Ecabet Sodium Research Articles

Antioxidant and Anti-Inflammatory Phytochemicals for the Treatment of Inflammatory Bowel Disease: A Systematic Review

Inflammatory bowel disease (IBD) remains a burden for patients with increasing prevalence in industrialized countries. Phytochemicals are non-nutrient plant derived bioactive substances with antioxidant and anti-inflammatory effects that may prove beneficial to IBD patients. This review aims to overview current evidence on the application and impact of isolated phytochemicals or phytochemicals contained in plant extracts and essential oils on patients suffering from IBD. A systematic literature search was conducted for studies relating to the use of phytochemicals for the treatment of IBD. Ultimately, 37 human clinical trials and 3 systematic reviews providing human IBD patient data relevant to phytochemicals as therapeutic agents were included. Phytochemicals in the form of curcumin, Plantago ovata seeds, polyphenon E, silymarin, resveratrol supplements or an herbal preparation of myrrh, chamomile and coffee charcoal have evidence from human clinical trials supporting their safety and beneficial effects. Cannabinoids improve quality of life but not IBD outcomes. The addition of probiotics like B. longum to fructo-oligosaccharides promote healthy composition of the gut microbiome. Phytochemicals like mastiha, anthocyanins, berberine, tormentil, T2, ecabet sodium and Pycnogenol need more well-designed trials. Systematic research on phytochemicals can lead to the discovery of useful therapeutics. These secondary metabolites can be incorporated in current IBD treatment strategies to limit side effects, promote mucosal healing and provide higher quality of life to patients.

Structural and mechanistic insights into the precise product synthesis by a bifunctional miltiradiene synthase.

Selaginella moellendorffii miltiradiene synthase (SmMDS) is a unique bifunctional diterpene synthase (diTPS) that catalyses the successive cyclization of (E,E,E)-geranylgeranyl diphosphate (GGPP) via (+)-copalyl diphosphate (CPP) to miltiradiene, which is a crucial precursor of important medicinal compounds, such as triptolide, ecabet sodium and carnosol. Miltiradiene synthetic processes have been studied in monofunctional diTPSs, while the precise mechanism by which active site amino acids determine product simplicity and the experimental evidence for reaction intermediates remain elusive. In addition, how bifunctional diTPSs work compared to monofunctional enzymes is attractive for detailed research. Here, by mutagenesis studies of SmMDS, we confirmed that pimar-15-en-8-yl+ is an intermediate in miltiradiene synthesis. Moreover, we determined the apo-state and the GGPP-bound state crystal structures of SmMDS. By structure analysis and mutagenesis experiments, possible contributions of key residues both in class I and II active sites were suggested. Based on the structural and functional analyses, we confirmed the copal-15-yl+ intermediate and unveiled more details of the catalysis process in the SmMDS class I active site. Moreover, the structural and experimental results suggest an internal channel for (+)-CPP produced in the class II active site moving towards the class I active site. Our research is a good example for intermediate identification of diTPSs and provides new insights into the product specificity determinants and intermediate transport, which should greatly facilitate the precise controlled synthesis of various diterpenes.

Mucoprotectants

The gastric mucosa is constantly exposed to gastric acid and pepsin. Moreover, various factors, such as nonsteroidal anti-inflammatory drugs, <i>Helicobacter pylori</i> infection, ethanol, stress, and aging, can damage the gastrointestinal mucosa. Nevertheless, even under these harsh conditions, the gastric mucosa is structurally maintained by various processes, referred to as “defense mechanisms.” Mucosal defense mechanisms are complicated; however, the most important elements are known to be the gastric epithelium and mucus layer, which are stimulated by prostaglandins and nitric oxide. Peptic ulcers result from an imbalance between these aggressive and defensive factors. Methods to prevent or treat peptic ulcers can be classified into two classes: 1) inhibition of gastric acid secretion and 2) promotion of mucosal defense factors. Drugs that reduce gastric acid secretion include proton pump inhibitors, histamine H2 antagonists, and potassium-competitive acid blockers. Mucoprotectants prevent peptic ulcers by promoting peptic ulcer healing. Mucoprotectants can work by two main mechanisms of action; one is independent of prostaglandins, and the other is related to prostaglandin activity. Bismuth, sucralfate, and misoprostol have been traditionally used to protect the gastric mucosa from gastric acid and pepsin. Currently, several mucoprotectants, such as rebamipide, ecabet sodium, polaprezinc, teprenone, and DA-9601, are prescribed in clinical practice. This review aims to provide information to clinicians by examining the characteristics of each drug, including their mechanism of action, research results, effective dose, and side effects.

