2. Disease Areas
  3. Digestive System Disease
  4. Peptic Ulcer Disease

Peptic Ulcer Disease

Peptic ulcer disease (PUD) is a condition characterized by the development of open sores or ulcers in the lining of the stomach, duodenum, or lower esophagus, primarily caused by *Helicobacter pylori* infection or long-term use of non-steroidal anti-inflammatory drugs (NSAIDs). It may also result from stress-related conditions such as severe illness, burns, surgery, or central nervous system trauma. Common symptoms include upper abdominal pain (often burning or gnawing, sometimes relieved by eating), nausea, vomiting, bloating, belching, weight loss, and fatigue. Complications can involve bleeding, perforation, or gastric outlet obstruction. Diagnosis is typically confirmed through endoscopy (esophagogastroduodenoscopy), along with testing for *H. pylori* via blood, breath, or stool samples. Treatment involves antibiotics to eradicate *H. pylori*, acid-reducing medications such as proton pump inhibitors or H2 blockers, and lifestyle modifications including stress management and dietary changes. In refractory cases, surgical intervention may be required. Associated genes include *S100A8*, and pathways involved include signal transduction and gastrin signaling. Drugs like metronidazole and naproxen are linked to the disorder, with affected tissues including the small intestine and liver.

 

Peptic Ulcer Disease (61):

