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Pantokart Box


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The lining of the stomach contains deep collections of cells organized into gastric glands. These gastric glands secrete various substances in the stomach.

The opening of the gastric glands into the surface of the stomach is called gastric pits.
1) Mucous Cells – They secrete mucus in the stomach
2) Parietal Cells – They secrete HCL
3) G Cells – They secrete gastrin, which increases the HCL production.
4) ECL Cells – These cells secrete histamine and chief cells secrete pepsinogen (an inactive form of the pepsin-digesting enzyme pepsin.

 Intrinsic factors needed for the absorption of vitamin-b12 is also secreted by the gastric mucosa (most likely the parietal cells).

There are three pathways leading to acid production by the parietal cells
a) Acetylcholine – It is secreted at the sight, smell and taste of food.
b) Histamine is released as a result of swallowed food in the stomach.
c) Gastrin

When Acetylcholine, Gastrin or Histamine binds to its receptor on the parietal cell, a process is initiated that results in acid production.

ULCER: Ulcers are the perforations in the mucous membrane resulting from the hyperacidity, side effects of the drugs etc. Peptic ulcers are ulcers that form in the stomach or the upper part of the small intestine, called the duodenum.

Causes of ULCER:

  • Excess alcohol
  • Severe stress response
  • Severe burns
  • Extreme hyperacidity
  • In Gastrin-secreting tumors (Zollinger-Ellison syndrome)
  • Bacteria-H-pylori
  • Gastritis
  • NSAID’s

In 1982, two doctors – Barry Marshall and Robin Warren – discovered a certain kind of bacteria that can live and grow in the stomach. The medical name for these bacteria is Helicobacter pylori (or H. pylori, for short). Today doctors know that most peptic ulcers are caused by an infection from H. pylori.

Experts believe that 90% of the people around the world who have ulcers are infected with H. pylori. Peptic ulcers may have something to do with the combination of H. pylori infection and the level of acid in the stomach.

When H. pylori bacteria do cause ulcers, here’s how doctors think these ulcers develop:

  1. Bacteria weaken the protective coating of the stomach and upper small intestine.
  2. Acid in the stomach then gets through to the sensitive tissues lining the digestive system underneath.
  3. Acid and bacteria directly irritate this lining resulting in sores, or ulcers.

PEPTIC ULCER: A peptic ulcer is an open sore or raw area in the lining of the stomach (gastric) or the upper part of the small intestine (duodenal).

Duodenal ulcers :

  • Increased acid levels
  • Increased duration of normal acid secretion
  • Genetic
  • Smoking
  • damage to surface epithelium

Symptoms : Stomach pain is the most common symptom of an ulcer. It usually feels like sharp aches between the breastbone and the belly button. This pain often comes a few hours after eating. It can also happen during the night or early in the morning, when the stomach is empty. Eating something or taking an antacid medication sometimes makes the pain go away for a while..

Other symptoms of ulcers can include:

  • loss of appetite
  • sudden, sharp stomach pains
  • nausea
  • frequent belching
  • weight loss
  • vomiting (if blood is in the vomit or the vomit looks like coffee grounds, which only happens with severe ulcers, call a doctor right away)
  • bloody or blackish bowel movements (this could indicate a serious problem, so call a doctor right away if you notice this)

Anyone who thinks he or she may have an ulcer needs to see a doctor. Over time, untreated ulcers grow larger and deeper and can lead to other problems.

Diagnosis of ulcer:


  • One test to check for an ulcer is called an (upper gastrointestinal (GI) series). This is a type of X-ray of the stomach, duodenum, and esophagus, the muscular tube that links the mouth to the stomach. A person drinks a whitish liquid called barium while getting an X-ray, and if he or she has an ulcer, it should be outlined on the X-ray.
  • Another common procedure to look for an ulcer is called an endoscopy (pronounced: en- dass-kuh-pee). During this test, the doctor uses an endoscope, a skinny, lighted tube with a special camera on the end.
  • A doctor can also do a blood test for H. pylori bacteria. This may be important if an ulcer is found in the upper GI series or is suspected before the endoscopy.
  • Sometimes a bowel movement or a person’s breath can also be specially tested to check for the H. pylori bacteria.
  • Ulcers caused by H. pylori bacteria are generally treated with a combination of medications; usually two to three medicines are taken every day for a few weeks. Antibiotics are prescribed to kill the H. pylori bacteria. The other medicines – acid blockers or proton pump inhibitors – lessen the amount of acid in the stomach and help protect the lining of the stomach so the ulcer can heal.

Helicobacter Pylori

Helicobacter pylori (H. pylori) is a type of bacteria. Researchers believe that H. pylorus is responsible for the majority of peptic ulcers.

  1. pylori infection is common in the United States: About 20 percent of people under 40 years old and half of those over 60 years have it. Most infected people, however, do not develop ulcers. Why H. pylori does not cause ulcers in every infected person is not known. Most likely, infection depends on characteristics of the infected person, the type of H. pylori, and other factors yet to be discovered.

Researchers have found H. pylori in the saliva of some infected people, so the bacteria may also spread through mouth-to-mouth contact such as kissing.

