2. Anti-infection Metabolic Enzyme/Protease Apoptosis Membrane Transporter/Ion Channel Neuronal Signaling
  3. Antibiotic Bacterial HIF/HIF Prolyl-Hydroxylase Apoptosis MDM-2/p53 Potassium Channel Calcium Channel
  4. Minocycline

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。

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Minocycline Chemical Structure

Minocycline Chemical Structure

CAS No. : 10118-90-8

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Minocycline 的其他形式现货产品:

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Minocycline 相关抗体

Top Publications Citing Use of Products

MCE 顾客使用本产品发表的 31 篇科研文献

Proliferation Assay
IF

    Minocycline purchased from MCE. Usage Cited in: J Neuroinflammation. 2018 Aug 30;15(1):245.  [Abstract]

    Immunostaining of the trigeminal nucleus caudalis (TNC) for Iba1 in the NTG group and the NTG+Minocycline (Mino) group on day 9.

    Minocycline purchased from MCE. Usage Cited in: Neurochem Res. 2017 Oct;42(10):2698-2711.  [Abstract]

    a Statistical analysis showing the prevention effect of minocycline pretreatment (40 mg/kg/day) on CUS-, CRS- or CSDS-induced decreases in hippocampal microglial numbers. b, c Statistical analysis showing the prevention effect of minocycline pretreatment (40 mg/kg/day) on CUS-, CRS- or CSDS-induced increases in the immobile time in the TST (b) and FST (c).

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    HIF-1α HIF

    • 生物活性

    • 纯度 & 产品资料

    • 参考文献

    生物活性

    Minocycline is an orally active, potent and BBB-penetrated semi-synthetic tetracycline antibiotic. Minocycline is a hypoxia-inducible factor (HIF)-1α inhibitor. Minocycline shows anti-cancer, anti-inflammatory, and glutamate antagonist effects. Minocycline reduces glutamate neurotransmission and shows neuroprotective properties and antidepressant effects. Minocycline inhibits bacterial protein synthesis through binding with the 30S subunit of the bacterial ribosome, resulting in a bacteriostatic effect[1][2][3][4][5][6][7].

    IC50 & Target

    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].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Minocycline 相关抗体:

    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 IC50 values 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].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    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
    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.
    纯度 & 产品资料
    参考文献

    Minocycline 相关分类

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    Keywords:

    Minocycline10118-90-8AntibioticBacterialHIF/HIF Prolyl-HydroxylaseApoptosisMDM-2/p53Potassium ChannelCalcium ChannelHypoxia-inducible factorsHIFsHIF-PHKcsACa2+ channelsCa channelscerebral ischemianeuroprotectivestrokeVentricular arrhythmiaMyocardial ischemiaPI3K/AktMitochondrial ATP-sensitive potassiumL-type Ca2+ channelacinetobacterinfectionovarian cancerInhibitorinhibitorinhibit

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