Ranitidine Medication’s Pharmaceutical Analysis


Ranitidine belongs to the category of H2-receptor blocker drugs. Its mechanism of action entails blocking histamine-2 receptors to prevent histamine from binding, effectively acid release by gastric parietal cells. Oral ranitidine tablets (150 mg) are indicated in the treatment of GERD, gastric and duodenal ulcers (GUs and DUs), hypersecretory states, and pyrosis (heartburn), among others. Its pharmacokinetic (ADME) properties include bioavailability rate of 50% and peaks of 450-545 ng/ml after 3 hours, serum distribution level of 1.4 L/kg, excretion of 4% nitric oxide metabolite, and a 24-hour clearance rate of 410 ml/min. Its pharmacodynamic properties include suppressed bioavailability of drugs with pKa < 3.5, interaction with pirenzepine, and antisecretory effects on reflexive gastric acid.

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The side/adverse effects of ranitidine use include CNS disturbances such as dizziness and hallucinations, cardiovascular complications, and GI effects like diarrhea, vomiting, and nausea. Other reported side effects include cholestatic hepatitis, hematologic disorders such as leucopenia, thrombopenia, and granulocytopenia, respiratory effects, and musculoskeletal complications. Ranitidine has been shown through clinical trials to be an effective treatment for DUs and GUs, GERD, Zollinger-Ellison syndrome, and pyrosis when used at appropriate dosage levels and frequency. The risks associated with this drug include drug interaction effects, porphyric attacks, and side effects on pediatric patients and pregnant mothers.

Ranitidine is an H2-receptor antagonist used as an anti-ulcer therapy. It works by blocking histamine from the H2 receptors in the parietal cells of the stomach (Hamilton, Sercombe, & Pounder, 2011). Histamine is an H2 receptor agonist that mediates gastric acid hypersecretion, causing gastrointestinal lesions. Ranitidine’s mechanism of action involves dampening histamine-mediated gastric acid release through inverse agonism of H2-receptors. The active agent in the drug is ranitidine hydrochloride (C13H22N4O3S.HCl) that has a molecular mass of 350.9 (Hamilton et al., 2011). Physically, ranitidine appears as yellow crystals that are highly soluble in water. Ranitidine content in each tablet (USP) administered orally is 300mg.

The drug is indicated for the prophylactic treatment of gastroesophageal reflux disease (GERD), gastric and duodenal lesions, and Zollinger-Ellison syndrome (Hamilton et al., 2011). Ranitidine, unlike similar H2-receptor antagonists such as cimetidine, has a high efficacy at lower dosage levels (75mg). It is a competitive, reversible H2-receptor blocker. It neither reduces the calcium level in hypercalcemic conditions, nor is it an anticholinergic drug. This paper examines Ranitidine’s classification, pharmacokinetic and pharmacodynamic properties, adverse and side effects, and risks and benefits based on scholarly evidence in the literature.

Class of the Drug and its Purpose

Ranitidine is an H2-antagonist or blocker. Other drugs in this class are cimetidine, famotidine, and nizatidine (Rey et al., 2014). Histamine-2 antagonist category of drugs specifically inhibits histamine binding to H2-receptors, which reflexly suppresses acid secretion by gastric parietal cells. The drugs are used to treat gastric ulcers and GERD symptoms resulting from gastric acid hypersecretion. H2 blockers, unlike proton pump inhibitors (PPIs), speed up gastric acid emptying, which leads to more acid being released in the presence of food. Therefore, complete remission of the symptoms is achieved through regular dosing.

Ranitidine (Zantac) is indicated in the treatment of gastroesophageal and gastrointestinal lesions and gastric ulcers (GU) aggravated by elevated acid in the gut. It is used to treat active duodenal ulcers (DU) at a daily dosage of 300 mg administered at bedtime (Hamilton et al., 2011). At this dosage, DU can be cured within 4 weeks. Ranitidine is also administered as a maintenance therapy in DU cases (150 mg) in recovering patients. Ranitidine (150 mg) is indicated in the treatment of Zollinger-Ellison syndrome that results from gastric acid hypersecretion (Hamilton et al., 2011).

Ranitidine, administered at a dose of 150 mg PD, provides symptomatic relief from GERD and erosive esophagitis conditions such as pyrosis (heartburn) and dyspepsia in patients (Kahrilas, 2011). The relief is achieved within a day upon starting the treatment. The same dosage is recommended for maintenance treatment of these conditions for patients aged over 12 years. For pediatric patients, a dosage level of 2-4 mg is recommended depending on the weight of the individual.

