Rebamipide

Last updated
Rebamipide
Rebamipide.svg
Clinical data
Trade names Mucosta (JP), Rebagen (KR, CN, IN), Rebagit (RU), Rebamax (ID)
AHFS/Drugs.com International Drug Names
Routes of
administration
By mouth (tablets)
ATC code
Identifiers
  • 2-[(4-chlorobenzoyl)amino]-3-(2-oxo-1H-quinolin-4-yl)propanoic acid
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEMBL
CompTox Dashboard (EPA)
Chemical and physical data
Formula C19H15ClN2O4
Molar mass 370.79 g·mol−1
3D model (JSmol)
  • Clc1ccc(cc1)C(=O)NC(C(=O)O)CC2=CC(=O)Nc3ccccc32
  • InChI=1S/C19H15ClN2O4/c20-13-7-5-11(6-8-13)18(24)22-16(19(25)26)9-12-10-17(23)21-15-4-2-1-3-14(12)15/h1-8,10,16H,9H2,(H,21,23)(H,22,24)(H,25,26) Yes check.svgY
  • Key:ALLWOAVDORUJLA-UHFFFAOYSA-N Yes check.svgY
 X mark.svgNYes check.svgY  (what is this?)    (verify)

Rebamipide, an amino acid derivative of 2-(1H)-quinolinone, is used for mucosal protection, [1] healing of gastroduodenal ulcers, and treatment of gastritis. [2] It works by enhancing mucosal defense, scavenging free radicals, [3] and temporarily activating genes encoding cyclooxygenase-2. [4]

Studies have shown that rebamipide can fight the damaging effects of NSAIDs on the GIT mucosa, [5] and more recently, the small intestine, but not for naproxen-induced gastric damage. [6]

Availability

Rebamipide is used in a number of Asian countries including Japan (marketed as Mucosta), South Korea, China [7] and India (where it is marketed under the trade name Rebagen). It is also approved in Russia under the brand name Rebagit. [8]

Related Research Articles

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Non-steroidal anti-inflammatory drugs (NSAID) are members of a therapeutic drug class which reduces pain, decreases inflammation, decreases fever, and prevents blood clots. Side effects depend on the specific drug, its dose and duration of use, but largely include an increased risk of gastrointestinal ulcers and bleeds, heart attack, and kidney disease.

Peptic ulcer disease (PUD) is a break in the inner lining of the stomach, the first part of the small intestine, or sometimes the lower esophagus. An ulcer in the stomach is called a gastric ulcer, while one in the first part of the intestines is a duodenal ulcer. The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain, and upper abdominal pain that improves with eating. With a gastric ulcer, the pain may worsen with eating. The pain is often described as a burning or dull ache. Other symptoms include belching, vomiting, weight loss, or poor appetite. About a third of older people have no symptoms. Complications may include bleeding, perforation, and blockage of the stomach. Bleeding occurs in as many as 15% of cases.

<span class="mw-page-title-main">Pepsin</span> Enzyme

Pepsin is an endopeptidase that breaks down proteins into smaller peptides. It is produced in the gastric chief cells of the stomach lining and is one of the main digestive enzymes in the digestive systems of humans and many other animals, where it helps digest the proteins in food. Pepsin is an aspartic protease, using a catalytic aspartate in its active site.

<i>Helicobacter pylori</i> Species of bacteria

Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, microaerophilic, spiral (helical) bacterium usually found in the stomach. Its helical shape is thought to have evolved in order to penetrate the mucoid lining of the stomach and thereby establish infection. The bacterium was first identified in 1982 by the Australian doctors Barry Marshall and Robin Warren. H. pylori has been associated with cancer of the mucosa-associated lymphoid tissue in the stomach, esophagus, colon, rectum, or tissues around the eye, and of lymphoid tissue in the stomach.

Alkaline mucus is a thick fluid produced by animals which confers tissue protection in an acidic environment, such as in the stomach.

