| 包装 | 价格(元) |
| 500ug | 电议 |
| 1mg | 电议 |
| 5mg | 电议 |
Cell lines | |
Preparation Method | PC12 cells were rinsed with serum-free medium and treated with serum-free medium (with or without 100 µm Decanoyl-RVKR-CMK) for 3 h (basal release) and finally with serum-free medium containing 50 mm KCl (with or without 100 µm Decanoyl-RVKR-CMK) for 3 h. |
Reaction Conditions | 100 µm Decanoyl-RVKR-CMK for 3h |
Applications | PC12 cells were treated with the PC enzyme inhibitor Decanoyl-RVKR-CMK to partially block the regulated release of VGF. VGF treatment in cell extracts and culture medium from Decanoyl-RVKR-CMK-treated PC12 reduced the culture, indicating extensive inhibition of invertase activity at these Decanoyl-RVKR-CMK concentrations. |
Animal models | K5-PACE4 transgenic mice |
Preparation Method | In mice topically treated with the hyperplasiogenic phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), a 2-day topical treatment of Decanoyl-RVKR-CMK at 300 uM. |
Dosage form | Decanoyl-RVKR-CMK was locally treated at 300 µM for 2 days; Once daily for 3 weeks |
Applications | When used Decanoyl-RVKR-CMK. PACE4 activity in skin squamous cell carcinoma cell lines resulted in impaired insulin-like growth factor 1 receptor maturation, diminished its intrinsic tyrosine kinase activity, and decreased tumor cell proliferation. Two-stage skin chemical carcinogenesis experiments, together with topical applications of CMK, demonstrated that Decanoyl- Decanoyl-RVKR-CMK markedly reduced tumor incidence, tumor multiplicity, and metastasis, pointing to a significant delay in tumor progression in wild-type and PACE4 transgenic mice. |
| 产品描述 | Decanoyl-RVKR-CMK is a subtilisin/Kex2p-like proprotein convertase inhibitor; blocks activity of all seven convertases (PC1, PC2, PC4, PACE4, PC5, PC7 and furin)[4]. Decanoyl-RVKR-CMK inhibits cleavage of SARS-CoV-2 spike protein by furin and blocks viral cell entry (IC50 = 57 nM in plaque reduction assay)[9]. PC12 cells were treated with the PC enzyme inhibitor Decanoyl-RVKR-CMK to partially block the regulated release of VGF. VGF treatment in cell extracts and culture medium from Decanoyl-RVKR-CMK-treated PC12 reduced the culture, indicating extensive inhibition of invertase activity at these Decanoyl-RVKR-CMK concentrations[2]. Decanoyl-RVKR-CMK inhibits cleavage of glycoprotein B of human cytomegalovirus[8]. Decanoyl-RVKR-CMK promotes ciliated cell differentiation and has no effect on the ciliary beat frequency in air-liquid interface (ALI) cultures of human nasal epithelial cells (HNECs). CMK considerably increases ciliogenesis-related gene expression. CMK inhibited Notch1 processing and promoted regeneration and ciliogenesis of the mouse nasal respiratory epithelium after ZnSO4 injury[7]. In LoVo cell, Decanoyl-RVKR-CMK strongly reduced the recovery of sAPPα, Overexpression of Decanoyl-RVKR-CMK at high concentrations did not completely eliminate sAPP α-secretion[3]. Decanoyl-RVKR-CMK blocked entry of MERS-CoV harboring an S protein lacking furin cleavage sites; it even blocked entry into furin-deficient LoVo cells. In addition, Decanoyl-RVKR-CMK inhibited not only the enzymatic activity of furin but also those of cathepsin L, cathepsin B, trypsin, papain, and TMPRSS2[5]. Decanoyl-RVKR-CMK inhibits HIV-2ROD replication by blocking envelope glycoprotein precursor processing in the Jurkat lymphocyte cell[1]. When used Decanoyl-RVKR-CMK. PACE4 activity in skin squamous cell carcinoma cell lines resulted in impaired insulin-like growth factor 1 receptor maturation, diminished its intrinsic tyrosine kinase activity, and decreased tumor cell proliferation. Two-stage skin chemical carcinogenesis experiments, together with topical applications of CMK, demonstrated that Decanoyl-RVKR-CMK markedly reduced tumor incidence, tumor multiplicity, and metastasis, pointing to a significant delay in tumor progression in wild-type and PACE4 transgenic mice[6]. References: |
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