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134
results.
Updated on
05/06/2025 [07:03:00]
Absstract of: EP4564005A1
The present invention refers to an in vitro method for diagnosing or screening a chronic inflammatory disease selected from the group comprising: Inflammatory bowel disease (IBD), arthritis or psoriasis.
Absstract of: WO2025107068A1
It is provided a method of detecting inflammatory bowel disease (IBD) in a patient comprising the step of measuring in a sample of said patient protein expression from the sample, and determining from the measured expression the presence or absence in the patient of inflammatory bowel disease. The method comprises measuring the protein expression level measured of S100-A9, neutral ceramidase, serum albumin, chymotrypsin-C, protein S100-A4, alpha-1-acid glycoprotein 1, neprilysin, lactotransferrin, immunoglobulin lambda-like polypeptide 5, immunoglobulin heavy variable 4-28, protein S100-A8, chymotrypsin-like elastase family member 3A, IgGFc-binding protein, mucin-2, antithrombin-l 11, myeloblastin, zymogen granule membrane protein 16, annexin A2, glyceraldehyde-3-phosphate dehydrogenase, chloride anion exchanger, and/or a combination thereof.
Absstract of: WO2025109148A1
The invention relates to methods for diagnosing inflammatory bowel disease (IBD) and for distinguishing between common gastrointestinal disease (principally functional bowel disease/irritable bowel syndrome and coeliac disease) and IBD, especially in children and in subjects with normal levels of C-reactive protein. The methods are based on measuring the methylation level of at least one CpG site in at least one gene.
Absstract of: WO2025109034A1
The present invention relates to a method of determining or predicting the sensitivity of a subject to an anti-inflammatory treatment against IBD using vedolizumab, comprising the steps of: Providing a biological sample of a subject suffering from IBD, determining the methylation status of at least one CpG selected from the group consisting of cg08081727, cg17830959, cg03455316, cg05197062, cg00441209, cg00706914, cg12906381, cg25299227, cg05338672, cg17764313, cg16467921, cg04674762, cg02601475, cg14115807, cg21070860, cg04546413, cg12667521, cg05062694, cg02229781, cg17096289, cg08017465, cg18319102, cg09659072, cg03161606, cg25267487, and determining the sensitivity based on said methylation status wherein a higher level of methylation of cg17830959, cg03455316, cg25299227, cg05197062, cg12906381, cg05338672, cg02601475, cg00706914, cg04674762, cg02229781, cg09659072, cg08017465, cg18319102, cg21070860, cg14115807, and a lower level of methylation of cg08081727, cg00441209, cg17764313, cg16467921, cg05062694, cg25267487, cg03161606, cg04546413, cg17096289, cg12667521 in comparison to a control value or control sample is indicative of an increased sensitivity to a therapy using vedolizumab.
Absstract of: PH12022550223A1
Provided is an antibody for the treatment or prevention of autoimmune diseases, comprising a heavy chain variable region represented by SEQ ID NO: 1 or SEQ ID NO: 24, and a light chain variable region represented by SEQ ID NO: 6, SEQ ID NO: 11, SEQ ID NO: 13, SEQ ID NO: 15, SEQ ID NO: 17, or SEQ ID NO: 25.
Absstract of: EP4285988A2
The invention relates to methods of treating fibrosis and inflammatory bowel disease. In one embodiment, the present invention treats gut inflammation by administering a therapeutically effective dosage of TL1A inhibitors and/or DR3 inhibitors to an individual. In another embodiment, the present invention provides a method of reversing tissue fibrosis in an individual by inhibiting TL1A-DR3 signaling function.
Absstract of: AU2023364180A1
Provided herein is a peptide array comprising a plurality of flagellin peptides corresponding to highly conserved peptide regions. For example, the peptide array comprises a plurality of
Absstract of: US2025154215A1
The present invention relates to a dual PRR-inhibiting peptide system consisting of TLR4- and RAGE-inhibiting motifs derived from S100A8 and S100A9 and conjugated with a CT peptide for colon-specific delivery. In human-derived monocyte THP-1 and mouse bone marrow-derived macrophages (BMDMs), S100A8/A9-derived peptides including TLR4 and RAGE-interacting motifs inhibit the binding of S100 to TLR4 or RAGE and the activation of the NLRP3 inflammasome in a dose-dependent manner. When the peptide according to the present invention is injected into mouse models of acute and chronic colitis, survival is significantly increased, and pathological damage to the colon is alleviated. In a mouse model of colitis-related colorectal cancer, when the peptide according to the present invention is injected, body weight is increased, tumor burden in the distal colon is decreased, and histological colon damage is significantly alleviated. When the peptide according to the present invention is injected into an oxaliplatin-resistant CRC xenograft mouse model, EMT-associated markers are reduced in tumor tissues and tumor growth is significantly inhibited.
