1. Disease Areas
  2. Inflammation or Immune System Disease Digestive System Disease
  3. Autoimmune Disease Peptic Ulcer Disease
  4. Ulcerative Colitis

Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory bowel disease characterized by diffuse mucosal inflammation starting in the rectum and extending proximally along the colon. Experimental models of ulcerative colitis replicate key features of the human disease, with emerging evidence highlighting a critical role for IL-13 in disease pathogenesis and its potential as a therapeutic target.

Ulcerative Colitis (39):

Cat. No. Product Name CAS No. Purity Chemical Structure
  • HY-P990007
    Tulisokibart 2648504-55-4 99.00%
    Tulisokibart (PRA023) is a humanized IgG1-κ monoclonal antibody. Tulisokibart targets to TNFSF15/TL1A. Tulisokibart can be used to study a variety of inflammatory/fibrotic diseases, such as Crohn's Disease (CD) and ulcerative colitis.
    Tulisokibart
  • HY-B1829A
    Dexamethasone phosphate disodium 2392-39-4 99.94%
    Dexamethasone phosphate (Dexamethasone 21-phosphate) disodium is a prodrug form of the glucocorticoid Dexamethasone (HY-14648). Dexamethasone phosphate disodium is produced by introducing a phosphate ester group at the 21-position of the Dexamethasone molecule, forming a salt with sodium ions, thereby significantly improving water solubility. Dexamethasone phosphate disodium inhibits LPS (HY-D1056)-induced degradation of IRAK-1 and IRAK-4, and blocks LPS-induced activation of TRAF6, p-TAK1 and p-JNK. Dexamethasone phosphate disodium inhibits the secretion of RANTES, TGF-β1 and NO, promotes the production of MIP-1α and IL-10, and blocks microglial migration. Dexamethasone phosphate disodium is almost completely converted to Dexamethasone in rat blood, and supports transdermal delivery via iontophoresis. Dexamethasone phosphate disodium can be used in research related to steroid-dependent ulcerative colitis, chemotherapy-induced vomiting, allergic asthma and acute colitis (inflammatory bowel disease).
    Dexamethasone phosphate disodium
  • HY-P990006
    Duvakitug 2750005-84-4 99.76%
    Duvakitug (TEV-48574) is a humanized IgG1-λ2 monoclonal antibody targeting to TNFSF15/TL1A. Duvakitug' main expression system is CHOK1SV cells endogenously expressing glutamine synthetase (GS). Duvakitug can be used in the study of Crohn's Disease (CD).
    Duvakitug
  • HY-108852
    Basiliximab 179045-86-4 ≥99.0%
    Basiliximab (CHI 621) is a recombinant chimeric murine/human IgG1 monoclonal anti-interleukin-2 receptor antibody. Basiliximab can be used for the research of renal transplantation.
    Basiliximab
  • HY-113227
    Oxoadipic acid 3184-35-8 99.86%
    Oxoadipic acid is a key intermediate metabolite in the lysine degradation pathway. The level of Oxoadipic acid is significantly negatively correlated with the abundance of Staphylococcus. That is, the higher the abundance of Staphylococcus-a potential pathogenic bacterium that usually increases in ulcerative colitis-the lower the level of Oxoadipic acid. Oxoadipic acid can be used in the research of ulcerative colitis.
    Oxoadipic acid
  • HY-P9S0062
    Rosnilimab (Mouse IgG2a) 98.0%
    Rosnilimab (Mouse IgG2a) is a mouse-derived IgG2a, Rosnilimab. Rosnilimab is a PD-1 agonistic monoclonal antibody. Rosnilimab (Mouse IgG2a) can be used in research related to ulcerative colitis.
    Rosnilimab (Mouse IgG2a)
  • HY-P992120
    Minokitug 3061919-24-9
    Minokitug is a humanized monoclonal antibody targeting the CCR2 protein. Minokitug can be used for the research of refractory/relapsed ulcerative colitis.
