The substance penetrates into almost all tissues; very high concentrations are found in the gallbladder and liver. It crosses the blood–brain barrier better than doxycycline and other tetracyclines, reaching therapeutically relevant concentrations in the cerebrospinal fluid and also in inflamed meninges.Minocycline is inactivated by metabolization in the liver to about 50%. The rest is predominantly excreted into the gut (in part via the gallbladder, in part directly from blood vessels) and eliminated via the feces. About 10–15% are eliminated via the kidneys. The biological half-life is 14–22 (11–26) hours in healthy people, up to 30 hours in those with kidney failure, and significantly longer in those with liver disease. Chemistry
The drug is used in form of minocycline hydrochloride dihydrate, which is sparingly soluble in water and slightly soluble in ethanol. Minocycline reacts acidic in aqueous solution. History
Minocycline was patented in 1961 and came into commercial use in 1971. A topical foam for treatment of acne was approved in 2019. Society and culture
Trade names
Many forms of minocycline are no longer covered by patent, so it is marketed under a variety of trade names:

Minomycin
Minostad (in Europe, for the treatment of acne)
Akamin
Minocin
Minoderm
Cyclimycin
Arestin (1-mg doses administered locally into periodontal pockets, after scaling and root planing, for treatment of periodontal disease.)
Despite a moderately high pretreatment relapse rate in the patient group prior to treatment (1.3/year pre-enrollment; 1.2/year during a three-month baseline period), no relapses occurred between months 6 and 24 on minocycline. Also, despite significant MRI disease-activity pretreatment (19/40 scans had gadolinium-enhancing activity during a three-month run-in), the only patient with gadolinium-enhancing lesions on MRI at 12 and 24 months was on half-dose minocycline. Levels of interleukin-12 (IL-12), which at high levels might antagonize the proinflammatory IL-12 receptor, were elevated over 18 months of treatment, as were levels of soluble vascular cell adhesion molecule-1 (VCAM-1). The activity of matrix metalloproteinase-9 was decreased by treatment. Clinical and MRI outcomes in this study were supported by systemic immunological changes and call for further investigation of minocycline in MS.The overall antidepressant effect size of minocycline compared to placebo in a meta-analysis was -0.78, indicative of a potential antidepressant effect.In ongoing research and trial minocycline demonstrated efficacy and seems a promising neuroprotective agent in acute stroke patients, especially in AIS subgroup. Further RCTs are needed to evaluate the efficacy and safety of minocycline among ICH patients. Data from cellular and animal models
PARP1 inhibition Ki = 13.8 nM
Neuroprotection IC50 = 10 nM
Microglia full inhibition = 20 nM
Suppression of the mouses locomotor activity = 0.5 mg/kg

References
External links
"Minocycline". Drug Information Portal. U.S. National Library of Medicine.