Minocycline

Minocycline
Clinical data
Trade names Minocin, Minomycin, Akamin
AHFS/Drugs.com Monograph
MedlinePlus a682101
License data
Pregnancy
category
  • US: D (Evidence of risk)
    Routes of
    administration    		 Oral, intravenous, topical
    ATC code
    Legal status
    Legal status
    Pharmacokinetic data
    Bioavailability 100%
    Metabolism Liver
    Elimination half-life 11–22 hours
    Excretion mostly fecal, rest renal
    Identifiers
    CAS Number
    PubChem CID
    DrugBank
    ChemSpider
    UNII
    KEGG
    ChEBI
    ChEMBL
    ECHA InfoCard 100.226.626 Edit this at Wikidata
    Chemical and physical data
    Formula C23H27N3O7
    Molar mass 457.483
    3D model (JSmol)
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    Minocycline is a broad-spectrum tetracycline antibiotic, and has a broader spectrum than the other members of the group. It is a bacteriostatic antibiotic, classified as a long-acting type. As a result of its long half-life, it generally has serum levels two to four times that of the simple water-soluble tetracyclines.

    Minocycline is the most lipid-soluble of the tetracycline-class antibiotics, giving it the greatest penetration into the prostate and brain, but also the greatest amount of central nervous system-related side effects, such as vertigo. A common side effect is diarrhea. Uncommon side effects (with prolonged therapy) include skin discolouration and autoimmune disorders that are not seen with other drugs in the class.

    Minocycline is a relatively poor tetracycline-class antibiotic choice for urinary pathogens sensitive to this antibiotic class, as its solubility in water and levels in the urine are less than all other tetracyclines. Minocycline is metabolized by the liver and has poor urinary excretion.

    Minocycline was patented in 1961 and came into commercial use in 1971.[2] It is not a naturally occurring antibiotic, but was synthesized semi-synthetically from natural tetracycline antibiotics by Lederle Laboratories in 1966, and marketed by them under the brand name Minocin.[3]

    Medical uses

    Minocycline 100-mg capsules manufactured by Ranbaxy Pharmaceuticals

    Minocycline and doxycycline are frequently used for the treatment of acne vulgaris.[4][5] Both of these closely related antibiotics have similar levels of efficacy, although doxycycline has a slightly lower risk of adverse side effects.[6] Historically, minocycline has been a very effective treatment for acne vulgaris.[7] However, acne that is caused by antibiotic-resistant bacteria is a growing problem in many countries.[8] In Europe and North America, a significant number of acne patients no longer respond well to treatment with tetracycline family antibiotics (e.g., tetracycline, doxycycline, and minocycline) because their acne symptoms are caused by bacteria (primarily Propionibacterium acnes) that are resistant to these antibiotics.[9]

    Minocycline is also used for other skin infections such as methicillin-resistant Staphylococcus aureus[10] as well as Lyme disease,[11] as the one pill twice daily 100-mg dosage is far easier for patients than the four times a day required with tetracycline or oxytetracycline. Its activity against Lyme disease is enhanced by its superior ability to cross the blood-brain barrier.

    Although minocycline's broader spectrum of activity, compared with other members of the group, includes activity against Neisseria meningitidis,[12] its use for prophylaxis is no longer recommended because of side effects (dizziness and vertigo).

    It may be used to treat certain strains of methicillin-resistant S. aureus infection and a disease caused by drug-resistant Acinetobacter spp.[13]

    Both minocycline and doxycycline have shown effectiveness in asthma due to immune-suppressing effects.[14] Minocycline and doxycycline have modest effectiveness in treating rheumatoid arthritis.[15] However, the 2015 American College of Rheumatology guideline for the treatment of rheumatoid arthritis does not include minocycline.[16]

    A list of indications for which minocycline has been used include:

    Cautions

    Increase in sebaceous can excretion continue after the end of treatment. Increases in the number of excreting pilosebaceous follicles also may occur.[19]

    Contrary to most other tetracycline antibiotics (doxycycline excluded), minocycline may be used in those with kidney disease, but may aggravate systemic lupus erythematosus.[20] It may also trigger or unmask autoimmune hepatitis.[21]

    Also, more so than other tetracyclines, minocycline can cause the rare condition of secondary intracranial hypertension, which has initial symptoms of headache, visual disturbances, dizziness, vomiting, and confusion. Brain swelling and rheumatoid arthritis are rare side effects of minocycline in some people.[22]

