Comparison
Cagrilintide vs. DSIP
Two peptides side-by-side — identity, evidence base, legal status and known adverse events.
Identity
Category
Metabolic
Research other
CAS no.
1415456-99-3
62568-57-4
Molecular weight
4253.7 g/mol
848.81 g/mol
Half-life
168 h
0.1 h
Sequence
KCNTATCATQRLANFLVRSSNNLGPVLPPTNVGSNTYTrp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-GluMechanism of action
Cagrilintide
Cagrilintide binds amylin receptors (AMY1, AMY3, formed by the calcitonin receptor plus RAMP proteins). Activation delays gastric emptying, inhibits postprandial glucagon secretion and modulates central satiety signalling via area postrema neurons. An acyl modification enables albumin binding and thereby weekly dosing.
DSIP
DSIP was described in 1977 by the Schoenenberger-Monnier group in Basel as a blood-borne substance reported to induce EEG changes similar to delta sleep in animal models. The exact mechanism remains undefined to this day: no defined receptor, proposed modulation of opioid, GABAergic and glutamatergic systems. Most mechanistic findings stem from preclinical studies of the 1980s and 1990s and were later subjected to contested replication attempts.
Evidence base
Highest evidence
Human RCT
Human trial
Studies
4
4
of which in humans
3
1
Effects recorded
3
3
Open conflicts
0
1
Documented adverse events
1
1