    Minokitug
  • HY-183370
    JAK2/STAT3-IN-2
    JAK2/STAT3-IN-2 is an orally active JAK2/STAT3 inhibitor. JAK2/STAT3-IN-2 inhibits the phosphorylation of tyrosine residues in JAK2 and STAT3, blocks downstream signal transduction, disrupts the dimerization and nuclear translocation of STAT3, and suppresses pro-inflammatory transcriptional activity. JAK2/STAT3-IN-2 inhibits the expression of IL-17A and IL-17F, reduces immune cell infiltration, and inhibits the production of NO simultaneously. JAK2/STAT3-IN-2 exerts a protective effect in a mouse model of ulcerative colitis induced by DSS (HY-116282C). JAK2/STAT3-IN-2 can be used for the research of ulcerative colitis.
    JAK2/STAT3-IN-2
  • HY-N0448
    10-Gingerol 23513-15-7 99.48%
    10-Gingerol is an AMPK agonist, which is found in the ginger oleoresin from fresh rhizome with anti-inflammatory, antioxidant and anti-proliferative activities. 10-Gingerol suppresses neointimal hyperplasia and inhibits vascular smooth muscle cell proliferation. 10-Gingerol exhibits substantial scavenging activities with an IC50 value of 10.47 μM against DPPH radical, an IC50 value of 1.68 μM against superoxide radical and an IC50 value of 1.35 μM against hydroxyl radical. 10-Gingerol inhibits the proliferation of MDA-MB-231 tumor cell line with an IC50 of 12.1 μM. 10-Gingerol suppresses the proliferation, migration, invasion, and induced apoptosis through targeting the PI3K/Akt signaling pathway in MDA-MB-231/IR cells. 10-Gingerol can be used in research on various common cancers such as ovarian cancer and colon cancer, as well as colitis and neurodegenerative diseases.
    10-Gingerol
  • HY-P990203
    Anti-Mouse LPAM-1/Integrin α4β7 Antibody (DATK32) 99.08%
    Anti-Mouse LPAM-1/Integrin α4β7 Antibody (DATK32) is a rat-derived anti-LPAM-1/Integrin α4β7 IgG2a, κ type antibody inhibitor. Anti-Mouse LPAM-1/Integrin α4β7 Antibody (DATK32) specifically reacts with both chains of the α4β7 heterodimer and blocks the adhesion to immobilized mucosal addressin cell adhesion molecule-1 (MAdCAM-1). Anti-Mouse LPAM-1/Integrin α4β7 Antibody (DATK32) suppresses the proliferation and cytokine secretion of CD8+ T cells. Anti-Mouse LPAM-1/Integrin α4β7 Antibody (DATK32) decreases Peyer’s patches and follicular B cells in mice. Anti-Mouse LPAM-1/Integrin α4β7 Antibody (DATK32) can be used for the researches of inflammation, such as ulcerative colitis.
    Anti-Mouse LPAM-1/Integrin α4β7 Antibody (DATK32)
  • HY-108610A
    Edelfosine 70641-51-9 99.0%
    Edelfosine (ET-18-OCH3) is an orally active lipid raft modulator and apoptosis inducer that alters membrane fluidity and preferentially inserts into tumor cell membranes. Edelfosine recruits death receptor ligands (FasL/CD95L, TRAIL) and Bid to lipid rafts to form death-inducing signaling complexes, thereby initiating mitochondria-dependent apoptosis and inducing cytochrome c release. Edelfosine also exerts anti-inflammatory effects, promotes L-Selectin shedding, and causes no gastrointestinal or organ toxicity. In addition, Edelfosine inhibits nucleic acid and protein synthesis in Leishmania donovani and exhibits antiproliferative activity. Edelfosine can be used in research on multiple myeloma, inflammatory bowel diseases (such as ulcerative colitis and Crohn's disease), and visceral leishmaniasis.