    Minocycline, like most tetracyclines, becomes dangerous past its expiration date.[23] While most prescription drugs lose potency after their expiration dates, tetracyclines are known to become toxic over time. Expired tetracyclines can cause serious damage to the kidney due to the formation of a degradation product, anhydro-4-epitetracycline.[23] Minocycline's absorption is impaired if taken at the same time of day as calcium or iron supplements. Unlike some of the other tetracycline group antibiotics, it can be taken with calcium-rich foods such as milk, although this does reduce the absorption slightly.[24]

    Minocycline, like other tetracyclines, is associated with esophageal irritation and ulceration if insufficient fluids are taken with the drug before sleep.[25]

    A 2007 study suggested that minocycline harms amyotrophic lateral sclerosis patients. Patients on minocycline declined more rapidly than those on placebo. The mechanism of this side effect is unknown, although a hypothesis is that the drug exacerbated an autoimmune component of the primary disease. The effect does not seem to be dose-dependent because the patients on high doses did not do worse than those on the low doses.[26]

    Side effects

    Minocycline may cause upset stomach, diarrhea, dizziness, unsteadiness, drowsiness, mouth sores, headache, and vomiting. It increases sensitivity to sunlight, and may affect the quality of sleep and rarely causes sleep disorders.[27] It has also been linked to cases of lupus.[28] Prolonged use of minocycline can lead to blue-gray staining of skin, fingernails, and scar tissue. This staining is not permanent, but can take a very long time for the skin color to return to normal; however, a muddy brown skin color in sun-exposed areas is usually permanent.[29] Permanent blue discoloration of gums or teeth discoloration may also occur. Rare but serious side effects include fever, yellowing of the eyes or skin, stomach pain, sore throat, vision changes, and mental changes, including depersonalization.[30][31]

    Occasionally, minocycline therapy may result in autoimmune disorders such as drug-related lupus and autoimmune hepatitis, which usually occurs in men who also developed minocycline-induced lupus; however, women are more likely to develop minocycline-induced lupus. Significant or complete recovery occurs in most people who develop minocycline-induced autoimmune problems within a period of a few weeks to a year of cessation of minocycline therapy. Autoimmune problems emerge during chronic therapy, but can sometimes occur after only short courses of a couple of weeks of therapy.[32][33] Drug reaction with eosinophilia and systemic symptoms syndrome can occur during the first few weeks of therapy with minocycline.[33]

    Minocycline, but not other tetracyclines, can cause vestibular disturbances with dizziness, ataxia, vertigo, and tinnitus. These effects are thought to be related to minocycline's greater penetration into the central nervous system. Vestibular side effects are much more common in women than in men, occurring in 50 to 70% of women receiving minocycline. As a result of the frequency of this bothersome side effect, minocycline is rarely used in female patients.[34]

    Symptoms of an allergic reaction include rash, itching, swelling, severe dizziness, and trouble breathing.[30] Minocycline has also been reported to very rarely cause idiopathic intracranial hypertension (pseudotumor cerebri),[35] a side effect also more common in female patients, potentially leading to permanent vision damage.

    Thyroid cancer has been reported in the postmarketing setting in association with minocycline products. When minocycline therapy is given over prolonged periods, monitoring for signs of thyroid cancer should be considered.

    In 2009, the FDA added minocycline to its Adverse Event Reporting System; a list of medications under investigation by the FDA for potential safety issues. It cites a potential link between the use of minocycline products and autoimmune disease in pediatric patients.[36]


    Neuropsychiatric effect

    Antidepressant effect

    The overall antidepressant effect size of minocycline compared to placebo was -0.78 (95% CI: -0.4 to -1.33, P=0.005), indicative of a large and statistically significant antidepressant effect.[37]

    Antipsychotic effect

    Improving negative symptoms of schizophrenia by using minocycline in combination with antipsychotic drugs has been shown in a meta-review based on four meta-analysis systematic reviews.[38]

    Pharmacology

    Anti-inflammatory and neuroprotective

    NMDA receptor antagonists induce cortical apoptosis in perinatal rodents and sustain schizophrenia-like alterations that are ameliorated by treatment with antipsychotics. Minocycline with antipsychotic and neuroprotective effects exacerbated dizocilpine (MK-801)-induced brain-cell apoptosis without protection.[42]

    In various models of neurodegenerative disease, minocycline has demonstrated both neurorestorative and neuroprotective properties. Neurodegenerative diseases such as Huntington's disease and Parkinson's disease have shown a particularly beneficial response to minocycline in research studies, and an antipsychotic benefit has been found in people with schizophrenia, and minocycline is proposed as a possible add-on therapy for some schizophrenics.[43][44][45] Current research is examining the possible neuroprotective and anti-inflammatory effects of minocycline against the progression of a group of neurodegenerative disorders including multiple sclerosis, rheumatoid arthritis, Huntington's disease, and Parkinson's disease.[46][47][48][49] As mentioned above, minocycline harms ALS patients.

