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BIO PANTO

Quick Overview

Our aim is to reach out to the globe within shortest possible time frame. 


To promote this objective, not only we distribute and market our Gastroenterology  range of products globally through our distribution channels but we also undertake ‘contract manufacturing’& ‘formulation development ’of our wide range of generic products such as  Bio panto which contains  Pantoprazole Sodium USP (as Sesquihydrate) Equivalent to Pantoprazole….40 mg


 


 

Bio Panto

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Details

Each enteric coated tablet contains:

Pantoprazole Sodium USP (as Sesquihydrate)

Equivalent to Pantoprazole….40 mg

Excipients…..q.s
Colour.

Sunset Yellow and

Titanium Dioxide BP

CHEMICAL NAME: 5-(Difluoromethoxy)-2-[[(3,4-dimethoxy-2-pyridyl)methyl] sulfinyl]benzimidazole, sodium salt, sesquihydrate.

CATEGORY: Proton pump inhibitor

DESCRIPTION: Light orange to orange colour round shape biconvex enteric coated tablet plain on both sides.

CLINICAL PHARMACOLOGY

MECHANISM OF ACTION:

Pantoprazole is a proton pump inhibitor (PPI) that suppresses the final step in gastric acid production by covalently binding to the (H +/K+)-ATPase enzyme system at the secretory surface of the gastric parietal cell. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. The binding to the (H+/K+)-ATPase results in a duration of ant secretory effect that persists longer than 24 hours for all doses tested (20 mg to 120 mg).

Pharmacokinetic Actions

Absorption

After administration of a single or multiple oral doses of pantoprazole sodium delayed-release tablets, the peak plasma concentration of pantoprazole was reported to be achieved in approximately 2.5 hours and Cmax was 2.5 mcg/ml. Pantoprazole undergoes little first-pass metabolism, resulting in an absolute bioavailability of approximately 77%. Pantoprazole absorption is not affected by concomitant administration of antacids. Administration of pantoprazole sodium delayed-release tablets with food may delay its absorption up to 2 hours or longer; however, the C and the extent of pantoprazole absorption (AUC) are not altered. Thus, pantoprazole sodium delayed-release tablets may be taken without regard to timing of meals.

Distribution

The apparent volume of distribution of pantoprazole is approximately 11.0 to 23.6 L, distributing mainly in extracellular fluid. The serum protein binding of pantoprazole is about 98%, primarily to albumin.

Metabolism

Pantoprazole is extensively metabolized in the liver through the cytochrome P450 (CYP) system. Pantoprazole metabolism is independent of the route of administration (intravenous or oral). The main metabolic pathway is de methylation, by CYP2C19, with subsequent sulfation; other metabolic pathways include oxidation by CYP3A4. There is no evidence that any of the pantoprazole metabolites have significant pharmacologic activity.

Elimination

After a single oral or intravenous dose of C-labeled pantoprazole to healthy, normal metabolizer volunteers, approximately 71% of the dose was excreted in the urine, with 18% excreted in the feces through biliary excretion. There was no renal excretion of unchanged pantoprazole.

Geriatric

Only slight to moderate increase in pantoprazole AUC (43%) and C (26%) were found in elderly volunteers (64 to 76 years of age) after repeated oral administration, compared with younger subjects. No dosage adjustment is recommended based on age.

Gender

There is a modest increase in pantoprazole AUC and Cmax in

Women compared to men. No dosage adjustment is recommended based on gender. In pediatric patients there were no relevant clinically reported effects of gender on clearance of pantoprazole.

Renal Impairment

In patients with severe renal impairment, pharmacokinetic parameters for pantoprazole were similar to those of healthy subjects. No dosage adjustment is necessary in patients with renal impairment or in patients undergoing hemodialysis.

Hepatic Impairment

In patients with mild to severe hepatic impairment (Child-Pugh A to C cirrhosis), maximum pantoprazole concentrations were reported to be increased slightly. No reported dosage adjustment is needed in patients with mild to severe hepatic impairment.

INDICATIONS:

1. Short-Term Treatment of Erosive Esophagitis Associated With Gastro esophageal Reflux Disease (GERD).

2. Maintenance of Healing of Erosive Esophagitis.

3. Pathological Hyper secretory Conditions Including Zollinger­Ellison Syndrome.

DOSAGE AND ADMINISTRATION

The tablet should be swallowed whole with water. It should not be chewed or crushed.

