Soothing relief from the top of the esophagus to the stomach

In addition to heartburn, acid indigestion and gas, Mylanta is indicated for symptomatic relief of hyperacidity associated with the diagnosis of peptic esophagitis.

Esophagitis patients treated with antisecretory drugs can use Mylanta for relief of occasional breakthrough symptoms caused by hyperacidity and gastroesophageal reflux1.

Mylanta Products

Available in several formulations, Mylanta products provide rapid symptom relief.

  • Works on contact to neutralize acid — from the esophagus to the stomach1
  • Increases pH in the esophagus, which may help to reduce the pH-dependent activity of pepsin2
  • Smooth, great tasting flavors
  • Quickly soothes breakthrough heartburn that can occur with PPIs and other therapies
  • 45% more acid neutralizing capacity (ANC) than TUMS®*
  • NEW! Mylanta ONE all-in-one relief in ONE tablet

Did you know?

A recent survey shows that only 7% of patients think antacids also work in the esophagus. Let your patients know that Mylanta works in the esophagus, as well as in the stomach.

Recommend Mylanta for symptoms related to excess acid

View Mylanta Products

*Based on 1 dose of Mylanta Maximum Strength versus 1 dose of TUMS® Extra Strength
† Based on 2018 survey of 1200 individuals who treat frequently with antacids


  1. 1. Kahrilas P. Gastroesophageal Reflux Disease. New England Journal of Medicine. 2008:1700–1707.
  2. 2. Waller D, Sampson A. In: Waller D, Sampson A. Medical Pharmacology and Therapeutics. 5th ed. London, England: Elsevier; 2017:401-410.
  3. 3. Hirschowitz BI. Pepsin and the esophagus. Yale J Bio Med. 1999;72:133-142.


For patients on existing prescriptions, consult the prescribing information of those medicines to check for potential interactions with the ingredients in the Mylanta product you are recommending.

Use with caution for patients on magnesium-restricted diets.

Prolonged use of aluminum-containing antacids in patients with renal failure may result in or worsen dialysis osteomalacia. Elevated tissue aluminum levels contribute to the development of the dialysis encephalopathy and osteomalacia syndromes. Small amounts of aluminum are absorbed from the gastrointestinal tract and renal excretion of aluminum is impaired in renal failure. Aluminum is not well removed by dialysis because it is bound to albumin and transferrin, which do not cross dialysis membranes. As a result, aluminum is deposited in bone, and dialysis osteomalacia may develop when large amounts of aluminum are ingested orally by patients with impaired renal function.
Aluminum forms insoluble complexes with phosphate in the gastrointestinal tract, thus decreasing phosphate absorption. Prolonged use of aluminum-containing antacids by normophosphatemic patients may result in hypophosphatemia if phosphate intake is not adequate. In its more severe forms, hypophosphatemia can lead to anorexia, malaise, muscle weakness and osteomalacia.