    Minocycline is also known to indirectly inhibit inducible nitric oxide synthase.[50][51][52]

    Minocycline may exhibit neuroprotective action against AIDS dementia complex by inhibiting macrophage inflammation and HIV replication in the brain and cerebrospinal fluid.[53] Minocycline may suppress viral replication by reducing T cell activation.[54][55] The neuroprotective action of minocycline may include its inhibitory effect on 5-lipoxygenase,[56] an inflammatory enzyme associated with brain aging, and the antibiotic is being studied for use in Alzheimer's disease patients.[57] Minocycline may also exert neuroprotective effects independent of its anti-inflammatory properties.[58] Minocycline also has been used as a "last-ditch" treatment for toxoplasmosis in AIDS patients.[59] Minocycline is somewhat neuroprotective in mouse models of Huntington's disease.[60]

    As an anti-inflammatory, minocycline inhibits apoptosis (cell death) via attenuation of TNF-alpha, downregulating proinflammatory cytokine output. This effect is mediated by a direct action of minocycline on the activated T cells and on microglia, which results in the decreased ability of T cells to contact microglia, which impairs cytokine production in T cell-microglia signal transduction .[61] Minocycline also inhibits microglial activation, through blockade of NF-kappa B nuclear translocation[62].

    A 2007 study reported the impact of the antibiotic minocycline on clinical and magnetic resonance imaging (MRI) outcomes and serum immune molecules in 40 MS patients over 24 months of open-label minocycline treatment. 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.[63][64][58][65]

    Patients taking 200 mg of minocycline for five days within 24 hours of an ischemic stroke showed an improvement in functional state and stroke severity over a period of 3 months compared with patients receiving placebo.[66]

    A double-blind, placebo-controlled study of minocycline for depression[67] in 2017, adds to the growing body of literature addressing whether depression can be treated with drugs which reduce inflammation and foster nerve growth. The result was significant, suggesting that, in select patients who have failed to respond fully to more commonly used antidepressant drugs, minocycline may be appropriate as an adjunctive therapy for depression,[68] especially considering its relatively good safety profile.

    Minocycline was shown to be highly effective in conferring neuroprotection during murine cerebral malaria.[69]

    Trade names and availability

    Minocycline is no longer covered by patent,so 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.)[70]
    • Aknemin
    • Solodyn (extended-release, for the treatment of acne)
    • Dynacin
    • Sebomin
    • Mino-Tabs
    • Acnamino
    • Minopen (in Japan)
    • Maracyn 2 (for treatment of bacterial infections in aquarium fish and amphibians)
    • Quatrocin (in Syria)
    • Minox (in Ireland)
    • Minoz (in India and Romania)
    • Divaine (in India)

    Dentomycin (2% minocylcine gel for use in periodontal pockets) StoneBridge Pharma also markets Minocycline as Cleeravue-M in combination with SteriLid eyelid cleanser in the treatment of rosacea blepharitis.

    Research

    Early research has found a tentative benefit from minocycline in schizophrenia,[71] with several trials underway.[72] A 2014 meta-analysis found minocycline may reduce negative and total symptom scores and was well tolerated.[73]

    Minocycline has been shown to reduce the risk of the honey trap effect in healthy human subjects. A 2013 study reported that male subjects in a control group rated attractive young females as more trustworthy compared to the subjects who had been treated with minocycline.[74]

