a diagnostic biomarker for non-small cell lung cancer (NSCLC) and its inhibitors, belonging to the field of biomedical technology. For the first time, this invention utilizes immunohistochemical analysis of tumor tissues from NSCLC patients and paired adjacent normal tissues to confirm that MRPS7 protein is significantly overexpressed in NSCLC tissues (p<0.001), and this difference is statistically significant in both lung adenocarcinoma and lung squamous cell carcinoma subtypes. Furthermore, this invention demonstrates through in vitro functional experiments that knocking down MRPS7 gene expression using siRNA targeting MRPS7 significantly inhibits the proliferation, migration, and invasion abilities of NSCLC cells (A549, SK-MES-1) (p<0.001). Therefore, reagents for detecting MRPS7 expression levels can be used to prepare NSCLC diagnostic products, and MRPS7 inhibitors can be used to prepare drugs for treating NSCLC. This invention provides a novel molecular biomarker for the diagnosis of NSCLC and a new strategy for targeted therapy of NSCLC.

This invention discloses the application of β-1,4-galactosyltransferase 1 and its inhibitors in liver diseases, particularly acute liver injury and liver failure. The application of β-1,4-galactosyltransferase 1 and its inhibitors in acute liver injury and liver failure provides the correlation between β-1,4-galactosyltransferase 1 and acute liver injury and liver failure, confirming that inhibiting the activity of β-1,4-galactosyltransferase 1 can alleviate acute liver injury and liver failure. β-1,4-galactosyltransferase 1 can serve as a drug target for screening acute and chronic hepatitis, liver injury, fatty liver, liver fibrosis, and acute and chronic liver failure. This invention also confirms the alleviating effect of β-1,4-galactosyltransferase 1 inhibitors on acute liver failure. β-1,4-galactosyltransferase 1 inhibitors improve acute liver failure by reducing the enzyme activity or protein expression of β-1,4-galactosyltransferase 1.

The invention relates to application of TRPV4 and an inhibitor thereof, a head and neck cancer medicine and an in-vitro non-therapeutic inhibition method. According to the application of the TRPV4 as a head and neck cancer treatment target, the TRPV4 protein is remarkably and highly expressed in head and neck cancer tissues, and proliferation and migration of head and neck cancer cells can be inhibited and apoptosis can be promoted by knocking down the expression of the TRPV4 protein. The invention provides a novel therapeutic target for the head and neck cancer, and the target can be effectively used for judging and / or treating the head and neck cancer, so that a novel diagnostic and / or therapeutic agent is provided for the field and has a clinical application prospect.

This invention proposes the application of hyaluronic acid synthase 2 (HAS2) and its inhibitors, belonging to the field of biomedical technology. This invention provides the application of HAS2 as a therapeutic target for diseases caused by hyaluronic acid accumulation. Experiments have demonstrated a correlation between HAS2 and hyaluronic acid accumulation, thus enabling the treatment of related diseases. Inhibiting the expression of HAS2 can reduce hyaluronic acid production, thereby significantly alleviating or preventing related diseases. This invention provides a novel use of HAS2 as a target for the treatment or prevention of diseases caused by hyaluronic acid accumulation, offering a new strategy for clinical practice.

The invention relates to the technical field of bioengineering, in particular to a coccinella septempunctata biological clock Timeless (Cs-Tims) gene as well as an inhibitor and application thereof. The invention provides a nucleotide sequence of a coccinella septempunctata biological clock Cs-Tima gene as shown in SEQ ID NO. 1 and an amino acid sequence as shown in SEQ ID NO. 2; the invention also provides an application of the biological clock Cs-Tims gene inhibitor in relieving biological diapause. After the biological clock Cs-Timm gene provided by the invention is subjected to dsRNA inhibition expression, the diapause of the coccinella septempunctata can be relieved, the dsRNA of the Cs-Timm gene can be used as a related preparation and product for relieving the diapause of the coccinella septempunctata, the development of the natural enemy industry is promoted, and the application prospect is wide.

This invention belongs to the field of biomedical technology and discloses the application of CCR2 inhibitors in the preparation of drugs for treating hemophagocytic lymphohistiocytosis (HLH). By establishing a mouse model of HLH, this invention reveals for the first time that CCR2 can serve as an effective drug target for treating HLH. Experiments showed that treatment with the CCR2-specific antagonist RS102895 significantly reduced splenomegaly, improved peripheral blood cell reduction, alleviated liver damage, corrected metabolic disorders in model mice, and effectively inhibited serum cytokine storm and abnormal activation of splenic macrophages. Based on these findings, CCR2 can serve as a novel target for HLH treatment, and its inhibitors can be used to prepare highly effective and low-toxicity drugs for treating HLH.

The invention relates to the technical field of medicines, in particular to miRNA-181a-5p and application of an inhibitor of miRNA-181a-5p in a medicine for treating lower limb arteriosclerosis obliterans. The research on disease pathogenesis finds that miRNA-181a-5p is particularly important in the occurrence and development process of lower limb arteriosclerosis obliterans, and the miRNA-181a-5p inhibitor is adopted to treat vascular endothelial cells, so that the functions of the vascular endothelial cells can be improved, including improvement of migration and tubular formation of the vascular endothelial cells; the proliferation function is improved; the ROS generation is reduced.

