Anti-Mycobacteria

Brefeldin A is an antibiotic derived from Penicillium brefeldianum. It is an anti-cancer agent which disrupts protein transport and causes apoptosis of tumor cells. Brefeldin A disrupts the function of the Golgi apparatus and blocks Golgi-COPI activity. ER vesicles are prevented from fusion with the Golgi and are secretion is inhibited. Additionally, Brefeldin A is an ARF inhibitor, sphingomyelin cycle activator, and caspase-3 activator. It has been shown to induce apoptosis in leukemia cells and colon cancer cells.

Capreomycin sulfate is a cyclic peptide antibiotic often classified with the aminoglycoside antibiotics. It is used as a second line antibiotic for studying multidrug resistant tuberculosis. Capreomycin is primarily used against Mycobacterium tuberculosis.

Clofazimine is an active phenazine composed of an imino group and aromatic tricyclic heterocycles that is used as an antimycobacterial, anti-inflammatory and anti-cancer compound. It has been shown to be a potent in vivo antimycobacterial agent toward Mycobacterium leprae and in vitro to Mycobacterium avium.

As an anti-inflammatory, clofazimine inhibits reactive oxygen species (ROS) formation within neutrophils by inhibiting myeloperoxidase catalyzed reactions. The formed ROS are responsible for activating tumor necrosis factor alpha (TNFα) and interleukin 8 (IL8), which are inflammatory cytokines.

D-Cycloserine is an amino acid analog antibiotic effective against a wide variety of bacteria. It is commonly used against Mycobacterium tuberculosis. It is suitable for use as a selection agent in a variety of isolation methods. D-cycloserine inhibits a variety of enzymes, is a partial NMDA receptor agonist, and may improve memory and cognition.

Ethambutol is an antitubercular antibiotic effective against Mycobacterium species, especially Mycobacterium tuberculosis. It has been used to study multidrug-resistant tuberculosis and in combination with other drugs to decrease the risk of developing additional multidrug resistant species.

Ethambutol DiHCl is a hydrochloride salt form of an ethylenediamine derivative that is used as an anti-mycobiotic. It has been used for studying multidrug resistance in Mycobacterium tuberculosis and to investigate effective antibiotic combinations for ethambutol DiHCl.

Ethionamide is a thioamide antibiotic. Primarily targeting Mycobacterium tuberculosis and Mycobacterium leprae, ethionamide is useful against tuberculosis and leprosy. Although the mechanism is not well known, it is thought that ethionamide prevents synthesis of mycolic acids which are a required component of Mycobacterium cell walls. It is sparingly soluble.

Isoniazid is a prodrug derivative of nicotinic acid that is used as an antibiotic compound against Mycobactrium tuberculosis, M. bovis, and other mycobacteria. This prodrug is transformed by catalase-peroxidases, where its active form inhibits an enoyl-reductase (InhA). Inhibition of InhA compromises bacterial cell walls by preventing mycolic acid synthesis, disrupting fluid homeostasis and leading to cell death.

Pyrazinamide is an anti-tubercular antibiotic. It is also used to study ways to prevent liver toxicity and in the formation of polymeric copper complexes.

Although the mechanism of action of pyrazinamide is not well understood, it is thought that upon entering a target cell, it is converted to pyrazinoic acid or POA. This conversion results in altered cellular permeability and decreased internal pH due to POA accumulation in the cytoplasm. This may inhibit fatty acid synthesis.

Rifampicin is a broad-spectrum antibiotic known for its efficacy against tuberculosis and other infections caused by Mycobacterium species. This semisynthetic antibiotic has also been shown to work against methicillin-resistant Staphylococcus aureus (MRSA), to activate nuclear pregnane x receptor (PXR), and to promote CYP2C-mediated metabolism.

Rifampicin functions by binding the β-subunit of RNA polymerase, inhibiting RNA synthesis. Resistance to this antibiotic develops from mutations on the binding site on RNA polymerase leading to a lower affinity for rifampicin.