OVCAR-3, SKOV-3, and A2780 pearl cotton lines are inhibited in terms of proliferation and clonogenic activity by minocycline hydrochloride (0-100 μM, 24-72 hours) [3]. Hydrochloride of minocycline (0-100 μM, 24-48 hours). In an oscilloscope, minocycline hydrochloride (0-100 μM, 72 h)) causes a cell cycle [3]. In addition to inhibiting both caspase-dependent and caspase-independent cell death, direct neural protection may also be linked to mitochondrial abnormalities and cytochrome c protection [2]. Examination of the proliferation of hypoxia-inducible factor (HIF) cells induced by minocycline hydrochloride [3]

In female nude mice, ovccrine hydrochloride (0–30 mg/kg) administered intravenously once daily for four weeks inhibits the growth of OVCAR-3 tumors [3]. In animal models of brain damage, minocycline hydrochloride (IP), a powerful medication, exhibits neuroprotective effects when administered intraperitoneally in high dosages [1]. METH-induced hyperlocomotion and behavioral sensitization in mice are markedly inhibited by minocycline hydrochloride (0–40 mg/kg, IP, once) [2]. In a model of temporary middle cerebral artery occlusion (TMCAO), minocycline hydrochloride (3 and 10 mg/kg IV once) effectively reduces infarct size [1]. The effects of minocycline hydrochloride (3–10 mg/kg IV once) on blood may be mitigated by potential-induced ventricular arrhythmias. This effect in humans at the standard 200 mg dose may be associated with mitochondrial KATP channels, PI3K/Akt signaling, and L-type levels (3 mg/kg) [1].

Cell Proliferation Assay[3]
Cell Types: human ovarian cancer cell line (OVCAR-1α inhibition, and regulation of up-p53 protein and AKT levels/mTOR/p70S6K/ Inactivation of 4E-BP1 dye [6]. 3. SKOV-3 and A2780) and primary cells (HEK-293, HMEC, HUVEC, ATCC)
Tested Concentrations: 0, 1, 10, 50 and 100 μM
Incubation Duration: 24 , 48 or 72 hrs (hours)
Experimental Results: Inhibition of the proliferation of OVCAR-3, SKOV-3 and A2780 cells was concentration-dependent, with IC50 values of 62.0, 56.1 and 59.5 μM respectively. There was no effect on the viability of HEK-293 or HUVEC.

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Western Blot Analysis[3]
Cell Types: OVCAR-3, SKOV-3 and A2780 Cell
Tested Concentrations: 0, 10, 50 and 100 μM
Incubation Duration: 72 hrs (hours)
Experimental Results: Cyclins A, B and E were expressed at low levels. caspase- increasing by 3 levels increased more than 3.0-fold at 100 μM. Minocycline-activated caspase-3 in turn leads to the cleavage of PARP-1. Caspase-3 increases the degradation product of PARP-1, p89.

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Cell cycle analysis[3]
Cell Types: OVCAR-3, SKOV-3 and A2

Animal/Disease Models: Female nude mice (6 weeks old, 9 mice per group, each mouse was injected with OVCAR-3 cells subcutaneously (sc) (sc) on the left side of the abdomen) [3]
Doses: 10 or 30 mg/kg
Route of Administration: Orally in drinking water Administration, starting on day 8 of cell inoculation, one time/day for 4 weeks.
Experimental Results: Inhibited OVCAR-3 tumor growth and diminished microvessel density in these female nude mice.

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Animal/Disease Models: Male Balb/cAnNCrICrIj mice (8 weeks old, 23-30 g, methamphetamine (METH, 3 mg/kg) subcutaneously (sc) (sc) (sc) in a volume of 10 ml/kg) [2]
Doses: 0, 10 , 20 or 40 mg/kg
Route of Administration: intraperitoneal (ip) injection, once, 30 minutes before METH administration
Experimental Results: 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.

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Animal/Disease Models: Male Sprague-Dawley rats (270-330 g, TMCAO model)[1]
Doses: 3 mg/kg and 10 mg/kg
Route of Administration: IV, once, 4, 5, or 6 hours post TMCAO
Experimental Results: 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.

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Animal/Disease Models: Male Sprague-Dawley rats (270-330 g)[1]
Doses: 3, 10, or 20 mg/kg
Route of Administration: IV, once
Experimental Results: 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.

[1]. Xu L, et al. Low dose intravenous minocycline is neuroprotective after middle cerebral artery occlusion-reperfusion in rats. BMC Neurol. 2004 Apr 26;4:7.
[2]. Zhang L, et al. Protective effects of minocycline on behavioral changes and neurotoxicity in mice after administration of methamphetamine. Prog Neuropsychopharmacol Biol Psychiatry. 2006 Dec 30;30(8):1381-93.
[3]. Pourgholami MH, et al. Minocycline inhibits growth of epithelial ovarian cancer. Gynecol Oncol. 2012 May;125(2):433-40.
[4]. Molina-Hernández M, et al. Antidepressant-like actions of minocycline combined with several glutamate antagonists. Prog Neuropsychopharmacol Biol Psychiatry. 2008 Feb 15;32(2):380-6.
[5]. Ritchie DJ, et al. A review of intravenous minocycline for treatment of multidrug-resistant Acinetobacter infections. Clin Infect Dis. 2014 Dec 1;59 Suppl 6:S374-80.
[6]. Ataie-Kachoie P, et al. Minocycline attenuates hypoxia-inducible factor-1α expression correlated with modulation of p53 and AKT/mTOR/p70S6K/4E-BP1 pathway in ovarian cancer: in vitro and in vivo studies. Am J Cancer Res. 2015 Jan 15;5(2):575-88.
[7]. Hu X, Wu B, Wang X, Xu C, He B, Cui B, Lu Z, Jiang H. Minocycline attenuates ischemia-induced ventricular arrhythmias in rats. Eur J Pharmacol. 2011 Mar 11;654(3):274-9.

C23H28CLN3O7

493.9373

13614-98-7

Minocycline;10118-90-8

O=C([C@@]1(O)[C@@](C[C@]2([H])C(C1=O)=C(O)C3=C(O)C=CC(N(C)C)=C3C2)([H])[C@@H]4N(C)C)/C(C4=O)=C(N)/O.[H]Cl

KDLQIOPKJDNQIM-YKWOUSISSA-N

InChI=1S/C23H27N3O7.ClH/c1-25(2)12-5-6-13(27)15-10(12)7-9-8-11-17(26(3)4)19(29)16(22(24)32)21(31)23(11,33)20(30)14(9)18(15)28;/h5-6,9,11,17,27-28,32-33H,7-8,24H2,1-4H3;1H/b22-16+;/t9-,11-,17+,23-;/m1./s1

(4S,4aR,5aS,12aR,E)-2-(amino(hydroxy)methylene)-4,7-bis(dimethylamino)-10,11,12a-trihydroxy-4a,5a,6,12a-tetrahydrotetracene-1,3,12(2H,4H,5H)-trione hydrochloride

NSC 141993; Minocycline HCl; NSC 141993; Mynocine hydrochloride; NSC141993; NSC-141993; Periocline; Klinomycin; Minocin; Solodyn; Mynocine; Tri-mino; Vectrin; Ximino; Minomax; Minomycin chloride; Mynocine hydrochloride

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~19.23 mg/mL (~38.93 mM)
H2O : ~9.09 mg/mL (~18.40 mM)

Solubility in Formulation 1: 7.69 mg/mL (15.57 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)