70563-58-5
Chemical Structure
Herbimycin A
- CAS No.: 70563-58-5
- Formula:C30H42N2O9
- Molecular Weight:574.66
IUPAC Name: (4E,6Z,8S,9S,10E,12S,13R,14S,16S,17R)-8,13,14,17-tetramethoxy-4,10,12,16-tetramethyl-3,20,22-trioxo-2-azabicyclo[16.3.1]docosa-1(21),4,6,10,18-pentaen-9-yl carbamate
InChIKey: MCAHMSDENAOJFZ-BVXDHVRPSA-N
SMILES: CO[C@H]([C@H](C[C@@H]([C@@H]([C@H](/C=C([C@@H]1OC(N)=O)\C)C)OC)OC)C)C(C(C(NC(/C(C)=C/C=C\[C@@H]1OC)=O)=C2)=O)=CC2=O
Biological Activity:
Herbimycin A is an antibiotic and protein tyrosine kinase inhibitor. Herbimycin A directly inhibits the autophosphorylation of p210 BCR-ABL with an IC50 of approximately 5 μM, and reduces Src kinase activity. Herbimycin A also induces the degradation of receptor tyrosine kinases such as insulin-like growth factor 1 receptor (IGF-1R), insulin receptor (IR) and epidermal growth factor receptor (EGFR) via the ubiquitin-20S proteasome pathway. Herbimycin A directly modifies NF-κB p50, with the main target site involving Cys62, thereby blocking the DNA binding of p50 and NF-κB-driven gene expression. Herbimycin A can be used in studies related to tyrosine kinase signaling, chronic myeloid leukemia, NF-κB signaling, osteoclast function, apoptosis and cellular stress[1][2][3][4][5][6][7][8][9][10].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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Herbimycin A | 99% | Herbimycin A is an antibiotic and protein tyrosine kinase inhibitor. Herbimycin A directly inhibits the autophosphorylation of p210 BCR-ABL with an IC50 of approximately 5 μM, and reduces Src kinase activity. Herbimycin A also induces the degradation of receptor tyrosine kinases such as insulin-like growth factor 1 receptor (IGF-1R), insulin receptor (IR) and epidermal growth factor receptor (EGFR) via the ubiquitin-20S proteasome pathway. Herbimycin A directly modifies NF-κB p50, with the main target site involving Cys62, thereby blocking the DNA binding of p50 and NF-κB-driven gene expression. Herbimycin A can be used in studies related to tyrosine kinase signaling, chronic myeloid leukemia, NF-κB signaling, osteoclast function, apoptosis and cellular stress. |
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References
- [1]. Sepp-Lorenzino L, et al. Herbimycin A induces the 20 S proteasome- and ubiquitin-dependent degradation of receptor tyrosine kinases. The Journal of biological chemistry. 1995 Jul 14;270(28):16580-7.
- [2]. Honma Y, et al. Induction of Erythroid Differentiation of K562 Human Leukemic Cells by Herbimycin A, an Inhibitor of Tyrosine Kinase Activity. Cancer Res. 1989;49:331-334.
- [3]. Mahon TM, et al. Studies into the Effect of the Tyrosine Kinase Inhibitor Herbimycin A on NF-κB Activation in T Lymphocytes: Evidence for Covalent Modification of the p50 Subunit. J Biol Chem. 1995;270(48):28557-28564.
- [4]. Yoneda T, et al. Herbimycin A, a pp60c-src tyrosine kinase inhibitor, inhibits osteoclastic bone resorption in vitro and hypercalcemia in vivo. The Journal of clinical investigation. 1993 Jun;91(6):2791-5.
- [5]. Uehara Y, et al. Inhibition of transforming activity of tyrosine kinase oncogenes by herbimycin A. Virology. 1988 May;164(1):294-8. [Content Brief]
- [6]. Fukazawa H, et al. Specific inhibition of cytoplasmic protein tyrosine kinases by herbimycin A in vitro. Biochemical pharmacology. 1991 Oct 09;42(9):1661-71.
- [7]. Hegde RS, et al. Short circuiting stress protein expression via a tyrosine kinase inhibitor, herbimycin A. Journal of cellular physiology. 1995 Oct;165(1):186-200.
- [8]. Murakami Y, et al. Induction of hsp 72/73 by herbimycin A, an inhibitor of transformation by tyrosine kinase oncogenes. Experimental cell research. 1991 Aug;195(2):338-44.
- [9]. Davis MA, et al. Herbimycin A and Geldanamycin Inhibit Okadaic Acid-Induced Apoptosis and p38 Activation in NRK-52E Renal Epithelial Cells. Toxicol Appl Pharmacol. 1999;161:59-74.
- [10]. Sachidhanandam SB, et al. Herbimycin A attenuates apoptosis during heat stress in rats. European journal of pharmacology. 2003 Aug 01;474(1):121-8.