Absstract of: US2025154591A1
The present invention is related to a method for determining or confirming chronic inflammatory intestinal disease or a risk thereof in a subject. The method comprises detecting the presence of keratin 7 (K7) mRNA or protein in a biological sample obtained from a subject.
Absstract of: CN119546632A
The present invention relates to a sandwich immunoassay for determining cross-linked collagen type V in a biological sample, and its use in identifying patients suffering from conditions associated with fibrosis, such as ankylosing spondylitis, inflammatory bowel disease, psoriasis and atopic dermatitis. The invention also relates to a kit for performing a sandwich immunoassay.
Absstract of: US2025146074A1
The invention relates to a method of determining whether a patient diagnosed with inflammatory bowel disease (will respond to 5-ASA therapy which includes the steps of: obtaining a stool sample from the patient, analyzing the sample for the presence of microbial acetyltransferase genes capable of converting 5-ASA to the clinically ineffective N-acetyl 5-ASA, if microbial acetyltransferase genes are not present in the sample, the patient will respond to 5-ASA therapy and such therapy should be administered; if microbial acetyltransferase genes are present in the sample, the patient will not respond to 5-ASA therapy and a second line therapy should be administered.
Absstract of: US2025144219A1
The present invention provides methods for facilitating cleansing of the gastrointestinal tract of a patient prior to a diagnostic, surgical or therapeutic procedure. The methods can improve patient compliance, and thus, efficacy of the preparation. Specifically, the present methods make the gastrointestinal tract preparation composition palatable for the patient to consume. For example, for a patient preparing to undergo colonoscopy, the present methods make the bowel preparation solution taste significantly less salty.
Absstract of: US2025146075A1
Among the various aspects of the present disclosure is the provision of methods of diagnosing and treating inflammatory bowel disease (IBD) including ulcerative colitis (UC) or Crohn's disease (CD). In particular, the present disclosure provides in part a panel of IBD biomarkers useful in diagnosing and making treatment decisions. In addition, the present disclosure provides methods of treating IBD with a plasminogen activator inhibitor-1 (PAI-1) inhibitor or tissue plasminogen activator (tPA).
Absstract of: WO2025089672A1
The present invention relates to inflammatory bowel disease model production using patient-derived intestinal organoids, and use thereof, wherein the inflammatory bowel disease model produced by an optimized production method for inflammatory bowel disease model production can be used as a patient-customized bowel disease model by constructing an evaluation method for inflammatory bowel disease drugs.
Absstract of: WO2025089672A1
The present invention relates to inflammatory bowel disease model production using patient-derived intestinal organoids, and use thereof, wherein the inflammatory bowel disease model produced by an optimized production method for inflammatory bowel disease model production can be used as a patient-customized bowel disease model by constructing an evaluation method for inflammatory bowel disease drugs.
Absstract of: WO2025089884A1
The present specification provides a method for providing information on ulcerative colitis by means of a processor, the method comprising: a step for receiving a Korean Ulcerative Colitis-Specific Questionnaire (K-UCSQ) score for an individual; and a step for determining an inflammatory bowel disease prognosis for the individual on the basis of the received K-UCSQ score.
Absstract of: WO2025085928A1
This disclosure relates generally to methods for treating an inflammatory bowel disease ("IBD", e.g., Crohn's disease or ulcerative colitis) in a patient. More particularly, this disclosure relates to methods for selecting a therapy for treating a patient suffering from an IBD. In embodiments, the foregoing can also be used to assess the severity of the IBD. The predictive aspects of said methods can facilitate and expedite the identification and stratification of IBD patient populations that are responsive to treatment with a RIPK2 inhibitor. The foregoing methods can further include treating the IBD by administering a RIPK2 inhibitor to the patient.