This invention relates to the application of PLEKHH1 and its inhibitors in the preparation of drugs or kits that induce ferroptosis, belonging to the field of tumor treatment technology. This invention discovers that knocking down the PLEKHH1 gene in liver cancer cells can induce ferroptosis. Therefore, this invention uses the PLEKHH1 gene as a novel target for cancer cells to resist ferroptosis. By knocking down this gene, it eliminates ferroptosis escape from cancer cells, induces ferroptosis, and thus exerts a therapeutic effect on tumors.

The present invention relates to the field of biopharmaceutical technology, and specifically to the application of ODC1 and its inhibitor in the diagnosis and treatment of tamoxifen resistance in breast cancer. The present invention has found that ODC1 is overexpressed in tamoxifen-resistant breast cancer cells, so ODC1 overexpression can be used as a marker for judging or predicting tamoxifen resistance in breast cancer; in addition, the present invention has found that the ODC1 inhibitor DFMO can significantly inhibit the proliferation of ERα-positive breast cancer cells and other tamoxifen-resistant breast cancer cells when used as a single drug or in combination with tamoxifen. Therefore, the present invention uses ornithine metabolism-related gene ODC1 as a diagnostic and predictive marker for tamoxifen resistance in breast cancer, and the combined therapy of ODC1 inhibitor DFMO combined with tamoxifen has great application value in the diagnosis and treatment of tamoxifen-resistant breast cancer.

The invention relates to the technical field of bioengineering, in particular to a coccinella septempunctata ion transport peptide Cs-ITP-L gene as well as an inhibitor and application thereof. The invention provides a nucleotide sequence of a coccinella septempunctata ion transport peptide Cs-ITP-L gene as shown in SEQ ID NO. 1 and an amino acid sequence as shown in SEQ ID NO. 2; the invention also provides an application of the ion transport peptide Cs-ITP-L gene inhibitor in the induction of biological diapause. After dsRNA expression inhibition, the Cs-ITP-L gene of the ion transport peptide can induce diapause of coccinella septempunctata, the dsRNA of the Cs-ITP-L gene can be used as a related preparation and product for inducing diapause of coccinella septempunctata, development of the natural enemy industry is promoted, and the Cs-ITP-L gene has a wide application prospect.

The present application relates to cancer, and particularly to the application of circPIAS1-108aa and its inhibitor in the preparation of antitumor drugs. The application of circPIAS1-108aa as a target in the development or screening or preparation of drugs for preventing or treating tumors is characterized in that the amino acid sequence of the circPIAS1-108aa is SEQ ID NO. 1. The present application finds the application of the inhibitor of the target circPIAS1-108aa in the treatment of cancer through experiments. The inhibitor plays a role in inhibiting proliferation in ten common cancers, including lung cancer, liver cancer, gastric cancer, melanoma, pancreatic cancer, breast cancer, nasopharyngeal carcinoma, colorectal cancer, esophageal cancer and prostate cancer; and the inhibitor of the target circPIAS1-108aa can significantly enhance the efficacy of immune checkpoint inhibitors, providing a new synergistic strategy for tumor immunotherapy.

The invention discloses an application of an FAM3A inhibitor in colorectal cancer treatment. Experiments prove that the FAM3A gene is a brand-new functional gene related to colorectal cancer morbidity, an inhibitor of the FAM3A gene can inhibit colorectal cancer cell proliferation, migration and invasion, and a new research strategy and tool are provided for colorectal cancer treatment.

The invention provides a preparation method of a human recombinant SPHK2 protein, and belongs to the technical field of biology. The amino acid sequence of the human recombinant SPHK2 protein prepared by the invention is as shown in SEQ ID NO. 1. The human-derived recombinant SPHK2 protein prepared by the preparation method disclosed by the invention is good in expression quantity, and the obtained human-derived recombinant SPHK2 protein is soluble protein, relatively high in purity and good in stability. The human-derived recombinant SPHK2 protein prepared by the invention can be used for screening and evaluating inhibitors of the human-derived recombinant SPHK2 protein, and has a good application prospect.

The present application relates to acetaldehyde dehydrogenase 1 family member A3, and particularly to the application of acetaldehyde dehydrogenase 1 family member A3 and its inhibitor in the preparation of a drug for chronic heart failure. The present application discloses the application of acetaldehyde dehydrogenase 1 family member A3 as a drug target in the preparation of a drug for chronic heart failure. The present application first discloses the correlation between acetaldehyde dehydrogenase 1 family member A3 and chronic heart failure, and confirms that the vascular endothelial injury can be improved by specific knockdown or interference of ALDH1A3 to treat chronic heart failure, which indicates that ALDH1A3 can become a new target for treating chronic heart failure or cardiovascular diseases. Therefore, acetaldehyde dehydrogenase 1 family member A3 can be used as a target for screening a drug for preventing, relieving and / or treating chronic heart failure.