Evaluating the mucoprotective effect of polydeoxyribonucleotide against indomethacin-induced gastropathy via the MAPK/NF-κB signaling pathway in rats

Non-steroidal anti-inflammatory drugs (NSAIDs) cause gastric mucosal damage and gastric ulceration. Among the most commonly used NSAIDs, indomethacin upregulates mucosal tumor necrosis factor-α, which activates nuclear factor-kappa B (NF-κB), and mitogen-activated protein kinases (MAPK) to induce various pro-inflammatory mediators. Polydeoxyribonucleotide (PDRN) is an adenosine A2A receptor agonist that exerts anti-inflammatory effects. In this study, we evaluated the efficacy of PDRN in the initial treatment of gastropathy against that of ecabet sodium and irsoglandin maleate, which are commonly used medications. The rats were administrated indomethacin once a day for 7 days after 24 h of fasting to induce gastropathy. Rats in the drug-treated groups were orally administrated 500 μl of distilled water containing the drug once daily for 7 days 1 h after indomethacin administration. Indomethacin administration caused mucosal damage and increased pro-inflammatory cytokine release. Both NF-κB and MAPK cascade factors were increased by indomethacin administration. PDRN therapy more potently suppressed the expressions of NF-κB and MAPK cascade factors compared to other drugs. The expression of cyclic adenosine-3′,5′-monophosphate was also increased by PDRN treatment in the indomethacin-induced gastropathy rats. These changes led to a reduction in pro-inflammatory cytokines and apoptotic factors, which ultimately promote recovery of damaged gastric tissue. Therefore, PDRN may serve as a new therapeutic option in the initial treatment of NSAIDs-induced gastropathy.

Simultaneous Control of Crystal Habit and Particle Size of Ecabet Sodium Hydrate with Rapid Cooling Crystallization and Temperature Cycling

Simultaneous Control of Crystal Habit and Particle Size of Ecabet Sodium Hydrate with Rapid Cooling Crystallization and Temperature Cycling

Efficacy of Ecabet Sodium for Helicobacter pylori Eradication with Sequential Therapy

Efficacy of Ecabet Sodium for Helicobacter pylori Eradication with Sequential Therapy

Preparation, Characterization, and In Vitro Release of Chitosan-Ecabet Electrolyte Complex for the Mucosal Delivery.

Ecabet has a mucosal protection and anti-Helicobacter pylori effect only by local action in the gastric mucous layer, due to an extremely poor absorption into the systemic blood circulation. The aim of the present work was to develop chitosan-ecabet electrolyte complex (ChE) for the enhanced mucosal drug delivery. ChEs were prepared with various ecabet-chitosan concentration ratios. Entrapment efficiency (%), sedimentation volume (%), transmission electron microscopy (TEM), FT-IR spectrum, and drug release were investigated. ChEs were prepared by the simple mixing method in a pH-adjusted solution based on the electrostatic interaction between the sulfonate (negatively charged) group from ecabet and the amine (positively charged) group from chitosan. Sedimentation volume and entrapment efficiency at the same concentration of ecabet sodium with that of chitosan resulted in 53.6% and 86.75%, respectively, suggesting a high degree of forming complex. In TEM images, the complex was approximately 200 nm in particle size and had loosely entangled particles. Forming complex of ChEs was supported by new bands appearance in the FT-IR spectrum. In the drug release study using dialysis membrane sac, ChEs showed a sustainable release up to 80% during 12 h as compared to ecabet sodium suspension at pH 1.2 medium. Based on the results of this work, ChE would be a promising drug delivery system for gastric mucosa.

Preventive effect of ecabet sodium on low-dose aspirin-induced small intestinal mucosal injury: a randomized, double-blind, pilot study

BackgroundWe aimed to investigate how high-dose ecabet sodium affects low-dose aspirin-induced small intestinal mucosal injury in healthy volunteers.MethodsHealthy volunteers were enrolled randomly into one of two groups with the following drug regimens for 2 weeks: group A, low-dose aspirin once per day and group B, low-dose aspirin and 4.0 g of ecabet sodium. Small bowel capsule endoscopy was performed before and 2 weeks after low-dose aspirin administration.ResultsA significant difference was found in the median number [range] of small intestinal lesions between baseline and two weeks after low-dose aspirin administration in group A (baseline: 1 [0–5], after: 5 [1–11]; p = 0.0059) but not in group B (baseline: 0.5 [0–9], after: 3 [0–23]; p = 0.0586). In group B, although the median number [range] of lesions in the first tertile of the small intestine did not increase two weeks after low-dose aspirin administration (baseline: 0 [0–4], after: 1.5 [0–8]; p = 0.2969), the number of lesions in the second and third tertiles of the small intestine increased significantly (baseline: 0 [0–5], after: 2 [0–15]; p = 0.0469).ConclusionsEcabet sodium had a preventive effect on low-dose aspirin-induced small intestinal mucosal injury in the upper part of the small intestine.Trial registrationISRCTN 99322160, 01/10/2018.

