Pharmacological Research review examines why amylin-based drugs cause nausea, and how that might be reduced
MechanismP1Primary public evidencePeer-reviewed publication
On 12 August 2026 Fischer and Borner published a review of amylin biology and the tolerability of long-acting amylin analogues, including eloralintide, in Pharmacological Research. It discusses how receptor pharmacology, hindbrain circuitry and drug exposure may shape nausea and vomiting.
Background and context
Who wrote it
Both authors are at the University of Southern California, in the Department of Human and Evolutionary Biology. The PubMed record lists no company affiliation for either author and does not show funding or competing-interest statements.
The distinction at the centre of the review
The abstract separates selective amylin receptor agonists from dual amylin and calcitonin receptor agonists. It names cagrilintide, eloralintide, petrelintide and NN1213 among the long-acting agents. It suggests that calcitonin receptor engagement, how drug levels build up and which brain circuits are recruited may decide whether reduced eating reflects normal fullness or an aversive signal.
What it does not settle
The abstract lists species differences among the factors that may shape nausea, so findings from animals may not carry over to people. It frames the discussion as a guide to designing future drugs. As a review it reports no new experiment on eloralintide.
Fischer SL, Borner T, Pharmacological Research, 2026, volume 232, article 108382, via PubMed (PMID 42586227). DOI 10.1016/j.phrs.2026.108382.
