79 results about "HER Inhibitors" patented technology

The present application describes the use of low HER3 as a selection criterion for treating patients with a HER inhibitor, such as pertuzumab.It also describes the use of high HER2:HER3 ratio as a selection criterion for treating cancer patients, such as ovarian cancer patients, with a HER inhibitor, such as pertuzumab.In addition, the application describes the use of high HER3 as a selection criterion for treating cancer patients with a chemotherapeutic agent, for instance gemcitabine.

The invention provides methods for the treatment of disease and promotion of healing that include providing a therapeutically effective amount of a mammalian antimicrobial peptide (AMP) or analog thereof, in particular a cathelicidin or cathelicidin fragment or cathelicidin analog, thereby treating the disease in the subject in need thereof. The invention also provides specific analogs or fragments of cathelicidin that function as agonists, as do endogenous cathelicidins, or as either dominant negatives or as inhibitors to endogenous cathelicidin or to other endogenous AMPs or that compete with pro-inflammatory agents or fragments of AMPs on cognate receptors without inducing disease.

A method for selecting patients for therapy with a HER inhibitor, such as pertuzumab, based on gene expression analysis is described. A method for assessing HER phosphorylation or activation in a biological sample via gene expression analysis is also described.

A method and a product for cleaning and / or whitening of teeth. Natural human cysteine proteinases are employed for cleaning and whitening purposes and this activity can be blocked by natural cysteine protease inhibitors, which are released secondarily from the product at a later stage. The use of natural cysteine proteinases and their inhibitors provides the advantage that they are man's own proteins, and therefore the risk of allegorization is minimized. In addition, their enzyme kinetics are will known.

This invention relates to the therapeutic, diagnostic and pharmacogenetic use of nucleic acids and proteins involved in human proteolytical system such as serine and cysteine proteases and their inhibitors and pharmaceutical agents and other therapies affecting these. This invention discloses methods for the treatment and prevention of cardiovascular diseases such as coronary heart disease (CHD), acute myocardial infarction (AMI), chronic CHD, arterial hypertension (HT) and cerebrovascular stroke and metabolic disorders such as the metabolic syndrome (MBO) and obesity and methods for detecting or diagnosing a risk of, or predisposition to the said diseases in a subject, for selecting treatment in a subject and for selecting subjects for studies testing cardiovascular, anti-diabetic and anti-obesity drugs, as well as to transgenic animals.

This application discloses methods for diagnosing and treating SUI. The treatment methods are directed to inhibiting elastolysis in affected tissues and correcting imbalances in the expression of elastase enzymes and their inhibitors.

The present invention relates to a new drug target for the prevention and the treatment of cerebrovascular diseases related to inflammation and the medical usage of the inhibitors thereof, more particularly, the present invention relates to the nonmuscle myosin heavy chain 9(MyH9) used as the new drug target for the prevention and the treatment of cerebrovascular diseases related to inflammation and the usage of the inhibitors ruscogenin and the genin in the prevention and the treatment of the tumor differentiation and metastasis, glaucoma and other diseases.

Provided are methods for the treatment of disease and promotion of healing that include providing a therapeutically effective amount of a mammalian antimicrobial peptide (AMP) or analog thereof, in particular a cathelicidin or cathelicidin fragment or cathelicidin analog, thereby treating the disease in the subject in need thereof. Also provided are specific analogs or fragments of cathelicidin that function as agonists, as do endogenous cathelicidins, or as either dominant negatives or as inhibitors to endogenous cathelicidin or to other endogenous AMPs or that compete with pro-inflammatory agents or fragments of AMPs on cognate receptors without inducing disease.

The invention provides methods for the treatment of disease and promotion of healing that include providing a therapeutically effective amount of a mammalian antimicrobial peptide (AMP) or analog thereof, in particular a cathelicidin or cathelicidin fragment or cathelicidin analog, thereby treating the disease in the subject in need thereof. The invention also provides specific analogs or fragments of cathelicidin that function as agonists, as do endogenous cathelicidins, or as either dominant negatives or as inhibitors to endogenous cathelicidin or to other endogenous AMPs or that compete with pro-inflammatory agents or fragments of AMPs on cognate receptors without inducing disease.

