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Systematic (IUPAC) name
Hexadeca-μ-hydroxytetracosahydroxy[μ8-[1,3,4,6-tetra-O-sulfo-β-Dfructofuranosyl-α-D-glucopyranoside tetrakis(hydrogen sulfato)8-)]]hexadecaaluminum[1]
Clinical data
Trade names Carafate
AHFS/ monograph
MedlinePlus a681049
  • B
Legal status
  • (Prescription only)
Routes of
oral, suspension, rectal suspension
Pharmacokinetic data
Bioavailability 3-5% (local acting)
Metabolism GI; liver: unknown
Biological half-life unknown
Excretion feces, urine
CAS Registry Number 54182-58-0 YesY
ATC code A02BX02
PubChem CID: 6398525
DrugBank DB00364 N
ChemSpider 4911161 N
Chemical data
Formula C12H54Al16O75S8
Molecular mass 2086.75 g/mol[1]
 N (what is this?)  (verify)

Sucralfate is a cytoprotective agent, an oral gastrointestinal medication primarily indicated for the treatment of active duodenal ulcers. Brand names include Sucramal in Italy; Carafate in U.S.A.; Sufrate, Sucralcoat, Pepsigard, Sucral, Sucrafil, Hapifate in India; Sutra or Musin in parts of South-East Asia; Sulcrate in Canada; Ulsanic in South Africa and Israel; and Antepsin in Turkey. Sucralfate is also used for the treatment of gastroesophageal reflux disease (GERD)[2] and stress ulcers. Unlike the other classes of medications used for treatment of peptic ulcers, sucralfate is a sucrose sulfate-aluminium complex that binds to the mucosa, thus creating a physical barrier that impairs diffusion of hydrochloric acid in the gastrointestinal tract and prevents degradation of mucus by acid. It also stimulates bicarbonate output and acts like an acid buffer with cytoprotective properties. Sucralfate was approved by the U.S. Food and Drug Administration (FDA) in 1981.

Mechanism of action[edit]

Sucralfate is a locally acting substance that in an acidic environment (pH < 4) reacts with hydrochloric acid in the stomach to form a cross-linking, viscous, paste-like material capable of acting as an acid buffer for as long as 6 to 8 hours after a single dose. It also attaches to proteins on the surface of ulcers, such as albumin and fibrinogen, to form stable insoluble complexes. These complexes serve as protective barriers at the ulcer surface, preventing further damage from acid, pepsin, and bile. In addition, it prevents back diffusion of hydrogen ions, and adsorbs both pepsin and bile acids. Recently, it has been indicated that sucralfate also stimulates the increase of prostaglandin E2, epidermal growth factors (EGF), bFGF, and gastric mucus.

Clinical uses[edit]

The only FDA-approved indication for sucralfate is for the treatment of active duodenal ulcers not related to NSAID usage because the mechanism behind these ulcers is secondary to acid oversecretion. It is not technically approved for gastric ulcers because the main mechanism is not due to acid oversecretion but rather from diminished protection. The use for sucralfate in peptic ulcer disease has diminished recently, but it is still the preferred agent for stress ulcer prophylaxis.


DUODENAL ULCER: It is used in the short-term (up to 8 weeks) treatment of duodenal ulcer.

Antacids may be used as adjuncts to sucralfate therapy to relieve pain, but should not be taken within 30 minutes before or after administration of sucralfate.

GASTRIC ULCER: Sucralfate has been used in the treatment of patients with gastric ulcer

Prevention and treatment of chemotherapy induced mucositis


Gastric ulcer



Stress ulcer prophylaxis

Ulcer of rectum

Adverse reactions[edit]

The most common side effect seen is constipation 2-3%. Less commonly reported include flatulence, cephalalgia (headache), hypophosphatemia, xerostomia (dry mouth), and bezoar[8] formation. Avoid using this drug in patients with chronic renal failure, it might cause them aluminum-induced nephropathy. Nursing mothers: Uncertain.


Onset: 1-2 hr (initial onset for PUD)

Absorption: <5% (PO)

Duration: Up to 6 hr due to high affinity for defective mucosa (PUD)

Bioavailability: 5% as sucralfate is considered non-systemic, sucrose octasulfate: 5%, aluminum:0.005%

Metabolism: Not metabolized, excreted unchanged in urine

Excretion: Primarily in urine as unchanged drug


  1. ^ a b Merck Index, 12th Edition, 9049.
  2. ^ Maton PN (2003). "Profile and assessment of GERD pharmacotherapy". Cleve Clin J Med. 70 Suppl 5: S51–70. doi:10.3949/ccjm.70.Suppl_5.S51. PMID 14705381. 
  3. ^ Jian-Min, Si; Liang-Jing, Wang; Shu-Jie, Chen; Lan, Zhao; Ning, Dai (2003). "Quality of life and cost-effectiveness of combined therapy for reflux esophagitis". Journal of Zhejiang University SCIENCE A 4 (5): 602–6. doi:10.1631/jzus.2003.0602. PMID 12958722. 
  4. ^ Aliment Pharmacol Ther. 2005 Nov 1;22(9):749-57.
  5. ^ Respir Care. 2005 Jun;50(6):725-39; discussion 739-41.
  6. ^ Surg Today. 2005;35(8):617-22.
  7. ^ International Journal Radiation Oncology Biological Physics, 2004 Jan 1;58(1):98-105
  8. ^
  • Katzung, Bertram G. Basic and Clinical Pharmacology, 9th ed. (2004).

External links[edit]