Efficacy of Ecabet Sodium for Helicobacter pylori Eradication with Sequential Therapy

Efficacy of Ecabet Sodium for <i>Helicobacter pylori</i> Eradication with Sequential Therapy

The Efficacy of Rebamipide or Ecabet Sodium Supplementation for Helicobacter pylori Eradication Therapy Compared with Quadruple (Concomitant) Regimen

Although some previous studies reported that a treatment combined with mucoprotective agent could improve the eradication rate in dual or triple therapy, there are other reports that question the efficacy of combining these drugs in concomitant therapy (CoCTx). The aim of this study was to investigate the effects of rebamipide or ecabet on the Helicobacter pylori (H. pylori) eradication combined with CoCTx. We retrospectively reviewed the medical records of 277 patients with proven H. pylori infection. They were assigned to one of 3 regimens for 10 days, twice daily: (a) CoCTx (n=118): lansoprazole 30 mg, amoxicillin 1 g, metronidazole 500 mg, and clarithromycin 500 mg; (b) CoCTx+rebamipide (100 mg) (n=85); (c) CoCTx+ecabet (1 g) (n=74). The baseline characteristics were not significantly different. H. pylori eradication rates were 82.2% (97/118) in CoCTx, 90.6% (77/85) in CoCTx+rebamipide, and 89.2% (66/74) in CoCTx+ecabet (p=0.17), which were statistically insignificant. Overall adverse events were more frequently reported in the CoCTx+rebamipide (50.6%. 43/85) and CoCTx+ecabet (44.6%, 33/74) groups than in the CoCTx (32.2%, 38/118) (p = 0.03) group. Drug compliances were not different between three groups (CoCTx: 95.8%, 113/118; CoCT+rebamipide: 92.9%, 79/85; CoCTx+ecabet 98.6%,73/74) (p=0.209). Multivariate analysis showed that the risk of eradication failure was significantly increased with decreased drug compliance (odds ratio 3.52, 95% confidence interval 1.00-12.32; p=0.05). Addition of these mucoprotective agent was not superior to CoCTx alone for eradicating H. pylori infection with frequent adverse events. Rather, drug compliance is the most related factor affecting the eradication rate. Our data suggest the importance of drug compliance over the drugs used.

Effect of Ecabet Sodium as an Adjuvant Therapy for Helicobacter pylori Eradication with Sequential Therapy

Effect of Ecabet Sodium as an Adjuvant Therapy for <i>Helicobacter pylori</i> Eradication with Sequential Therapy

Irsogladine maleate, a gastric mucosal protectant, suppresses intestinal polyp development in Apc-mutant mice.

This study aimed to identify gastric mucosal protectants that suppress intestinal tumorigenesis in a mouse model. We chose six gastric mucosal protectants (ecabet sodium hydrate, irsogladine maleate, rebamipide, sofalcone, teprenone and troxipide) and examined their effects on the activity of oxidative stress-related transcriptional factors, including AP-1, NF-jB, NRF2, p53 and STAT3, in Caco-2 cells using a luciferase reporter gene assay. Among the six protectants, irsogladine maleate clearly inhibited NF-jB and AP-1 transcriptional activity. Furthermore, the chemopreventive property of irsogladine maleate was examined in a Min mouse model of familial adenomatous polyposis. Treatment with irsogladine maleate at doses of 5 and 50 ppm significantly reduced the number of intestinal polyps to 69% and 66% of the untreated control value, respectively. In these polyps, mRNA levels of the downstream targets of NF-jB, such as IL-1β and IL-6, were decreased by irsogladine maleate treatment. Moreover, the levels of oxidative stress-related markers, reactive carbonyl species, in the livers of Min mice were clearly decreased following the administration of irsogladine maleate. This study demonstrated that irsogladine maleate suppresses intestinal polyp formation in Min mice partly through the NF-jB signaling pathway, thus reducing oxidative stress.

