npr 1

NPR-C activator 1 (Compound 1) is a potent agonist (EC50 ~ 1 μM) of natriuretic peptide receptor C (NPR-C), which plays a crucial role in regulating vascular homeostasis, and demonstrates promising in vivo pharmacokinetic properties [1].

Norchlorcyclizine (C-10) is a partially selective NPR-B inhibitor. It also is an inhibitor of human tyrosyl-DNA phosphodiesterase 1.

C-Type Natriuretic Peptide (CNP) (1-22), human, is the 1-22 fragment of the parent C-Type Natriuretic Peptide.

C-Type Natriuretic Peptide (CNP) (1-22), human acetate is an agonist of natriuretic peptide receptor B (NPR-B), an endothelial-derived relaxant and growth inhibitory factor. C-Type Natriuretic Peptide (CNP) (1-22), human acetate inhibits cAMP synthesis stimulated by histamine and 5-HT or directly by Forskolin.

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.

Vosoritide (BMN 111), a modified recombinant C-type natriuretic peptide (CNP) analogue, engages with natriuretic peptide receptor type B (NPR-B) to diminish the function of fibroblast growth factor receptor 3 (FGFR3). This compound is employed in the study of achondroplasia and dwarfism [1] [2] [3].

PL-3994, a natriuretic peptide receptor-A (NPR-A) agonist resistant to neutral endopeptidase, functions as a bronchodilator, eliciting a concentration-dependent relaxation of pre-contracted guinea-pig trachea, evidenced by an IC50 of 42.7 nM [1].

Atrial Natriuretic Peptide (ANP) (1-28), human, porcine Acetate is an atrial natriuretic peptide (ANP) hormone secreted by atrial myocytes that is capable of acting as an natriuretic peptide receptor-A(NPR-A) agonist, used in the treatment of acute decompensated heart failure (ADHF). By binding to specific receptors on the surface of the kidney, blood vessel, and heart cells, Carperitide causes an increase in cyclic guanosine monophosphate (cGMP) levels and induces vasodilatation, diuresis, and sodium excretion, which in turn reduces the heart's workload.

dCNP binds to NPR-B C receptors (NPR-B C receptor), initiating the cGMP signaling pathway and regulating vascular function. It exhibits anti-hypoxic effects by downregulating hypoxia-related genes such as HIF1α and HIF2α. Additionally, dCNP inhibits tumor stroma induction, demonstrating antifibrotic properties. It also enhances immune response by upregulating CTL, NK cells, and conventional type 1 dendritic cells in tumors.