EC359

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

EC359 是一种有效的，选择性的，高亲和力的和口服的生物利用度白血病抑制因子受体 (LIFR) 抑制剂，其 Kd 值为 10.2 nM，可直接与 LIFR 相互作用以有效阻断 LIF/LIFR 相互作用。EC359 是一种点击化学试剂。它含有 Alkyne 基团，可以和含有 Azide 基团的分子发生铜催化的叠氮-炔环加成反应 (CuAAc)。

EC359 is a potent, selective, high affinity and orally active leukemia inhibitory factor receptor (LIFR) inhibitor with a Kd of 10.2 nM, which directly interacts with LIFR to effectively block LIF/LIFR interactions. EC359 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

EC359 (0-100 nM; 3 days; BT-549, SUM-159, MDA-MB-231, MDA-MB-468, and HCC1806 cells) treatment reduces cell viability in a dose-dependent manner.EC359 (20 nM, 25 nM; 72 hours; MDA-MB-231 and BT-549 cells) treatment significantly increases caspase-3/7 activity and Annexin V-positive cells in both MDAMB-231 and BT-549 cells. EC359 exhibits significant inhibitory activity on invasion and promotes apoptosis of TNBC cells.EC359 (100 nM; 12 hours; BT549 cells) treatment significantly reduces the expression of several (such as STAT1 TGFB1, JUNB, MCL-1, etc) known STAT3 target genes.EC359(100 nM; 1 hour; MDA-MB-231 and BT-549 cells) treatment substantially reduces the LIF activation of STAT3, also reduces the STAT3 activation by OSM and CNTF. EC359 treatment substantially decreases the phosphorylation of AKT, mTOR, S6, and ERK1/2 in MDA-MB231 and BT-549 cells. EC359 treatment also increases the phosphorylation of proapoptotic p38MAPK in BT549 cells.:Cell Viability Assay Cell Line:BT-549, SUM-159, MDA-MB-231, MDA-MB-468, and HCC1806 cells Concentration:0 nM, 1.5 nM, 12.5 nM, 25 nM, 50 nM, 100 nM Incubation Time:3 days Result:Reduced cell viability in a dose-dependent manner.Apoptosis Analysis Cell Line:MDA-MB-231 and BT-549 cells Concentration: 20 nM, 25 nM Incubation Time:72 hours Result:Promoted apoptosis of TNBC cells.RT-PCR Cell Line:BT549 cells Concentration:100 nM Incubation Time:12 hours Result:Reduced the expression of several known STAT3 target genes.Western Blot Analysis Cell Line:MDA-MB-231 and BT-549 cells Concentration:100 nM Incubation Time:1 hour Result:Substantially reduced the LIF activation of STAT3, reduced the STAT3 activation by OSM and CNTF, decreased the phosphorylation of AKT, mTOR, S6, and ERK1/2 in both BT-549 and MDA-MB-231 cells andincreased the phosphorylation of proapoptotic p38MAPK in BT549 cells.

EC359 (5 mg/kg; subcutaneous injection; 3 days per week; for 25 days; female athymic nude mice) treatment significantly reduces the tumor progression. The body weights of mice in EC359-treated groups remains unchanged confirming the low toxicity of EC359.Animal Model:8-week-old female athymic nude mice with MDA-MB-231 cells Dosage:5 mg/kg Administration:Subcutaneous injection; 3 days per week; for 25 days Result:Significantly reduced the tumor progression.

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Apoptosis

Apoptosis

Apoptosis

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2012591-09-0

540.68

C36H38F2O2

>98% (HPLC)

In Vitro:?DMSO 中的溶解度 : 125 mg/mL (231.19 mM; 超声助溶 )

[H][C@@]12CC[C@@](O)(C(F)(F)C#C)[C@@]1(C)C[C@@H](C1=C3CCC(=O)C=C3CC[C@@]21[H])c1ccc(cc1)-c1c(C)cc(C)cc1C

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(-20℃)

With Ice Pack

≥ 2 years