    References

    1. ↑ DrugBank: DB01017 (Minocycline)
    2. ↑ Fischer, Janos; Ganellin, C. Robin (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 489. ISBN 9783527607495.
    3. ↑ Redin, G. S. (1966). Antibacterial activity in mice of minocycline, a new tetracycline. Antimicrobial Agents and Chemotherapy, 6, 371.
    4. ↑ Strauss; et al. (2007). "Guidelines of care for acne vulgaris management". Journal of the American Academy of Dermatology. 56 (4): 651–63. doi:10.1016/j.jaad.2006.08.048. PMID 17276540.
    5. ↑ "Minocycline, Doxycycline and Acne Vulgaris". ScienceOfAcne.com. 07/11/2011. Retrieved 2012-08-07. Check date values in: |date= (help)
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    7. ↑ Hubbell; et al. (1982). "Efficacy of minocycline compared with tetracycline in treatment of acne vulgaris". Archives of Dermatology. 118 (12): 989–92. doi:10.1001/archderm.1982.01650240033017. PMID 6216858.
    8. ↑ Eady; et al. (2003). "Propionibacterium acnes resistance: a worldwide problem". Dermatology. 206 (1): 54–6. doi:10.1159/000067822. PMID 12566805.
    9. ↑ Ross; et al. (2003). "Antibiotic-resistant acne: lessons from Europe". British Journal of Dermatology. 148 (3): 467–78. doi:10.1046/j.1365-2133.2003.05067.x. PMID 12653738.
    10. ↑ Rogers RL, Perkins J (September 2006). "Skin and soft tissue infections". Prim. Care. 33 (3): 697–710. doi:10.1016/j.pop.2006.06.005. PMID 17088156.
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    12. ↑ Fraser A, Gafter-Gvili A, Paul M, Leibovici L (March 2005). "Prophylactic use of antibiotics for prevention of meningococcal infections: systematic review and meta-analysis of randomised trials". Eur. J. Clin. Microbiol. Infect. Dis. 24 (3): 172–81. doi:10.1007/s10096-005-1297-7. PMID 15782277.
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    16. ↑ "Clinical Practice Guidelines: Rheumatoid Arthritis". American College of Rheumatology. Retrieved 13 May 2017.
    17. ↑ Copeland KF, Brooks JI (15 April 2010). "A Novel Use for an Old Drug: The Potential for Minocycline as Anti-HIV Adjuvant Therapy" (PDF). J Infect Dis. 201 (8): 1115–7. doi:10.1086/651278. PMID 20205572.
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    23. 1 2 "Principles and methods for the assessment of nephrotoxicity associated with exposure to chemicals". Environmental health criteria: 119. World Health Organization (WHO). ISBN 92-4-157119-5. ISSN 0250-863X. 1991
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    30. 1 2 MedicineNet: Minocycline Oral (Dynacin, Minocin) - side effects, medical uses, and drug interactions
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    36. ↑ ov/Drugs/GuidanceComplianceRegulatoryInformation/Surveillance/AdverseDrugEffects/ucm185260.htm FDA Adverse Events Reporting System Retrieved on January 16, 2011
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    41. ↑ minomycin-if
    42. ↑ Inta I, Vogt MA, Vogel AS, Bettendorf M, Gass P, Inta D (October 2016). "Minocycline exacerbates apoptotic neurodegeneration induced by the NMDA receptor antagonist MK-801 in the early postnatal mouse brain". European Archives of Psychiatry and Clinical Neuroscience. 266 (7): 673–7. doi:10.1007/s00406-015-0649-2. PMID 26482736. Retrieved 2017-12-21.
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    45. ↑ Chaudhry, I. B.; Hallak, J.; Husain, N.; Minhas, F.; Stirling, J.; Richardson, P.; Dursun, S.; Dunn, G.; Deakin, B. Similar preliminary findings have also been shown in depression (Dean et al. 2017). (2012). "Minocycline benefits negative symptoms in early schizophrenia: A randomised double-blind placebo-controlled clinical trial in patients on standard treatment". Journal of Psychopharmacology. 26 (9): 1185–1193. doi:10.1177/0269881112444941. PMID 22526685.
    46. ↑ "Preliminary Study Shows Creatine and Minocycline May Warrant Further Study In Parkinson's Disease" (Press release). National Institute of Health. February 23, 2006.