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Ranitidine’s pharmacokinetics profile is characterized by the “double peak phenomenon” after oral administration (Hamilton et al., 2011, p. 581). Its pharmacokinetic properties, i.e., absorption, distribution, metabolism, and excretion (ADME), are described below.


The bioavailability of 150 mg oral Ranitidine tablets, USP, is 50% after 2-3 hours, absorbed mainly through the ileac lining (Schuck, Costa, de Barros, Gruber, & Schapoval, 2012). In contrast, IV administration peaks at 450-545 ng/ml. The absorption rate of the syrup is equivalent to that of the tablets. Acids in food and antacids have no significant impact on the absorption rate. However, in one trial, propantheline (150 m/mol) was found to slow down absorption and serum ranitidine peaks and bioavailability (Schuck et al., 2012). It was suggested that repressed gastric emptying rate accounts for the delayed bioavailability. Low intestinal permeability also causes a slow release of the drug. However, ranitidine microemulsion in nut oil has enhanced bioavailability that is 1.4 times higher than that of the normal formulation (Jha, Karki, Puttegowda, & Ghosh, 2014).


The serum level of Ranitidine is estimated to be 1.4 L/kg. Its mean plasma protein binding ability is 15% (Ranitidine, 2016).


The main metabolite excreted in urine after oral ranitidine administration is nitric oxide, accounting for 4% of the dosage (Ranitidine, 2016). Urine also contains sulfur oxide and desmethyl ranitidine at 1% each. Additional metabolites also occur in fecal materials. Hepatic dysfunction has been shown to alter the “half-life, distribution, and bioavailability” of the drug (Ranitidine, 2016, para. 5).


Ranitidine is mainly excreted in urine, which accounts for a third of the oral dose administered within 24-hour duration (Ranitidine, 2016). Clearance is estimated to be 410 ml per minute through the renal tubes. The drug has an elimination half-life of 2-3 hours. In one study, subjects with renal impairment had repressed drug clearance rate (29 ml/min), increased distribution rate (1.76 L/kg), and elevated half-life (4.8 hrs) after ranitidine (50 mg) IV administration (Ranitidine, 2016). Thus, renal impairment due to age suppresses the Ranitidine clearance rate.

In geriatric patients, ranitidine half-life and clearance from the blood is repressed because of impaired renal function. This increases the elimination time to 4 hours and raises the peak levels to 526-530 ng/ml after a 3-hour period. In young people (1-16 years), the mean bioavailability of the drug when administered orally is 49% (Ranitidine, 2016). Estimated pharmacokinetic parameter values (Cmax and Tmax) for pediatric patients are shown in Table 1 below.

Table 1. Ranitidine Pharmacokinetic Parameter Values.

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Age Dose Cmax (ng/mL) Tmax(hrs)
DU or GU (3-16 years) Tablets (2mg per Kg) 54-490 2.0
Healthy people (1-14 years) – one dose Syrup (2mg per Kg) 244 1.61
Healthy people (1-14 years) – double dose Syrup (2mg per Kg) 320 1.66


The pharmacodynamic effects of ranitidine relate to competitive inhibition of H2-receptors (Jha et al., 2014). Thus, the drug reverses the effects of H2-receptor agonists such as histamine-2. The pharmacodynamic interaction between this drug and pirenzepine has been found to affect its bioavailability and clearance rates (Jha et al., 2014). Ranitidine’s pharmacodynamic effects are discussed below.

Effects on Bioavailability/Absorption

Ranitidine suppresses histamine-mediated release of gastric acid, resulting in elevated pH. Jha et al. (2014) suggest that the drug affects the absorption or bioavailability of other drugs. Further, ranitidine may limit the absorption rate of drugs with low solubility in elevated intra-gastric pH conditions. Therefore, ranitidine has a direct effect on pH-dependent absorption rate in the stomach for weakly alkaline drugs due to an elevated pH of 4-5. This slows the absorption of drugs such as aspirin (pKa 3.5) and diazepam that are soluble in weakly alkaline conditions (Jha et al., 2014).

Ranitidine also has an indirect effect on drugs with low solubility in weakly alkaline conditions. The dissolution of such a drug depends on its pKa and intra-gastric pH (Jha et al., 2014). Weakly alkaline drugs have a high solubility in acidic conditions. Therefore, the solubility and absorption of such drugs in the stomach may be affected by ranitidine.

