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2206-20-4

中文名稱 3-Α-氨基膽甾烷(3AC)
英文名稱 Cholestan-3-aMine, (3α,5α)-
CAS 2206-20-4
分子式 C27H49N
分子量 387.68
MOL 文件 2206-20-4.mol
更新日期 2023/03/20 15:41:27
2206-20-4 結(jié)構(gòu)式 2206-20-4 結(jié)構(gòu)式

基本信息

中文別名
3Α-氨基膽甾烷
3-Α-氨基膽甾烷(3AC)
3偽-AMINOCHOLESTANE
5ALPHA-膽甾烷-3ALPHA-胺
SHIP1抑制劑(3Α-AMINOCHOLESTANE)
英文別名
3α-Aminocholestane
3alpha-Aminocholestane
(3α,5α)-Cholestan-3-amine
3-a-aMinocholestane (3AC)
Cholestan-3-aMine, (3α,5α)-
5alpha-Cholestan-3alpha-amine

物理化學(xué)性質(zhì)

熔點104.5-105.5℃ (methanol )
沸點160 °C(Press: 0.1 Torr)
密度0.930±0.06 g/cm3(Predicted)
儲存條件-20°C儲存
溶解度Chloroform: 30 mg/ml
酸度系數(shù)(pKa)10.94±0.70(Predicted)
形態(tài)固體
顏色White to off-white

常見問題列表

生物活性
3α-Aminocholestane 是含有選擇性 SH2 結(jié)構(gòu)域的肌醇-5'-磷酸酶 1 (SHIP1) 的抑制劑,其 IC50 值約為 2.5 μM。
靶點

IC50: 2.5 μM (SHIP1)

體外研究

OPM2 cell viability is effectively reduced by 3α-Aminocholestane (3AC) treatment. RPMI8226 and U266 cells show significantly less sensitivity to 3α-Aminocholestane treatment when compare with OPM2 cells, although viability is decreased significantly at concentrations of ≥12.5 μM. Treatment with 3α-Aminocholestane for 36 h severely reduces the percentage of cells in the S phase, which is accompanied by an increase of cells in the G2/M phase. In contrast, in the less proliferative RPMI8226 and U266 cells, cell cycle progression is blocked in the G0/G1 phase upon 3α-Aminocholestane treatment, in conjunction with a reduced percentage of cells undergoing the S phase.

體內(nèi)研究

It is found that 3α-Aminocholestane (3AC) results in reduced multiple myeloma (MM) growth in vivo , as determined by quantitation of free human Igλ light chain in the plasma after OPM2 challenge. In addition, reduced numbers of circulating OPM2 cells, as determined by human HLA-ABC staining, is observed in peripheral blood from 3α-Aminocholestane-treated mice compare with vehicle controls. Most importantly, 3α-Aminocholestane treatment results in significantly enhanced survival of mice after tumor challenge. In 3α-Aminocholestane-treated mice that resist treatment, it is found that MM tumors exhibit an upregulation of SHIP2, reminiscent of in vitro treatment of OPM2 cells and suggesting that SHIP1 inhibition may select for tumor cells with increased SHIP2 expression.

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