Adults: one 40 mg tablet daily for 2-4 weeks (duodenal ulcer) or 4- 8 weeks (gastric ulcer and reflux esophagitis). Longer term therapy may be prescribed in individual cases.

H. pylon eradication regimens: 40 mg tablet twice daily in combination with twice daily in combination with daily doses of clarithromycin 500 mg and amoxicillin 1 g, taken for 7 days.

Elderly: Dose adjustment is not necessary.

Children: Not recommended.

Impaired renal function: Do not exceed 40 mg daily.

Impaired hepatic function: Reduce dose of one tablet on alternate days.

A daily dose of 40 mg pantoprazole should not be exceeded in elderly patients or in those with impaired renal function.

CONTRA-INDICATIONS

Pantoprazole sodium delayed-release tablets are contraindicated in patients with known hypersensitivity to any component of the formulation or any substituted benzimidazole.

WARNINGS AND PRECAUTIONS

Concurrent Gastric Malignancy

Symptomatic response to therapy with pantoprazole does not preclude the presence of gastric malignancy.

Atrophic Gastritis

Atrophic gastritis has been noted occasionally in gastric corpus biopsies from patients treated with long-term pantoprazole, particularly in patients who were H. pylori positive.

Cyanocobalamin (Vitamin B-12) Deficiency

Generally, daily treatment with any acid-suppressing medications over a long period of time (e.g., longer than 3 years) may lead to malabsorption of Cyanocobalamin (Vitamin B-12) caused by hypo or achlorhydria. Rare reports of cyanocobalamin deficiency occurring with acid-suppressing therapy have been reported in the literature. This diagnosis should be considered if clinical symptoms consistent with cyanocobalamin deficiency are observed.

For adult patients who have not healed after 8 weeks of treatment, an additional 8 week course of pantoprazole sodium delayed- release tablets may be considered. Dosage regimens should be adjusted to individual patients need and should continue for as long as clinically indicated. Doses up to 240 mg daily have been administered.

Patients should be cautioned that pantoprazole sodium delayed- release tablets USP should not be split, chewed or crushed. Diagnosis should be considered if clinical symptoms consistent with cyanocobalamin deficiency are observed.

Bone Fracture

Several published observational studies suggest that proton pump inhibitor (PPI) therapy may be associated with an increased risk for osteoporosis-related fractures of the hip, wrist or spine. The risk of fracture was increased in patients who received high-dose, defined as multiple daily doses and long-term PPI therapy (a year or longer).

Patients should use the lowest dose and shortest duration of PPI therapy appropriate to the condition being treated. Patients at risk for osteoporosis-related fractures should be managed according to established treatment guidelines.

Tumorigenicity

Due to the chronic nature of GERD, there may be a potential for prolonged administration of pantoprazole. In long-term rodent studies, pantoprazole was carcinogenic and caused rare types of gastrointestinal tumors. The relevance of these findings to tumor development in humans is unknown.

Hypomagnesaemia

Hypomagnesaemia, symptomatic and asymptomatic, has been reported in patients treated with PPIs for at least three months, in most cases after a year of therapy. Serious adverse events include tetany, arrhythmias and seizures. In most patients, treatment of hypomagnesaemia required magnesium replacement and discontinuation of the PPI. For patients expected to be on prolonged treatment or who take PPIs with medications such as digoxin or drugs that may cause hypomagnesemia (e.g., diuretics), health care professionals may consider monitoring magnesium levels prior to initiation of PPI treatment and periodically.

DRUG INTERACTIONS

Interference with Antiretroviral Therapy

Concomitant use of atazanavir or nelfinavir with proton pump inhibitors is not recommended. Coadministration of atazanavir or nelfinavir with proton pump inhibitors is expected to substantially decrease atazanavir or nelfinavir plasma concentrations and may result in a loss of therapeutic effect and development of drug resistance.

Coumarin Anticoagulants: There have been reports of increased INR and prothrombin time in patients receiving proton pump inhibitors, including pantoprazole and warfarin concomitantly. Increase in INR and prothrombin time may lead to abnormal bleeding and even death. Patients treated with proton pump inhibitors and warfarin concomitantly should be monitored for increases in INR and prothronnbin time.