Absstract of: WO2025085674A1
In one aspect, the present disclosure provides a method for selecting a subject having ulcerative colitis for treatment with ADS051, or a pharmaceutically acceptable salt thereof, the method comprising: (a) measuring MRP2 seRNA in a stool sample obtained from the subject; and (b) selecting the subject for treatment when the level of MRP2 seRNA in the stool sample exceeds a threshold value. In some embodiments, the subject has moderate or severe ulcerative colitis.
Absstract of: US2025129422A1
The invention relates to methods of monitoring treatment response, disease resolution, and disease progression in subjects having inflammatory bowel disease (IBD).
Absstract of: EP4541373A1
The present invention provides a therapeutic agent for sepsis and/or septic shock, comprising, as an active ingredient, a compound capable of suppressing phosphorylation of threonine at position 749 in human STAT1; a method for screening for a candidate compound serving as an active ingredient of a therapeutic agent for sepsis and/or septic shock, the method comprising selecting a compound capable of suppressing phosphorylation of threonine at position 749 in human STAT1; a therapeutic agent for colitis, comprising, as an active ingredient, a compound capable of promoting phosphorylation of threonine at position 749 in human STAT1; a method for screening for a candidate compound serving as an active ingredient of a therapeutic agent for colitis, the method comprising selecting a compound capable of promoting phosphorylation of threonine at position 749 in human STAT1; a therapeutic agent for systemic lupus erythematosus, comprising, as an active ingredient, a compound capable of inhibiting human STAT1; and a method for screening for a candidate compound serving as an active ingredient of a therapeutic agent for systemic lupus erythematosus, the method comprising selecting a compound capable of inhibiting human STAT1.
Absstract of: WO2025079348A1
It has been revealed that, from an analysis of the mechanism regarding the action of sulfasalazine which is a therapeutic drug for inflammatory bowel disease, an anti-inflammatory action occurs by increasing intracellular glutamate. As a result of a detailed analysis, it has been revealed that a glutamine synthetase inhibitor or an xCT inhibitor which increases intracellular glutamate has a therapeutic effect on inflammatory bowel disease. Further, it is considered that a compound that suppresses expression of a glutamine synthesis inhibiting enzyme or xCT also has a therapeutic effect. An xCT inhibitor or a glutamine synthetase inhibitor is useful as a prophylactic/therapeutic drug that is for inflammatory diseases, particularly inflammatory bowel disease, and that has no serious side effects such as immunosuppression.
Absstract of: US2025122569A1
The invention relates to methods of predicting a patient's responsiveness to treatment (e.g., vedolizumab treatment) for inflammatory bowel disease (IBD).
Absstract of: WO2025076081A1
The disclosure herein relates to the development and production of novel antibodies and antigen binding fragments thereof that bind TL1 A and that are useful in the treatment, prevention and diagnosis of a disease, disorder or inflammation including, for example, autoimmune diseases including rheumatoid arthritis, inflammatory bowel disease, atopic dermatitis, systemic lupus erythematosus, asthma, ulcerative colitis, Crohn's disease, psoriasis, primary biliary cirrhosis, primary biliary cholangitis, ankylosing spondylitis, and fibrosis including intestinal fibrosis, pulmonary fibrosis, and liver fibrosis. Some of the elements of final antibody structure being designed de novo by a computer system and its data training set without reference to a specific reference molecule.
Absstract of: WO2025075714A1
Described herein is a method of diagnosing and/or treating irritable bowel syndrome (IBS) in a subject. The method comprises determining a fatty acid profile in a stool sample of the subject; and comparing the fatty acid profile with a first reference profile indicating an absence of IBS or a second reference profile indicating IBS. Also described herein is a composition for treating IBS, which comprises two or more of a Monoglobaceae bacterium, a Lachnospiraceae bacterium; and a Ruminococcaceae bacterium, as well as a method of treating IBS using the same.
Nº publicación: WO2025076414A1 10/04/2025
Applicant:
THE CHILDRENS MEDICAL CENTER CORP [US]
ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI [US]
SNAPPER SCOTT [US]
COLLEN LAUREN [US]
SCHADT ERIC [US]
ARGMANN CARMEN [US]
BECKMANN NOAM [US]
THE CHILDREN'S MEDICAL CENTER CORPORATION,
ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI,
SNAPPER, Scott,
COLLEN, Lauren,
SCHADT, Eric,
ARGMANN, Carmen,
BECKMANN, Noam
Absstract of: WO2025076414A1
The disclosure provides methods for predicting response in a subject having IBD to anti-IL12 and/or anti-IL23-based therapies, and selecting an effective therapy.
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