Ranitidine

314.4

314.40

266-332-5

884KT10YB7

C29412

A02BA02

2932999099

112

1.93

tan solid

1.184±0.06 g/cm3(Predicted)

69-70 °C

437.1ºC at 760 mmHg

1.558

H2O: 24.7 mg/mL

Desiccate at +4°C

LD50 oral in rat: > 5gm/kg

Characteristic

Bitter taste

8.2 and 2.7

2

22-24/25

KM6557000

Ranitidine hydrochloride injection is stable for up to 48 hr @ room temp when added to or diluted with most IV soln. The commercially available IV infusion soln of the drug in 0.45% sodium chloride is stable through the expiration date noted on the container when stored as recommended. When the pharmacy bulk package is used, infusion soln of ranitidine hydrochloride should be prepared within 24 hr after the vial is first entered; any drug remaining in the bulk package after this period should b

P261, P264, P270, P271, P272, P280, P285, P301+P312, P302+P352, P304+P340, P304+P341, P305+P351+P338, P312, P321, P330, P332+P313, P333+P313, P337+P313, P342+P311, P362, P363, P403+P233, P405, P501

H302

Oral doses of 1,000 mg/kg in mice and rats were not found to be lethal. Intravenous LD50 values in mice and rats were 77 and 83 mg/kg, respectively. Overdose information There has been limited experience with ranitidine overdose. Reported acute ingestions of up to 18 grams orally were followed by temporary adverse effects similar to the normal adverse effects of this drug, including tachycardia, bradycardia, dizziness, diarrhea, nausea, and vomiting, among other effects. Gait abnormalities and hypotension have also been observed. When an overdose with ranitidine is suspected, remove unabsorbed ranitidine from the gastrointestinal tract if possible, and monitor the patient and provide supportive therapy as required.

The plasma protein binding of ranitidine is approximately 15%.

This drug is used alone or with concomitant antacids for the following conditions: short-term treatment of active duodenal ulcer, treating gastric acid hypersecretion due to Zollinger-Ellison syndrome, systemic mastocytosis, and other conditions that may pathologically raise gastric acid levels. It also used in the short term treatment of active benign gastric ulcers and maintenance therapy of gastric ulcers at a reduced dose. In addition to the above, ranitidine can be used for the treatment of GERD symptoms, treatment of erosive esophagitis (endoscopically diagnosed) and the maintenance of gastric or duodenal ulcer healing.|FDA Label

Ranitidine decreases the secretion of gastric acid stimulated by food and drugs. It also reduces the secretion of gastric acid in hypersecretory conditions such as Zollinger-Ellison syndrome. Marked improvements in the appearance of the esophageal tissues have been observed by endoscopic imaging after ranitidine therapy.

Various agents with different action mechanisms used to treat or ameliorate PEPTIC ULCER or irritation of the gastrointestinal tract. This has included ANTIBIOTICS to treat HELICOBACTER INFECTIONS; HISTAMINE H2 ANTAGONISTS to reduce GASTRIC ACID secretion; and ANTACIDS for symptomatic relief. (See all compounds classified as Anti-Ulcer Agents.)|Drugs that selectively bind to but do not activate histamine H2 receptors, thereby blocking the actions of histamine. Their clinically most important action is the inhibition of acid secretion in the treatment of gastrointestinal ulcers. Smooth muscle may also be affected. Some drugs in this class have strong effects in the central nervous system, but these actions are not well understood. (See all compounds classified as Histamine H2 Antagonists.)

Ranitidine is rapidly absorbed with peak concentrations reached within 1-3 hours after administration, and varying greatly among patients. Bioavailability is about 50%-60% due to hepatic metabolism. In a pharmacokinetic study of healthy males, the AUC 0-infinity was about 2,488.6 ng x h/mL and the median Tmax was 2.83 hours. Food or antacids have limited effects on absorption. One clinical study found that the administration of a potent antacid (150 mmol) in subjects in the fasted state led to decreased absorption of ranitidine.|This drug is mainly excreted in the urine but also excreted in the feces. About 30% of a single oral dose has been measured in the urine as unchanged drug within 24 hours of ingestion.|The volume of distribution is higher than body volume, and measures at approximately 1.4 L/kg. It concentrates in breast milk, but does not readily distribute into the cerebrospinal fluid.|Renal clearance is about 410 mL/min according to FDA prescribing information. Another resource mentions a plasma clearance of approximately 600 ml/min. Clearance is decreased in the elderly and those with impaired or hepatic renal function. It is recommended to decrease the dose of ranitidine by one-half in patients with renal impairment.

The major metabolite in the urine is N-oxide, which represents less than 4% of the dose. Other metabolites of ranitidine include S-oxide (1%) and desmethyl ranitidine (1%). The feces contain the remainder of the excreted ranitidine dose. Liver dysfunction has been shown to cause small, but clinically insignificant, changes in various ranitidine pharmacokinetic parameters.

The elimination half-life or ranitidine is about 2.5-3 hours. It may be longer after oral administration versus injection. The plasma half-life is longer for elderly patients population due to a decrease in renal function, and is measured at 3-4 hours.

After a meal, the hormone gastrin, produced by cells in the lining of the stomach, stimulates the release of histamine, which then binds to histamine H2 receptors, leading to the secretion of gastric acid. Ranitidine reduces the secretion of gastric acid by reversible binding to histamine (H2) receptors, which are found on gastric parietal cells. This process leads to the inhibition of histamine binding to this receptor, causing the reduction of gastric acid secretion. The relief of gastric-acid related symptoms can occur as soon as 60 minutes after administration of a single dose, and the effects can last from 4-10 hours, providing fast and effective symptomatic relief.

AH 19065