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  3. Minocycline hydrochloride

Minocycline hydrochloride 

Cat. No.: HY-17412 Purity: 99.71%
Handling Instructions

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

For research use only. We do not sell to patients.

Minocycline hydrochloride Chemical Structure

Minocycline hydrochloride Chemical Structure

CAS No. : 13614-98-7

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Customer Review

Based on 19 publication(s) in Google Scholar

Top Publications Citing Use of Products

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

    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).

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

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

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    Description

    Minocycline hydrochloride is an orally active, potent and BBB-penetrated semi-synthetic tetracycline antibiotic. Minocycline hydrochloride is a hypoxia-inducible factor (HIF)-1α inhibitor. Minocycline hydrochloride shows anti-cancer, anti-inflammatory, and glutamate antagonist effects. Minocycline hydrochloride reduces glutamate neurotransmission and shows neuroprotective properties and antidepressant effects. Minocycline hydrochloride 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

     

    In Vitro

    Minocycline hydrochloride (0-100 μM, 24-72 h) suppresses proliferation and clonogenic activity of ovarian cancer cell-lines (OVCAR-3, SKOV-3 and A2780)[3].
    Minocycline hydrochloride (0-100 μM, 24-48 h)arrests cell cycle through inhibition of cyclins and suppression of DNA incorporation[3].
    Minocycline hydrochloride (0-100 μM, 72 h) induces cell apoptosis in ovarian cancer cell lines[3].
    Minocycline hydrochloride 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 hydrochloride 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.

    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.

    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.

    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.
    In Vivo

    Minocycline hydrochloride (0-30 mg/kg, orally, daily for 4 weeks) suppresses OVCAR-3 tumor growth in female nude mice[3].
    Minocycline hydrochloride (IP) is an effective neuroprotective agent in animal models of cerebral ischemia when given in high doses intraperitoneally[1].
    Minocycline hydrochloride (0-40 mg/kg, IP, once) significantly attenuats METH-induced hyperlocomotion and the development of behavioral sensitization in mice[2].
    Minocycline hydrochloride (3 and 10 mg/kg, IV, once) is effective at reducing infarct size in a Temporary Middle Cerebral Artery Occlusion model (TMCAO)[1].
    Minocycline hydrochloride (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 hydrochloride 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
    Molecular Weight

    493.94

    Formula

    C23H28ClN3O7

    CAS No.
    SMILES

    OC1=C(C(N)=O)C([[email protected]@]2(O)C(O)=C3C(C4=C(O)C=CC(N(C)C)=C4C[[email protected]@]3([H])C[[email protected]@]2([H])[[email protected]@H]1N(C)C)=O)=O.Cl

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

    4°C, sealed storage, away from moisture

    *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

    Solvent & Solubility
    In Vitro: 

    H2O : 10 mg/mL (20.25 mM; Need ultrasonic)

    DMSO : 0.49 mg/mL (0.99 mM; Need ultrasonic and warming)

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.0245 mL 10.1227 mL 20.2454 mL
    5 mM 0.4049 mL 2.0245 mL 4.0491 mL
    10 mM 0.2025 mL 1.0123 mL 2.0245 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  PBS

      Solubility: 7.69 mg/mL (15.57 mM); Clear solution; Need ultrasonic

    *All of the co-solvents are available by MCE.
    References

    Purity: 99.71%

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    Minocycline hydrochloride
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