Ecabet sodium alleviates neomycin-induced hair cell damage

Ecabet sodium (ES) is currently applied to some clinical gastrointestinal disease primarily by the inhibition of the ROS production. In this study, the protective role of ES was evaluated against the neomycin-induced hair cell loss using zebrafish experimental animal model.Zebrafish larvae (5–7 dpf), were treated with each of the following concentrations of ES: 5, 10, 20, 40, and 80μg/mL for 1 h, followed by 125μM neomycin for 1h. The positive control group was established by 125μM neomycin-only treatment (1h) and the negative control group with no additional chemicals was also established. Hair cells inside four neuromasts ( SO1, SO2, O1, OC1) were assessed using fluorescence microscopy (n=10). Hair cell survival was calculated as the mean number of viable hair cells for each group. Apoptosis and mitochondrial damage were investigated using special staining (TUNEL and DASPEI assay, respectively), and compared among groups. Ultrastructural changes were evaluated using scanning electron microscopy.Pre-treatment group with ES increased the mean number of viable hair cells as a dose-dependent manner achieving almost same number of viable hair cells with 40μM/ml ES treatment (12.98±2.59 cells) comparing to that of the negative control group (14.15±1.39 cells, p=0.72) and significantly more number of viable hair cells than that of the positive control group (7.45±0.91 cells, p<0.01). The production of reactive oxygen species significantly increased by 183% with 125μM neomycin treatment than the negative control group and significantly decreased down to 105% with the pre-treatment with 40μM/ml ES (n=40, p=0.04). A significantly less number of TUNEL-positive cells (reflecting apoptosis, p<0.01) and a significantly increased DASPEI reactivity (reflecting viable mitochondria, p<0.01) were observed in 40μM/ml ES pre-treatment group.Our data suggest that ES could protect against neomycin-induced hair cell loss possibly by reducing apoptosis, mitochondrial damages, and the ROS generation.

Dietary Intervention of Artemisia and Green Tea Extracts to Rejuvenate Helicobacter pylori-Associated Chronic Atrophic Gastritis and to Prevent Tumorigenesis.

As nonmicrobial dietary approach is capable of controlling Helicobacter pylori infection, we evaluated the efficacy of long-term dietary administration of Artemisia and/or green tea extracts on H. pylori-initiated, high-salt-promoted chronic atrophic gastritis and gastric tumorigenesis mouse model. Helicobacter pylori-infected and high-salt-diet-administered C57BL/6 mice were administered with Artemisia extracts (MP group) and/or green tea extracts (GT group) for 36 weeks in addition to the control group (ES group, gastroprotective drug, ecabet sodium 30 mg/kg, diet pellet). Gross and pathological gastric lesions were evaluated after 24 and 36 weeks, respectively, and their underlying molecular changes were measured in gastric homogenates. Detailed mechanisms were further evaluated in in vitro cell models. The erythematous and nodular changes and mucosal ulcerative and erosive lesions were noted in the control group at 24 weeks. MP, GT, MPGT, and ES groups all showed significantly ameliorated pathologic lesion compared to the control group (p < .05). After the 36 weeks, scattered nodular masses with some central ulcers and thin gastric surface were noted in the control stomach, whereas no tumorous lesion and milder atrophic changes were observed in all MP, GT, and MPGT groups except ES group (p < .05). On molecular analysis, increased expressions of COX-2, TNF-α, IL-6, lipid peroxide, and activated STAT3 relevant to H. pylori infection were significantly decreased with MPGT administration (p < .01), whereas HSP70 was significantly increased. PGDH expressions, core tumor suppressor involved in carcinogenesis, were significantly decreased with H. pylori infection (p < .05), but significantly increased in MPGT group (p < .05). Increased mucosal apoptotic index noted in the control group was significantly decreased with MP and/or GT along with significantly preserved gastric gastroprotective mediators (p < .01) such as mucins, HSP27, and HSP70. H. pylori-induced serum TNF-α and NF-κB activations were significantly decreased with MPGT administration (p < .05). Long-term dietary intake of MP and/or GT can be an effective strategy either to rejuvenate H. pylori atrophic gastritis or to suppress tumorigenesis.

The effect of sequential therapy with lansoprazole and ecabet sodium in treating iatrogenic gastric ulcer after endoscopic submucosal dissection: a randomized prospective study.

