cnp

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

CNP-AFU (2-Chloro-4-nitrophenyl α-L-fucopyranoside) serves as the substrate for alpha-L-fucosidase.

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.

CNP-38, a C-type natriuretic peptide (CNP) analog.

Gal-G2-CNP is a pyranosyl galactoside maltoside, which serves as a substrate for the assay of novel amylases and pancreatic-type amylases.

G3-CNP is a substrate for α-amylase and the hydrolysis product is 2-chloro-4-nitrophenol, which can be used to determine the enzyme activity by colorimetric assay at 405 nm.

CNP0296775 is an inhibitor of dengue virus methyltransferase (DENV MTase) with the potential to disrupt the viral replication process.

G108 is an inhibitor of human cGAS and is used in the study of autoimmune diseases associated with human cGAS.

Umibecestat is an inhibitor of beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1), with IC50s of 11 nM and 10 nM for human BACE-1 and mouse BACE-1, respectively. Umibecestat can be used for the research of alzheimer's disease.

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.

Indantadol HCl (CHF-3381) is a NMDA antagonist and nonselective MAO inhibitor.

Umibecestat HCl (CNP520 HCl) is a highly efficient β-secretase (BACE1/BACE2) inhibitor, lowering Aβ levels in mice and rats, used in Alzheimer's disease research.

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.

GlcNPhth[36Bn,4Ac]-β-MP is a biochemical reagent that can be used as a biomaterial for life science related research and as a sulfonylation reagent for organic synthesis and drug discovery.

Triciribine phosphate (VD 002) is a highly selective AKT inhibitor that induces cell cycle arrest and cysteinyl asparagin-dependent apoptosis, inhibits neovascularization, and can be used in the study of leukemia.

Boc-N-PEG1-C2-NHS ester, a PEG-based linker, finds utility in PROTAC synthesis[1].

Boc-N-PEG5-C2-NHS ester is a PEG-based linker used in PROTACs to join two essential ligands, facilitating selective protein degradation by harnessing the ubiquitin-proteasome system within cells.

endo-BCN-PEG2-acid, a PEG-based linker for PROTACs, connects two essential ligands necessary for PROTAC molecule formation. This linker facilitates selective protein degradation by utilizing the ubiquitin-proteasome system within cells.

endo-BCN-PEG2-alcohol, a PEG-based linker for PROTACs, facilitates the connection of two essential ligands, critical for the formation of PROTAC molecules, and enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

Endo-BCN-PEG2-PFP ester, a PEG-based linker, serves as a valuable component in PROTAC synthesis[1].

endo-BCN-PEG3-acid is a PEG-based linker for PROTACs, joining two essential ligands to facilitate selective protein degradation via the ubiquitin-proteasome system within cells.

endo-BCN-PEG3-NH-Boc is a PEG-based linker for PROTACs, joining two essential ligands integral to PROTAC molecule formation, facilitating selective protein degradation via the ubiquitin-proteasome system within cells.

endo-BCN-PEG4-acid is a PEG-based linker for PROTACs that joins two essential ligands, crucial for the formation of PROTAC molecules, enabling selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

endo-BCN-PEG4-Boc is a PEG-based linker for PROTACs that combines two essential ligands, facilitating the formation of PROTAC molecules and enabling selective protein degradation via the ubiquitin-proteasome system within cells.