Troxipide

Last updated
Troxipide
Troxipide.png
Clinical data
Trade names Troxip (India), Anytoral (Japan), Aplace (Japan), Aplace (South Korea), Defensa (South Korea), Ke Fen Qi (China), Shugi (China), Troxsin (Japan)
AHFS/Drugs.com International Drug Names
Routes of
administration 		Oral
ATC code
Legal status
Legal status
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability 99.6%
Elimination half-life 7.5 hours
Excretion Excreted in urine
Identifiers
  • 3,4,5-Trimethoxy-N-(piperidin-3-yl)benzamide
CAS Number
PubChem CID
ChemSpider
UNII
KEGG
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard 100.232.894 OOjs UI icon edit-ltr-progressive.svg
Chemical and physical data
Formula C15H22N2O4
Molar mass 294.351 g·mol−1
3D model (JSmol)
  • COc1cc(cc(c1OC)OC)C(=O)NC2CCCNC2
  • InChI=1S/C15H22N2O4/c1-19-12-7-10(8-13(20-2)14(12)21-3)15(18)17-11-5-4-6-16-9-11/h7-8,11,16H,4-6,9H2,1-3H3,(H,17,18) X mark.svgN
  • Key:YSIITVVESCNIPR-UHFFFAOYSA-N X mark.svgN
 X mark.svgNYes check.svgY  (what is this?)    (verify)

Troxipide is a drug used in the treatment of gastroesophageal reflux disease. Troxipide is a systemic non-antisecretory gastric cytoprotective agent with anti-ulcer, anti-inflammatory and mucus secreting properties irrespective of pH of stomach or duodenum. Troxipide is currently marketed in Japan (Aplace), [1] China (Shuqi), [2] South Korea (Defensa), [3] and India (Troxip). [4] It is used for the management of gastric ulcers, and amelioration of gastric mucosal lesions in acute gastritis and acute exacerbation of chronic gastritis.

Contents

Mechanism of action

The gastric pH and content independent properties of troxipide include the following:

Gastric mucosal protection

Gastric mucosa typically is composed of salts and other dialyzable components, free proteins, carbohydrate rich glycoprotein and water. Troxipide fortifies this gastric mucosal barrier by increasing the content of glucosamine, mucopolysaccharides and collagen. [5] [6] Glucosamine is an amino-sugar that is known to stimulate glycoprotein synthesis and protective mechanisms of the gastric mucosa, thereby aiding in ulcer healing. [7] Mucopolysaccharides impart structural integrity to the gastric mucosa and collagen imparts properties like ionic capability to attract blood components essential to tissue regeneration, mechanical protection, high tensile strength and slow digestibility to the gastric mucosa. [8] [9]

Stimulation of cytoprotective prostaglandins

Almost all of the gastric mucosal defense mechanisms are stimulated and/or facilitated by prostaglandins (PGs), especially PGE2. [10] These cytoprotective PGs stimulate mucus, bicarbonate, and phospholipid secretion; increase mucosal blood flow; and accelerate epithelial restitution and mucosal healing. They also inhibit mast cell activation, and leukocyte and platelet adherence to the vascular endothelium. Thus, continuous generation of PGE2 by gastric mucosa is crucial for the maintenance of mucosal integrity and protection against ulcerogenic and necrotizing agents. [10] Troxipide is known to stimulate the release of PGE2 and PGD2 in experimental as well as clinical studies. Troxipide has been observed to enhance PG-stimulated increase in gastric mucosal output, accelerated epithelial restitution and mucosal healing. [11]

Suppression of gastric inflammation

Gastric inflammation is a highly complex biochemical protective response to cellular injury. [12] In the multitude of mechanisms involved in the development of gastric mucosal inflammation, derangement of the microcirculatory system is a common initial pathway. [13]

Troxipide inhibits various proinflammatory mediators present at different stages of the microcirculatory system, thereby restoring the normal gastric mucosa. Troxipide caused the inhibition of recombinant interleukin-8 (IL-8) induced migration of the inflammatory cells. [14] Two other pro-inflammatory mediators causing oxidative stress that are inhibited by Troxipide include the formyl-methionyl-leucyl-phenylalanine (fMLP) and the Platelet Activating Factor (PAF). [14]