Pharmacodynamic Interaction

Pirenzepine has been shown to interact with ranitidine to produce synergistic inhibitory effects on the gastric acid release (Rey et al., 2014). Pirenzepine belongs to the anticholinergic class of drugs that inhibits the “effects of acetylcholine” on gastric parietal cells (Rey et al., 2014, p. 684). Simultaneous IV administration of the two drugs increased the inhibition rate to 97% compared to 79.5% and 42% for ranitidine and pirenzepine, respectively. Thus, pirenzepine reinforces the anti-secretory effects of ranitidine on the parietal cells. Further, pirenzepine extends ranitidine’s inhibitory effects on elevated acid secretion in Zollinger-Ellison syndrome (Rey et al., 2014).

Antisecretory effects

The presence of ranitidine represses hypersecretion of acid through H2-receptor blockage. Goldstein, Johanson, Suchower, and Brown (2005) found that the drug also inhibits reflexive gastric acid release due to “food, betazole, and pentagastrin” (p. 2652). Oral ranitidine causes 92% and 99% suppression the secretory effects of 150 mg betazole and pentagastrin on the parietal cells. Elevated ranitidine (35-94 ng/ml) in the plasma causes acid inhibition by 50% for up to 12 hours (Goldstein et al., 2005). Thus, ranitidine has antisecretory effects on acid secretion.

Adverse Effects, Side effects

H2-antagonists such as ranitidine have a range of adverse effects on patients. Clinical trials report common side/adverse effects of ranitidine use as headaches, CNS disturbances, cardiovascular problems, and gastrointestinal discomfort, among others.

Central Nervous System Disturbances

Ranitidine administration has been associated with dizziness, confusion, insomnia, and hallucinations. The disturbances have been reported in elderly patients with renal dysfunction within 14 days after starting ranitidine therapy (Ranitidine, 2016). The drug may also cause disorientation, psychotic states, and paranoia in this patient population. In rare cases, the drug causes locomotor disturbances and visual impairments.

Cardiovascular Complications

Ranitidine, like other H2-antagonists, has been associated with cases of cardiac arrhythmia, bradycardia, and irregular ventricular contractions (Ranitidine, 2016).

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Gastrointestinal Effects

The gastrointestinal side effects reported due to ranitidine administration include “constipation, nausea, diarrhea, and abdominal pain” compared to the placebo group (Ranitidine, 2016, para. 15). The H2-blocker also inhibits the absorption of weakly basic drugs.

Hepatic Effects

Hepatocellular/cholestatic hepatitis has been reported in some patients receiving ranitidine therapy (DeVault & Castell, 2015). Occasional renal failure and fatalities have also been reported. Elevated blood SGPT levels have also been observed in patients administered with a daily dose of 400 mg IV given in 100 mg tablets (DeVault & Castell, 2015). Elevated plasma SGPT levels indicate hepatic or cardiovascular damage.

Hematologic Complications

Patients receiving ranitidine therapy have been found to have low blood cell count. The cell count causes reversible conditions such as leucopenia, thrombopenia, and granulocytopenia, which are characterized by abnormally low levels of white blood cells, platelets, and granulocytes, respectively. Some reports indicate that the drug sometimes causes agranulocytosis and hypoplasia.

Adverse Effects on the Endocrinal System

Studies show that ranitidine causes impotence and suppressed libido in elderly subjects. Further, instances of galactorrhea and gynecomastia, a disorder characterized by enlarged breasts, have been reported patients (Rey et al., 2014). The drug is indicated in cases of cimetidine-induced gynecomastia in patients.

Respiratory Side Effects

Studies have found a causal relationship between H2-receptor antagonists, such as ranitidine, and pneumonia (Rey et al., 2014). This class of drugs increases the pneumonia risk significantly (RR = 1.65) in patients with hypersecretion of gastric acid.

Musculoskeletal Effects

Some reports indicate that the drug causes joint pains and sometimes myodynias or skeletal muscle pains (Rey et al., 2014). Other adverse effects of ranitidine include alopecia and blood vessel inflammation. Some patients experience side effects like bronchospasm, allergies, elevated plasma creatinine, and skin rash. The reported effects of overdose (18g daily) include hypotension and tremors in animal models.

