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Sucralfate Sale

(Synonyms: 硫糖铝; Sucrose octasulfate-aluminum complex) 目录号 : GC44964

A basic aluminum sucrose sulfate complex with gastroprotective activity

Sucralfate Chemical Structure

Cas No.:54182-58-0

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实验参考方法

Animal experiment:

Thirty-six male Wistar rats (300 to 350 g) are used in this study. The animals are divided into two experimental groups with 18 animals in each group. Each experimental group is divided into six subgroups (n=6) according to the intervention solution employed and time of intervention. In the first and second subgroups, 12 animals receive daily rectal enemas containing 40 mL of 0.9% saline solution (control subgroup) at 37°C for two weeks (n=6) and four weeks (n=6). In the second subgroup, 12 animals receive daily rectal enemas containing 40 mL of Sucralfate (SCF) at a concentration of 1.0 g/kg for two weeks (n=6) and four weeks (n=6). Finally, 12 animals of the third subgroup receive daily enemas containing 40 mL of Sucralfate at a concentration of 2.0 g/kg for two weeks (n=6) and four weeks (n=6). In order to standardize the speed and time of application, the enemas are administered in all animals with an infusion pump whose speed is standardized at 2/mL/min[1].

References:

[1]. Chaim FM, et al. Evaluation of the application of enemas containing sucralfate in tissue content of neutral and acid mucins in experimental model of diversion colitis. Acta Cir Bras. 2014 Sep;29(9):544-52.

产品描述

Sucralfate is a cytoprotective agent which has been employed for prevention and treatment of several gastrointestinal diseases.

Sucralfate is a cytoprotective agent which has been employed for prevention and treatment of several gastrointestinal diseases. Enemas containing Sucralfate improves the inflammation and increases the tissue contents of neutral and acid mucins. The content of neutral mucins does not change with the time or concentration of Sucralfate used, while acid mucins increases with concentration and time of intervention. A significant increase in tissue content of neutral mucins in animals subjected to irrigation with Sucralfate (SCF) is found compare to animals irrigated with S.F. 0.9%, regardless of the concentration and duration of intervention[1].

References:
[1]. Chaim FM, et al. Evaluation of the application of enemas containing sucralfate in tissue content of neutral and acid mucins in experimental model of diversion colitis. Acta Cir Bras. 2014 Sep;29(9):544-52.

Chemical Properties

Cas No. 54182-58-0 SDF
别名 硫糖铝; Sucrose octasulfate-aluminum complex
分子式 C12H54Al16O75S8 分子量 2086.7
溶解度 aqueous acid: slightly soluble 储存条件 Store at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
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1 mM 0.4792 mL 2.3961 mL 4.7923 mL
5 mM 0.0958 mL 0.4792 mL 0.9585 mL
10 mM 0.0479 mL 0.2396 mL 0.4792 mL
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Research Update

Topical Sucralfate for treatment of mucocutaneous conditions: A systematic review on clinical evidences

Dermatol Ther 2022 Apr;35(4):e15334.PMID:35080090DOI:10.1111/dth.15334.

Sucralfate is an aluminum salt of sucrose octasulfate, generally considered safe in terms of adverse effects. Systemic Sucralfate is FDA-approved for the treatment of duodenal ulcers. Since 1991, topical Sucralfate has been used in various mucocutaneous conditions, but it is not approved by the FDA yet. In this systematic review, the online databases were searched with appropriate keywords, and the papers were screened by the authors. After screening steps, the relevant articles were selected according to the inclusions and exclusions criteria. Finally, the full texts of 18 articles were included for final evaluations. In conclusion, topical Sucralfate has some clinical benefit in several mucocutaneous conditions, including mucocutaneous inflammatory conditions (e.g., post-radiotherapy reaction, diaper dermatitis, keratoconjunctivitis sicca, etc.), mucocutaneous infectious disorders (e.g., peristomal wound reaction/infection); ulcers; burns, and also pain relief.

Sucralfate--safety and side effects

Scand J Gastroenterol Suppl 1991;185:36-42.PMID:1957123doi

The safety of Sucralfate in terms of aluminium absorption, excretion, tissue accumulation, and toxicity is discussed, with special reference to the small amount of aluminium absorbed, its ready excretion by the normal kidney, and the hazard of toxicity in patients with advanced renal failure. The various manifestations of aluminium toxicity are described, and the notion that Alzheimer's disease should be included in this category is refuted. The clinical relevance of possible intraluminal binding and drug-drug interactions in patients receiving Sucralfate therapy is also considered. Evidence is presented to show that Sucralfate reduces the hyperphosphataemia in chronic uraemia, albeit at the risk of raised blood aluminium levels, but has no measurable effect on normal phosphate levels in patients with good renal function. The bioavailability of phenytoin, fluoroquinolone antibiotics, and H2-receptor blockers may be impaired by concomitant dosing with Sucralfate, but normal kinetics are restored by administering the drug 2 h before Sucralfate.

Sucralfate versus histamine 2 receptor antagonists for stress ulcer prophylaxis in adult critically ill patients: A meta-analysis and trial sequential analysis of randomized trials

J Crit Care 2017 Aug;40:21-30.PMID:28315586DOI:10.1016/j.jcrc.2017.03.005.

