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Herbimycin A is a **benzoquinone ansamycin antibiotic** originally isolated from *Streptomyces hygroscopicus*. It acts as a **small molecule inhibitor** of **heat shock protein 90 (Hsp90)**, interfering with the protein’s role as a molecular chaperone. By binding to Hsp90 and its ER homolog GP96, herbimycin A impairs the conformational maturation and stabilization of client proteins—including mutated tyrosine kinases such as **v-Src**, **Bcr-Abl**, **ErbB2**, **Raf-1**—and promotes their degradation via the ubiquitin-proteasome pathway[1][4][5][7]. Herbimycin A is a **cell-permeable inhibitor of non-receptor tyrosine kinases**, reducing tyrosine phosphorylation and blocking oncogenic signal transduction. It has shown **anti-tumor and anti-angiogenic activity** in preclinical models, including chronic myeloid leukemia (CML), retinopathy of prematurity, and proliferative vitreoretinopathy[3][4][6][9][12][16]. It is not approved for human or diagnostic use and remains in preclinical development.
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