The present invention discloses the application of the MDH2 gene and its inhibitors in resisting ZEA toxin, which relates to the field of biotechnology. In the present invention, a cell line lacking the MDH2 gene was obtained through CRISPR gene editing. Compared with the cells expressing the wild-type MDH2 gene, under the influence of ZEA, the cell viability was extremely significantly improved, and the apoptosis rate of the cells was extremely significantly reduced. In addition, inhibiting the MDH2 activity of wild-type IPEC-J2 cells with the LW6 inhibitor can also improve the tolerance of the cells to ZEA. Thus, knocking out, mutating or inhibiting the activity of the MDH2 gene can improve the ability of humans, animals and plants to resist ZEA. The present invention provides a potential solution to solve the adverse reactions caused by ZEA.

The invention discloses application of STMP1 and an inhibitor thereof in preparation of a medicine for treating diabetic retinopathy. A mouse STMP1 knock-down / knock-out model (KO) is constructed by utilizing a CRISPR-Cas9 technology, comparison is performed in an STZ (streptozotocin) induced diabetes animal model, and a result shows that compared with a wild type (WT) mouse, a KO + STZ group mouse has better performance in the aspects of insulin secretion and insulin sensitivity; meanwhile, electrophysiological detection and eye movement reaction test detection show that the visual function of a KO + STZ mouse is obviously superior to that of a WT + STZ mouse, and it is indicated that STMP1 knock-down can have a protective effect on visual impairment caused by diabetic retinopathy. A novel intervention strategy and medicine taking STMP1 as a treatment target are established on the basis of STMP1, so that the pathological mechanism of diabetic retinopathy can be disclosed, and a safer treatment method and medicine with higher compliance can be provided for patients with diabetic retinopathy.

This invention discloses a long non-coding RNA that regulates protease degradation, its inhibitor, and its applications, belonging to the field of cell biology. The nucleotide sequence of the long non-coding RNA is shown in SEQ ID NO.1, and the reagent for inhibiting the long non-coding RNA includes knocking out the shRNA expressed by the long non-coding RNA. This invention enhances the ubiquitination modification of HK1 by knocking down lncHBHK1 (NONCODE database name: RP11-675F6.3), thereby accelerating the degradation of HK1 protein and inhibiting the proliferation of liver cancer cells. Combined with animal experiments, it is further confirmed that knocking down the expression level of this lncRNA in vivo can inhibit the growth of liver cancer tumors, indicating that this lncRNA has the potential to serve as a novel therapeutic target for liver cancer and provides a new strategy for developing drugs to treat liver cancer.

The invention discloses application of HRD1 and an inhibitor thereof in prevention and treatment of myocardial ischemia-reperfusion injury. According to the invention, an endodermis-specific HRD1 gene knockout mouse (Hrd1f / f; a myocardial ischemia-reperfusion injury model is formed by ligating a left anterior descending coronary artery (LAD) of a mouse heart by taking Hrd1f / f (Cd, Cdh5Cre) as an experimental subject, and a result shows that compared with an Hrd1f / f mouse, the Hrd1f / f mouse is Hrd1f / f; the cardiac infarction area of the Cdh5Cre mouse is reduced, the myocardial injury marker level is reduced, the heart microcirculation perfusion is increased, and the inflammatory cell infiltration is reduced; the invention discloses that the HRD1 gene promotes mouse myocardial infarction induced by myocardial ischemia reperfusion injury for the first time, and the HRD1 gene has an important deterioration effect in a myocardial ischemia reperfusion injury model; the invention provides a new drug action target for prevention and treatment of myocardial ischemia reperfusion injury, and has very important clinical transformation value.

The present invention relates to a biomarker composition for cancer diagnosis comprising KSR1 (Kinase Suppressor of RAS1) as an active ingredient. By confirming that the expression of KSR1 (Kinase Suppressor of RAS1) increases in cancer patient groups compared to normal groups, that cancer development is promoted when KSR1 is overexpressed, and that cancer activity is suppressed when KSR1 is knocked down, it was confirmed that the KSR1 or its inhibitor can be utilized for the diagnosis, prevention, treatment, or improvement of cancer or for screening purposes for said disease treatments.

This invention provides the application of GCKR and its inhibitors in the preparation of drugs for treating pancreatic cancer, belonging to the field of biomedical technology. The application of GCKR and its inhibitors in the preparation of drugs for treating pancreatic cancer reveals for the first time that GCKR is a key metabolic switch driving liver metastasis in pancreatic cancer, and that high expression of the GCKR gene can promote the growth and liver metastasis of pancreatic cancer in mice. The proliferation, invasion, and migration abilities of pancreatic cancer cells in the GCKR low-expression group were significantly lower than those in the normal control group. Using a pancreatic cancer orthotopic xenograft model constructed in highly immunodeficient mice, the invention demonstrated in vivo that knocking out GCKR can inhibit the growth of pancreatic cancer, indicating that GCKR inhibitors block the progression of pancreatic cancer by downregulating GCKR; conversely, overexpression plasmids that promote GCKR expression can upregulate GCKR expression and promote pancreatic cancer progression. This provides a new application of GCKR and offers new ideas for the treatment of pancreatic cancer.