Risk versus Benefits – Literature Review

Ranitidine is indicated in the treatment and maintenance of DUs and Gus, GERD, and Zollinger-Ellison syndrome in adult and pediatric patients at appropriate dosage levels. The benefits of the drug outweigh its risks or adverse events when used in the correct dosage. The benefits include short-term and maintenance treatment of GUs and DUs, heartburns (pyrosis), GERD, and hypersecretory conditions. Ranitidine provides a fast onset effect that causes a rapid symptomatic relief. Ranitidine, like other H2-receptor blockers, induces a faster symptom relief from GERD compared to protein-pump inhibitors (PPIs) (Kahrilas, 2011). Its ‘onset effect’ occurs about two hours earlier than that of the PPIs.

The results of a meta-analysis by Tran, Lowry, and El-­serag (2006) indicate that healthy subjects receiving an oral 150 mg dose of ranitidine experience a faster gastric pH rise (>4) than those receiving omeprazole. Similarly, Hedenstrom, Alm, Kraft, and Grahnen (2007) establish that the drug’s intra-gastric pH increase is higher than that of omeprazole in GERD cases within the first four hours. Thus, ranitidine provides fast-relief from the symptoms of GERD and heartburns. On the other hand, omeprazole has no significant effect on gastric pH change within the first four hours after oral administration. This indicates that ranitidine is effective in bringing a faster remission of heartburns/dyspepsia in the short-term compared to PPIs.

H2-receptor blockers, such as ranitidine, have a superior long-term efficacy in preventing GERD symptoms compared to a placebo (DeVault & Castell, 2015). Ranitidine used as a single dose provides complete remission from GERD symptoms after a period of 2-4 weeks compared with antacids. Evidence further shows that the drug’s healing rate lie between 40% and 80%, depending on “dosage and dosing frequency” (Cremonini et al., 2010, p. 38). Greater efficacy is achieved when higher doses are administered regularly to the GERD patient.

Another beneficial effect of ranitidine is decreasing reflex symptoms resulting from acidic meals. Consuming meals containing acids increases the risk of reflux symptoms. Goldstein et al. (2005) found that H2-receptor blockers, including ranitidine prevent acid reflux symptoms when taken before a meal. Additionally, ranitidine, besides its fast onset effect, is a long-acting drug. It brings relief from esophagitis for over 10 hours; hence, ranitidine is more beneficial than short-acting antacids. However, antacids and H2-receptor antagonists have equivalent peak potency.

Ranitidine has also been shown to protect the gastric mucosa from ethanol-related damage. Ethanol increases the risk of DUs and GUs in patients. It damages the mucosal barrier, exposing it to “proteolytic and hydrolytic” effects of gastric hydrochloric acid (Rey et al., 2014, p. 686). Ranitidine micro-emulsion formulation was found to reduce the ethanol-induced ulcer and mucosal damage by 80.8% (Jha et al., 2014). This indicates that the drug offers protection to the gastric mucosa against ethanol-induced effects.

The drug is indicated in the treatment of pyrosis (heartburns) episodes (OTC only). Treatment success in patients with episodic heartburns was found to be higher in the ranitidine group (75 mg) than in the placebo patients (Ciociola, Pappa, & Sirgo, 2001). In this study, ranitidine treatment reduced episodic heartburns by >10% within 45-60 minutes after administration with 75 mg of the drug. Additionally, the remission of nocturnal episodes improved in this group compared to the control group. The subjects under the 75 mg therapy received lower amounts of antacids compared to the control group.

Therefore, ranitidine is an effective treatment for pyrosis episodes, regardless of severity, age, sex, and daily cycles (nocturnal or diurnal). In addition, 1-2 tablets (75 mg) can provide complete relief from heartburns, especially nocturnal episodes (Gardner, Ciociola, Robinson, & McIsaac, 2008). However, oral ranitidine administration has been linked to adverse GI events in elderly subjects. Nevertheless, tablets (75 mg) can offer effective relief to patients when administered PD for two weeks (Gardner et al., 2008). Thus, the recommended maximum daily dosage of 150 mg taken for 14 days can prevent the adverse events associated with overdosing.

Ranitidine is indicated in the treatment of GU and DU for a period of 6-8 weeks. The drug is also useful as maintenance therapy of gastric and duodenal ulcers at a lower dose for up to 12 months. Ranitidine and other H2-receptor blockers have shown high efficacy in the treatment of DUs by reducing nocturnal acid level by up to 96% (Yeomans, Svedberg, & Naesdal, 2006). Further, the 6-week healing rate of DUs is 80-90%, indicating that the drug is effective as a short-term treatment. Bedtime dosing is particularly beneficial for treating the DUs in the short term.