Cat. No. Nombre del producto No. CAS Pureza Estructura química
  • 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-B1820
    Zinc sulphate 7733-02-0 99.85%
    Zinc sulphate is an orally active inhibitor of tyrosinase and glutathione reductase. Zinc sulphate enhances the activity of dopachrome tautomerase. Zinc sulphate delays anagen-related eumelanin production, induces hair hypopigmentation in mice, and accelerates wound healing. Zinc sulphate can be used in research related to benign gastric ulcers. Zinc sulphate can be used in research related to rheumatoid arthritis.
    Zinc sulphate
  • 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-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-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-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-181872
    JAK1-IN-20 3106963-85-0
    JAK1-IN-20 (Compound 38) is a gut-restricted, orally active, selective JAK1 inhibitor with an IC50 of <0.5 nM. JAK1-IN-20 inhibits the enzymatic activity of JAK1, reduces the production of proinflammatory cytokines (TNF-α, IL-6), and suppresses the phosphorylation of STAT3. JAK1-IN-20 ameliorates ulcerative colitis. JAK1-IN-20 can be used for the research of inflammatory bowel disease.
    JAK1-IN-20
  • 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-N0340
    Scopolamine butylbromide 149-64-4 99.97%
    Scopolamine butylbromide (Hyoscine butylbromide) is an orally active anticholinergic agent and spasmolytic. Scopolamine butylbromide binds with high affinity to rat cardiac M2 (Ki 83 nmol/L), hM2 (Ki 233 nmol/L), rat intestinal M3 (Ki 290 nmol/L) and hM3 (Ki 643 nmol/L) muscarinic receptors. Scopolamine butylbromide exerts a dose-dependent antagonistic effect on Carbachol-induced gastrointestinal smooth muscle spasm. Scopolamine butylbromide can be used for the research of abdominal colic and pain associated with gastrointestinal spasm, functional abdominal pain, chronic gastropathy and gastric ulcer.
    Scopolamine butylbromide
  • 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-N3031
    Grosvenorine 156980-60-8 99.64%
    Grosvenorine is an orally active flavonoid glycoside found in S. grosvenorii. Grosvenorine exhibits antibacterial, antioxidant and antiinflammation activities. Grosvenorine can induce apoptosis and increases anti-apoptotic Bcl-2 protein expression and reduces pro-apoptotic P53 protein expression in gastric tissues. Grosvenorine enhances mucin/glycoprotein secretion, regulates gastric pH, and reduces gastric lesion incidence.Grosvenorine increases glutathione peroxidase, catalase, and SOD levels, reduces lipid peroxidation (MDA), and lowers TNF-α and IL-6 levels. Grosvenorine can be used for the researches of bacterial infection and Gastric ulcer.
    Grosvenorine
  • HY-126848
    Diclofenac acyl glucuronide 64118-81-6 98.34%
    Diclofenac acyl glucuronide (D-1-O-G) is an orally active glucuronide metabolite of Diclofenac (HY-15036). Diclofenac acyl glucuronide exhibits SOD inhibitory activity, COX-1 inhibitory activity (IC50 = 0.620 μM), and COX-2 inhibitory activity (IC50 = 2.91 μM). Diclofenac acyl glucuronide induces reactive oxygen species (ROS) production and acts as a substrate of OATP2B1. Diclofenac acyl glucuronide induces small intestinal ulcers. Diclofenac acyl glucuronide can be used in research related to intestinal diseases and small intestinal ulcers.
    Diclofenac acyl glucuronide
  • HY-G0007
    Omeprazole sulfone 88546-55-8 99.23%
    Omeprazole sulfone (Omeprazole sulphone) is one of the major circulating metabolites of Omeprazole (HY-B0113) in vivo, and belongs to class 4 non-mutagenic impurities. Omeprazole sulfone does not bind to the aryl hydrocarbon receptor (AhR), nor does it induce the expression of CYP1A1 or CYP1A2. However, Omeprazole sulfone promotes the migration of gastric epithelial cells under basal conditions and reverses the inhibitory effect of Indomethacin (HY-14397) on cell migration. Omeprazole sulfone does not promote cell proliferation, nor does it upregulate COX-2 expression or activate signaling pathways such as ERK, P38 MAPK and PI3K. Omeprazole sulfone maintains basal ulcer healing under non-acid-dependent conditions and can be used in studies related to gastric ulcer repair.
    Omeprazole sulfone
  • 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-B0327
    Irsogladine 57381-26-7 99.88%
    Irsogladine (Dicloguamine) is an orally active gastric mucosal protective agent. Irsogladine inhibits breast cancer recurrence and lung metastasis in nude mice. Irsogladine inhibits the transcriptional activities of NF-κB and AP-1, suppresses the activities of PDE and PDE4 to elevate intracellular cAMP levels, and activates TRPV1 and KATP channels. Irsogladine enhances iNOS expression, NO production, and the activation of cAMP-responsive elements. Irsogladine inhibits the development and progression of intestinal polyps in Apc-mutant mice. Irsogladine alleviates oxidative stress, increases gastric mucosal blood flow, and stimulates the production of endogenous prostaglandins. Irsogladine promotes insulin secretion in MIN6 cells. Irsogladine inhibits tumor angiogenesis, cancer cell proliferation, and the production of proinflammatory cytokines. Irsogladine exerts protective effects on astrocytes in ethanol/hydrochloric acid-induced gastric ulcers in mice. Irsogladine prevents colitis in IL-10 gene-deficient mice by reducing the production of IL-12 and IL-23. Irsogladine upregulates gap junction intercellular communication in pancreatic cancer cells via the PKA pathway. Irsogladine is applicable to research related to breast cancer, intestinal polyposis, gastric ulcer, spontaneous colitis, glioma, liver cancer, and pancreatic cancer[5][6].
    Irsogladine
  • HY-N12717
    Casuarinin 79786-01-9 98.24%
    Casuarinin is an orally active antiproliferative, anti-inflammatory, antifungal, virucidal and gastroprotective agent. Casuarinin upregulates the expression of p21/WAF1, Fas/APO‑1, mFasL, sFasL and HSP‑70, arrests cell cycle, induces apoptosis and inhibits cancer cell proliferation. Casuarinin inhibits TNF‑α-induced phosphorylation of MAPK and activation of NF‑κB, downregulates the expression of iNOS, NF‑κB, COX‑2 and ICAM‑1, and reduces the production of proinflammatory mediators. Casuarinin attenuates ethanol-induced activation of caspase‑3 and elevation of TNF‑α, inhibits the growth of Candida albicans, and inhibits HSV‑2. Casuarinin can be used in research related to mammary adenocarcinoma, inflammatory skin diseases, gastric ulcers, candidiasis and herpes simplex virus infections.
    Casuarinin
  • HY-126941
    Hecogenin acetate 915-35-5 98.57%
    Hecogenin acetate is an orally active steroid saponin aglycone with extensive biological activities. Hecogenin acetate inhibits the phosphorylation of NF-κB and p38 MAPK signaling pathways, antagonizes TRPA1/TRPM8 channels, inhibits the production of pro-inflammatory cytokines, and has anti-inflammatory and analgesic effects. Hecogenin acetate inhibits the production of ROS and the activation of NLRP3 inflammasome; downregulates the expression of MMP-2, and has neuroprotective and anti-tumor activities. Hecogenin acetate enhances gastric mucosal defense and promotes ulcer healing. Hecogenin acetate can be used in combination with certain antibiotics to regulate bacterial efflux pumps and restore antibiotic sensitivity.
    Hecogenin acetate