<span class="mw-page-title-main">Esomeprazole</span> Medication that suppresses stomach acidity

Esomeprazole, sold under the brand name Nexium [or Neksium] among others, is a medication which reduces stomach acid. It is used to treat gastroesophageal reflux disease, peptic ulcer disease, and Zollinger–Ellison syndrome. Its effectiveness is similar to that of other proton pump inhibitors (PPIs). It is taken by mouth or injection into a vein.

<span class="mw-page-title-main">Gastritis</span> Stomach disease that is an inflammation of the lining of the stomach

Gastritis is inflammation of the lining of the stomach. It may occur as a short episode or may be of a long duration. There may be no symptoms but, when symptoms are present, the most common is upper abdominal pain. Other possible symptoms include nausea and vomiting, bloating, loss of appetite and heartburn. Complications may include stomach bleeding, stomach ulcers, and stomach tumors. When due to autoimmune problems, low red blood cells due to not enough vitamin B12 may occur, a condition known as pernicious anemia.

<span class="mw-page-title-main">Atrophic gastritis</span> Medical condition

Atrophic gastritis is a process of chronic inflammation of the gastric mucosa of the stomach, leading to a loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. As a result, the stomach's secretion of essential substances such as hydrochloric acid, pepsin, and intrinsic factor is impaired, leading to digestive problems. The most common are vitamin B12 deficiency possibly leading to pernicious anemia; and malabsorption of iron, leading to iron deficiency anaemia. It can be caused by persistent infection with Helicobacter pylori, or can be autoimmune in origin. Those with autoimmune atrophic gastritis (Type A gastritis) are statistically more likely to develop gastric carcinoma, Hashimoto's thyroiditis, and achlorhydria.

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<span class="mw-page-title-main">Gastrinoma</span> Medical condition

Gastrinomas are neuroendocrine tumors (NETs), usually located in the duodenum or pancreas, that secrete gastrin and cause a clinical syndrome known as Zollinger–Ellison syndrome (ZES). A large number of gastrinomas develop in the pancreas or duodenum, with near-equal frequency, and approximately 10% arise as primary neoplasms in lymph nodes of the pancreaticoduodenal region.

Gastric hydrogen potassium ATPase, also known as H+/K+ ATPase, is an enzyme which functions to acidify the stomach. It is a member of the P-type ATPases, also known as E1-E2 ATPases due to its two states.

<span class="mw-page-title-main">Enprostil</span> Chemical compound

Enprostil is a synthetic prostaglandin designed to resemble dinoprostone. Enprostil was found to be a highly potent inhibitor of gastric HCl secretion. It is an analog of prostaglandin E2 but unlike this prostaglandin, which binds to and activates all four cellular receptors viz., EP1, EP2, EP3, and EP4 receptors, enprostil is a more selective receptor agonist in that it binds to and activates primarily the EP3 receptor. Consequently, enprostil is expected to have a narrower range of actions that may avoid some of the unwanted side-effects and toxicities of prostaglandin E2. A prospective multicenter randomized controlled trial conducted in Japan found combining enprostil with cimetidine was more effective than cimetidine alone in treating gastric ulcer.

Timeline of peptic ulcer disease and <i>Helicobacter pylori</i>

This is a timeline of the events relating to the discovery that peptic ulcer disease and some cancers are caused by H. pylori. In 2005, Barry Marshall and Robin Warren were awarded the Nobel Prize in Physiology or Medicine for their discovery that peptic ulcer disease (PUD) was primarily caused by Helicobacter pylori, a bacterium with affinity for acidic environments, such as the stomach. As a result, PUD that is associated with H. pylori is currently treated with antibiotics used to eradicate the infection. For decades prior to their discovery, it was widely believed that PUD was caused by excess acid in the stomach. During this time, acid control was the primary method of treatment for PUD, to only partial success. Among other effects, it is now known that acid suppression alters the stomach milieu to make it less amenable to H. pylori infection.

