The Active Ingredient of GASTROPIDE is Troxipide, a new Gastric Cytoprotective Agent, which neither inhibits acid secretion nor has acid neutralizing activity, but has been clinically proven to heal Gastritis and Gastric Ulcers .Troxipide has shown to inhibit Neutrophil mediated Inflammation and Oxidative stress in addition to improving the Gastric Mucus composition and output.
Each Tablet Contains Troxipide 100mg.
Pack size: 10*10 Blisters.
Troxipide is known to treat Gastritis and Gastric Ulcer, through a multimodal action. It is proposed to act by the inhibition of Neutrophil functions in the Gastric Mucosa, thereby inhibiting Interleukin 8 (IL-8)-stimulated migration of Neutrophils in the Gastric Mucosa, suppressing the Formyl-Methionyl-Leucyl-Phenylalanine (fMLP) or Platelet Activating Factor (PAF)-stimulated Superoxide generation and decreasing the inflammation in Mucosal Tissues. Troxipide prevents Mucosal Fragility and disruption of Gastric Mucosal barrier by regeneration of collagen fibers and also increasing the Gastric Mucosal Muco Polysaccharidosis content. Troxipide increases Gastric Mucosal blood flow, Prostaglandin Synthesis and Glycoprotein Excretion in the Gastric Mucosa. Therapeutically active concentrations in the Small Intestine, Liver and Stomach. It has a half-life of 7.615+/- 0.3782 hrs.’, and is mainly Excreted in the urine (96%) as Metabolites.
Pharmacodynamics Properties
Mechanism of Action
The gastric pH and content independent properties of Troxipide include the following:
Troxipide is known to treat Gastritis and Gastric Ulcer, through a multimodal action. It is proposed to act by the inhibition of Neutrophil functions in the Gastric Mucosa, thereby inhibiting Interleukin 8 (IL-8)-stimulated migration of Neutrophils in the Gastric Mucosa, suppressing the Formyl-Methionyl-Leucyl-Phenylalanine (fMLP) or Platelet Activating Factor (PAF)-stimulated Superoxide generation and decreasing the inflammation in Mucosal Tissues. Troxipide prevents Mucosal Fragility and disruption of Gastric Mucosal barrier by regeneration of collagen fibers and also increasing the Gastric Mucosal Muco Polysaccharidosis content. Troxipide increases Gastric Mucosal blood flow, Prostaglandin Synthesis and Glycoprotein Excretion in the Gastric Mucosa. Therapeutically active concentrations in the Small Intestine, Liver and Stomach. It has a half-life of 7.615+/- 0.3782 hrs.’, and is mainly Excreted in the urine (96%) as Metabolites.
Almost all of the gastric mucosal defense mechanisms are stimulated and/or facilitated by Prostaglandins (PGs), especially PGE2. 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. 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.
Gastric inflammation is a highly complex biochemical protective response to cellular injury. In the multitude of mechanisms involved in the development of Gastric Mucosal inflammation, derangement of the microcirculatory system is a common initial pathway. Troxipide inhibits various pro inflammatory 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. 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).
Troxipide directly acts on the enzymes such as Xanthine Oxidase and Myeloperoxidase that generate free Oxygen radicals in Gastric Mucosa. Experimental studies have demonstrated that Troxipide restrains NSAID-induced generation of Porphyrins, Tissue peroxidation and Gastric lesion formation.
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, 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, thereby elevating the tissue Respiration and Energy Metabolism.
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. The increment in Mucosal Blood Flow with Troxipide is more pronounced in the Gastric Antrum than in the Gastric Corpus.
Troxipide inhibits H. pylori-derived urease, a Multimeric nickel-containing enzyme that catalyzes 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.
Pharmacodynamics Properties
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, Muco -polysaccharides and Collagen. Glucosamine is an Amino-Sugar that is known to stimulate Glycoprotein synthesis and Protective mechanisms of the Gastric Mucosa, thereby aiding in Ulcer healing. Muco -polysaccharides 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.
Stimulation of Cytoprotective Prostaglandins
Suppression of gastric inflammation
In addition to inhibition of pro-inflammatory mediators
Enhancement of mucosal metabolism
Stimulation of mucosal microcirculation
Anti-Helicobacter pylori Action
Troxipide is well absorbed throughout the Gastrointestinal Tract after administration. Troxipide is detected in plasma from 0.05 hr. after oral administration of 100 mg of film coated tablets, suggesting a rapid absorption.
Bioavailability of Troxipide is 99.40%.
A peak serum concentration of 1052.471 ± 51.9318 ng/ml is obtained within 3.042 ± 0.1896 hrs.’ of drug administration and the resultant area under the curve is 8737.481 ± 315.4253 ng/ml*hr.
It is found that, at any time, a mean concentration of 5.3 – 8.9 µg 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.
Troxipide has a half-life of 7.615 ± 0.3782 hrs.
And is mainly excreted in the Urine (96%) as Metabolites (61% after 24hrs and 87% after 48 hrs.).
Amelioration of gastric mucosal lesions (Erosion, Hemorrhage, Redness and Edema) in the following diseases:
The most commonly reported adverse reactions include:
If any of following symptoms occur, stop taking this medicine and see your doctor immediately.
Hepatic Dysfunctions
Jaundice, Hepatic Dysfunction or Jaundice with increased AST (GOT), ALT (GPT), Al-P, and γ -GTP and/or LDH may occur. Patients should be carefully monitored. If any symptoms are observed, administration should be discontinued and appropriate therapeutic measures must follow.
Use in the Elderly
In general, elderly patients often have physiological hypo function, therefore these products should be administered carefully.
Use during Pregnancy, Delivery or Lactation
The safety of this product in pregnant women has not been established. Therefore, these drugs should be used in pregnant women or in women who may possibly be pregnant only if the expected therapeutic benefits outweigh the possible risks associated with treatment. Breast-feeding must be discontinued during treatment. Troxipide is shown to be excreted in breast milk in animal studies with rats.
Pediatric Use
The safety of these products in children has not been established. (Insufficient clinical data)
Other Precautions