Drugs for which Gastric pH can affect bioavailability Pantoprazole causes long-lasting inhibition of gastric acid secretion. Therefore, pantoprazole may interfere with absorption of drugs where gastric pH is an important determinant of their bioavailability (e.g., ketoconazole, ampicillin esters and iron salts).

False Positive Urine Tests for Tetrahydrocannabinol (THC) There have been reports of false positive urine screening tests for Tetrahydrocannabinol (THC) in patients receiving proton pump inhibitors. An alternative confirmatory method should be considered to verify positive results.

USE IN SPECIFIC POPULATIONS Pregnancy

Teratogenic Effects

Pregnancy category B

Reported reproduction studies in rats at oral doses up to 88 times the recommended human dose and in rabbits at oral doses up to 16 times the recommended human dose and have revealed no evidence of impaired fertility or harm to the fetus due to pantoprazole. This drug should be used during pregnancy only if clearly needed.

Nursing Mothers

In a reported pre-clinical study, pantoprazole and its metabolites are excreted in the milk of rats. Pantoprazole excretion in human milk has also been reported in nursing mother. Many drugs which are excreted in human milk have a potential for serious adverse reactions in nursing infants. Based on the potential for tumorigenicity shown for pantoprazole in rodent carcinogenicity studies, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the benefit of the drug to the mother.

Pediatric Use

The effectiveness of pantoprazole for treating symptomatic GERD in pediatric patients has not been established.

Geriatric Use

In short-term reported US clinical trials, erosive esophagitis healing rates in the 107 elderly patients 65 years old) treated with pantoprazole were similar to those found in patients under the age of 65. The incidence rates of adverse reactions and laboratory abnormalities in patients aged 65 years and older were similar to those associated with patients younger than 65 years of age.

Gender:

Erosive esophagitis healing rates in the women treated with

Pantoprazole sodium delayed-release tablets in reported US clinical trials were similar to those found in men. In the women

Treated long-term with pantoprazole 40 mg or 20 mg, healing was maintained at a rate similar to that in men. The incidence rates of adverse reactions were also similarfor men and women.

Patients with Hepatic Impairment

Doses higher than 40 mg/day have not been studied in patients with hepatic impairment [see Clinical Pharmacology].

OVERDOSAGE

Experience in patients taking very high doses of pantoprazole (>240 mg) is limited. Spontaneous post marketing reports of overdose are generally within the known safety profile of pantoprazole.

Pantoprazole is not removed by hemodialysis. In case of over dosage,treatment should be symptomatic and supportive. The reported symptoms of acute toxicity were hypo activity, ataxia, hunched sitting, limb-splay, lateral position, segregation, absence of ear reflex and tremor.

ADVERSE EFFECTS:

  • General: Headache, nausea, abdominal pain, vomiting, flatulence, dizziness and arthralgia.
  • Body as a Whole: Allergic reaction, pyrexia, photosensitivity reaction and facial edema.
  • Gastrointestinal: Constipation, dry mouth and hepatitis.
  • Hematologic: Leucopenia and thrombocytopenia.
  • Metabolic/Nutritional: Elevated CK (creatine kinase), generalized edema, elevated triglycerides and liver enzymes elevated.
  • Musculoskeletal: Myalgia.
  • Nervous: Depression and vertigo.
  • Skin and Appendages: Urticaria, rash and pruritus.
  • Special Senses: Blurred vision.
  • Zollinger-Ellison Syndrome
    • Immune System Disorders: Anaphylaxis (including anaphylactic shock).
    • Skin and Subcutaneous Tissue Disorders: Severe dermatologic reactions (some fatal), including erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis (TEN, some fatal) and angioedema (Quincke's edema).
    • Musculoskeletal and Connective Tissue Disorders: Rhabdomyolysis and bone fracture.
    • Metabolism and Nutritional Disorders: Hypomagnesaemia.
    • Renal and Urinary Disorders: Interstitial nephritis.
    • Hepatobiliary Disorders: Hepatocellular damage leading to jaundice and hepatic failure.
    • Psychiatric Disorders: Hallucination and confusion.
    • Zollinger-Ellison syndrome: Adverse reactions were reported in patients taking pantoprazole 80 mg/day to 240 mg/day for upto 2 years were similar to those reported in adult patients with GERD.

Packing: Blister of 10 tablets.

Storage: Store in a cool and dry place below 30° C. Protect from moisture.

Shelf Life: 36 months

 

 
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