Evidence for ranitidine’s efficacy in treating gastric ulcers has been reported. The drug is efficacious in treating active GUs for a period of six weeks (Yeomans et al., 2006). It is also the recommended maintenance therapy for treated GUs to avoid relapse. The drug is also effective in the treatment of hypersecretory conditions. Hedenstrom et al. (2007) found that ranitidine suppresses acid secretion that increase the risk of “diarrhea, anorexia, and pain” in patients diagnosed with Zollinger-Ellison syndrome (p. 1139). Additionally, healing of GUs is achieved in patients who do not respond to other treatments.

The risks associated with ranitidine are related to hypersensitivity and drug interactions. Further, precautions (dosage and dosing frequency) should be taken when administering the drug to patients with hepatic dysfunction (Hamilton et al., 2011). The drug increases the risk of porphyric attacks in subjects with a history of the disease. Ranitidine affects the bioavailability of most drugs by altering the intra-gastric pH (Hedenstrom et al., 2007). Ranitidine interaction with drugs such as procainamide, warfarin, and atazanavir has been shown to affect the absorption of these drugs. Thus, it should not be given to patients using these drugs.


Ciociola, A., Pappa, K., & Sirgo, M. (2011). Nonprescription doses of ranitidine are effective in the relief of episodic heartburn. American Journal of Therapeutics, 8, 399-408.

Cremonini, F., Ziogas, D., Chang, H., Kokkotou, E., Kelley, J., Conboy, L.,…Lembo, A. (2010). Meta-analysis: The effects of placebo treatment on gastro-oesophageal reflux disease. Alimentary Pharmacology & Therapeutics, 32(1), 29-­42.

DeVault, K., & Castell, D. (2015). Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. American Journal of Gastroenterology, 100, 190-200.

Gardner, J., Ciociola, A., Robinson, M., & McIsaac, R. (2008). Determination of the time of onset of action of ranitidine and famotidine on intra-gastric acidity. Alimentary Pharmacology & Therapeutics, 16(7), 1317-1326.

Goldstein, J., Johanson, J., Suchower, L., & Brown, K. (2005). Healing of gastric ulcers with esomeprazole versus ranitidine in patients who continued to receive NSAID therapy: A randomized trial. American Journal of Gastroenterology, 100, 2650–2657.

Hamilton, M., Sercombe, J., & Pounder, R. (2011). Control of intragastric acidity with over-the-counter doses of ranitidine or famotidine. Alimentary Pharmacology & Therapeutics, 15(10), 579-583.

Hedenstrom, H., Alm, C., Kraft, M., & Grahnen, A. (2007). Intragastric pH after oral administration of single doses of ranitidine effervescent tablets, omeprazole capsules and famotidine fast-dissolving tablets to fasting healthy volunteers. Alimentary Pharmacology & Therapeutics, 11(1), 1137-1141.

Jha, S., Karki, R., Puttegowda, V., & Ghosh, A. (2014). Pharmacodynamics and pharmacokinetics evaluation of ranitidine microemulsion on experimental animals. Advances in Pharmaceutics, 3(2), 1-6.

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Rey, E., Poves-Frances, C., Sanchez, G., Fueyo, A., Badiola, C., & Diaz-Rubio, M. (2014). Effect of effervescent ranitidine on gastric pH: Comparison with almagate and placebo in fasting and postprandial conditions. Alimentary Pharmacology & Therapeutics, 15(6), 683-688.

Schuck, V., Costa, T., de Barros, S., Gruber, C., & Schapoval, E. (2012). Compartmental analysis of ranitidine doubled peak plasma profile after oral administration to healthy volunteers. Brazilian Journal of Pharmaceutical Sciences, 38(2), 183-189.

Tran, T., Lowry, A., & El-­serag, H. (2006). Meta-­analysis: The efficacy of over-­the-­counter gastro-­oesophageal reflux disease therapies. Alimentary Pharmacology & Therapeutics, 25(1), 143-­153.

Yeomans, D., Svedberg, L., & Naesdal, J. (2006). Is ranitidine therapy sufficient for healing peptic ulcers associated with non-steroidal anti-inflammatory drug use? International Journal of Clinical Practice, 60(11), 1401-1407.

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