The invention discloses a method to screen compounds which can suppress tumor cells multiplication by suppressing TRPC ion channel. Use of TRPC inhibitor in preparing medicine for curing tumor is also disclosed. The invention firstly testifies the correlation on cells of TRPC ion channel and tumor cells multiplication, which offers a new path to suppress tumor cells multiplication by suppressing TRPC ion channel.

The invention discloses a detection reagent containing nano mimic enzyme. The invention further discloses a visual detection method of bio-enzyme or protein and its inhibitor on the basis of nano mimic enzyme technology. The method shows good pH dependence for the oxidization reaction of many developing agents on the basis of some nano materials capable of simulating natural oxidase, and many oxidase or proteins can release / consume H+ characteristics in the biological catalysis process, and uses the in-site change of pH of reaction system to influence the catalytic oxidization ability of the nano material, thus the detection reagent has color change at different levels, and the visual detection of bio-enzyme or protein activity is realized, and further the visual detection of corresponding inhibitor is realized. The physical signal output by the detection method can show a very good linear relationship for the bio-enzyme or protein activity within a certain concentration scale, and thereby realizing the high-sensitivity detection of a target to be tested.

The invention relates to a probe used for detecting acetylcholin esterase and its inhibitor activity, an application and a preparation method. The probe is polymerized by 10,12-diyne pentacosanoic acid and a compound in a formula I according to weight ratio of 7:3, The vesicle probe presents blue color and no fluorescence in 4-(2-Hydroxyethyl)-1-piperazineethanesulfonic acid buffer, and presents red color and emit fluorescence after being reacted with Myristoylcholine chloride (the fluorescence emission wavelength is 550nm), the sensitivity is high, the operation is easy, and the fluorescence detection method of the probe has great application prospect in biological medicine field.

This invention relates to a method of screening active natural medicines by immobilization model of alpha-glucosaccharase. It belongs to chemical craft domain of new drug screening, characters: immobilizing alpha-glucosaccharase, make screening model of its inhibitor, and validate model efficiency efficaciously of representative alpha-glucosaccharase inhibitor acarbose. We use this model to select Huzhang and Xuehe, first fix the alpha-glucosaccharase, enclose it into chromatographic column with pH=6.8 KxH3-xPO4 buffer solution at 4Deg.C. When selecting Huzhang and Xuehe, we add 4-nitrobenzene- alpha -galactopyranose, Huzhang and Xuehe, and then collect the buffer solution eluted, test its absorption in the Ultraviolet spectrophotometer, count the suppression rate by formulae, draw work curve of the corresponding suppression solution density, obtain half suppression solution density IC50 at the point of 50% suppression rate, as the thereunder of selection material activity.

The invention discloses a miRNA-155 and an application of its inhibitor in a DC-CIK cell culture; the miRNA-155 can be used as a drug target and applied to improve the killability of a CIK cell co-cultured and enhanced by a DC cell to a cancer cell. The applicant study finds that the DC-CIK cell under down-regulated expression of miRNA-155 has higher killability than the DC-CIK cell under normal expression of miRNA-155, and the killability of the DC cell under down-regulated expression of miRNA-155 is basically consistent with the killability of the DC cell under the normal expression of miRNA-155, there is no significant difference. It indicates that the miRNA-155 down-regulation cannot directly improve the killability of the DC cell to leukemia cell, but the down-regulated DC cell of the miRNA-155 can significantly enhance the killability of the cancer cell through co-culture. The applicant further finds that radix pseudostellariae cyclic peptide B and radix pseudostellariae cyclic peptide C are effective inhibitors of miRNA-155.

A method of treating or preventing adhesion formation during or following a surgical procedure comprising administering to a patient in need thereof at least one medicament selected from the group consisting of potassium channels; modulators of macrophage activation and leucocyte attraction through cytokines, or their inhibitors, antibodies or inhibitors blocking the effect of VEGF expression; prostaglandin E1; free radical scavengers, lipid peroxysomes; pregnatrienes; calcium antagonists; hypoxia; acidosis; MP; dopamine; and ATP-MgCl2, wherein the method prevents adhesion formation by preventing anoxemia.

