Golden line indicates disulfide bond
Clinical data
Trade names Symlin
AHFS/ Monograph
MedlinePlus a605031
  • US: C (Risk not ruled out)
Routes of
ATC code A10BX05 (WHO)
Legal status
Legal status
Pharmacokinetic data
Bioavailability 30 to 40%
Protein binding ~60%
Metabolism Renal
Biological half-life ~48 minutes
CAS Number 151126-32-8 YesY
PubChem (CID) 16132446
DrugBank DB01278 N
KEGG D05595 N
Chemical and physical data
Formula C171H269N51O53S2
Molar mass 3951.41 g/mol
 NYesY (what is this?)  (verify)

Pramlintide (trade name Symlin) is an injectable amylin analogue drug for diabetes (both type 1 and 2), developed by Amylin Pharmaceuticals (now a wholly owned subsidiary of AstraZeneca).[1] Pramlintide is sold as an acetate salt.


Pramlintide is an analogue of amylin, a small peptide hormone that is released into the bloodstream by the β cells of the pancreas along with insulin after a meal.[2] Like insulin, amylin is completely absent in individuals with Type I diabetes.[3]

By augmenting endogenous amylin, pramlintide aids in the cellular absorption and regulation of blood glucose by slowing gastric emptying, promoting satiety via hypothalamic receptors (different receptors than for GLP-1), and inhibiting inappropriate secretion of glucagon, a catabolic hormone that opposes the effects of insulin and amylin. Pramlintide also has effects in raising the acute first-phase insulin response threshold following a meal.

Both a reduction in glycated hemoglobin and weight loss have been shown in insulin-treated patients with type 2 diabetes taking pramlintide as an adjunctive therapy.[4]


Pramlintide has been approved by the FDA, for use by type 1 and type 2 diabetic patients who use insulin.[5] Pramlintide allows patients to use less insulin, lowers average blood sugar levels, and substantially reduces what otherwise would be a large unhealthy rise in blood sugar that occurs in diabetics right after eating. Apart from insulin analogs, pramlintide is the only drug approved by the FDA to lower blood sugar in type 1 diabetics since insulin in the early 1920s.

Design and structure

Since native human amylin is highly amyloidogenic and potentially toxic, the strategy for designing pramlintide was to substitute residues from rat amylin, which is not amyloidogenic (but would presumably retain clinical activity). Proline residues are known to be structure-breaking residues, so these were directly grafted into the human sequence.

Amino acid sequences:


Pramlintide as protein is (positively charged).


  1. Taylor, Phil (19 December 2013). "AstraZeneca buys BMS out of diabetes alliance". Retrieved 16 June 2014.
  2. Jones MC (2007). "Therapies for diabetes: pramlintide and exenatide" (pdf). American Family Physician. 75 (12): 1831–5. PMID 17619527.
  3. Edelman, Steve; Maier, Holly; Wilhelm, Ken (2008). "Pramlintide in the Treatment of Diabetes Mellitus". BioDrugs. 22 (6): 375–386. doi:10.2165/0063030-200822060-00004. ISSN 1173-8804.
  4. Hollander, Priscilla; Maggs, David G.; Ruggles, James A.; Fineman, Mark; Shen, Larry; Kolterman, Orville G.; Weyer, Christian (2004). "Effect of Pramlintide on Weight in Overweight and Obese Insulin-Treated Type 2 Diabetes Patients" (pdf). Obesity. 12 (4): 661–668. doi:10.1038/oby.2004.76. ISSN 1930-7381.
  5. Ryan GJ, Jobe LJ, Martin R (2005). "Pramlintide in the treatment of type 1 and type 2 diabetes mellitus". Clinical therapeutics. 27 (10): 1500–12. doi:10.1016/j.clinthera.2005.10.009. PMID 16330288.
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