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    48. ↑ Tikka TM, Koistinaho JE (15 June 2001). "Minocycline provides neuroprotection against N-methyl-D-aspartate neurotoxicity by inhibiting microglia" (PDF). Journal of Immunology. 166 (12): 7527–33. doi:10.4049/jimmunol.166.12.7527. PMID 11390507.
    49. ↑ Nirmalananthan N, Greensmith L (2005). "Amyotrophic lateral sclerosis: recent advances and future therapies". Current Opinion in Neurology. 18 (6): 712–9. doi:10.1097/01.wco.0000187248.21103.c5. PMID 16280684.
    50. ↑ Amin, AR; Attur, MG; Thakker, GD; Patel, PD; Vyas, PR; Patel, RN; Patel, IR; Abramson, SB (November 1996). "A novel mechanism of action of tetracyclines: Effects on nitric oxide synthases". Proceedings of the National Academy of Sciences of the United States of America. 93 (24): 14014–14019. doi:10.1073/pnas.93.24.14014. PMC 19486. PMID 8943052.
    51. ↑ Chen, M; Ona, VO; Li, M; Ferrante, RJ; Fink, KB; Zhu, S; Bian, J; Guo, L; Farrell, LA; Hersch, SM; Hobbs, W; Vonsattel, JP; Cha, JH; Friedlander, RM (July 2000). "Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington disease". Nature Medicine. 6 (7): 797–801. doi:10.1038/77528. PMID 10888929.
    52. ↑ Sadowski, T; Steinmeyer, J (February 2001). "Minocycline inhibits the production of inducible nitric oxide synthase in articular chondrocytes". Journal of Rheumatology. 28 (2): 336–340. PMID 11246672.
    53. ↑ Zink MC, Uhrlaub J, DeWitt J, Voelker T, Bullock B, Mankowski J, Tarwater P, Clements J, Barber S (April 2005). "Neuroprotective and anti-human immunodeficiency virus activity of minocycline". JAMA. 293 (16): 2003–11. doi:10.1001/jama.293.16.2003. PMID 15855434.
    54. ↑ Szeto, G.; Brice, A.; Yang, H.; Barber, S.; Siliciano, R.; Clements, J. (2010). "Minocycline attenuates HIV infection and reactivation by suppressing cellular activation in human CD4+ T cells". The Journal of Infectious Diseases. 201 (8): 1132–1140. doi:10.1086/651277. PMC 3739045. PMID 20205570.
    55. ↑ Szeto, G; Brice, A; Yang, H; Barber, S; Siliciano, R; Clements, J (April 2010). "Minocycline attenuates HIV infection and reactivation by suppressing cellular activation in human CD4+ T cells". The Journal of Infectious Diseases. 201 (8): 1132–40. doi:10.1086/651277. PMC 3739045. PMID 20205570.
    56. ↑ Song Y, Wei EQ, Zhang WP, Zhang L, Liu JR, Chen Z (2004). "Minocycline protects PC12 cells from ischemic-like injury and inhibits 5-lipoxygenase activation". NeuroReport. 15 (14): 2181–4. doi:10.1097/00001756-200410050-00007. PMID 15371729.
    57. ↑ Uz T, Pesold C, Longone P, Manev H (1 April 1998). "Aging-associated up-regulation of neuronal 5-lipoxygenase expression: putative role in neuronal vulnerability" (PDF). FASEB J. 12 (6): 439–49. PMID 9535216.
    58. 1 2 Maier K, Merkler D, Gerber J, Taheri N, Kuhnert AV, Williams SK, Neusch C, Bähr M, Diem R (2007). "Multiple neuroprotective mechanisms of minocycline in autoimmune CNS inflammation". Neurobiol. Dis. 25 (3): 514–25. doi:10.1016/j.nbd.2006.10.022. PMID 17239606.
    59. ↑ Lacassin, F; Schaffo, D; Perronne, C; Longuet, P; Leport, C; Vilde, JL (January 1995). "Clarithromycin-Minocycline Combination as Salvage Therapy for Toxoplasmosis in Patients Infected with Human Immunodeficiency Virus" (PDF). Antimicrobial Agents and Chemotherapy. 39 (1): 276–277. doi:10.1128/AAC.39.1.276. PMC 162527. PMID 7695324.
    60. ↑ Beal F, Ferrante J (2004). "Experimental Therapeutics in Transgenic Mouse Models of Huntington's Disease". Nature Reviews Neuroscience. 5: 373–84. doi:10.1038/nrnl1386.
    61. ↑ Giuliani F, Hader W, Yong VW (2005). "Minocycline attenuates T cell and microglia activity to impair cytokine production in T cell-microglia interaction". J. Leukoc. Biol. 78 (1): 135–43. doi:10.1189/jlb.0804477. PMID 15817702.
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