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1784282-12-7

中文名稱 鹽酸KHS101
英文名稱 KHS101 hydrochloride
CAS 1784282-12-7
更新日期 2024/06/25 17:15:55
分子式 C18H22ClN5S
分子量 375.92
MOL 文件 1784282-12-7.mol
1784282-12-7 結(jié)構(gòu)式 1784282-12-7 結(jié)構(gòu)式

基本信息

中文別名
鹽酸KHS101
英文別名
KHS101 hydrochloride
所屬類別
生物化工:抑制劑

物理化學性質(zhì)

溶解度Soluble to 50 mM in DMSO and to 50 mM in ethanol
形態(tài)Solid
顏色White to off-white

常見問題列表

生物活性
KHS101是TACC3的小分子抑制劑,TACC3是中心體微管動態(tài)網(wǎng)絡中的關(guān)鍵組分。
靶點
TargetValue
TACC3
()
體外研究

KHS101 increases neuronal differentiation of adherently cultured rat NPCs in a dose-dependent fashion (EC 50 ~1 μM). KHS101-induced neuron formation (40-60% TuJ1+ cells at 1.5–5 μM KHS101) is also observed under neurosphere-forming conditions in secondary neurospheres derived from both the hippocampus and the subventricular zone (SVZ) of adult rats. Moreover, hippocampal NPCs treated with KHS101 and cultured adherently on microelectrode arrays for 12 d exhibit neuronal morphologies as well as spontaneous spiking activity, hence indicating the presence of functional, maturing neurons. KHS101 markedly attenuates tumor cell growth as compared to the cells treated with the vehicle [dimethyl sulfoxide (DMSO)]. TACC3 is a known target of KHS101 in rodent neural progenitor cells. KHS101 has been shown to cause cellular destabilization of TACC3, hence reducing endogenous TACC3 protein levels over time .

體內(nèi)研究

Tumor cell proliferation is markedly reduced in KHS101-treated tumors (about twofold). KHS101-treated tumors show signs of elevated cell death (reduced cellularity/increased pyknosis) compared with tumors treated with vehicle control. KHS101 treatment markedly reduces both frontal-to-caudal tumor expansion and corpus callosum invasion of vimentin-positive GBM1 cells. It is also found that the survival of animals carrying GBMX1 tumors (established 2 or 6 weeks before treatment) is markedly increased by the KHS101 treatment regimen for 10 weeks. None of the mice have to be removed from the study because of adverse side effects of the treatment. An additional experiment using a continuous KHS101 treatment regimen until the experimental endpoints also shows a marked increase in the survival of GBMX1-bearing animals. Histological endpoint analysis of KHS101- and vehicle-treated animals confirms a significantly decreased tumor size in KHS101-treated mice.

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