The present invention relates to the field of medicine, in particular to regulators for regulating the invasion behavior of glioma stem cells. The application of tumor stem cell invasion inhibitor; the expression of miRNA-20a in GSC was significantly higher than that in GC, and the expression of TIMP-2 in GSC was significantly lower than that in GC regardless of mRNA level or protein level; the inhibitor of miRNA-20a can significantly inhibit Invasion ability of GSC; after inhibiting the expression of miRNA-20a, the expression of TIMP-2 mRNA level and protein level was significantly increased, and the luciferase reporter gene experiment confirmed that miRNA-20a can not only negatively regulate the expression of TIMP-2, but also through and The 3'UTR of TIMP-2 directly regulates the expression of TIMP-2.

The crystal structure at 2.16 Å resolution of the full-length bacterial bifunctional transglycosylase penicillin-binding protein 1b (PBP1b) from Escherichia coli, in complex with its inhibitor moenomycin, is provided. The atomic coordinates of the complex as well as the moenomycin binding site are provided. Three dimensional structures of amino acid residues involved in moenomycin binding and transglycosylation activity are identified. Binding site for peptidoglycan synthesis inhibitors comprising inhibitor-binding site comprises amino acid residues from at least one of transglycosylase (TG), UvrB domain 2 homolog (UB2H) and transmembrane (TM) domains of PBP1b are identified at an atomic level of resolution. Methods for rational drug design based on the atomic coordinates are provided. Methods for screening for antibiotics based on anisotropic binding assay and transglycosylase inhibitor assays are provided. Novel antibiotics based on the screening assays of the invention are disclosed.

A gene construct comprising a programmed-cell-death executioner gene having a nuclear localization signal, a deleted signal peptide, an inhibitor-resistant binding site, a promoter, and an activator. A method of making a gene construct, by modifying a programmed-cell-death executioner gene by adding a nuclear localization signal, deleting a signal peptide, mutating a binding site for an inhibitor to make it inhibitor-resistant, adding a promoter for exclusive expression in selected cells, and adding an activator. A method of eliminating undesired cells from a patient. A method of treating cancer. An array comprising at least two gene constructs wherein all of the gene constructs differ with respect to the programmed-cell-death executioner gene and the nuclear localization signal. A method of personalizing anti-cancer treatment. A method of increasing DNase 1 resistance to actin binding. A method of increasing catalytic activity of DNase 1 binding.

The invention relates to a GADD45beta protein and relative restrainer, in the application of atrophic arthritis treatment. Said agent comprises GADD45beta protein and cell factor, one or combination of descending kinases of GADD45beta protein, wherein, said cell factor comprises IFN-gamma and TNF-alpha for improving the expression of GADD45beta and the effective inducing agent IL-12 and IL-18 for improving the expression of GADD45beta. And the inventive drug compound comprises the restrainer with safe amount of GADD45beta protein which comprises GADD45beta protein antibody, reverse sequence of GADD45beta protein code sequence, natural vegetable extractive or chemical agent and IL-12 / 18 antibody, GADD45beta nucleic acid specific small molecule RNA, acceptable carrier of shaping agent, while said safe amount is that one to five 1micrograms of restrainer can be used in one kilogram weight.

This invention relates to a new cell receptor of the PRRS virus, i.e. as non-muscle myosin II-A (NMHC II-A)and its inhibitor blebbistatin, which can be used as a drug for suppressing PRRS virus infection of cells. The invention provides a method of utilizing purified NMHC II-A protein, artificially synthesized polypeptides and blebbistatin to prevent PRRS viruses from infecting cells. It also offers the antibodies generated by NMHC II-A protein and polypeptides. The purified NMHC II-A protein or artificially synthesized polypeptides and blebbistatin as well as anti-NMHC II-A protein and anti-polypeptide antibodies all have inhibitory effects on cell infection from the PRRS virus, and can be developed into drugs for preventing and treating infections of the PRRS virus.