    Edelfosine
  • HY-N3415
    Kumatakenin 3301-49-3 99.31%
    Kumatakenin is an orally active apoptosis inducer and autophagy inhibitor, with a Kd value of 2.94 μM for mouse ATG5. Kumatakenin increases the activities of caspase-3, caspase-8 and caspase-9, thereby inducing caspase-dependent apoptosis in ovarian cancer cells. Kumatakenin reduces the expression of chemokines and pro-oncogenic factors in ovarian cancer cells, and inhibits M2 macrophage polarization. Kumatakenin inactivates TRIM65 function, reduces the expression and stability of FASN, and thus inhibits the proliferation, migration, invasion and tumor progression of esophageal cancer cells. Kumatakenin interacts with ATG5 to reduce its protein level, decrease LC3 level, and reduce the number of autophagosomes in the hippocampus. Kumatakenin binds to Eno3 to upregulate its expression, reduce the stability and expression level of IRP1 mRNA, inhibit ferroptosis, alleviate intestinal inflammation, and restore epithelial barrier function. Kumatakenin enhances the efficacy of antibiotics against pathogenic bacteria, inhibits SARS-CoV-2 replication, and reduces cytokine production. Kumatakenin is applicable to research related to ovarian cancer, esophageal cancer, depression and colitis.
    Kumatakenin
  • HY-172208
    PROTAC cGAS degrader-1 3118499-89-8 99.07%
    PROTAC cGAS degrader-1 is a potent and selective cGAS PROTAC degrader, with DC50 values of 0.9 μM and 4.6 μM in THP-1 and RAW 264.7 cells, respectively. PROTAC cGAS degrader-1 induces proteasome-mediated degradation of cGAS, inhibits the cGAS signaling pathway, and attenuates double-stranded DNA-induced activation of cGAS in human and mouse cells. PROTAC cGAS degrader-1 is applicable to research related to ulcerative colitis.
    PROTAC cGAS degrader-1
  • HY-P5522A
    TriDAP dihydrochloride 99.16%
    TriDAP dihydrochloride (L-Ala-γ-D-Glu-meso-diaminopimelic acid dihydrochloride) is a NOD1 agonist with a Kd value of 34.5 μM. TriDAP dihydrochloride enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP dihydrochloride downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP dihydrochloride decreases IκBα levels and increases p65 levels. TriDAP dihydrochloride induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP dihydrochloride increases the RANKL/OPG ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP dihydrochloride can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection.
    TriDAP dihydrochloride
  • HY-N0442
    5-O-Methylvisammioside 84272-85-5 99.90%
    5-O-Methylvisammioside (4'-O-β-D-Glucosyl-5-O-methylvisamminol) is an orally active natural chromone glycoside and multiple biological activities. 5-O-Methylvisammioside inhibits ferroptosis by activating the Nrf2/HO-1 signaling axis. 5-O-Methylvisammioside alleviates intestinal barrier damage by inhibiting the ROS/NF-κB/NLRP3 pathway. 5-O-Methylvisammioside exerts a protective effect against acute liver injury by reducing ALT/AST, decreasing inflammatory infiltration, and inhibiting IκB-α phosphorylation and NF-κB nuclear translocation. 5-O-Methylvisammioside blocks the HMGB1/RAGE/MEK/ERK signaling axis to exert anti-tumor and anti-angiogenic effects. 5-O-Methylvisammioside improves depression-like behaviors by inhibiting Src kinase and the NF-κB pathway.
    5-O-Methylvisammioside
  • HY-P99728
    Melredableukin alfa 2056881-92-4
    Melredableukin alfa (RG7835) is a bivalent conjugate composed of a human IL-2 mutant (T3A, N88D, C125A) and human IgG1. Melredableukin alfa exhibits enhanced Treg cell selectivity in cynomolgus monkey and humanized mouse models. Melredableukin alfa can be used in research related to ulcerative colitis and autoimmune hepatitis.
