Minocycline is a semi-synthetic second-generation tetracycline antibiotic. Synthesized in 1967, it is a broad-spectrum antibiotic used in the management and treatment of many infectious and non-infectious diseases, with similar anti-infectious activity to that of other tetracyclines. Aside from anti-infectious activity against both gram-positive and gram-negative bacteria, it also has anti-inflammatory, anti-oxidant, anti-apoptotic, and immunomodulatory effects. It is known to be the most effective tetracycline derivative at providing neuroprotective effects, as it is a highly lipophilic molecule that can cross the blood-brain barrier.[1]

Susceptibility to tetracycline is typically predictive of susceptibility to minocycline.[2] Minocycline covers Borrelia recurrentis, Mycobacterium marinum, Mycoplasma pneumoniae, Staphylococcus aureus (including MRSA), Acinetobacter baumannii, Vibrio vulnificus, and susceptible strains of vancomycin-resistant enterococcus (VRE). Minocycline is also used to treat rickettsial infections, chlamydial infections, syphilis, pelvic inflammatory disease, acne, nocardiosis, brucellosis, ehrlichiosis, amebiasis, actinomycosis, anaplasmosis, leptospirosis, melioidosis, tularemia, traveler's diarrhea, Lyme disease (early stage), legionnaire's disease, and Whipple disease.[3] 

Nonantibiotic indications for minocycline include rosacea, bullous dermatoses, neutrophilic diseases, pyoderma gangrenosum, sarcoidosis, aortic aneurysms, cancer metastasis, periodontitis, as well as autoimmune disorders such as rheumatoid arthritis and scleroderma.[4][5]

In both eukaryotic and prokaryotic cells, protein synthesis occurs through the use of ribosomes, which translate messenger RNA (mRNA) codes into functioning proteins. Prokaryotic cells use the 30S, and 50S subunits of ribosomes and eukaryotic cells use the 40S and 60S subunits of ribosomes. In both prokaryotic and eukaryotic organisms, the two ribosomal subunits combine at the mRNA template to allow for transfer RNA (tRNA) to bring an amino acid and form cellular proteins via elongation of amino acid chains. 

Tetracyclines, and by extension minocycline, bind to the 30S ribosomal subunit, preventing the charged tRNA from bringing an amino acid to elongate the amino acid chain and form a cellular protein. Halting this process results in a bacteriostatic effect on the prokaryotic cell, wherein the organism can no longer grow or replicate.[6]

Tetracyclines are lipid-soluble compounds capable of transportation across hydrophobic barriers such as biological membranes. Due to their lipophilicity, they are rapidly absorbed and distributed throughout the organism.

Minocycline is more lipophilic than other tetracyclines, such as doxycycline; thus, it achieves higher concentrations in the central nervous system (CNS) and skin.[7] 

Minocycline is available for administration in both oral and parenteral forms. Oral forms are absorbed in the stomach and proximal small intestine. Absorption rates are dependent on the presence of food, particularly products containing divalent cations such as calcium, which chelates minocycline and other tetracyclines rendering them unabsorbable. It can also be administered intravenously (IV). The IV route has seen use in the treatment of pneumonia, bloodstream infections, as well as skin and skin structure infections.[8]

More common adverse effects of minocycline include gastrointestinal distress and photosensitivity. Hyperpigmentation of skin and discoloration of nails is also possible. Staining of teeth and bone growth inhibition is more likely to occur in children than adults, although it has been reported in adults as well. The prevalence of tooth discoloration due to minocycline is 3 to 6%.[9][10] 

Hepatotoxicity may occur due to minocycline use, and exacerbation of preexisting renal failure is also a risk to consider. Pill esophagitis - symptoms of which present as chest pain, odynophagia, and dysphagia - have also been reported and may be avoided by taking oral forms of minocycline with adequate water and standing upright after intake. 

Although side effects are rare, the higher concentrations of minocycline in the CNS as compared to other tetracyclines are thought to contribute to the dose-limiting vestibular side effects (such as nausea, vomiting, vertigo, dizziness or change in hearing).[11][12] Research has also found a correlation between tetracycline use and idiopathic intracranial hypertension (pseudotumor cerebri).

There is a reported association between systemic lupus erythematosus (SLE) with minocycline use (risk of 8.8 cases per 100,000 person-years).[13] Tetracycline use also has correlations with drug-induced pancreatitis.[14]

As with all antibiotics, minocycline increases the risk of developing Clostridium difficile infection; however, the risk is lower as compared to other antibiotics.[15]

All tetracyclines can cross the placental barrier and are contraindicated in pregnancy, and this is no less true for minocycline. Due to their potential for permanent discoloration of teeth and impairment of long bone growth in the fetus, pregnant women should avoid tetracyclines.[16] Hepatotoxicity in the pregnant mother is also a risk factor to consider and another reason not to use it.[17][18]

Generally, any patients under the age of 16 should avoid using minocycline as the risk of permanent teeth discoloration in unerupted teeth is present. Ideally, avoid minocycline until after all crowns are complete (13 to 19 years).[19]

Although most tetracycline group medication should be avoided in patients with chronic renal failure, minocycline elimination is independent of renal function.[20] High doses of minocycline have been shown to increase urea excretion in healthy subjects. In patients with kidney impairment, On the other hand, aggravation of uremia may occur due to minocycline's catabolic effects. Therefore it is important to monitor both the therapeutic doses of minocycline and renal function in patients with renal failure to avoid further aggravation of uremia.[21]