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Minocycline
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。
Minocycline图片
CAS NO:10118-90-8
包装与价格:
包装价格(元)
100mg电议
250mg电议
500mg电议

产品介绍
Minocycline 是一种口服有效、能透过血脑屏障的半合成四环素类抗生素。Minocycline 是一种缺氧诱导因子 (HIF-1α) 抑制剂。Minocycline 具有抗癌(anti-cancer),抗炎(anti-inflammatory) 和谷氨酸 (glutamate) 拮抗作用。Minocycline 降低谷氨酸神经传递,显示神经保护特性和抗抑郁作用。Minocycline 通过与细菌核糖体 30S 亚基结合,抑制细菌蛋白的合成,从而产生抑菌 (bacteriostatic) 作用。
生物活性

Minocycline is an orally active, potent and BBB-penetrated semi-synthetictetracyclineantibiotic. Minocycline is ahypoxia-inducible factor (HIF)-1αinhibitor. Minocycline showsanti-cancer,anti-inflammatory, andglutamateantagonist effects. Minocycline reduces glutamate neurotransmission and shows neuroprotective properties and antidepressant effects. Minocycline inhibitsbacterialprotein synthesis through binding with the 30S subunit of thebacterialribosome, resulting in abacteriostaticeffect[1][2][3][4][5][6][7].

IC50& Target

Tetracycline

 

L-type calcium channel

 

体外研究
(In Vitro)

Minocycline (0-100 μM, 24-72 h) suppresses proliferation and clonogenic activity of ovarian cancer cell-lines (OVCAR-3, SKOV-3 and A2780)[3].
Minocycline (0-100 μM, 24-48 h)arrests cell cycle through inhibition of cyclins and suppression of DNA incorporation[3].
Minocycline (0-100 μM, 72 h) induces cell apoptosis in ovarian cancer cell lines[3].
Minocycline shows direct neuronal protection, and this mode of protection is likely to be associated with the preservation of mitochondrial integrity and cytochrome c, followed by the suppression of caspase-dependent as well as caspase-independent cell death[2].
Minocycline leads to suppression of Hypoxia-inducible factor (HIF)-1α accompanied by up-regulation of p53 protein levels and inactivation of AKT/mTOR/p70S6K/4E-BP1 pathway[6].

Cell Proliferation Assay[3]

Cell Line:Human ovarian cancer cell lines (OVCAR-3, SKOV-3 and A2780) and primary cells (HEK-293, HMEC, HUVEC, ATCC)
Concentration:0, 1, 10, 50 and 100 μM
Incubation Time:24, 48 or 72 h
Result:Inhibited proliferation of OVCAR-3, SKOV-3 and A2780 cells in a concentration-dependent manner, with IC50values of 62.0, 56.1 and 59.5 μM, respectively. Had no effect on the viability of HEK-293 or HUVEC.

Cell Cycle Analysis[3]

Cell Line:OVCAR-3, SKOV-3 and A2780 cells
Concentration:0, 10, 50 and 100 μM
Incubation Time:24 or 48 h
Result:Arrested cells in the G0-G1 phase in a concentration and time-dependent manner. Declined percentage of cells in the S and G2-M phases in excess of 80% each at 100 μM.

Western Blot Analysis[3]

Cell Line:OVCAR-3, SKOV-3 and A2780 cells
Concentration:0, 10, 50 and 100 μM
Incubation Time:72 h
Result:Expressed lower levels of cyclins A, B and E. Increased caspase-3 levels by more than 3.0 fold in the 100 μM. Minocycline-activated caspase-3 in turn led to cleavage of PARP-1. Increased the degradation product p89 of PARP-1 by caspase-3.
体内研究
(In Vivo)

Minocycline (0-30 mg/kg, orally, daily for 4 weeks) suppresses OVCAR-3 tumor growth in female nude mice[3].
Minocycline (IP) is an effective neuroprotective agent in animal models of cerebral ischemia when given in high doses intraperitoneally[1].
Minocycline (0-40 mg/kg, IP, once) significantly attenuats METH-induced hyperlocomotion and the development of behavioral sensitization in mice[2].
Minocycline (3 and 10 mg/kg, IV, once) is effective at reducing infarct size in a Temporary Middle Cerebral Artery Occlusion model (TMCAO)[1].
Minocycline (3-10 mg/kg, IV, once) results in serum levels (at 3 mg/kg) similar to that achieved in humans after a standard 200 mg dose[1].
Minocycline attenuates ischemia-induced ventricular arrhythmias in rats. This effect may be associated with activations of PI3K/Akt signaling pathway, mitochondrial KATP channels and L-type Ca2+ channels[7].

Animal Model:Female nude mice (6 weeks old, 9 per group, OVCAR-3 cells were injected s.c. into the left flank of each mouse)[3]
Dosage:10 or 30 mg/kg
Administration:Administered orally in the drinking water, initiated on day 8 of cell inoculation, daily for 4 weeks
Result:Suppressed OVCAR-3 tumor growth in these female nude mice, and reduced microvessel density.
Animal Model:Male Balb/cAnNCrICrIj mice (8 weeks old, 23-30 g, methamphetamine (METH, 3 mg/kg) was injected subcutaneously (s.c.) in a volume of 10 ml/kg)[2]
Dosage:0, 10, 20, or 40 mg/kg
Administration:IP, once, 30 min before the administration of METH
Result:Significantly attenuated METH-induced hyperlocomotion and the development of behavioral sensitization in mice at 40 mg/kg. Did not exert any effect on the induction of METH-induced hyperthermia in mice. Significantly attenuated the reduction of DA and DOPAC in the striatum. Significantly attenuated the reduction of DAT-immunoreactivity in the mouse striatum. Significantly attenuated the increase in MAC1-immunoreactivity in the striatum after the administration of METH.
Animal Model:Male Sprague-Dawley rats (270-330 g, TMCAO model)[1]
Dosage:3 mg/kg and 10 mg/kg
Administration:IV, once, 4, 5, or 6 hours post TMCAO
Result:Reduced infarct size by 42% while 10 mg/kg reduced infarct size by 56% at doses of 3 mg/kg; significantly reduced infarct size at 5 hours by 40% at doses of 10 mg/kg and the 3 mg/kg dose significantly reduced infarct size by 34%. With a 6 hour time window there was a non-significant trend in infarct reduction.
Animal Model:Male Sprague-Dawley rats (270-330 g)[1]
Dosage:3, 10, or 20 mg/kg
Administration:IV, once
Result:Peak concentrations of serum levels of minocycline averaged 3.6, 13.0 and 28.8 mg/L with 3, 10 and 20 mg/kg doses respectively. The serum levels of minocycline at a 3 mg/kg dose (3.6 mg/L) were similar to that reported in humans after a standard 200 mg dose. Did not significantly affect hemodynamic and physiological variables.
Clinical Trial
分子量

457.48

Formula

C23H27N3O7

CAS 号

10118-90-8

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.