Sucralfate exerts its antiulcer effect by forming a protective barrier on ulcer base. The sub-mechanism critical to its action at the molecular level is:

• A Sucralfate inhibits H+/K+-ATPase, reducing acid secretion in the gastric lumen
• B In acidic conditions, sucralfate polymerizes into a gel that binds positively-charged proteins in the ulcer base via electrostatic interaction with its highly negative sulfate groups, forming a protective paste that also adsorbs pepsin and bile acids ✓
• C Sucralfate is a basic aluminum salt that neutralizes gastric acid by stoichiometric reaction
• D Sucralfate activates prostaglandin E2 synthesis stimulating mucus and bicarbonate secretion

Explanation

Sucralfate is a complex of aluminum hydroxide and sucrose octasulfate. At low pH (<4), aluminum dissociates, and sucrose octasulfate polymerizes into a viscous, sticky gel. The eight negatively-charged sulfate groups bind electrostatically to positively-charged amino acid residues (lysine, arginine) on proteins in the ulcer crater (albumin, fibrinogen), forming a tenacious protective coating that adheres to the ulcer base for 4–6 hours. This coating physically excludes gastric acid, pepsin, and bile acids from the ulcer. Sucralfate also adsorbs pepsin and bile acids, further protecting the mucosa. It does NOT inhibit acid secretion (unlike PPIs), does NOT neutralize acid (unlike antacids), and while it does stimulate some prostaglandin production, this is not the primary mechanism.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.