Purpose: To determine the impact of using Sucralfate versus H2RAs for SUP on patient important outcomes. Materials and methods: We searched CENTRAL, MEDLINE, EMBASE, ACPJC, clinical trials registries, and conference proceedings through June 2016 for randomized controlled trials (RCTs) comparing Sucralfate to H2RAs for SUP in adult critically ill patients. Results: 21 RCTs enrolling 3121 patients met inclusion criteria. There was no significant difference between Sucralfate compared to H2RAs in the risk of clinically important GI bleeding (risk ratio [RR] 1.19; 95% CI [confidence interval] 0.79, 1.80; P=0.42; I2=0%; low quality evidence). However, there was a statistically significant lower risk of ICU acquired pneumonia with Sucralfate compared to H2RAs (RR 0.84; 95% CI 0.72, 0.98; P=0.03; I2=0%; moderate quality evidence). Sucralfate did not significantly affect the risk of death (RR 0.95; 95% CI 0.82, 1.10; P=0.51; I2=0%; high quality evidence), or duration of ICU stay in days (mean difference-0.39; 95% CI [-1.12, 0.34]; P=0.29; I2=0%; moderate quality evidence). Trial sequential analysis adjusted estimates were consistent with conventional estimates. Conclusion: Moderate quality evidence suggests that Sucralfate reduced ICU acquired pneumonia compared to H2RAs in adult critically ill patients, with no significant impact on GI bleeding or death.

Comparison of topical Sucralfate with dexpanthenol in rat wound model

Int J Exp Pathol 2022 Aug;103(4):164-170.PMID:PMC9264344DOI:10.1111/iep.12441.

Wound healing is a dynamic process initiated in response to injury. There are many factors that have detrimental effects on the wound healing process. Numerous studies have been conducted for improving wound healing processes. Dexpanthenol is widely used to accelerate wound healing. Sucralfate is used for the treatment of peptic ulcers. We aimed to compare the efficacy of topical Dexpanthenol and Sucralfate in an experimental wound model in rats via histopathological examinations and immune histochemical determinations, as well, to evaluate their effects on EGF levels. Three different groups were formed: the Control Group, the Dexpanthenol Group and the Sucralfate Group. Full-thickness skin wounds were created on the back of each rat and isotonic saline was applied to the wounds of the rats in the control group, Bepanthol® cream was applied in Dexpanthenol Group and 10% Sucralfate cream was applied in Sucralfate Group, once a day. On the 7th, 14th and 21st days the wounds were measured and seven rats from each group were sacrificed and the wounds were excised for histopathological examination. Sucralfate increased wound healing rates by increasing neovascularization, fibroblast activation, reepithelialization and collagen density, as well as dexpanthenol. Our study revealed that the dexpanthenol and Sucralfate groups were better than the control group in terms of their effects on wound healing, however there was no statistically significant difference among these two groups. Sucralfate improves EGF expression in skin wounds and has positive results on skin wound healing comparable to dexpanthenol.

Why do ulcers heal with Sucralfate?

Scand J Gastroenterol Suppl 1990;173:6-16.PMID:2190306DOI:10.3109/00365529009091918.

It is unknown why ulcers in general heal. Some clues are worth considering. What is known is (i) that ulcer healing occurs spontaneously, (ii) that ulcers heal more quickly in the duodenum than in the stomach, (iii) that mucosal blood flow at ulcer edge improves with healing, and (iv) that healing can be speeded up by (a) not smoking, (b) removing acid from the stomach, and (c) using non-antisecretory mucosal protective agents such as Sucralfate and colloidal bismuth. The difference in healing rates between duodenal and gastric ulcers may be related to ulcer size, duodenal alkalinity due to the secretion of the Brunner's glands, and other uninvestigated factors such as epidermal growth factor and mucosal blood flow. The difference between smokers and non-smokers may be related to inhibition of prostaglandin synthesis and impairment of mucosal blood flow due to smoking and to higher acid secretion in smokers. The success with antisecretory agents indicates that acid inhibits the healing process. The success of Sucralfate and bismuth indicates that cytoprotective mechanisms play a role in ulcer healing. The literature also shows that ulcer healing is less affected by smoking in patients treated with Sucralfate than in those treated with antisecretory agents, suggesting that cytoprotective mechanisms play a more important part than acid inhibition in counteracting the adverse effects of smoking on healing. Furthermore, ulcer relapse occurs sooner in patients treated with antisecretory agents than in those treated with Sucralfate or bismuth, suggesting that withdrawal of antisecretory agents speeds up relapse and/or that cytoprotective mechanisms are associated with longer-lasting remission. It is concluded that Sucralfate healing involves cytoprotective mechanisms and that these cannot be ignored in the planning of any anti-ulcer therapy. Despite the understanding of the various site-protective and cytoprotective mechanisms, as discussed in the previous article, it is not clear why ulcers heal with Sucralfate. In fact, there is no clear answer to the fundamental question as to why ulcers in general heal with the known therapeutic agents, including H2-receptor antagonists, antacids, proton pump inhibitors, anticholinergics, site-protective agents, and cytoprotective agents. This review examines this question, using Sucralfate as a model.