| 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 |
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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. |
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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. |
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| 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. |
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