CC-885

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CC-885

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。

CAS NO:	1010100-07-8
规格:	≥98%

包装与价格：

包装	价格(元)
10mg	询价
25mg	询价
50mg	询价
100mg	询价
250mg	询价
500mg	询价

理化性质和储存条件

	Name: CC-885 CAS#: 1010100-07-8 Chemical Formula: C22H21ClN4O4 Exact Mass: 440.1251 Molecular Weight: 440.884
Storage	-20℃ for 3 years in powder form
Storage	-80℃ for 2 years in solvent
Technical Information	Synonym: CC885, CC-885, CC 885. Chemical Name: N-(3-chloro-4-methylphenyl)-N'-[[2-(2,6-dioxo-3-piperidinyl)-2,3-dihydro-1-oxo-1H-isoindol-5-yl]methyl]-urea InChi Key: DOEVCIHTTTYVCC-UHFFFAOYSA-N InChi Code: InChI=1S/C22H21ClN4O4/c1-12-2-4-15(9-17(12)23)25-22(31)24-10-13-3-5-16-14(8-13)11-27(21(16)30)18-6-7-19(28)26-20(18)29/h2-5,8-9,18H,6-7,10-11H2,1H3,(H2,24,25,31)(H,26,28,29) SMILES Code: O=C(NCC1=CC2=C(C(N(C(CC3)C(NC3=O)=O)C2)=O)C=C1)NC4=CC=C(C)C(Cl)=C4

实验参考方法

In Vitro	Acute myeloblatlic leukemia (AML) cell lines, human liver epithelial cell line (THLE-2) and human peripheral blood mononuclear cells (PBMC) are treated with varying concentrations of CC-885, with IC50s of 10×-6-1 μM. The effect of CC-885 on cell proliferation in AML cell lines, THLE-2 and human PBMC is more powerful than Lenalidomide and Pomalidomide with IC50s>10 μM. To address whether the cereblon-dependent degradation of GSPT1 is responsible for the cytotoxic effects of CC-885, a GSPT1 mutant that retains its normal function, but loses CC-885-dependent cereblon binding, is used to distinguish the role of GSPT1 from that of other substrates. CC-885 is tested in 293T HEK cells stably expressing the CC-885-sensitive or -resistant GSPT1 variants. Overexpression of a resistant variant GSPT1Δ(1–138)/(G575N) completely abrogate the CC-885-induced anti-proliferation, whereas overexpression of a CC-885-sensitive variant GSPT1Δ(1-138) only confer partial protection. Similar results are obtained in AML cell lines[1].
In Vivo	The study assessed the therapeutic efficacy of this combination in vivo by using nude mice bearing tumors. While volasertib and CC-885 alone inhibited tumor growth, the combination of both small molecular drugs markedly inhibited tumor growth and reduced tumor weights (Figures 1I and IJ). Taken together, these data clearly show that CC-885 synergizes with volasertib against NSCLC cells both in vitro and in vivo.

In Vitro

Acute myeloblatlic leukemia (AML) cell lines, human liver epithelial cell line (THLE-2) and human peripheral blood mononuclear cells (PBMC) are treated with varying concentrations of CC-885, with IC50s of 10×-6-1 μM. The effect of CC-885 on cell proliferation in AML cell lines, THLE-2 and human PBMC is more powerful than Lenalidomide and Pomalidomide with IC50s>10 μM. To address whether the cereblon-dependent degradation of GSPT1 is responsible for the cytotoxic effects of CC-885, a GSPT1 mutant that retains its normal function, but loses CC-885-dependent cereblon binding, is used to distinguish the role of GSPT1 from that of other substrates. CC-885 is tested in 293T HEK cells stably expressing the CC-885-sensitive or -resistant GSPT1 variants. Overexpression of a resistant variant GSPT1Δ(1–138)/(G575N) completely abrogate the CC-885-induced anti-proliferation, whereas overexpression of a CC-885-sensitive variant GSPT1Δ(1-138) only confer partial protection. Similar results are obtained in AML cell lines[1].

In Vivo

The study assessed the therapeutic efficacy of this combination in vivo by using nude mice bearing tumors. While volasertib and CC-885 alone inhibited tumor growth, the combination of both small molecular drugs markedly inhibited tumor growth and reduced tumor weights (Figures 1I and IJ). Taken together, these data clearly show that CC-885 synergizes with volasertib against NSCLC cells both in vitro and in vivo.