Arabinosyltransferase (Mycobacterium tuberculosis)

**Ethambutol’s primary molecular targets are the arabinosyltransferases EmbA, EmbB, and EmbC in Mycobacterium tuberculosis, which are enzymes essential for the biosynthesis of arabinogalactan and lipoarabinomannan—major cell wall components of mycobacteria. Inhibiting these enzymes prevents the formation of a functional cell wall, increasing cell permeability and halting bacterial replication, conferring a bacteriostatic effect[3][4][5][6][7][8]. Ethambutol also acts synergistically with isoniazid by interacting with a TetR family transcriptional repressor (EtbR), which suppresses the inhA gene involved in mycolic acid synthesis, further compromising cell wall integrity and enhancing isoniazid’s bactericidal activity[1][2]. Ethambutol is a central therapeutic target and selective for mycobacterial infections, notably tuberculosis, but is associated with notable safety concerns such as optic neuritis, especially at higher doses and prolonged therapy[4][5]. **Note regarding "Ethambutol mechanism":** The requested target name, "Ethambutol mechanism," does **not** refer to a specific molecule or receptor but instead describes a drug action. The actual target is the *arabinosyltransferase* enzyme complex (EmbA/EmbB/EmbC) in *Mycobacterium tuberculosis*, and for molecular targeting, this should be used as the canonical form. "Ethambutol mechanism" is thus not a valid target name and is marked as incorrect.

Other names

EmbAEmbBEmbCembAembBembCarabinosyl transferaseEtbR regulatory protein (regulatory factor, not direct target)

Inhibition of arabinosyltransferase activity, blocking arabinogalactan and lipoarabinomannan cell wall biosynthesis, leading to bacteriostatic effect and increased cell wall permeability[1][3][5][6][7][8]. Ethambutol indirectly enhances the activity of isoniazid by binding to EtbR, a transcriptional repressor, which suppresses inhA gene expression, thereby increasing susceptibility to isoniazid[1][2].