NADI-351|CAS 2503017-11-4|DC Chemicals

Cas No.:	2503017-11-4
Chemical Name:	NADI-351
Synonyms:	3-Thiazolidineacetamide, 5-[1-[3-fluoro-5-methoxy-4-(1H-1,2,4-triazol-5-ylmethoxy)phenyl]ethylidene]-N,N-dimethyl-4-oxo-2-thioxo-, (5Z)-
SMILES:	S1/C(=C(\C2=CC(OC)=C(OCC3NN=CN=3)C(F)=C2)/C)/C(=O)N(CC(N(C)C)=O)C1=S
Formula:	C₁₉H₂₀FN₅O₄S₂
M.Wt:	465.521604537964
Purity:	>98%
Sotrage:	2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

Cat. No.	Product name	Field of application
DC74459	Z271-0326	Z271-0326 is a first-in-class, potent and specifc inhibitor of NACK (Notch activation complex kinase) with SPR KD value of 0.89 uM, directly blocks NACK recruitment to the Notch ternary complex (NTC).
DC70635	NADI-351	NADI-351 is a specific small-molecule inhibitor of Notch1 transcriptional complexes with IC50 of 8.8 uM in cellualr reporter assays.NADI-351 inhibited OE33 cell growth in single dose MTT assays (EC50= 10 uM) and, more potently, in multi-dose colony formation assays (EC50=1.3 uM)NADI-351 is 15 times more potent than IMR-1 in an NTC AlphaScreen assay.NADI-351 selectively disrupted Notch1 transcription complexes, inhibited recruitment of Notch1 to the NTC (Notch Ternary Complex) and to the HES1 promoter, and reduced Notch1 recruitment to target genes.NADI-351 inhibits tumor growth in Notch-dependent cancers and does not exert gastrointestinal toxicity associated with goblet cell metaplasia.NADI-351 selectively inhibits stem-like esophageal adenocarcinoma (EAC) cell populations.
DC28774	CB-103	CB-103 is a notch signaling pathway inhibitor extracted from patent US9296682B2. CB-103 is developed for the treatment of cancers.
DC11017	ZLDI-8	ZLDI-8 (IAC-8) is a novel Notch signaling pathway inhibitor for Notch activating/cleaving enzyme ADAM-17, significantly decreases the level of NICD and accumulation of NICD in the nucleus; exhibits cytotoxic acitviity against MHCC97-H cells with IC50 of 5.32 uM, reduces the expression of pro-survival/anti-apoptosis regulators, Survivin and cIAP1/2, also increases the expression of epithelial marker E-Cadherin and reduces mesenchymal markers N-Cadherin and Vimentin in HCC cells; significantly disrupted the activity of Notch pathway in HCC cells and inhibits the epithelial-mesenchymal transition (EMT) process of HCC cells; ZLDI-8 treatment enhances the susceptibility of HCC cells to Sorafenib, Etoposide, and Paclitaxel both in vitro and in vivo.