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SR-4370
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
SR-4370图片
CAS NO:1816294-67-3
规格:≥98%
包装与价格:
包装价格(元)
5mg电议
10mg电议
25mg电议
50mg电议
100mg电议
250mg电议
500mg电议

产品介绍
理化性质和储存条件
Molecular Weight (MW) 304.34
Formula C17H18F2N2O
CAS No. 1816294-67-3
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)DMSO: ≥ 150 mg/mL
Water:
Ethanol:
Chemical Name N'-butyl-2',3'-difluoro-[1,1'-biphenyl]-4-carbohydrazide
Synonyms SR4370; SR 4370; SR-4370
SMILES Code O=C(C1=CC=C(C2=CC=CC(F)=C2F)C=C1)NNCCCC
实验参考方法
In Vitro

In vitro activity: SR-4370 is an inhibitor of HDAC with IC50 values of 0.13 μM, 0.58 μM, 0.006 μM, 2.3 μM, and 3.4 μM for HDAC1, HDAC2, HDAC3, HDAC8, and HDAC6, respectively. SR-4370 is cytotoxic to the breast cancer cells (MDA-MB-231), with an IC50 of 12.6 μM.


Kinase Assay:


Cell Assay: To assess the ability of the compounds to kill cancer cells, cancer cell lines were treated with various compounds, as shown in FIG. 4. Liver cancer cell line HepG2 was exposed to several compounds with various in vitro HDAC inhibition potencies. The data show that HDAC inhibition potencies of these analogs exhibited excellent correlation with their inhibiton of HepG2 (FIG. 4(A)). Indeed, RLS2- 131 that is 2 to 5-fold more potent than UF010 in inhibiting HDAC1, HDAC2 and HDAC3 is 3-fold more potent against HepG2. By contrast, RLS2-125 that inhibited HDACs to a lesser degree exerted little to no growth inhibition for HepG2. Similar effects were also observed in other cancer cell lines (HCT116, colon; MDA-MB-231 and HCC1957, breast cancer; FIGs. 4 (B)-(D)). These data suggest that HDAC inhibition may be one mechanism for halting cancer cell growth and proliferation. HDAC1, HDAC2 or HDAC3 were depleted with shRNAs to further examine the importance of HDACs for UFO 10 's cellular effects. The cells with shRNA expression were treated with UF010 or RLS2-131. The data presented in Table 3 indicate that HDAC2 shRNA expression reduced UFOlO's cytotoxic potency by about 2-fold in both HepG2 and breast cancer MDA-MB-468 cell lines. HDAC1 depletion also reduced UFOlO-mediated cytotoxicity in HepG2. Similarly, depletion of HDAC1 or HDAC2 also reduced sensitivity of HepG2 cells to RLS2-131. In contrast, HDAC3 depletion markedly sensitized HepG2 cells to both UFO 10 and RLS2-131 (Table 3). One explanation of this may be that pharmacological HDAC3 inhibition coupled with its genetic depletion might result in a dramatic suppression of its functions, leading to a potential synthetic lethal effect. In sum, these data suggest that one mechanism that UFO 10 and other analogs kill cancer cells may be through pharmacological inhibition of HDACs 1-3.

In Vivo
Animal model
Formulation & Dosage
References.html