cnp

C-Type Natriuretic Peptide (CNP) (1-22), human 是一种利钠肽受体 B (NPR-B) 激动剂，是一种 CNP 的 1-22 片段。它对生理激动剂组胺和 5-HT 刺激或直接由 Forskolin 刺激的 cAMP 合成具有抑制作用。其中CNP 是一种有效的、内皮衍生的松弛剂和生长抑制因子。

CNP-AFU (2-Chloro-4-nitrophenyl α-L-fucopyranoside) 是 α-L-岩藻糖苷酶的底物。

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

CNP-38是C型钠尿肽，具有调节血压和体液平衡的生物活性。

Gal-G2-CNP 是吡喃半乳糖基麦芽糖苷，适用于新型淀粉酶和胰型淀粉酶的测定作为基质。

G3-CNP是一种α-淀粉酶的底物，水解产物为2-chloro-4-nitrophenol，可在405 nm处用比色法测定酶的活性。

CNP0296775 是一种针对登革热病毒甲基转移酶 (DENV MTase) 的抑制剂，具有中断病毒复制过程的潜力。

G108 是一种人 cGAS 的抑制剂，二可用于研究与人类 cGAS 相关的自身免疫性疾病。

Umibecestat 是一种β-位点淀粉样前体蛋白裂解酶-1 (BACE-1) 抑制剂，对人 BACE-1 和小鼠 BACE-1 的 IC50 分别为 11 nM 和 10 nM，可用于阿尔茨海默病的研究。

C-Type Natriuretic Peptide (CNP) (1-22), human acetate 是一种利钠肽受体 B (NPR-B) 的激动剂，一种内皮衍生的松弛剂和生长抑制因子。 C-Type Natriuretic Peptide (CNP) (1-22), human acetate 抑制由组胺和 5-HT 或直接由毛喉素刺激的 cAMP 合成。

Indantadol HCl (CHF-3381) 是一种 NMDA 拮抗剂和非选择性 MAO 抑制剂。

Umibecestat HCl (CNP520 HCl) 是一种高效性的 β-分泌酶 （BACE1/BACE2） 抑制剂，可降低小鼠和大鼠的 Aβ 水平，可用于研究阿尔茨海默病。

dCNP 结合 NPR-B/C 受体 (NPR-B/C receptor)，激活 cGMP 信号通路以调节血管功能。通过下调 HIF1α、HIF2α 等基因，dCNP 发挥抗缺氧作用，并抑制肿瘤基质诱导，体现其抗纤维化效能。同时，dCNP 上调肿瘤中的 CTL、NK 细胞和常规 1 型树突状细胞，增强免疫反应。

GlcNPhth[36Bn,4Ac]-β-MP是一种高纯度生化试剂，适合作为生物材料或有机合成中间体，广泛应用于生命科学领域的研究与实验。

Triciribine phosphate (VD 002) 是一种高选择性的 AKT 抑制剂，可诱导细胞周期停滞和半胱天冬酶依赖性细胞凋亡，抑制新生血管的生成，可用于研究白血病。

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 for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

endo-BCN-PEG2-acid is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

endo-BCN-PEG2-alcohol is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker 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 which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

endo-BCN-PEG3-NH-Boc is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.

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

endo-BCN-PEG4-Boc is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.