Ecabet sodium (ES) is a new non-systemic anti-ulcer agent belonging to the category of gastroprotective agents. In this study we aimed to compare the efficacy of a combination therapy with lansoprazole (LS) followed by ES with LS alone in treating endoscopic submucosal dissection (ESD)-induced iatrogenic gastric ulcers. Patients diagnosed with gastric adenomas or early gastric cancer were randomly divided into either the LS group (30 mg once daily for 4 weeks; n = 45) or the LS + ES group (LS 30 mg once daily for one week followed by ES 1500 mg twice daily for 3 weeks; n = 45). Four weeks after ESD, a follow-up endoscopy was conducted to evaluate the proportions of ulcer reduction and ulcer stages in the two groups. In all, 79 patients were included in the final analyses. Both treatment modalities were well-tolerated in most patients, with a drug compliance of over 80%. There were no significant differences between the two groups in terms of the proportions of ulcer reduction (0.9503 ± 0.1215 in the LS group vs 0.9192 ± 0.0700 in the LS + ES group, P = 0.169) or ulcer stage (P = 0.446). The prevalence of adverse events related to drugs and bleeding were also similar between the two groups. Sequential therapy with LS + ES is as effective as LS alone against ESD-induced gastric ulcers.

Efficacy and Safety of Ecabet Sodium as an Adjuvant Therapy forHelicobacter pyloriEradication: A Systematic Review and Meta-Analysis

Several studies have reported that the application of ecabet sodium during the eradication of Helicobacter pylori can improve the eradication rate and reduce therapy-associated side effects. However, the efficacy and safety of this therapy are controversial. To determine whether ecabet sodium improves the eradication rate of H. pylori and examine treatment safety by conducting a meta-analysis based on randomized controlled trials (RCTs). Literature searches were conducted in the following databases: PubMed, Embase, the Cochrane Library, the Science Citation Index, the China National Knowledge Infrastructure Database, and the Wanfang Database. A meta-analysis of all RCTs comparing ecabet sodium supplementation with nonecabet sodium-containing therapy was performed. Thirteen RCTs that included a total of 1808 patients were assessed. The meta-analysis showed that the eradication rate in the ecabet sodium-containing quadruple therapy group was higher than that in the standard triple therapy group (84.5% vs 74.55%, OR 1.757 (95%CI: 1.307 to 2.362), p < .001). The analysis also showed that the eradication rate in the ecabet sodium-containing triple therapy group was significantly higher than that in the PPI plus amoxicillin or clarithromycin therapy group (74.6% vs 43.9%,OR 3.727 (95%CI: 2.320 to 5.988), p < .001)(ITT), (74.6% vs 43.9%,OR 3.863 (95%CI: 2.369 to 6.298), p < .001) (PP). Furthermore, our meta-analysis suggested that the occurrence of side effects did not significantly differ between patients receiving ecabet sodium-containing therapy and patients receiving nonecabet sodium-containing therapy (14.0% vs 13.3%, OR 1.055 (95%CI: 0.632 to 1.759), p = .839). Supplementation with ecabet sodium during H. pylori eradication therapy improves the eradication rate. The use of ecabet sodium does not increase the side effects based on our meta-analysis.

Freeze-Dried Highly Porous Matrix as a New Gastroretentive Dosage Form for Ecabet Sodium: In Vitro and In Vivo Characterizations

AbstractThe aims of the present study were to prepare hydroxypropylmethyl cellulose-based matrix tablets prepared using the freeze-drying method for gastroretentive delivery of ecabet sodium (ECS), a locally acting antigastric ulcer drug, and to perform in vitro/in vivo characterizations.The freeze-dried gastroretentive tablets (FD-GRTs) had porous structures, while they had good friability as a pharmaceutical dosage form. The porous structures lowered the tablet density, allowing the tablet to float without any lag time. Buoyancy of FD-GRT was maintained until they were entirely disintegrated during an in vitro release study. Release rate of ECS could be controlled by the amount of ethylcellulose (EC) in FD-GRT. As amount of EC in the composition was increased, there was a decrease in both release rate and erosion rate of FD-GRT. When administered to a miniature pig, FD-GRT remained in the stomach for more than 12h, which was significantly longer than a conventional sustained release tablet. The new FD-GRT do not contain any excipients for buoyancy and do not require any lag time for buoyancy, consequently it could be considered to be safer and more effective than conventional floating-type GRT.