<span class="mw-page-title-main">NFE2L2</span> Human protein and coding gene

Nuclear factor erythroid 2-related factor 2 (NRF2), also known as nuclear factor erythroid-derived 2-like 2, is a transcription factor that in humans is encoded by the NFE2L2 gene. NRF2 is a basic leucine zipper (bZIP) protein that may regulate the expression of antioxidant proteins that protect against oxidative damage triggered by injury and inflammation, according to preliminary research. In vitro, NRF2 binds to antioxidant response elements (AREs) in the promoter regions of genes encoding cytoprotective proteins. NRF2 induces the expression of heme oxygenase 1 in vitro leading to an increase in phase II enzymes. NRF2 also inhibits the NLRP3 inflammasome.

Prostaglandin EP<sub>3</sub> receptor Protein-coding gene in the species Homo sapiens

Prostaglandin EP3 receptor (53kDa), also known as EP3, is a prostaglandin receptor for prostaglandin E2 (PGE2) encoded by the human gene PTGER3; it is one of four identified EP receptors, the others being EP1, EP2, and EP4, all of which bind with and mediate cellular responses to PGE2 and also, but generally with lesser affinity and responsiveness, certain other prostanoids (see Prostaglandin receptors). EP has been implicated in various physiological and pathological responses.

<span class="mw-page-title-main">NFE2L1</span> Protein-coding gene in the species Homo sapiens

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<span class="mw-page-title-main">HOXC6</span> Protein-coding gene in the species Homo sapiens

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<span class="mw-page-title-main">Aceglutamide</span> Chemical compound

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Zinc L-carnosine, often simply called zinc carnosine, and also known as polaprezinc, is a mucosal protective chelate compound of zinc and L-carnosine invented by Hamari Chemicals, Ltd. It is a quadridentate 1:1 complex of a polymeric nature. Although it contains 23% zinc and 77% L-carnosine by mass, zinc carnosine is a molecule and not a mixture of zinc and L-carnosine.

References

  1. Arakawa T, Kobayashi K, Yoshikawa T, Tarnawski A (September 1998). "Rebamipide: overview of its mechanisms of action and efficacy in mucosal protection and ulcer healing". Digestive Diseases and Sciences. 43 (9 Suppl): 5S–13S. PMID   9753220.
  2. Arakawa T, Watanabe T, Fukuda T, Yamasaki K, Kobayashi K (November 1995). "Rebamipide, novel prostaglandin-inducer accelerates healing and reduces relapse of acetic acid-induced rat gastric ulcer. Comparison with cimetidine". Digestive Diseases and Sciences. 40 (11): 2469–72. doi:10.1007/bf02063257. PMID   7587834. S2CID   22807270.
  3. Takumida M, Anniko M (January 2009). "Radical scavengers for elderly patients with age-related hearing loss". Acta Oto-Laryngologica. 129 (1): 36–44. doi:10.1080/00016480802008215. PMID   18607930. S2CID   16906464.
  4. Tarnawski AS, Chai J, Pai R, Chiou SK (February 2004). "Rebamipide activates genes encoding angiogenic growth factors and Cox2 and stimulates angiogenesis: a key to its ulcer healing action?". Digestive Diseases and Sciences. 49 (2): 202–9. doi:10.1023/b:ddas.0000017439.60943.5c. PMID   15104358. S2CID   31756608.
  5. Zhang S, Qing Q, Bai Y, Mao H, Zhu W, Chen Q, Zhang Y, Chen Y (July 2013). "Rebamipide helps defend against nonsteroidal anti-inflammatory drugs induced gastroenteropathy: a systematic review and meta-analysis". Digestive Diseases and Sciences. 58 (7): 1991–2000. doi:10.1007/s10620-013-2606-0. PMID   23456504. S2CID   4887031.
  6. Gagliano-Jucá T, Moreno RA, Zaminelli T, Napolitano M, Magalhães AF, Carvalhaes A, Trevisan MS, Wallace JL, De Nucci G (June 2016). "Rebamipide does not protect against naproxen-induced gastric damage: a randomized double-blind controlled trial". BMC Gastroenterology. 16 (1): 58. doi:10.1186/s12876-016-0472-x. PMC   4893238 . PMID   27259970.
  7. "Rebamipide". Drugs.com.
  8. "Registration Sertificate: Rebagit (rebamipide) Film-Coated Tablets" (in Russian). Russian State Register of Medicines. Retrieved 10 June 2017.