In addition to inhibition of pro-inflammatory mediators, troxipide directly acts on the enzymes such as xanthine oxidase and myeloperoxidase that generate free oxygen radicals in gastric mucosa. [15] Experimental studies have demonstrated that troxipide restrains NSAID-induced generation of porphyrins, tissue peroxidation and gastric lesion formation. [16]

Enhancement of mucosal metabolism

Gastric parietal cells are rich in mitochondria which provide energy in the form of ATP for cells by oxidative phosphorylation, critical to maintain the proper morphology and function of gastric mucosa. The mitochondrion is the major target of intracellular oxidative stress associated with aggressive factors like H. pylori , alcohol and NSAIDs, [17] which disturb the energy metabolism of mitochondria. Troxipide accelerates oxygen intake of marginal gastric mucosa and glycogen consumptive stimulation of the gastric mucosa of the corpus, [18] thereby elevating the tissue respiration and energy metabolism.

Stimulation of mucosal microcirculation

Troxipide enhances mucosal blood flow, which is the secondary defense barrier of gastric mucosa that supplies nutrients and oxygen to the epithelium, and removes, dilutes and neutralizes toxic substances that have diffused into the mucosa from the lumen. [19] [20] The increment in mucosal blood flow with troxipide is more pronounced in the gastric antrum than in the gastric corpus. [20]

Anti-Helicobacter pylori action

Troxipide inhibits H. pylori -derived urease, a multimeric nickel-containing enzyme that catalyses the hydrolysis of urea to yield ammonia and carbonic acid, which damage host tissues and trigger inflammatory response, including recruitment of leukocytes and triggering of the oxidative burst in neutrophils. [14] [21]

Pharmacokinetics

Troxipide is well absorbed throughout the gastrointestinal tract with a relative bioavailability of 99.6%. [22] At any time, a mean concentration of 5.3- 8.9 μg of troxipide is present per gram of tissue, which is capable of inhibiting the chemotactic migration and superoxide generation in the gastric mucosa. Thus, even 3 hrs after attaining peak serum levels, troxipide is found in therapeutically active concentrations in the small intestine, liver and stomach. [14] The elimination half-life of troxipide is 7.5 hours, and is mainly excreted in urine (96% as metabolites). [6]

Clinical experience

Troxipide has been well established in the treatment of gastric ulcers showing an overall amelioration rate of 79.4%. [6] An overall endoscopic healing rate of 66.7% after 8 weeks and 80% after 12 weeks of drug administration was achieved with troxipide (100 mg t.i.d. (three times a day)). In patients with duodenal ulcers, troxipide showed endoscopic healing rate of 53.3% and 73% at 8 weeks and 12 weeks respectively. At the end of the treatment, an overall improvement of 86.6% and 93.3% was achieved in patients with gastric ulcer and duodenal ulcer respectively. [23] In patients with acute gastritis and acute gastric mucosal lesions, an overall amelioration rate of 82.9% has been observed with troxipide. [6] In a comparative study evaluating the efficacy of troxipide (100 mg t.i.d.) with Ranitidine (150 mg b.i.d. (two times a day)), administered over 28 days in patients with gastritis, troxipide was statistically superior to Ranitidine, both with respect to resolution of gastritis clinical signs (abdominal pain, bloating, belching and heartburn) as well as the endoscopic evidences (erosion, oozing, redness and edema). [24] A study comparing the efficacy of troxipide (100 mg t.i.d for 28 days) with Rabeprazole (20 mg o.d. for 28 days) in patients suffering from gastritis showed that improvement in abdominal pain and nausea was significantly superior with troxipide at the end of 14 days. Troxipide administration caused a marked reduction in clinical (abdominal pain, bloating, belching, nausea, vomiting, loss of appetite and heartburn) and endoscopic signs of gastritis by the end of the treatment, though it did not significantly differ from that of Rabeprazole. [25] In patients with APDs like dyspepsia, gastritis, GERD and/or gastric ulcer, uncontrolled with acid inhibitors viz. proton pump inhibitors (PPIs), histamine receptor antagonists (H2RAs) etc., troxipide (100 mg t.i.d. for 28 days) showed significant improvement in all major symptoms such as nausea, vomiting, belching, heartburn, epigastric pain, acid regurgitation, abdominal bloating & loss of appetite. [26]