How does H. pylori cause a peptic ulcer?
H. pylori weakens the protective mucous coating of the stomach and duodenum, which allows acid to get through to the sensitive lining beneath. Both the acid and the bacteria irritate the lining and cause a sore, or ulcer.
H. pylori is able to survive in stomach acid because it secretes enzymes that neutralize the acid

How are H. pylori peptic ulcers treated?
H. pylori peptic ulcers are treated with drugs that kill the bacteria, reduce stomach acid, and protect the stomach lining. Antibiotics are used to kill the bacteria.

Two types of acid-suppressing drugs might be used:

H 2 blockers work by blocking histamine, which stimulates acid secretion. They help reduce ulcer pain after a few weeks. Proton pump inhibitors suppress acid production by halting the mechanism that pumps the acid into the stomach. H 2 blockers and proton pump inhibitors have been prescribed alone for years as treatments for ulcers. But used alone, these drugs do not eradicate H. pylori and therefore do not cure H. pylori-related ulcers.

The use of only one medication to treat H. pylori is not recommended. At this time, the most proven effective treatment is a 2-week course of treatment called triple therapy.

Another option is 2 weeks of dual therapy. Dual therapy involves two drugs: an antibiotic and an acid suppressor. It is not as effective as triple therapy.

Two weeks of quadruple therapy, which uses two antibiotics, an acid suppressor, and a stomach-lining shield, looks promising in research studies. It is also called bismuth triple therapy


Antacids: They provide temporary relief, as they are not able to inhibit the factors that stimulate acid secretion e.g. Wisfast
Anticholinergics: These drugs are capable of inhibiting only Acetylcholine e.g. Pirenzipine

H2 receptor antagonists: These drugs are capable of inhibiting only Histamine e.g. Ranitidine

Proton Pump Inhibitors (PPIs): These agents provide complete control of acid secretion by inhibiting all the factors that stimulate acid secretion e.g. patoprazole
The final step in the acid secretion is an enzyme – the H+/ K+ ATPase (PROTON PUMP)) located on the surface of Parietal cells
These agents have the ability to block acid secretion by inhibiting this proton pump.


Pantokart tablet:
Composition: Pantoprazole- 40mg.Tab.

MODE OF ACTION of Pantoprazole:
Benz imidazole derivative blocks the proton pump by reacting with (H+/k+)-ATPase enzyme by causing it’s inhibition of action resulting long lasting inhibition of gastric acid secretion.


Proton Pump Inhibitors binds Proton Pump (H+K+ (-ATPase enzyme) that results in irreversible inhibition of acid secretion by the proton pump.

Their duration of action is much longer because of their unique mechanism of action

  • PPl only effective when proton pump is actively making acid.
  • Proton pump is lost after PPI interaction.
  • Proton pumps are reactivated after pumps are renewed.
  • Peak serum level post dose 1.5 hrs.
  • PPI must be closed before a meal for maximal efficacy.


  • Peptic Ulcers
  • Gastric Ulcers
  • Duodenal Ulcers
  • NSAID Induced gastritis
  • Helicobacter Pylori
  • Reflux Esophagitis

Zollinger Elison’s Syndrome


Proton Pump Inhibitor Bioavailability (%) Cmax (µmol/L) Duration of Effect (Hrs) Protein Binding (%) Drug Interaction
Pantoprazole 77 5.73 5 (40 mg) 24-72 98 None
Omeprazole 30-40 0.70 5 (20 mg) 24-72 95 Diazepam, Warfarin, Digoxin, Phenytoin, Ketoconazole
Lansoprazole 77-80 2.25 5 (30 mg) 24 97 Ketoconazol


Rabeprazole 52 0.48 6 (20 mg) 24 96 None
Esomeprazole 64 1.86 2 (20 mg) 24-72 97 None
2.38 2 (40 mg)


Different Proton Pump Inhibitors available in the market

  • Omeprazole
  • Lansoprazole
  • Pantoprozole
  • Rabeprazole
  • Esomeprazole


It has least drug interaction More drug interaction because has greater interaction with cytochrome system. It has drug interaction with Diazepam, Phenytoin , Warfarin.
Bioavailability is 77% Bioavailability is 30-40%
Pantoprazole is a category-B drug. Pantoprazole is a category-C drug
Can be used for maintenance therapy in duodenal ulcer. Can not be used for maintenance therapy in duodenal ulcer



It has least drug interaction It has drug interaction with Ketoconazole, Theophylline.
Duration of action is 24-72 hr. Duration of action 24 hr.
It does not have drug food interaction It has drug food interaction


Duration of action is 24-72 hr. Duration of action 24 hr.
Bioavailability is 77% Bioavailability is 54%
Protein binding of Pantoprazole

is 97%

Protein binding ofRabeprazole

is 95%

Mechanism of action is to bind both Cysteine 813 & 833 Cysteine It binds to Cystein 813 and not to Cysteine 822



  • 40 mg once daily for 6-8 week.
  • 20 mg once daily for maintenance therapy for healed esophagitis low grade reflux esophagitis.
  • Do not break, crush or chew tablets.


  • Less or no drug interaction.
  • For H Pylori eradication.
  • FDA approved ( Feb 2, 2000)
  • No interaction with antacids

Drug Interactions
Not significant

Advise patient to avoid alcohol, products containing NSAIDs and foods that may cause an increase in GI irritation.


  • Hepatic impairment
  • Pregnancy