The invention discloses a function of tumor progress site 2 in treatment of fatty liver and type 2 diabetes as well as an application thereof. According to the invention, TPL2 gene knockout mice and wild type mice are taken as the experiment objects, through a high-fat diet-induced obesity mice model, the result shows that compared with the wild type C 57 mice, body weight of the TPL2 gene knockout mice is mitigated, the fasting blood glucose level is lower than that of a control group WT mice, and the hepatic dysfunction is obviously mitigated. Through intraperitoneal glucose tolerance experiment, the endurance of the TPL2 gene knockout mice on glucose is obviously enhanced. the mice liver tissue cholesterol content change result instructs that TPL2-KO mice fatty liver pathology of a HFD group (High fat diet) is obviously mitigated, and the lipid accumulation is obviously reduced. TPL2 can be taken as a drug target for treating fatty liver and / or type 2 diabetes, and its inhibitor can be used for preparing a drug to treating fatty liver and / or type 2 diabetes.

A generic biosensor strategy was developed for the construction of switchable antibody reporter enzymes that allow direct detection of antibodies in solution including serum. The biosensor principle is based on the antibody-induced disruption of the intramolecular interaction between a reporter enzyme and its inhibitor and takes advantage of a unique structural property shared by all antibody classes, the presence of two identical antigen binding sites separated by a distance of approximately 100 Å. Unlike previous strategies, this biosensor design is intrinsically modular, allowing the construction of e.g. β-lactamase reporter enzymes for in principle any target antibody without cumbersome optimization / screening procedures. General guidelines are provided for the construction of reporter enzymes using enzyme-inhibitor pairs.

Provided are methods for the treatment of disease and promotion of healing that include providing a therapeutically effective amount of a mammalian antimicrobial peptide (AMP) or analog thereof, in particular a cathelicidin or cathelicidin fragment or cathelicidin analog, thereby treating the disease in the subject in need thereof. Also provided are specific analogs or fragments of cathelicidin that function as agonists, as do endogenous cathelicidins, or as either dominant negatives or as inhibitors to endogenous cathelicidin or to other endogenous AMPs or that compete with pro-inflammatory agents or fragments of AMPs on cognate receptors without inducing disease.

The present invention provides methods for using the level of caspase 3 activity for determining or prognosticating likelihood of cancer recurrence or relapse in a patient after the treatment for cancer. The present invention also provides methods for treating cancer in a patient using a caspase 3 inhibitor in conjunction with a conventional cancer treatment.

Proteases regulate a wide range of normal cellular functions where dysregulated activity is observed in various diseases. Compositions and methods use protease activity multiplexed bead-based immunoassays to profile protease activity. This platform technology integrates protease activity measurements with total protein quantification techniques. It represents a significant improvement over existing detection techniques by allowing for multiplexed, sensitive active protease measurements in complex biological samples. Exemplary multiplexed detections are realized in a single assay using a minute sample amount (e.g., 5 μl) for active recombinant MMP-1, -2, -3, -7, 9, and 12 and those same MMPs in cell culture supernatant, menstrual fluid effluent, and peritoneal aspirates. This multiplexed platform achieves high level of sensitivities equal to or better than existing leading single-plex detection strategies. It also allows for high throughput screening to identify inhibitors of proteases in complex, donor-derived samples.

Crystal structure at 2.16 Å resolution of full-length Escherichia coli penicillin-binding protein 1b (PBP1b) in complex with its inhibitor moenomycin, is provided. 3D structures of amino acid residues involved in moenomycin binding and transglycosylation activity are identified. Binding sites for peptidoglycan synthesis inhibitors comprising amino acid residues from transglycosylase (TG), UvrB domain 2 homolog (UB2H) and transmembrane (TM) domains of PBP1b are identified at atomic level resolution. Rational drug design, based on the atomic coordinates, are disclosed. Methods for screening for antibiotics using anisotropic binding and transglycosylase inhibitor assays and novel antibiotics based on the screening assays are provided.