C-Type Natriuretic Peptide (CNP) (1-22), human (TFA), is a 22 amino acid fragment of CNP that functions as an agonist for the natriuretic peptide receptor B (NPR-B). It can inhibit cAMP synthesis induced by histamine, 5-HT, or Forskolin, while exhibiting strong endothelial-derived relaxation properties and acting as a growth inhibitor.

C-Type Natriuretic Peptide (CNP) (1-22), human (TFA) (0.01, 0.1, 1, 10, 100, 1000 nM) enhances cGMP production in CHO cells express ng human NPR-B in a concentration-dependent manner[1]. PK parameters of CNP immunoreactivity after a s ngle intravenous dose of CNP (1-22), human (TFA)[1]: 20 nM/kg dose—AUC 0→∞: 320±54 pMmin/mL, MRT 0→∞: 1.02±0.18 min, T1/2: 1.42±0.45 min, CL tot: 63.9±11.9 mL/min/kg, Vd ss: 64.2±5.1 mL/kg. PK parameters after a s ngle subcutaneous dose of CNP (1-22), human (TFA)[1]: 50 nM/kg dose—Cmax: 9.02±3.74 pM/mL, Tmax: 5.0±0.0 min, AUC 0→∞: 152±73pM·min/mL, MRT 0→∞: 13.9±3.4 min, T1/2: 10.0±5.0 min, BA: 19±9%. Values represent the mean±SD of 3 rats. i.c.v. administration of CNP (1-22) at 2 nM increases the severity of picrotoxin-kindled convulsions 24 and 48 hours post-application[3].