Background:

Herbimycin A is an antibiotic and a selective inhibitor of non-receptor tyrosine kinases [1].

Antibiotics are a type of antimicrobial used in the treatment of bacterial infection. Non-receptor tyrosine kinases (nRTKs) are cytoplasmic enzymes and catalyse the transfer of a phosphate group from a nucleoside triphosphate donor to tyrosine residues in proteins.

Herbimycin A is a selective non-receptor tyrosine kinases inhibitor. Herbimycin A bound to the reactive SH domains of p60v-src and p210BCR-ABL and inactivated their activity [1].

In a retinopathy prematurity rat model, Herbimycin A inhibited capillary tube formation and bovine retinal microvascular endothelial cell proliferation induced by vascular endothelial growth factor in a dose-dependent way. Also, Herbimycin A reduced pre-retinal neovascularization by 63% and 41% in oxygen-treated rats and herbimycin-injected eyes, respectively [2]. In rats exposed to heat stress, Herbimycin A exhibited thermotolerance and significantly reduced apoptosis of hepatocytes. Also, Herbimycin A inhibited caspase-3 activation [3].

参考文献:
[1].  Fukazawa H, Uehara Y, Murakami Y, et al. Labeling of v-Src and BCR-ABL tyrosine kinases with [14C]herbimycin A and its use in the elucidation of the kinase inactivation mechanism. FEBS Lett, 1994, 340(3): 155-158.
[2].  McCollum GW, Rajaratnam VS, Bullard LE, et al. Herbimycin A inhibits angiogenic activity in endothelial cells and reduces neovascularization in a rat model of retinopathy of prematurity. Exp Eye Res, 2004, 78(5): 987-995.
[3].  Sachidhanandam SB, Lu J, Low KS, et al. Herbimycin A attenuates apoptosis during heat stress in rats. Eur J Pharmacol, 2003, 474(1): 121-128.