Safety and tolerability

A post-marketing study, conducted by the innovator, in over 12,000 patients showed that only 0.75% of them developed adverse events attributable to the drug. [6] The adverse reactions were mild to moderate, which resolved when the drug was discontinued. Commonly observed adverse events included constipation (0.19%) and increase in levels of liver enzymes, AST (0.17%) and ALT (0.25%). In a post-marketing study conducted in 1500 Indian patients, only 9 adverse events were reported in 9 patients (0.63%) that were of mild to moderate intensity. [26] Adverse events observed included constipation, acidity, nausea, fatigue and headache, and were of mild to moderate intensity. [26] In all clinical studies, troxipide was well tolerated. In a comparative study with ranitidine, troxipide was assessed as a more tolerable medication than ranitidine. A favorable tolerability profile for troxipide was reported by 95.45% of the investigators as compared to 65.45% for ranitidine while favorable tolerability profile was reported by 93.67% of the patients for troxipide and 64.55% for ranitidine. [24]

Related Research Articles

Peptic ulcer disease 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 with peptic ulcers have no symptoms. Complications may include bleeding, perforation, and blockage of the stomach. Bleeding occurs in as many as 15% of cases.

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

Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, flagellated, helical bacterium. Mutants can have a rod or curved rod shape, and these are less effective. Its helical body is thought to have evolved in order to penetrate the mucous lining of the stomach, helped by its flagella, and thereby establish infection. The bacterium was first identified as the causal agent of gastric ulcers in 1983 by the Australian doctors Barry Marshall and Robin Warren.

<span class="mw-page-title-main">Barry Marshall</span> Australian physician (born 1951)

Barry James Marshall is an Australian physician, Nobel Laureate in Physiology or Medicine, Professor of Clinical Microbiology and Co-Director of the Marshall Centre at the University of Western Australia. Marshall and Robin Warren showed that the bacterium Helicobacter pylori plays a major role in causing many peptic ulcers, challenging decades of medical doctrine holding that ulcers were caused primarily by stress, spicy foods, and too much acid. This discovery has allowed for a breakthrough in understanding a causative link between Helicobacter pylori infection and stomach cancer.

Coffee ground vomitus refers to a particular appearance of vomit. Within organic heme molecules of red blood cells is the element iron, which oxidizes following exposure to gastric acid. This reaction causes the vomitus to look like ground coffee.

<span class="mw-page-title-main">Famotidine</span> Medication that reduces stomach acid

Famotidine, sold under the brand name Pepcid among others, is a histamine H2 receptor antagonist medication that decreases stomach acid production. It is used to treat peptic ulcer disease, gastroesophageal reflux disease, and Zollinger-Ellison syndrome. It is taken by mouth or by injection into a vein. It begins working within an hour.

<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.

A Cushing ulcer, named after Harvey Cushing, is a gastric ulcer associated with elevated intracranial pressure. It is also called von Rokitansky–Cushing syndrome. Apart from the stomach, ulcers may also develop in the proximal duodenum and distal esophagus.

<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.

<span class="mw-page-title-main">Sucralfate</span> Chemical compound and gastrointestinal medication

Sucralfate, sold under various brand names, is a medication used to treat stomach ulcers, gastroesophageal reflux disease (GERD), radiation proctitis, and stomach inflammation and to prevent stress ulcers. Its usefulness in people infected by H. pylori is limited. It is used by mouth and rectally.

<span class="mw-page-title-main">Rebamipide</span> Amino acid derivative

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

<span class="mw-page-title-main">Ménétrier's disease</span> Medical condition

Ménétrier disease is a rare, acquired, premalignant disease of the stomach characterized by massive gastric folds, excessive mucous production with resultant protein loss, and little or no acid production. The disorder is associated with excessive secretion of transforming growth factor alpha (TGF-α). It is named after a French physician Pierre Eugène Ménétrier, 1859–1935.

<span class="mw-page-title-main">Vagotomy</span> Surgical procedure

A vagotomy is a surgical procedure that involves removing part of the vagus nerve. It is performed in the abdomen.

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.

A stress ulcer is a single or multiple mucosal defect usually caused by physiological stress which can become complicated by upper gastrointestinal bleeding. These ulcers can be caused by shock, sepsis, trauma or other conditions and are found in patients with chronic illnesses. These ulcers are a significant issue in patients in critical and intensive care.

