Doxycycline Capsules

Overview of Doxycycline Capsules

Dosage Strength

Doxycycline Monohydrate 100 mg Capsule

General Information

The tetracycline class of antibiotics, including doxycycline, are semi-synthetic and generated from oxytetracycline. It is a bacteriostatic agent, but at high concentrations, it also has bactericidal properties. Similar to other tetracycline group members, doxycycline has broad-spectrum activity against a variety of gram-positive, gram-negative, and atypical species. Additionally, the medication works to combat several protozoan diseases. Doxycycline is a medication that doctors frequently use to control and treat a variety of mild-to-moderate infectious illnesses. 78 multidrug-resistant strains of Acinetobacter baumannii9 and Stenotrophomonas maltophilia10, 123 penicillin-resistant strains of Staphylococcus aureus, 56 -lactamase-producing strains of Moraxella catarrhalis, and strains of organisms resistant to additional tetracyclines.

Doxycycline has a low binding affinity for calcium (Ca2+) ions and excellent oral bioavailability. But it has a longer serum half-life and is more lipid-soluble than other tetracyclines. 1112 Additionally, doxycycline has a high level of stability in healthy human serum, and therapeutic drug monitoring is incredibly uncommon. There are numerous dose forms for the medication, including tablets, capsules, syrup, oral suspension, and reconstituted powder for IV. Doxycycline and minocycline can be taken without regard to meals. Doxycycline was initially approved by the US-FDA in 1967 and is currently categorized as a medication with a broad therapeutic index. 13 The World Health Organization lists it as one of the essential medicines because it is the first line of defense against Chlamydia trachomatis-related STIs. 14 Doxycycline mostly enters cells via the transcellular transport pathway and passes through the susceptible bacteria’s outer cell membrane via hydrophilic pores. 16 It is believed to reach the inner cytoplasmic membrane by an active transport pathway that is pH-dependent before becoming chelated in the cytoplasm. 1217 When the charged aminoacyl transfer RNA (aa-tRNA) is prevented from binding to the ribosomal A site, RNA-dependent protein synthesis is stopped. As a result, the aa-tRNA is unable to interact with the messenger RNA-ribosome complex, which stops bacterial translation and interferes with the creation of crucial proteins. 1518 The germs eventually perish in this stagnant state.

Late in the cell cycle, apicoplast gene expression in Plasmodium falciparum has been found to be inhibited by doxycycline. When apicoplasts are blocked, fatty acid production is hampered, which prevents the development of parasites. 19 Due to its increased lipophilicity compared to other tetracyclines and reduced resistance rate of P. acnes strains against cyclines, doxycycline, along with minocycline and other 2nd generation tetracyclines, is a recommended antibiotic in the treatment of acne vulgaris. The precise mechanism(s) via which doxycycline combats acne is/are not completely understood. It is believed to inhibit P. acnes-derived lipase and downregulate inflammatory mediators, which ultimately leads to a reduction in the number of lipase-producing bacteria by lowering the levels of follicular-free fatty acids. 20212223

Additionally, it has been discovered that doxycycline has the capacity to inhibit collagenase in people with periodontitis. The peptide bonds in collagen are broken down by collagenase, which finally causes the gum and the tooth to separate. Subantimicrobial dosages (SD) of doxycycline have been demonstrated to have anti-collagenolytic, matrix metalloproteases (MMPs) degrading, and cytokine down-regulating effects in the treatment of periodontitis. 23242526 SD However, the concentration of doxycycline is insufficient to demonstrate a direct antimicrobial action; as a result, it shouldn’t be administered as an antibacterial drug in individuals with periodontitis. Doxycycline also promotes wound healing, inhibits angiogenesis and apoptosis, and promotes attachment of gingival fibroblasts. 12

Tetracycline resistance in bacteria is generally brought on by ribosomal protection proteins like Tet(O), Tet(K), and Tet(M). To stop the function of tetracyclines, these proteins use a variety of resistance mechanisms, including as efflux, rRNA alterations, permeability decrease, and enzymatic destruction. 2728 They increase the disassociation constant and prevent tetracyclines from interacting with the target ribosomal subunit (Kd). By enabling tRNA to connect to the ribosome, these processes finally allow protein synthesis to resume. 15 Therefore, it is advised to conduct susceptibility testing and culture before using tetracyclines.


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Mechanism of Action
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