Antiblastin
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| Category | Antibiotics |
| Catalog number | BBF-00051 |
| CAS | 544-51-4 |
| Molecular Weight | 198.22 |
| Molecular Formula | C13H10O2 |
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Description
Antiblastin is an antifungal antibiotic produced by Monilia antipiriculariae. Catalytic hydrogenation to generate tridecane.
Specification
| Synonyms | Mycomycin; UNII-398491Y0IE |
| Canonical SMILES | C#CC#CC=C=CC=CC=CCC(=O)O |
| InChI | InChI=1S/C13H10O2/c1-2-3-4-5-6-7-8-9-10-11-12-13(14)15/h1,5,7-11H,12H2,(H,14,15)/b9-8-,11-10+ |
| InChI Key | APNPVBXEWGCCLU-QNRZBPGKSA-N |
Properties
| Appearance | White columnar Crystal |
| Antibiotic Activity Spectrum | fungi |
| Boiling Point | 402.9°C at 760 mmHg |
| Density | 1.075 g/cm3 |
Reference Reading
1. Metabolomic Profiles on Antiblastic Cardiotoxicity: New Perspectives for Early Diagnosis and Cardioprotection
Luca Fazzini, Ludovica Caggiari, Martino Deidda, Carlotta Onnis, Luca Saba, Giuseppe Mercuro, Christian Cadeddu Dessalvi J Clin Med. 2022 Nov 15;11(22):6745. doi: 10.3390/jcm11226745.
Antiblastic drugs-induced cardiomyopathy remains a relevant cause of morbidity and mortality, during and after chemotherapy, despite the progression in protective therapy against cardiovascular diseases and myocardial function. In the last few decades, many groups of researchers have focused their attention on studying the metabolic profile, first in animals, and, subsequently, in humans, looking for profiles which could be able to predict drug-induced cardiotoxicity and cardiovascular damage. In clinical practice, patients identified as being at risk of developing cardiotoxicity undergo a close follow-up and more tailored therapies. Injury to the heart can be a consequence of both new targeted therapies, such as tyrosine kinase inhibitors, and conventional chemotherapeutic agents, such as anthracyclines. This review aims to describe all of the studies carried on this topic of growing interest.
2. Novel insights in pathophysiology of antiblastic drugs-induced cardiotoxicity and cardioprotection
Martino Deidda, Rosalinda Madonna, Ruggiero Mango, Pasquale Pagliaro, Pier P Bassareo, Lucia Cugusi, Silvio Romano, Maria Penco, Francesco Romeo, Giuseppe Mercuro J Cardiovasc Med (Hagerstown). 2016 May;17 Suppl 1:S76-83. doi: 10.2459/JCM.0000000000000373.
Despite advances in supportive and protective therapy for myocardial function, heart failure caused by various clinical conditions, including cardiomyopathy due to antineoplastic therapy, remains a major cause of morbidity and mortality. Because of the limitations associated with current therapies, investigators have been searching for alternative treatments that can effectively repair the damaged heart and permanently restore its function. Damage to the heart can result from both traditional chemotherapeutic agents, such as anthracyclines, and new targeted therapies, such as trastuzumab. Because of this unresolved issue, investigators are searching for alternative therapeutic strategies. In this article, we present state-of-the-art technology with regard to the genomic and epigenetic mechanisms underlying cardiotoxicity and cardioprotection, the role of anticancer in influencing the redox (reduction/oxidation) balance and the function of stem cells in the repair/regeneration of the adult heart. These findings, although not immediately transferable to clinical applications, form the basis for the development of personalized medicine based on the prevention of cardiotoxicity with the use of genetic testing. Proteomics, metabolomics and investigations on reactive oxygen species-dependent pathways, particularly those that interact with the production of NO and energy metabolism, appear to be promising for the identification of early markers of cardiotoxicity and for the development of cardioprotective agents. Finally, autologous cardiac stem and progenitor cells may represent future contributions in the field of myocardial protection and recovery in the context of antiblastic therapy.
3. Novel insights in pathophysiology of antiblastic drugs-induced cardiotoxicity and cardioprotection
Martino Deidda, Rosalinda Madonna, Ruggiero Mango, Pasquale Pagliaro, Pier P Bassareo, Lucia Cugusi, Silvio Romano, Maria Penco, Francesco Romeo, Giuseppe Mercuro J Cardiovasc Med (Hagerstown). 2016 May;17 Suppl 1 Special issue on Cardiotoxicity from Antiblastic Drugs and Cardioprotection:e76-e83. doi: 10.2459/JCM.0000000000000373.
Despite advances in supportive and protective therapy for myocardial function, heart failure caused by various clinical conditions, including cardiomyopathy due to antineoplastic therapy, remains a major cause of morbidity and mortality. Because of the limitations associated with current therapies, investigators have been searching for alternative treatments that can effectively repair the damaged heart and permanently restore its function. Damage to the heart can result from both traditional chemotherapeutic agents, such as anthracyclines, and new targeted therapies, such as trastuzumab. Because of this unresolved issue, investigators are searching for alternative therapeutic strategies. In this article, we present state-of-the-art technology with regard to the genomic and epigenetic mechanisms underlying cardiotoxicity and cardioprotection, the role of anticancer in influencing the redox (reduction/oxidation) balance and the function of stem cells in the repair/regeneration of the adult heart. These findings, although not immediately transferable to clinical applications, form the basis for the development of personalized medicine based on the prevention of cardiotoxicity with the use of genetic testing. Proteomics, metabolomics and investigations on reactive oxygen species-dependent pathways, particularly those that interact with the production of NO and energy metabolism, appear to be promising for the identification of early markers of cardiotoxicity and for the development of cardioprotective agents. Finally, autologous cardiac stem and progenitor cells may represent future contributions in the field of myocardial protection and recovery in the context of antiblastic therapy.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