    Melredableukin alfa
  • HY-W324435
    2,4-Dinitrobenzenesulfonic acid sodium salt 885-62-1 99.98%
    2,4-Dinitrobenzenesulfonic acid (DNBS; DNBSO) sodium salt (Sodium 2,4-dinitrobenzenesulfonate) is a classic colitis inducer that relies on activation of the NF-κB p65/COX-2/p38 pathway. As a hapten, 2,4-Dinitrobenzenesulfonic acid sodium salt stimulates the production of immune responses in colonic tissues, triggers oxidative stress and inflammatory reactions, and thereby leads to colonic injury. 2,4-Dinitrobenzenesulfonic acid sodium salt successfully induces models of colitis and ulcerative colitis in rats, causing pathological changes such as ulcers, edema, stenosis, shortening and organ adhesion in the distal colon, along with significant increases in the levels of inflammatory indicators and endoplasmic reticulum stress marker proteins. 2,4-Dinitrobenzenesulfonic acid sodium salt is widely used in studies on the mechanisms related to colitis and ulcerative colitis.
    2,4-Dinitrobenzenesulfonic acid sodium salt
  • HY-147240
    Acloproxalap 1824609-67-7 99.92%
    Acloproxalap (ADX-629) is an orally active reactive aldehyde species (RASP) inhibitor. Acloproxalap binds covalently to free aldehydes, sequesters reactive aldehyde species, malondialdehyde, acetaldehyde and preformed malondialdehyde-acetaldehyde adducts, and reduces elevated RASP levels. Acloproxalap decreases the formation of aldehyde adducts, reduces liver and serum triglyceride levels, hepatic fat accumulation, circulating anti-malondialdehyde-acetaldehyde adduct antibody levels, and inhibits the release of IL-6 and MCP-1. Acloproxalap improves cell viability of liver slices exposed to ethanol. Acloproxalap blocks ethanol-induced damage in animal models of alcoholic liver disease. Acloproxalap is applicable to research related to alcoholic liver disease, alcoholic fatty liver disease, non-alcoholic steatohepatitis, chronic cough, rheumatoid arthritis, ulcerative colitis and mild atopic asthma.
    Acloproxalap
  • HY-N7695
    Physalin B 23133-56-4
    Physalin B is an orally active anti-inflammatory and anticancer agent. Physalin B can be isolated from Physalis alkekengi L. var. Franchetii. Physalin B inhibits the activation of the NF-κB, NLRP3 inflammasome, STAT3, PI3K/Akt and Hedgehog signaling pathways, regulates the phosphorylation levels of GSK-3β, p38 MAPK, ERK1/2 and JNK, and promotes the nuclear translocation of NRF2. Physalin B reduces the levels of pro-inflammatory cytokines and factors, induces mitochondrial reactive oxygen species (mito-ROS) production, Apoptosis, G2/M cell cycle arrest and incomplete Autophagy, alters cytoskeleton structure and alleviates oxidative stress. Physalin B reduces cancer cell viability, ameliorates liver and lung tissue damage and alleviates liver fibrosis. Physalin B can be used in research related to ulcerative colitis, breast cancer, acute lung injury, colon cancer, non-alcoholic steatohepatitis, liver fibrosis, lung cancer, pancreatic cancer, lymphoma, ovarian cancer, sarcoma and leukemia.
    Physalin B
  • HY-158990
    GE1111 2883669-12-1
    GE1111 is a MRGPRX2 antagonist (IC50 = 9.4 μM). GE1111 inhibits MRGPRX2/MRGPRB2-mediated mast cell activation. GE1111 reduces the expressions of TSLP, IL-13, MCP-1, TNF-α, IL-1β and periostin, maintains the expression levels of claudin 1 and involucrin, restores the phagocytic activity of macrophages, and attenuates the activation of STIM1 and phosphorylated AKT. GE1111 exerts anti-inflammatory and anti-allergic effects in multiple animal models. GE1111 is applicable to the research related to rosacea, atopic dermatitis and ulcerative colitis.
    GE1111