Helicobacter pylori eradication protocols is a standard name for all treatment protocols for peptic ulcers and gastritis in the presence of Helicobacter pylori infection. The primary goal of the treatment is not only temporary relief of symptoms but also total elimination of H. pylori infection. Patients with active duodenal or gastric ulcers and those with a prior ulcer history should be tested for H. pylori. Appropriate therapy should be given for eradication. Patients with MALT lymphoma should also be tested and treated for H. pylori since eradication of this infection can induce remission in many patients when the tumor is limited to the stomach. Several consensus conferences, including the Maastricht Consensus Report, recommend testing and treating several other groups of patients but there is limited evidence of benefit. This includes patients diagnosed with gastric adenocarcinoma, patients found to have atrophic gastritis or intestinal metaplasia, as well as first-degree relatives of patients with gastric adenocarcinoma since the relatives themselves are at increased risk of gastric cancer partly due to the intrafamilial transmission of H. pylori. To date, it remains controversial whether to test and treat all patients with functional dyspepsia, gastroesophageal reflux disease, or other non-GI disorders as well as asymptomatic individuals.

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<span class="mw-page-title-main">Gastric folds</span>

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<span class="mw-page-title-main">Acid peptic diseases</span> Overview of the acid peptic diseases of the stomach and gastrointestinal tract

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Ranitidine bismuth citrate - drug, which has antisecretory and bactericidal action.

