Minocycline

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]}. 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]. 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 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].