Efficacy of gastro-retentive forms of ecabet sodium in the treatment of gastric ulcer in rats

The purpose of the present study is to investigate the influence of gastric retention of ecabet sodium (ECS) on its mucoprotective effect in rat ulcer models. Mini-tablets containing 9 mg ECS were prepared using the direct compression method. The release rates of ECS mini-tablets were controlled by the amount and viscosity grade of hydroxypropylmethyl cellulose incorporated. Gastric retention of ECS mini-tablets after oral administration to rats was visually confirmed using a fluorescence imaging system. Because ECS mini-tablets exhibited size-dependent gastric retention, their gastric retention time was prolonged as the release rate decreased. In the in vivo efficacy study, gastro-retentive dosage forms of ECS did not influence the mucoprotective effect in the immediate irritation model but enhanced the effect in the delayed irritation model compared with ECS suspension. This finding indicates that the duration of the mucoprotective effect of ECS can be extended by the employment of gastro-retentive dosage formulations and provides a rationale for development of ECS gastro-retentive dosage forms.

Curcumin and Anthocyanin Inhibit Pepsin-Mediated Cell Damage and Carcinogenic Changes in Airway Epithelial Cells

Laryngopharyngeal reflux (LPR) is associated with inflammatory and neoplastic airway diseases. Gastric pepsin internalized by airway epithelial cells during reflux contributes to oxidative stress, inflammation, and carcinogenesis. Several plant extracts and compounds inhibit digestive enzymes and inflammatory or neoplastic changes to the esophagus in models of gastroesophageal reflux. This study examined the potential of chemoprotective phytochemicals to inhibit peptic activity and mitigate pepsin-mediated damage of airway epithelial cells. Cultured human laryngeal and hypopharyngeal epithelial cells were pretreated with curcumin (10 micromol/L), ecabet sodium (125 microg/mL), and anthocyanin-enriched black-raspberry extract (100 microg/mL) 30 minutes before treatment with pepsin (0.1 mg/mL; 1 hour; pH 7). Controls were treated with media pH 7 or pepsin pH 7 without phytochemicals. Cell damage and proliferative changes were assessed by electron microscopy, cell count, thymidine analog incorporation, and real-time polymerase chain reaction array. Pepsin inhibition was determined by in vitro kinetic assay. Micromolar concentrations of curcumin, ecabet sodium, and black-raspberry extract inhibited peptic activity and pepsin-induced mitochondrial damage and hyperproliferation. Curcumin abrogated pepsin-mediated depression of tumor suppressor gene expression and altered the subcellular localization of pepsin following endocytosis. Several phytochemicals inhibit the pepsin-mediated cell damage underlying inflammatory or neoplastic manifestations of LPR. Dietary supplementation or adjunctive therapy with phytochemicals may represent novel preventive or therapeutic strategies for LPR-attributed disease.

Helicobacter pylori Eradication with Ecabet Sodium, Omeprazole, Amoxicillin, and Clarithromycin Versus Bismuth, Omeprazole, Amoxicillin, and Clarithromycin Quadruple Therapy: A Randomized, Open‐Label, Phase IV Trial

Helicobacter pylori infection is a substantial public health problem and plays etiological role in the pathogenesis of many gastroduodenal disorders. The addition of ecabet sodium is proven to improve the efficacy of the standard triple therapy. Our aim was to assess the efficacy and safety of ecabet sodium-containing quadruple therapy versus 10-day bismuth-containing quadruple therapy for H. pylori eradication. We did a randomized, open-label, phase IV trial in four cities (eight sites) in China, comparing the efficacy and safety of 10-days ecabet sodium-containing versus bismuth-containing quadruple therapy in adults with H. pylori infection. Eligible patients were randomly assigned treatment and monitored H. pylori eradication by negative [13C]/[14C] urea breath test 28 days after the treatment as the primary outcome. Symptoms improvement and side effects were the secondary outcome. A total of 311 H. pylori-positive subjects were enrolled: 155 were assigned ecabet sodium quadruple therapy and 156 bismuth quadruple therapy. The eradication rates with ecabet sodium-containing and bismuth-containing quadruple regimens were 68.4% (106/155) and 68.0% (106/156) p = .9339 intention-to-treat (ITT) and 75.4% (104/138) and 77.0% (104/135) p = .7453 per-protocol (PP), respectively. The eradication rates for the ecabet sodium quadruple regimen differed significantly between cities (e.g., 81.2% ITT and 89.6% PP in Shanghai and 50% ITT and 53.5% PP in Xi'an). The symptom improvements and safety profiles were also similar for both treatments. Neither 10-day Ecabet sodium-containing quadruple therapy or 10-day bismuth-containing quadruple therapy can be recommended as empiric therapy in cities with high antibiotic resistance rate of China.