Cell lines

CHO cells

Preparation Method

To evaluate the human NPR (hNPR) agonist activities of the test compounds(C-type natriuretic peptide (1-22) (human, rat, swine)), Using Chinese hamster ovarian (CHO) cells stably expressing hNPR-A or hNPR-B. Each compound was added to the cells in duplicate and incubated for 15 min. Cells were lysed.

Reaction Conditions

0.01-1000nM C-type natriuretic peptide (1-22) (human, rat, swine)for 15 min

Applications

C-type natriuretic peptide (1-22) (human, rat, swine) increased cGMP production in CHO cells expressing human NPR-B in a concentration-dependent manner.

Animal models

Sprague Dawley (SD) rats

Preparation Method

Rats received C-type natriuretic peptide (1-22) (human, rat, swine) or ASB20123 by intravenous (iv) injection into the tail vein or subcutaneous (sc) injection into the back.

Dosage form

C-type natriuretic peptide (1-22) (human, rat, swine) iv (20 nmol/kg) or sc (50 nmol/kg)

Applications

C-type natriuretic peptide (1-22) (human, rat, swine) could be transported across the vascular wall and reach NPR-B in peripheral tissues.

C-type natriuretic peptide (1-22) (human, rat, swine) is an endogenous peptide found in plasma and cerebrospinal fluid^[2]. C-type natriuretic peptide (CNP) is a member of the natriuretic peptide (NP) family^[3]. It is also a potent, endothelial-derived relaxant and growth-inhibitory factor^[6]. C-type natriuretic peptide (1-22) (human, rat, swine) is an agonist for the natriuretic peptide receptor NPR2 (NPRB) and has an affinity for NPR3 (NPRC). C-type natriuretic peptide (1-22) (human, rat, swine) can inhibit L-type calcium current in cardiomyocytes, has anti-proliferation effect in cardiac fibroblasts in vitro, and can promote vasodilation^[7].

C-type natriuretic peptide (1-22) (human, rat, swine) increased cGMP production in CHO cells expressing human NPR-B in a concentration-dependent manner^[1].

C-type natriuretic peptide (1-22) (human, rat, swine) could be transported across the vascular wall and reach NPR-B in peripheral tissues^[1]. exogenous CNP(1-22) improved endochondral ossification and accelerated bone growth in mice after constant intravenous infusion at a large dose only^[4]. I.c.v. administration of C-type natriuretic peptide (1-22) (human, rat, swine) in a dose of 2 nmol induced an increase in the severity of picrotoxin-kindled convulsions 24 and 48 hrs after application of the peptide^[5].

References:
[1]. Morozumi N, Yotsumoto T, et,al. ASB20123: A novel C-type natriuretic peptide derivative for treatment of growth failure and dwarfism. PLoS One. 2019 Feb 22;14(2):e0212680. doi: 10.1371/journal.pone.0212680. PMID: 30794654; PMCID: PMC6386482.
[2]. Minamino N, Makino Y, et,al.Characterization of immunoreactive human C-type natriuretic peptide in brain and heart. Biochem Biophys Res Commun. 1991 Aug 30;179(1):535-42. doi: 10.1016/0006-291x(91)91404-z. PMID: 1831979.
[3]. Potter LR, Yoder AR, et,al. Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applications. Handb Exp Pharmacol. 2009;(191):341-66. doi: 10.1007/978-3-540-68964-5_15. PMID: 19089336; PMCID: PMC4855512.
[4]. Yasoda A, Kitamura H, et,al. Systemic administration of C-type natriuretic peptide as a novel therapeutic strategy for skeletal dysplasias. Endocrinology. 2009 Jul;150(7):3138-44. doi: 10.1210/en.2008-1676. Epub 2009 Mar 12. PMID: 19282381; PMCID: PMC2703521.
[5]. Mazarati AM, HalÁszi E, et,al. ANP(1-28), BNP(1-32) and CNP(1-22) increase the severity of picrotoxin-kindled seizure syndrome in rats. Life Sci. 1993;52(3):PL19-24. doi: 10.1016/0024-3205(93)90227-t. PMID: 8423706.
[6]. Buckley MG, Jenkins GH, et,al. Circulating C-type natriuretic peptide is increased in orthotopic cardiac transplant recipients and associated with cardiac allograft vasculopathy. Clin Sci (Lond). 2000 Nov;99(5):467-72. PMID: 11052928.
[7]. Pejchalova K, Krejci P, et,al.C-natriuretic peptide: an important regulator of cartilage. Mol Genet Metab. 2007 Nov;92(3):210-5. doi: 10.1016/j.ymgme.2007.06.014. Epub 2007 Aug 6. PMID: 17681481.