References

  1. ↑ Aplace tablets, Kyorin Pharmaceutical Co., Ltd., Japan
  2. ↑ Shuqi tablets, Zhongzhu Holding Co., Ltd., China
  3. ↑ Defensa tablets, Il Hwa, Korea
  4. ↑ Troxip tablets, Zuventus Healthcare Ltd., India
  5. ↑ Abe Y, Sekiguchi H, Tsuru K, Irikura T (1984). "Effects of 3,4,5-trimethoxy-N-(3-piperidyl) benzamide (KU-54) on the incorporation (excretion) of 14C-glucosamine in the gastric mucosa and the liver of rats (Article in Japanese)". Nihon Yakurigaku Zasshi. 84 (1): 11–8. doi: 10.1254/fpj.84.11 . PMID   6489865.
  6. 1 2 3 4 5 Prescribing information of APLACE (Troxipide). 2008. Kyorin Pharmaceutical Co., Ltd., Japan
  7. ↑ Santhosh S, Anandan R, Sini TK, Mathew PT (2007). "Protective effect of glucosamine against ibuprofen-induced peptic ulcer in rats". J Gastroenterol Hepatol. 22 (6): 949–53. doi:10.1111/j.1440-1746.2007.04840.x. PMID   17504261. S2CID   33620936.
  8. ↑ Clamp JR, Cooper B, Creeth JM, Ene D, Barrett J, Gough M (1983). "The presence of polysaccharide in normal human gastric mucus". Biochem J. 215 (2): 421–3. doi:10.1042/bj2150421. PMC   1152412 . PMID   6651769.
  9. ↑ Castro GA, Sgarbieri VC, Carvalho JE, Tinti SV, Possenti A (2007). "Protective effect of collagen derivates on the ulcerative lesions caused by oral administration of ethanol". J Med Food. 10 (1): 154–8. doi:10.1089/jmf.2006.262. PMID   17472480.
  10. 1 2 Laine L, Takeuchi K, Tarnawski A (2008). "Gastric mucosal defense and cytoprotection: bench to bedside". Gastroenterology. 135 (1): 41–60. doi:10.1053/j.gastro.2008.05.030. PMID   18549814.
  11. ↑ Mine T, Kataoka A, Fujisaki J. "Effects of cimetidine and troxipide on gastric mucosal prostaglandin synthesis in patients with chronic gastric ulcer". Curr Ther Res. 50 (6): 878–87.
  12. ↑ Yoshikawa T, Naito Y (2000). "The role of neutrophils and inflammation in gastric mucosal injury". Free Radic Res. 33 (6): 785–94. doi:10.1080/10715760000301301. PMID   11237100. S2CID   8106545.
  13. ↑ Suzuki H, Masaoka T, Suzuki M, Ishii H (2005). "Microvascular Pathophysiology in Gastric Mucosal Inflammation Associated with Helicobacter pylori Infection". Keio Univ Symp Life Sci Med. Keio University International Symposia for Life Sciences and Medicine. 13: 63–72. doi:10.1007/4-431-27174-0_8. ISBN   4-431-22135-2.
  14. 1 2 3 4 Kusugami K, Ina K, Hosokawa T, Kobayashi F, Kusajima H, Momo K, Nishio Y (May 2000). "Troxipide, a novel antiulcer compound, has inhibitory effects on human neutrophil migration and activation induced by various stimulants". Dig Liver Dis. 32 (4): 305–11. doi:10.1016/S1590-8658(00)80023-7. PMID   11515628.
  15. ↑ Momo K, Hoshina K, Ishibashi Y, Saito T (1994). "Preventive effects of troxipide on a newly developed model of acute gastric mucosal lesion (AGML) induced by ischemia/reperfusion plus ammonia in the rat (Article in Japanese)". Nihon Yakurigaku Zasshi. 104 (4): 313–23. doi: 10.1254/fpj.104.313 . PMID   7959422.
  16. ↑ Matsui H, Murata Y, Kobayashi F, Shiba R, Momo K, Kondo Y, Nakahara A, Muto H (2001). "Diclofenac-induced gastric mucosal fluorescence in rats". Dig Dis Sci. 46 (2): 338–44. doi:10.1023/A:1005656916830. PMID   11281183. S2CID   20655506.
  17. ↑ Pan JS, He SZ, Xu HZ, Zhan XJ, Yang XN, Xiao HM, Shi HX, Ren JL (2008). "Oxidative stress disturbs energy metabolism of mitochondria in ethanol-induced gastric mucosa injury". World J Gastroenterol. 14 (38): 5857–67. doi: 10.3748/wjg.14.5857 . PMC   2751896 . PMID   18855985.
  18. ↑ Abe Y, Sekiguchi H, Tsuru K, Irikura T (1984). "Effects of 3,4,5-trimethoxy-N-(3-piperidyl) benzamide (KU-54) on respiration of the gastric mucosa and liver in rats (Article in Japanese)". Nihon Yakurigaku Zasshi. 83 (4): 317–24. doi: 10.1254/fpj.83.317 . PMID   6745811.
  19. ↑ Wallace JL, Granger DN (1996). "The cellular and molecular basis of gastric mucosal defense" . FASEB J. 10 (7): 731–40. doi: 10.1096/fasebj.10.7.8635690 . PMID   8635690. S2CID   34936755.
  20. 1 2 Abe Y, Irikura T (1980). "Influence of 3-(3, 4, 5-trimethoxybenzamido) piperidine (KU-54) on gastric mucosal blood flow (author's transl)". Nihon Yakurigaku Zasshi. 76 (5): 355–61. doi: 10.1254/fpj.76.355 . PMID   7203276.
  21. ↑ Mobley HL (1996). "The role of Helicobacter pylori urease in the pathogenesis of gastritis and peptic ulceration". Aliment Pharmacol Ther. 10 (Suppl 1): 57–64. doi:10.1046/j.1365-2036.1996.22164006.x. PMID   8730260. S2CID   35566040.
  22. ↑ Zhao Y, Qiu R, Wang W, Sun H, Dai M, Yang Q, Mao G (June 2003). "Relative bioavailability and bioequivalance of troxipide capsule in healthy volunteers after a single oral administration". The Chinese Journal of Clinical Pharmacology.
  23. ↑ Hyeoyun (1989). "Peptic ulcers for the clinical effectiveness of Troxipide". Latest Med. 32 (2): 125–31.
  24. 1 2 Dewan B, Balasubramanian A (2010). "Troxipide in the management of gastritis: a randomized comparative trial in general practice". Gastroenterol Res Pract. 2010: 758397. doi: 10.1155/2010/758397 . PMC   2992815 . PMID   21127703.
  25. ↑ A Parallel, Randomized, Comparative, Double-Blind, Double-Dummy Clinical Trial to Evaluate the Efficacy and Safety of Troxipide versus Rabeprazole in the Treatment of Gastritis. Data on file (appears on zuventus healthcare website www.zuventus.co.in).
  26. 1 2 3 An Open-Label, Multicentric Study to Assess the Symptomatic Efficacy and Safety of Troxipide [TroxipTM] In the Management of Acid Peptic Disorders in Indian Patients. Data on file (appears on zuventus healthcare website www.zuventus.co.in).
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